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Aiheen aloittaja HopeSprings Pvm 04.03.2012 - 14:39:30

Aihe: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.03.2012 - 14:39:30

Aikaisemmin on keskusteltu keuhkoklamydiasta ja borrelioosista.  Saattaa tuntua toistolta puhua samoista asioista uudestaan, mutta halusin jakaa kokemukseni  kroonisista bakteeri-infektioista, joita voi sairastaa tietämättään,  koska testit ovat olleet negatiiviset.

MS diagnoosini yhteydessä minulle tehtiiin seuravat neuropakettitutkimuksen virus- ja lisäksi parit bakteeri-infektiotestit: herpes virus 6. herpes simplex, human T-cell leukemia virus, vesirokkovirus, HIV (?), adenovirus, Coxsackie B5, enterovirukset, influenssa A, influenssa B, parainfluenssa 1, respiratory syncytial-virus; ja bakteereista  mykoplasma ja  borreliosis.  Mykoplasma lausunnossa sanottiin seuraavasti: ”likvorissa ei normaalisti esiinny mykoplasma vasta-aineita”.  Kuulostaa melko turhalta edes tehdä tälläista testiä, mutta onneksi seerumista löytyi vasta-aineita, vaikka sitä ei minulle mainittu eikä sille tehty mitään. Kaikki muut testit olivat negatiivisia, joten luonnollisesti  IgG-indeksi päätti sairaudekseni MS-taudin, vaikka labran lausunnossa IgG-indeksistä sanotaan, että ”Selvä positiivinen tulos.. Sopii MS-tautiin tai keskushermoston infektioon.”
Mikä sitten voisi olla keskushermoston infektio? Huslabin ohjekirjan mukaan keksushermostoinfektioita voivat aiheuttaa mm. respiratoriset ja enterovirukset, Chlamydia pneumoniae, Dengue-virus, EBV, CMV, HIV, Inkoovirus, Japanin enkefaliittivirus, Puumalavirus, puutiaisenenkefaliittivirus (TBE), West Nile-virus, borreliat ja Toxoplasma gondii. Näiden taudinaiheuttajien diagnosoimiseksi tutkimukset tulee pyytää erikseen eivätkä ne kuulu normaalin Neuropakettitutkimuksen hintaan eli näitä (lukuunottamatta borreliaa) ei tehty. Näistä on ainakin Chlamydia pneumonia, Ebstein-Barr-virus (EBV) ja borreliabakteerit löydetty MS-potilaista monissa tutkimuksissa.

Yhden tutkimuksen mukaan lähes 50%:lla  potilaista erilaiset infektiot pahensivat tautia. (www.ncbi.nlm.gov/pubmed/8534384). Sinänsä tämä ei ole uutinen – jokainen tietää miten pienikin flunssa saattaa vetää jalat alta. Mutta jospa syynä on olemassolevan bakteeri-infektion reakoiminen uuteen infektioon?
Garth Nicolsonin tutkimuksessa vuodelta 2007 jopa 80% MS potilailla oli yksi tai useampi solunsisäinen bakteeri-infektio kuten mykoplasma, keuhkoklamydia jne.  Mykoplasmaa oli päälle 50%:lla, herpes 6 virus noin 30%:lla, keuhkoklamydiaa alle 15%:lla, borrelioosia noin 35%:lla, enteroviruksia ei löytynyt lainkaan ja hepatitisvirusta alle 10%:lla. http://www.immed.org/NeuroDiseases/SIBI.Myco.Clam.Borr.NeuroMS.ALS.BhavDis.pdf. Häneltä on myös toinen tutkimus vuodelta 2009: http://www.bjmp.org/content/role-chronic-bacterial-and-viral-infections-neurodegenerative-neurobehavioral-psychiatric-au.

BORRELIOOSI
Neuroborrelioosilla eli kroonisella borrelioosilla on samanlaiset oireet ja plakit kuin MS-taudilla. Borrelioosin oireet voivat ilmaantua yllättäen erittäin voimakkaina tai vähitellen harmittoman tuntuisesti viikkojen, kuukausien tai vuosien aikana. Borrelia bakteeri kuuluu spirokeettoihin, aivan kuten syfiliksen aiheuttaja. Siksi on epäilty, että borrelia bakteeri kykenee olemaan lepotilassa vuosien ajan, jolloin se ei aiheuta oireita. Epäillään, että se voi aktivoitua uudelleen esim. silloin, kun ihmisen immuunijärjestelmä heikkenee syystä tai toisesta. Borrelioosin oireet voivat vaihdella eri henkilöillä suuresti. Neurologiset oireet: Borrelia bakteeri kykenee siirtymään verenkierrosta keskushermostoon nopeasti.  Borrelioosi vaikuttaa keskushermostoon monin tavoin. Yleisimpiä oireita ovat esim. päänsärky, huimaus, vapina, polttava tunne eri puolilla kehoa, heikotus, halvaus, paineen tunne päässä, tasapainohäiriöt, kävelyhäiriöt (joskus myös iskias), lisääntynyt matkapahoinvointi, häiriöt ajattelussa, masennus, yöhikoilu, puutuminen ja pistely raajoissa, mielialan vaihtelu ja vaikea uupumustila jne.Psykologiset oireet: esim. muistihäiriöt, mielialan vaihtelu, masennus, unettomuus, levottomuus, puhehäiriöt, keskittymiskyvyn puute jne.  Enemmän borrelioosi epidemiasta”Under our skin” dokumentissa, joka esitettiin viime heinäkuussa Teemalla: http://www.megaupload.com/?d=N2U4M9NA.  Borrelioosin oireista enemmän: http://www.borrelioosi.net/ARTIKKELI-BORRELIOOSISTA.php.

Borrelioosin sairastuneiden hoidossa käytetään kortikosteroideja tulehdusten ja kivun hoitoon, mikä itse asiassa pahentaa tautia painamalla immuunijärjestelmää alas joten bakteeri pääsee leviämään huoletta. Bakteeri  pitää erityisesti  verisuonten endoteeli soluista synnyttäen tulehduksen. Hermojen, ihon, lihasten, jänteiden ja kudosten verisuonten tulehdus (vaskulitis) kuvaa tautia. Bakteerit elävät solujen sisällä immuunijärjestelmän koskettamattomissa. Se ei ainoastaan piiloudu immuunijärjestelmältä, mutta myös ”nukkuu” pitkiä aikoja aiheuttamatta mitään oireita.  Taudin toteamiseen ei ole yhtä luotettavaa testiä ja usein diagnoosi joudutaan tekemään kliinisesti oireiden perusteella. Krooninen väsymyssyndrooma ja fibromyalgia ovat ehkä osa samaa tautia tai sitten ne ovat keuhkoklamydiabakteerin aiheuttamat.

KEUHKOKLAMYDIA
Keuhkoklamydia leviää pisaratartuntona ja voi aiheuttaa vakavan hengitysteiden infektion. Jos immuunijärjestelmä ei onnistu  pääsemään eroon bakteerista, se leviää verenkierron mukana esim. verisuonten seinämiin, hermokudokseen, aivoihin, lihaksiin ja jopa immuunisoluihin. Bakteeri käyttää solujen energian lisääntymiseen. Koska bakteeri on solunsisäinen, sillä ei ole soluseinämää, ja sitä on vaikea todeta verikokeissa. Edes immuunijärjestelmä ei löydä sitä ja kaiken lisäksi se korruptoi immuunisoluja.  Bakteeri hakeutuu myös uusiin infektioihin aiheuttaen toisasteisen infektion. On todettu, että bakteeri aiheuttaa atheroskleroosia valtimoissa ja muita kroonisia tauteja. http://www.ktl.fi/portal/suomi/julkaisut/kansanterveyslehti/lehdet_1996/7_1996/chlamydia_pneumoniae_liittyy_lukuisiin_kroonisiin_sairauksiin/
Keuhkoklamydia voi saastuttaa selkäytimessä muodostuvat immuunisolut, se altistaa  lisäinfektioille (virukset, bakteerit, hiivat, mykoplasmat jne) jotka kuormittavat immuunijärjestelmää entistä enemmän,  sydänlihaksessa se pienentää sydämen tehokkuutta ennen kaikkea fyysisissä tehtävissä ja palautumiskykyä.Se aiheuttaa myös  mm. suoliston häiriöitä,  nukkumisvaikeuksia, masennusta ja ahdistusta, glukoosin häiriöitä, päänsärkyä, korkeaa verenpainetta, verisuonten tulehduksia (myös aivoihin menevien verisuonten),  ”velton” olon, tietynlaisen liikkumattomuuden, jonka syynä on kehon pyrkimys energian säästämisen.  
Keuhkoklamydiaa on löydetty MS-potilaiden selkäydinnesteestä ja ainakin yksi MS-potilas on parantunut taudista pitkän antibioottikuurin ansiosta. Hänen miehensä, mikrobiologi Dr Wheldon kehitti MS-potilaille sopivan hoidon. Lisätietoja: http://www.cpnhelp.org/, klikkaa multiple sclerosis ja saat tietoja bakteerista ja hoidosta.  Jo vuonna 1960 Paul Le Gac yhdisti bakteerit, verenkierron ongelmien aiheuttamat plakit aivoissa ja antibioottihoidon.  
Nykyisin PK Thibault (http://www.ncbi.nlm.nih.gov/pubmed/22240624) kallistuu Le Gac’n puolelle CCSVI:n taudinkuvassa eli laskimoiden viat johtuvat  keuhkoklamydiasta eivätkä synnynnäisistä vioista kuten Prof. Zamboni esittää.  Täten olisi loogista, että laskimolaajennus parantaa MS-oireet vain jos se on synnynnäinen vika. Jos verenkierto-ongelmat johtuvat bakteerista, niin silloin ne täytyisi hoitaa antibiooteilla.  Tutkijat Prioneas ja Parratt Austraaliasta tulivat siihen tulokseen, että ennen myeliinikatoa astrosyytit aivoissa kuolivat.  Astrosyytit ovat soluja aivoissa, jotka ohjaavat paljon toimintoja, esim. kertovat oligodendrosyyteille milloin rakentaa myeliiniä, pitävät yllä veriaivoestettä  jne. Vasta veriaivoesteen heikentyessä valkosolut pääsevät sisään ja korjaamaan kuolleita soluja. Astrosyyttien joukkokuoleman aiheuttajaa etsitään, mutta on tutkimuksia joissa keuhkoklamydiaa on löydetty astrosyyteistä (katso Cpn.org).  

JA SITTEN
On siis olemassa bakteereita, jotka piiloutuvat solujen sisälle ja joita ei voida helposti todeta verikokeista tai selkäydinnesteestä, ja kaiken lisäksi ne vahingoittavat verisuonten seinämiä ja tykkäävät tuhota hermosoluja. Se, että laskimolaajennukset eivät tuottaneet minulle pysyvää hyötyä, ja epätietoisuus mahdollisesta borrelioosista saivat minut tutkimaan enemmän kroonisia bakteeri-infektioita.
Minulla diagnoosin aikana tehdyn likvorin borrelioositesti oli negatiivinen, mutta Huslabin ohjekirjan mukaan ” Negatiivinen vasta-ainemäärityksen tulos ei siten sulje pois Borrelia burgdorferi –infektiota”.   Myöhemmin  terveyskeskuksessa otetun testin lausunnossa sanottiin, että ”Lievästi positiivinen.. kyseessä voi olla jolloinkin menneisyydessä koetun borreliakontaktin jättämä vanha immuniteetti..” En ollut tietääkseni sairastanut borrelioosia, joten luonnollisesti halusin enemmän tietoa, mutta minulle vakuutettiin että sillä ei ollut merkitystä. Myöhemmin halusin kuitenkin selvyyttä ja sen vuoksi pyysin jatkotutkimusta. HYKS:n vastaus oli kielteinen, koska minulle oli tehty MS diagnoosin yhteydessä borrelioositesti, joka oli negatiivinen. He yksinkertaisesti kieltäytyivät, vaikka teoriassa olisin voinut saada infektion diagnoosin jälkeen.  Menin kuitenkin yksityiselle puolelle selvittämään asiaa ja Prof Valtonen (HYKS:n sisätautien ylilääkäri ennen kun jäi eläkkeelle) tuli puolentoista tunnin kliinisen tutkimuksen  jälkeen siihen johtopäätökseen, että minulla oli kuin olikin borrelioosi ja määräsi doksisykliiniä yhteensä viideksi kuukaudeksi, josta oli hieman hyötyä.
Loppujen lopuksi otin yhteyttä Borreliose Centrum Augsburg:iin, joiden mukaan minulla on borrelioosi (neljällä testillä varmistettu, joista kahta ei edes tehdä Suomessa), krooninen mykoplasma pneumonia,  ja ehrilichioosi (ei edes tutkita Suomessa).    Ei ihme, jos olo tuntuu heikolta.. Edessä on pitkä  antibioottikuuri näiden bakteereiden voittamiseksi. Jos se onnistuu, jäljelle jää MS. Vai jääkö?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Milena Pvm 05.03.2012 - 13:35:50

HopeSprings, kiva kuulla sinusta pitkästä aikaa! Kuulostaa kyllä aika hurjalta taistelusi.

Osaatko arvella, mikä siihen voi olla syynä, ettei noita kannattaisi kaikilta mäsiltä tutkia perinpohjin yleisessä terveydenhuolossa? Eikö se tulisi halvemmaksi sulkea noi pois ja sitten vasta hoitaa kalliilla lääkkeillä? Jos kyseiset infektiot ovat noin yleisiä, ei kai ole ihme, ettei MS-lääkkeet pure kovinkaan hyvin. Miten ne voisivatkaan.

Mielenkiintoinen aihe, mutta vaatii varmaan ihan hirveästi ponnisteluja, että saa itselleen asianmukaisia testejä. Mitä kautta näytteesi menivät ulkomaille Borreliose Centrum Augsburg:iin?

Bakteeri-infektioihin antibiootit, mutta jos onkin krooninen virusinfektio?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 05.03.2012 - 18:46:08

Hei Milena!

Tämä on mennyt lääketieteelliseksi salapoliisitarinaksi... Olisi tietysti järkevää tutkia kaikki mahdolliset krooniset bakteeri-infektiot ennen lääkityksen aloittamista, mutta kroonisia tartuntoja on vaikea todeta. Tietysti kokemuksesta viisastuneena, minun olisi pitänyt testauttaa bakteeri-infektiot ennen laskimolaajennuksia, mutta en tiennyt silloin mitä tiedän nyt.  Ja infektiot eivät myöskään kuulu neurologien alaan - tarvittaisiin yhteistyötä infektiolääkäreiden ja myös verisuonikirurgien kanssa. That would be the day.. Kävin Suomessa myös keuhkoklamydia ja mykoplasma kokeissa, joiden mukaan minulla ei ollut aktiivista infektiota. Tulokset siten negatiivisia. Ihan turhaan tuhlasin nuo rahat. Jos haluaa tietää mitä infektioita itse kantaa, täytyisi ensin varmistaa, että otettavat testit paljastavat krooniset infektiot.

Otin sähköpostitse yhteyttä Borreliose Centrum Augsburgiin (BCA) kerroin että minulla oli MS-tauti ja halusin tietää onko minulla borrelioosi tai muita infektioita. He lähettivät melkein parikymmentä sivua pitkän kyselylomakkeen oireista, englanniksi. Siinä piti miettiä mistä alkaen, kuinka usein ja kuinka voimakkaana oireet esiintyivät. Tietysti luettelossa oli enemmän oireita kuin mitä itselläni on enkä muistanut kaikkia. Lähetin lomakkeen postissa ja myöhemmin sain laatikon, jossa verikokeisiin neulat ja putkilot. Sekä lista kokeista ja niiden hinta. Koska klinikka on yksityinen, kokeet eivät ole halpoja. Minulla oli 11 verikoetta, joiden hinta oli 1100 euroa. Mutta siihen kuului tietenkin se, että infektiolääkäri luki oireet läpi ja mietti mitkä verikokeet täytyy ottaa. Kävin terveyskeskuksessa otattamassa verinäytteet ja lähetin Saksaan FedEx:llä (79 euroa). Kahta viikkoa myöhemmin sain yksityiskohtaiset tulokset sähköpostitse. Kävin Saksassa vielä kliinisissä tutkimuksissa, mutta se ei ole pakollista, jos haluaa vain tulokset ja tietää hyvän lääkärin Suomessa. He ovat testanneet ja myös hoitaneet MS-potilaita, joten tauti ei ole este.
On muitakin paikkoja, joissa voi tutkituttaa kroonisia infektiota, kuulemma Norjassa ja Saksassa lähimmät, mutta en tiedä tarkemmin. Voin aina tarvittaessa etsiä tietoja.

En tiedä virus infektioista sen enempää, minulla tarkistettiin Saksassa EBV-virus, mikä osoitti että minulla on vasta-aineita viitaten vanhaan tartuntaan. Eikö viruksia voi hoitaa antiretroviraalisella hoidolla - ainakin joitain retroviruksia.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja merikihu Pvm 05.03.2012 - 23:40:10

EBV-vasta-aineita löytyy lähes kaikilta aikuisilta. Joten en siitä olisi kovin huolissani. Toivottavasti oireittesi syy selviää.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.03.2012 - 11:42:07

Oireiden syynä ovat neuroborrelioosi (eli krooninen borrelioosi), mykoplasma ja ehrlichioosi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Milena Pvm 06.03.2012 - 13:26:29

Sanot, että neuroborrelioosilla olisi vastaavat plakitkin kuin MS-taudilla. Siitä heräsi kysymys, miten neuroborrelioosin oireet voidaan saada pois, jos se on aiheuttanut jotakin pysyvää? Plakit tuskin katoavat antibiooteilla, luulen.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Milena Pvm 06.03.2012 - 13:27:47


HopeSprings 06.03.2012 - 11:42:07:
Oireiden syynä ovat neuroborrelioosi (eli krooninen borrelioosi), mykoplasma ja ehrlichioosi.

Huomataan vielä se, ettei kyseiset infektiot sulje pois MS-tautia. Sinullahan voi olla ne kaikki?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 07.03.2012 - 16:38:23

Tässä onkin lääketieteellinen identiteettikriisi - mitä oikein sairastan? Jos bakteeri-infektiot saadaan parannettua, niin jäljelle jää MS. Ainakin teoriassa ja varmasti neurologien mielestä. Jotkut ovat sanoneet, että borrelioosi johtaa MS-tautiin, toisten mielestä taudit sekoitetaan ja potilaita diagnoisoidaan väärin. Pitää katsoa, mitä tulee eteen antibioottikuurin jälkeen.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Keltanokka Pvm 11.03.2012 - 00:50:57

Heii.. nyt liipataan niin läheltä mun henk.koht. kriisiä koskien ms-taudin käsitettä, että on pakko purkaa. Mielestäni ms-tauti on lääketieteen sukkakori joukolle kroonisia keskushermostoinfektioita joita ei ole tutkittu ja/tai vielä edes löydetty ja muille erilaisille aineenvaihdunnan epätasapainotiloille, joiden aiheuttaja voi olla mitä tahansa ympäristömyrkkyjen ja epäsopivan lääkitysyhdistelmän välillä. Pelkkä autoimmuuniteoria tuntuu vain ontuvalta. Ms-taudin diagnosointihan perustuu siihen että poissuljetaan ns. muut todennäköiset ja tunnetut infektionaiheuttajat vasta-ainekokeilla. Tunnetaan kuitenkin useita kroonisia keskushermostoinfektioita, joiden oireet ja mri-löydökset vastaavat ms-tautia. Tunnetaaan myös useita ympäristömyrkkyjä jotka aiheuttavat hermostossa immuno-aktiivisuutta.
Ja vielä HopeSprings:hienoa kuulla että joku oikeasti avautuu myös näistä abcr-lääkkeiden vaihtoehdoista. Kuulisin mielelläni kokemuksiasi enemmänkin.
Ei enempää näin lauantai-illalle, kiitos ja anteeksi, hiljenen  :-X

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.03.2012 - 11:24:41

Olen samaa mieltä siitä, että nykyinen diagnosointi perustuu muiden todennäköisten taudinaiheuttajien poissulkemisella. Ongelma onkin se, että vasta-ainekokeet eivät ole luotettavia. Kroonisessa borrelioosissa on arvioitu, että jopa 70% negatiivisista vastauksista on vääriä negatiivisia. Huslabin ohjekirjan mukaan mikä tahansa negatiivinen tulos ei sulje pois borrelioosia.
Ehkä taudin määrittelemisessä voisi alkaa etsiä syitä, jotka dominoiden tavalla aiheuttavat MS-oireet. Oireitahan on moninaisia, joten syitäkin voisi olla erilaisia. Näitä voisi olla autoimmuunisairaus (abcr-lääkkeet), synnynnäiset laskimoviat (laskimolaajennus hoitokeinona), bakteeri-infektiot (antibiootit lääkkeenä), selkärankaan tai päähän kohdistunut trauma, tai raskasmetallit veressä.  

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Milena Pvm 11.03.2012 - 18:33:34

HopeSprings, kerrotko vielä, mitä antibioottia otat ja millä annostuksella? Tää on ihan hirmu mielenkiintoinen aihe. Pidä meidät ajan tasalla, miten tilasi etenee, kun otat lääkettä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja elisabet Pvm 12.03.2012 - 00:12:40

mielenkiintoinen postaus, ja ajankohtainen aihe täälläkin, kun monen vuoden tauon jälkeen ilmaantui neurologinen oire.

omalla kohdallani olen aika varma immunologian ja oireilun jonkinlaisesta yhteydestä, mutta nyt kun pysyvää haittaa ei ole pahemmin kertynyt, olen itsekin epäillyt oireilulla olevan suorempi yhteys infektioihin. eli vähän vaikea määritellä mikä siinä sitten olisi MS-tautia, kun eteneminen ei ole kovinkaan selvää. voisihan tuo olla jotain muutakin keskushermostotulehdusta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.03.2012 - 14:55:10

Antibioottikuurin määrää infektio eli ensin pitäisi tietää mitä bakteereita kantaa ja kuurin pituuden määrää bakteereiden esiintyminen elimistössä, eli testit ovat tärkeitä. Suomessa ei anneta helposti antibioottikombinaatioita, ainoastaan yhtä antibioottia. Keuhkoklamydiaan hoitona on http://www.davidwheldon.co.uk/ms-treatment1.html: doksisykliiniä päivittäin, aluksi 100mg ja sitten 200mg, azithromysiiniä (tai roxithromysiiniä) kolme kertaa viikossa, ja parin kuukauden jälkeen metronidazole viitenä päivänä kuukaudessa. Jokainen antibiootti tuhoaa yhden vaiheen bakteerin lisääntymisestä, mutta koska se elää solun sisällä, kuuri on pitkä. Tämä kuuri vuoden ajan ja sitten kaksi viikkoa kuukausittain.  Borrelioosin sain Suomesta doksisykliiniä 100mg kahdesti päivässä, ja Saksasta kombin azithromysiiniä, refampinia ja minosykliiniä. Jotkut MS-potilaat ovat käyttäneet Marshallin protokollaa, joka koostuu olmesartaanista (korkean verenpaineen lääke) ja antibiootista (joko minosykliini tai doksisykliini) ja D-vitamiinin välttämisestä. Protokolla on kehitetty sarkoidoosin hoitoon, joten en tiedä siitä enempää. Lisää tietoja http://mpkb.org/home/mp#starting_a_patient_on_the_marshall_protocol.
MS-tautiin on kokeiltu rebif+minosykliini ja betainterferoni+doksisykliini yhdistelmiä erittäin positiivisin tuloksin. Muistaakseni annostukset olivat 100mg kahdesti päivässä, mutta asia on syytä tarkastaa. Infektiolääkärini mielestä antibiootti MS-lääkkeen kanssa toimii, koska alla on bakteeri-infektio, luonnollisesti.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Ruusu Pvm 23.03.2012 - 05:14:02

Tämä on mielenkiintoinen juttu. Osuu omien pohdintojen kanssa yksiin nuo krooniset bakteeri-infektiot ja MS yhteys. Sain just diagnoosin, että sylkirauhasissa krooninen tulehdustila. Jokin infektio on myös tuhonnut kilpirauhasen josta seurauksena sen vajaatoiminta.

Otin sikainfluenssarokotuksen syksyllä 2009. Sitä ennen oli ollut ekaa kertaa elämässä tiukka virtsatieinfektio ja yksi epileptinen kohtaus. Seuraavana talvena oli vaihtelevaa uupumusta ja oireilua sen jälkeen. Uusi epileptinen kohtaus keväällä 2010. Syksyllä kohdunkaulantulehdus. Kohonneet borrelioosiarvot syksyllä 2010 punkin jäljiltä. Kahden viikon antibioottikuuri. Uudet testit syksyllä 2011, nyt borrelioosiarvo lievästi koholla mutta vain akuutti ja tutkimukset jäi siihen, koska uutta punkkia ei ollut ollut, eli lääkärin mukaan ei voinut olla borrelioosi.

Aloin viime vuoden kuluessa epäillä MSää koska niin monet oireet täsmäsi uupumuksesta neurologisiin oireisiin. Toki myös CFSään kuten täältä sainkin hyvän vinkin. Epäilin näköhermon tulehdusta mutta silloin näköongelmia ei ollut, kipua vain. MRI puhdas. Likvoria ei otettu. Diagnoosiksi migreeni.

Olen vahvasti eri mieltä. Musta tuo krooninen tulehdus sylkirauhasissa, tuhoutunut kilpirauhanen, borrelioosiarvot, 2008 puhjennut astma, epilepsiakohtaukset ja muut oireet ja kenties myös sikainfluenssarokote liittyy jotenkin yhteen mutten vaan ihan tajua miten. Tilasin magneettikuvat kotiinkin ja ajattelin vielä kiikuttaa jollekulle. Jos joku haluaa vinkata pätevää neuroradiologia olisin onnellinen! Tai vinkata miten tästä edetä :)


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja elisa Pvm 23.03.2012 - 09:08:28


Ruusu 23.03.2012 - 05:14:02:
Kohonneet borrelioosiarvot syksyllä 2010 punkin jäljiltä. Kahden viikon antibioottikuuri. Uudet testit syksyllä 2011, nyt borrelioosiarvo lievästi koholla mutta vain akuutti ja tutkimukset jäi siihen, koska uutta punkkia ei ollut ollut, eli lääkärin mukaan ei voinut olla borrelioosi.

Minulla oli borrelioosi vuonna 2007. Luulin, että lääkekuurin jälkeen käyn verikokeessa, mutta lekuri sanoi, että vereen jää pysyvästi kohonnut vasta- ainetaso.

Helikobakteeri löytyi minulta sattumalta vatsan tähystyksen yhteydessä, elettiin kai vuotta 2009 silloin(hitostako näitä kaikkia voi muistaa). Lääkekuuri paransi minut siitä vaivasta, joka minulla oli ollut varmaan koko pienen ikäni.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Ruusu Pvm 23.03.2012 - 12:35:21

Näin minullekin vasta-ainetasoista sanottiin. Jokin ero vain tuntuu olevan sillä kroonisella ja akuutilla tasolla. Mun lääkäri sanoi että vasta-aineiden pitäisi näkyä siellä kroonisella tasolla hoidetun borrelioosin jäljiltä. Ja että akuutti taso voi kertoa jostain muusta infektiosta. Mulla oli salmonella tuliaisina Intiasta syksyllä 2008. Voihan noistakin tietty jäädä jotain.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.03.2012 - 14:35:48

Ruusu,

Borrelioosi ei parane kahden viikon antibioottikuurilla, vaikka suomalaiset lääkärit niin väittävät. Sinun olisi parasta tutkituttaa se jollain infektiolääkärillä, tai lähettää verinäytteet ulkomaille tutkituttavaksi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 24.06.2012 - 16:33:21

Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable?

http://www.lymepa.org/Chronic%20Lyme%20borreliosis%20at%20the%20root%20of%20Multiple%20Sclerosis%20and%20a%20possible%20cure%20with%20antibiotics.pdf

Artikkelissa on verrattu MS:n ja borreliosin esiintymistä. MS-tautia esiintyy niillä alueilla joille linnut levittävät punkkeja. Esimerkiksi Uudessa Seelannissa esiintyy vähemmän MS-tautia kuin Australiassa, koska muuttolinnut pohjoisesta saapuvat aikaiasemmin Austraaliaan kuin Uuteen Seelantiin. Tutkimuksessa on myös mielenkiintoinen osa antibiooteista MS-taudin hoidossa eli  borrelioosin hoidossa käytetyt minosykliini, tinidazole ja hydroxychloroquine (malarialääke) auttaisivat myös MS-oireisiin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 24.06.2012 - 17:11:24

Antibiotic Use and Risk of Multiple Sclerosis

http://aje.oxfordjournals.org/content/163/11/997.full.pdf

Tämä tutkimus keskittyy puolestaa keuhkoklamydiaan ja lääkärien määräämiin antibiootteihin (enintään kaksi viikkoa).

"If a causal relation between a particular bacterial infection and MS indeed exists, then it is conceivable that persons who have been treated, for whatever indication, with antibiotics active against that bacteria might be at a lower risk of developing MS than those who have not received such antibiotic treatment."

"  Our prospective study shows that overall use of antibiotics, and use of antibiotics active against C.pneumoniae during the 3 years before the index date did not  reduce the risk of developing MS in this British population. However, in all the analytical scenarios, more than two weeks of penicillin use was associated with a 50 percent reduction in the risk of MS."

Tetrasykliinien käyttö myös vähensi MS riskiä, mutta tutkijat olettivat sen johtuvan muuttuvista variaabeleista. Penisilliinejä ja tetrasykliinejä on käytetty borrelioosin hoidossa. Antibioottien käyttö joko vähentää MS riskiä poistamalla infektioita aiheuttavat mikro-organismit tai suojelemalla hermoja ja siten vähentämällä neurologisia tuhoja.  

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.06.2012 - 10:34:23

Hyviä uutisia niille, joilla on mahdollinen borrelioosi ja haluavat hoitoa ulkomailta. Borrelioosi ja muutamat lisäinfektiot ovat orpha.netin listaamia harvinaisia sairauksia ja vuoden 2009 Euroopan neuvoston suosituksen ja uuden potilasdirektiivin mukaan harvinaisia sairauksia sairastavien potilaiden on mahdollista lähteä muihin jäsenvaltioihin diagnooseja ja hoitoja varten joita ei vakuutusjäsenvaltiossa ole saatavilla.

Nojaten lakiin sosiaaliturvajärjestelmien yhteensovittamisesta (352/2010, 14 art., Euroopan parlamentin ja neuvoston asetukseen sosiaaliturvajärjestelmien yhteensovittamisesta (883/2004) 30.2 artikla ja 27.3-5 artikla, ja Euroopan parlamentin ja neuvoston asetus sosiaaliturvajärjestelmien yhteensovittamisesta annetun asetuksen 883/2004 täytäntöönpanomenenttelystä  (987/09) 26 artikla, ja sairaanvakuutuslakiin (1224/2004) 15 lukuun 16 artiklaan, Kela on suostunut maksamaan borrelioosihoitoni Saksassa.

Eli ensin pitää hakea lupaa ja sitten kustannusten korvaamista. Itse hain molempia samaan aikaan ja jälkikäteen. Sain luvan vuodeksi eli hämmästyttävän pitkäksi aikaa, kun Suomessa kuvitellaan, ettei kroonista borrelioosia ole olemassa eikä kombinaatio-antibioottihoitoa sallita. Eläköön EU!

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.07.2012 - 22:55:59

Borrelioosin ja lisäinfektioiden oireiden lista, josta jokainen tunnistaa paljon oireita ja ehkä sellaisiakin jotka eivät ole tyypillisiä MS-taudille:

http://www.lyme-symptoms.com/LymeCoinfectionChart.html

Olisinpa nähnyt tämän vuosia sitten, koska olen vuosia etsinyt selitystä sille miksi minulle kehittyi hidas syke  ja "incomplete heart block". Neurologin mielestä ei ollut syytä huoleen, sillä minulla oli (huippu)urheilijan sydän.(Sen saa kävelemällä heikommin ja heikommin vuosi vuodelta). Ja sitä paitsi häiriöt olivat ilmeisesti MS-taudin syytä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 31.07.2012 - 20:39:52

It's not in veins - it's in the blood!

Uudenlainen teoria tai taru, joka yhdistää MS-taudin, CCSVI:n ja krooniset infektiot: veressä on biofilmiä rakentava protozoa (alkueläin).

http://www.iadvocatehealth.org/protozoal_infection0.aspx

"Fry: Well, they are doing -- this goes back to Paulo Zamboni’s work. I think he’s a vascular specialist at the University of Ferrara in Italy. His wife came down with multiple sclerosis and he wanted to find out what it was and hypothesized it was a vascular problem, and then after a lot of work developed an ultrasound technique and was able to visualize, using ultrasound, a defect in flow in either the deep cerebral veins or the petrosal veins of the brain or the internal jugular veins coming down from the brain. The next step to that was that he was able to show that in patients who had internal jugular vein obstruction or decreased flow he could go in with a balloon catheter and open this up. Some of these MS patients could get improvements and some dramatic improvements in their condition. Of course there’s a relapse rate with this that is actually quite high.

But it makes sense if it’s a microorganism that is growing there and you’re kind of, you know, clearing things up -- that would make a lot of sense. So now this has been repeated by Dr. Hubbard, who’s just recently submitted a 265 patient study showing similar results. Actually, that was a 6-month study. So these patients with MS have obstruction in the flow of the brain, and Dr. Hubbard used the word “swamp”. There’s reduced flow, bad flow, backflow. We feel the same way, that the brain is probably a sensitive organ or tissue. So if you change the flow environment in any way, whether it is less oxygenation, less nutrients, you are going to see some subtle changes and thus demyelination. It would be a subtle change, and I want you to know that they have documented remyelination in some of these patients where they have done this balloon procedure.
********
Fry: Yes, and when you see these vegetations, some are valves, and actually they categorize the type of vegetations. Or actually, they don’t use the word vegetations as Zamboni does, and I use that vegetation concept or idea. But there are growths, or filaments, or webs, or other structures that they see, that certainly aren’t normally found in the vasculature. And if you look at Zamboni’s work -- there is one you can see online -- Paolo Zamboni, you can pull it up, and there is an ultrasound and you can see the valve moving, but also you see a lot of other smaller and filamentous type material. Actually we have seen in blood samples filamentous material similar to that in patients with chronic fatigue. I think it is the same thing, and what we are seeing in the blood are really material that has just detached from the vasculature in long linear strands.
******
Now if you throw in this concept that these patients might have gross obstructive disease with a biofilm-forming protozoan, then it’s sort of...kind of brings all this thought together. So really in these patients they have -- for instance, in the CSF of fibro patients, they have brain fog -- I think that’s due primarily to sluggish flow either through some obstructive process due to these vegetations that I’m talking about, or even just the viscosity issue with a larger microorganism forming biofilm communities in the circulatory system. "

Koska biofilmit suojelevat bakteereita, olisi ensin ryhdyttävä vähärasvaiselle ruokavaliolle, jotta biofilmit eivät saa ravintoa (ei rasvoja, sokeria, rautaa, kalsiumia tai magnesiumia), sen jälkeen minosykliiniä tai doksisykliiniä, ja sen jälkeen azithromysiiniä tai malarialääkkeitä. Tepsii myös borrelioosiin ja useisiin bakteeri-infektioihin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Rami Pvm 01.08.2012 - 12:01:17


HopeSprings 31.07.2012 - 20:39:52:
It's not in veins - it's in the blood!

Uudenlainen teoria tai taru, joka yhdistää MS-taudin, CCSVI:n ja krooniset infektiot: veressä on biofilmiä rakentava protozoa (alkueläin).


Koska biofilmit suojelevat bakteereita, olisi ensin ryhdyttävä vähärasvaiselle ruokavaliolle, jotta biofilmit eivät saa ravintoa (ei rasvoja, sokeria, rautaa, kalsiumia tai magnesiumia), sen jälkeen minosykliiniä tai doksisykliiniä, ja sen jälkeen azithromysiiniä tai malarialääkkeitä. Tepsii myös borrelioosiin ja useisiin bakteeri-infektioihin.


Mutta jos nyt jo syö parsakaalia ja Goji-marjoja eikä liikaa kahvia (korkeintaan 12 [tusina]isoa kahvia päivässä)??? Varmaan paranee sairauksista, joita ei ole vielä olemassakaan

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.08.2012 - 00:46:40

Itse en usko ruokavalion parantavan kroonisia infektioita tai MS-tautia, vaikka kannattaakin syödä terveellisesti. Mutta kuten artikkelissa todettin, pöpöjä tuhoamaan tarvitaan antibiootteja ja/tai malarialääkkeitä.  

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.08.2012 - 21:06:19

Borrelioosi ja MS-tauti: onko yhteyttä? Tutkimus Puolassa v.2000

http://www.aaem.pl/pdf/aaem0024.pdf

Abstract: A total of 769 adult neurological patients hospitalised in clinics and hospitals
situated in the Lublin region (eastern Poland) were examined during the years 1997-
2000 with ELISA test for the presence of anti-Borrelia burgdorferi sensu lato
antibodies. A statististically significant (p = 0.0422) relationship was found between the
clinically confirmed diagnosis of multiple sclerosis and the positive serologic reaction
with Borrelia antigen. Ten out 26 patients with multiple sclerosis (38.5%) showed
positive serologic reaction to Borrelia, whereas among the total number of examined
neurological patients the frequency of positive findings was twice as low (19.4%). The
result suggests that multiple sclerosis may be often associated with Borrelia infection.
***********
The nature of the stated relationship between infection with LB agent and MS disease remains obscure. In some
cases, neuroborreliosis may be misdiagnosed as MS. A direct provoking of MS by B. burgdorferi does not look
probable, but it cannot be excluded that the LB agent may aggravate the pathogenic processes in the initial stage of
MS and thus increase a number of the symptomatic, clinically diagnosed cases. This hypothesis, similar to that
proposed by Karussis et al. [8], may be supported by the resemblance of the pathologic processes in both diseases:
activation of the lymphocytic system [6], inducing of the matrix metalloproteinases (MMPs) production [15],
inducing of the autoantibodies production, including antibodies to neuronal proteins [7] and to myelin basic
protein [8, 23]. In the late period of neuroborreliosis, demyelinating involvement of CNS can develop, similarly
as in MS [5].


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Tripp Pvm 13.08.2012 - 22:36:14

Hei!

Olen uusi kirjoittaja täällä.
Olisin hyvin kiinnostunut kuulemaan lisää tästä aiheesta.
Kävin koko kevään tutkimuksissa ja itse epäilin MS tautia.
Neuroborrelioosi diagnosoitiin kliinisin perustein.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.08.2012 - 16:13:42

Hei!

Tämäpä on mielenkiintoista, koska suomalaiset lääkärit eivät usko kroonisen borrelioosin olemassaoloon eivätkä neuroborrelioosiin. Borrelioosin voi parantaa parin viikon antibioottikuurilla, kun muualla maailmassa se on vaikea parannettava.. Missä neuroborrelioosi diagnosoitiin ja minkälaisen lääkityksen olet saanut?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.08.2012 - 16:52:46

Tämän viikon The Economist lehdessä on seuraava artikkeli: Me, myself, us  ihmisen ekosysteemistä (omat geenit plus 3 miljoona mikrobien geeniä):
http://www.economist.com/science-technology

" For, from obesity and diabetes, via heart disease, asthma and multiple sclerosis, to neurological conditions such as autism, the microbiome seems to play a crucial role."

"In the case of multiple sclerosis... showed, again in mice, that gut bacteria are indeed involved in triggering the reaction that causes the body's immune system to turn against certain nerve cells and strip away their insulation in precisely the way that leads to multiple sclerosis."

"If gut bacteria make you ill, can sapping make you healthy?"

"Clinical trials have indeed shown that probiotics (a mixture of bacteria found, for example, in yogurt) ease the symptoms of people with irritable-bowel syndrome, who often have slightly abnormal gut microbiomes. Whether they can cause a beneficial shift in other people is not known. A paper published last year by Dr Gordon’s group reported that in healthy identical twins the microbiome is unaffected by yogurt; when one twin was asked to eat yogurt regularly for a couple of months while his sibling did not, no change in the microbiome was seen.

Yogurts are limited in the range of bacteria they can transmit. Another intervention, though, allows entire bacterial ecosystems to be transferred from one gut to another. This is the transplanting of a small amount of faeces. Mark Mellow of the Baptist Medical Centre in Oklahoma City uses such faecal transplants to treat infections of Clostridium difficile, a bug that causes severe diarrhoea and other symptoms, particularly among patients already in hospital."

"there is no doubt that the microbiome does feed people, does help keep their metabolisms ticking over correctly and has at least some, and maybe many, ways of causing harm. And it may do one other thing: it may link the generations in previously unsuspected ways. A lot of the medical conditions the microbiome is being implicated in are puzzling. They seem to run in families, but no one can track down the genes involved. This may be because the effects are subtly spread between many different genes. But it may also be that some—maybe a fair few—of those genes are not to be found in the human genome at all."

"This is of more than merely intellectual interest. Known genetic diseases are often hard to treat and always incurable. The best that can be hoped for is a course of drugs for life. But the microbiome is medically accessible and manipulable in a way that the human genome is not. It can be modified, both with antibiotics and with transplants. If the microbiome does turn out to be as important as current research is hinting, then a whole new approach to treatment beckons."



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.08.2012 - 17:10:13

Leena62 lähetti seuraavan artikkelin, joka käsittelee haitallisia mikrobeja, jotka leviävät borrelioosin mukana ja aiheuttavat lisä-infektioita. Kiitos!

http://www.care2.com/greenliving/why-is-lyme-disease-not-just-tick-borne-anymore.html


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 24.08.2012 - 20:29:49

Lisää tuosta The Economist-lehden artikkelista:
"Two other areas look promising. One is more sophisticated deployment of the humble antibiotic, arguably the pharma industry's most effective invention. At the moment antibiotics are mainly used to kill infections. In the future they might have a more subtle use - to manipulate the mix of bugs within a human, so that good bugs spread at the expense of the bad ones.
The other field that may be changed is genetics. Many of the diseases in which the microbiome is implicated seem to run in families. .. In a lot, though, most notably autism, the genetic link is obscure. This may be because geneticists have been looking at the wrong set of genes - the 23,000 rather than the 3m. For those 3m are still inherited. They are largely picked up from your mother during the messy process of birth. Though no example is yet known, it is possible that particular disease-inducing strains are being passed down the generations in this way.
As with all such upheavals,  it is unclear where the microbiome revolution will end up. Doctors and biologists may come to think of people as superorganisms. Then again, they may not. What is clear, though, is that turning thinking inside out this way is yielding new insights into seemingly intractable medical problems, and there is a good chance cures will follow. Vive la revolution!"


Bakteeri-infektioihin määrätään antibiootteja, jotka tappavat myös hyviä bakteereita, mutta pahojen hävittämiseksi se on välttämätöntä. Kunnes yllämainitut uuden sukupolven valikoivat antibiootit keksitään. Antibiooteissa suurimmat haittavaikutukset liittyvätkin suoliston toimintaan. Iitselläni ei ole ollut mitään haittavaikutuksia, mutta olenkin syönyt säännöllisesti probiootteja ja tiedän että joudun syömään niitä kauan aikaa. Kefiiri ja muut maitotuotteet ovat myös hyväksi vatsalle.

Yksi usein kuultu väite on se, että syömällä antibiootteja liikaa, bakteerit tulevat immuuneiksi eikä niihin sen jälkeen tehoa mitkään antibiootit.  Ensiksi,  väite ei päde kaikkiin bakteereihin, tai bakteeri-antibiootti yhdistelmiin. Esimerkiksi Flagyl viitenä päivänä kuukaudessa pulssihoitona ei aiheuta keuhoklamydia-bakteerin vastustuskykyä ko antibioottiin. Ja toiseksi, jos sinulla on bakteerimäärä  jonka tuhoamiseen tarvitsee, sanotaan 5,5 viikkoa antibiootteja, ja saat kahden viikon kuurin, niin bakteeri ei kuole, jolloin tarvitset uuden kuurin. Vaara on siinä, että antibioottikuuri ei tapa kaikkia pahoja bakteereita: joko kuuri on liian lyhyt bakteerimäärään verrattuna, tai potilat lopettavat sen liian aikaisin, jolloin jotkut pahat bakteerit (ei kaikki) oppivat vastustamaan antibioottia. Eli on tärkeää saada tarpeeksi pitkät antibioottikuurit, vaikka haittavaikutukset voivat olla karmeat, kuten ripuli (hoidettavissa). Lisäksi on tauteja joihin hoitona on pitkä 1-2 vuoden antibioottikuuri, kuten tuberkuloosi, joten aihe ei ole vieras lääketieteelle. Se, että muualla määrätään pitkiä antibioottikuureja borrelioosin ja lisä-infektioiden kuten keuhkoklamydian hoitoon, ei ole myöskään täysin outoa tai vastuutonta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.08.2012 - 16:20:53

Ainakin borrelioosin hoidossa ulkomailla tähdätään oman immuunipuolustuksen vahvistamiseen. Hoitona käytetään antibiootti-komboja, luonnonlääkkeitä ja ruokavaliota. Yksi suomalainen lääketieteen kandi naureskeli halveksuen luonnonlääkkeiden käyttämistä, vaikka Euroopassa niitä yhdistellään tarpeen mukaan.  Mutta herääkin kysymys miten MS-taudin hoidossa käytetyt immunosuppresiiviset lääkkeet joko edistävät kroonisten infektioiden leviämistä tai haittaavat paranemista. Potilaiden paranemista borrelioosista pitkittää aikaisempi immunosuppresiivisten lääkkeiden käyttäminen ja käytön kesto. Muistaakseni tämä mainittiin jossain ILADSin artikkeleissa. En tiedä onko asia samoin muiden kroonisten infektioiden, esimerkiksi keuhkoklamydian eli Cpn:n  kanssa. En myöskään tiedä mitä lääkärit suosittelevat sillä hetkellä kun aloittaa antibiootti + luonnonlääkekuurin, mutta loogisesti tuntuisi väärältä jatkaa immunosuppressiivista lääkitystä ja aloittaa immunostimulatiivinen lääkitys. Kaksi lääkitystä, kotka vetävät immunijärjestelmää eri suuntiin.  

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.08.2012 - 15:15:29


Minosykliini auttaa neurodegeneratiivisien sairauksien hoidossa:

A Novel Target of Action of Minocycline in NGF-Induced Neurite Outgrowth in PC12 Cells: Translation Initiation Factor eIF4AI


Kenji Hashimoto*, Tamaki Ishima

Division of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan

Abstract
Background

Minocycline, a second-generation tetracycline antibiotic, has potential activity for the treatment of several neurodegenerative and psychiatric disorders. However, its mechanisms of action remain to be determined.

Methodology/Principal Findings
We found that minocycline, but not tetracycline, significantly potentiated nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells, in a concentration dependent manner. Furthermore, we found that the endoplasmic reticulum protein inositol 1,4,5-triphosphate (IP3) receptors and several common signaling molecules (PLC-γ, PI3K, Akt, p38 MAPK, c-Jun N-terminal kinase (JNK), mammalian target of rapamycin (mTOR), and Ras/Raf/ERK/MAPK pathways) might be involved in the active mechanism of minocycline. Moreover, we found that a marked increase of the eukaryotic translation initiation factor eIF4AI protein by minocycline, but not tetracycline, might be involved in the active mechanism for NGF-induced neurite outgrowth.

Conclusions/Significance
These findings suggest that eIF4AI might play a role in the novel mechanism of minocycline. Therefore, agents that can increase eIF4AI protein would be novel therapeutic drugs for certain neurodegenerative and psychiatric diseases.

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0015430

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.09.2012 - 20:11:32

Diagnosis and Treatment of Chronic Mycoplasmal Infections in Fibromyalgia and Chronic Fatigue Syndromes: Relationship to Gulf War Illness

http://www.biopathica.co.uk/Articles/Immune%20System/5%20-%20Diagnosis%20and%20Treatment%20of%20Chronic%20Mycoplasmal%20Infection.pdf

Mielenkiintoista oli tässä jo 1998 julkaistussa tutkimuksessa seuraava:

Interestingly, as chronic illnesses, such as CFS (Chronic Fatigue Syndrome), FMS (Fibromyalgia Syndrome) and GWI (Gulf War Illness)progress, there are a number of accompanying clinical problems, particularly autoimmune problems. These include in some patients the signs and symptoms of  multiple sclerosis (MS), amyotropic lateral sclerosis (ALS), lupus, Graves' Disease, arthritis, and other complex autoimmune diseases. Such usually rare autoimmune responses are consistent with certain chronic infections, such as mycoplasmal infections that penetrate into nerve cells, synovial cells, and other cell types. We speculate that these autoimmune signs and symptoms are caused when intracellular pathogens, such as mycoplasmas, escape from cellular compartments and incorporate into their own structures pieces of host cell membranes that contain important host membrane antigens that can trigger autoimmune responses. Alternatively, the antigents on the mycoplasma cell surface may directly stimulate an autoimmune response.

Eli solujen sisäiset bakteerit kuten mykoplasma, keuhkoklamydia tai borrelia purkautuessaan solun sisältä (käytettyään ensin solun ravinnon) ja etsiessään uutta isäntää, kantavat mukanaan osia käyttämästään solusta, antigeenejä, joihin immunijärjestelmä reagoi. Tämän prosessin selitän huonosti, mutta kroonisia infektioita kuten borrelioosia hoitavilta lääkäreiltä kuulee MS:n selitykseksi juuri tämänlaisen bakteerin aiheuttaman autoimmuunireaktion.
Luonnollisesti krooninen väsymys johtuu bakteereista, jotka käyttävät lisääntymiseensä solujen ravinnon.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 26.09.2012 - 19:44:50

Lyme Disease Pathology - Central Nervous System
http://lymediseaseguide.org/lyme-disease-pathology-central-nervous-system

The spread of the Lyme disease bacteria into the central nervous system varies in incidence and speed between individuals but when it does happen the spirochaetes may fundamentally alter brain function. It appears that astrocytes in the brain are involved in the pathogenesis of Lyme disease as these are glial cells providing support for endothelial cells that constitute the blood-brain barrier that protects the brain from damage by closely guarding entrance to brain circulation. The astrocytes are also important in maintaining nutrient supply to brain tissue, and in the repair process, and scarring, following trauma to the spinal cord or brain itself. The Borrelia bacteria induce astrogliosis in the astrocytes, a process where the cells rapidly reproduce and then die (proliferation followed by apoptosis). The effectiveness of the blood-brain barrier, the supply of nutrients to neural tissue, and the balance of ions in the brain can all be compromised through such events.

Mielenkiintoista on astrosyyttien tuhoutuminen ja sitä kautta veriaivoesteen murtuminen ja ravinteiden pääseminen hermokudokseen. Zambonin mielestä veriaivoesteen läpäisykyky muuttui ja aivoihin pääsi ylimääräistä rautaa veren mukana.  Muistaakseni myös Prof. Thibault puhui astrosyyttien massakuolemasta syynä veriaivoesteen murenemiselle.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.09.2012 - 14:57:19

Infectious Agents and Neurodegeneration

http://www.springerlink.com/content/gh5u4k7118274q46/fulltext.pdf?MUD=MP

Conclusions
Advances in microbiological research have led to indepth understanding of the structure and replication mechanisms of several pathogens, as well as of their interactions with host cells. However, a growing body of evidence suggests that when an infectious agent reaches sites different from those of its primary replication it may produce mild infections that eventually cause additional and unexpected effects. This is the case for persistent CNS infections caused by continuous pathogen replications (e.g. HIV and C. pneumoniae infections), repeated infections (e.g. influenza virus) or latent infections followed by life-long reactivations (as in the case of HSV-1). Repeated cycles of pathogen replication within the CNS produce functional and molecular hallmarks of neurodegeneration, including protein misfolding, deposition of misfolded protein aggregates, alterations of autophagic pathways, oxidative stress, neuronal functional alterations and apoptotic cell death (Fig. 7). These effects accumulate over time, thus contributing to neurodegeneration. The pathogen-induced effects add to and are possibly amplified by several factors such as metabolic disorders, genetic alterations and other environmental risk factors, involved in the pathogenesis of neurodegenerative diseases.

As a result, the pathogen-induced damage amplifies and accelerates the neurodegenerative process, whose signs are usually manifested during aging. The data reviewed in our paper suggest that more detailed understanding of the molecular mechanisms underlying pathogen-mediated neuronal damage may pave the way to the identification of new preventive and/or therapeutic strategies aimed at counteracting the progression of these devastating pathologies.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.09.2012 - 19:54:11

Our self-cleansing brain
Fluids coursing through the nervous system could help clear the brain of toxic detritus that leads to Alzheimer's


http://www.salon.com/2012/08/16/brains_drain_neuroscientists_discover_cranial_cleansing_system_salpart/

The brain can be a messy place. Thankfully, it has good plumbing: Scientists have just discovered a cleansing river inside the brain, a fluid stream that might be enlisted to flush away the buildup of proteins associated with Alzheimer’s, Huntington’s and other neurodegenerative disorders.

Scientific American The researchers, based at the University of Rochester (U.R.), University of Oslo and Stony Brook University, describe this new system in the journal Science Translational Medicine today. The study adds to the evidence that the star-shaped cells called astrocytes play a leading role in keeping the nervous system in good working order...The researchers observed that, like a river, cerebrospinal fluid carried these molecules rapidly along specific channels. Glial cells along the outside of arteries form these channels, creating a flume for cerebrospinal fluid that follows the brain’s blood vessels. In addition, the researchers found that these glial cells mediate the channel’s activity, assisting the flow of fluid through the channel.

From channels alongside arteries, the tracer-bearing fluid then passes through brain tissues. At the other end of tissues, it flows into similar channels along veins. The fluid follows these veins then either returns to the subarachnoid space, enters the bloodstream or eventually drains into the body’s lymphatic system. The researchers christened the network the “glymphatic” system, a nod to both glial cells and its functional similarity to the lymphatic system.

Iliff hypothesizes that a faulty glymphatic system may bear the blame for the over-accumulation of proteins seen in Alzheimer’s, amyotrophic lateral sclerosis, Huntington’s and other neurodegenerative disorders—and further study may even reveal a way to dispose of these clumps.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.10.2012 - 23:13:48

SPECT Brain Imaging in Chronic Lyme Disease.

http://www.ncbi.nlm.nih.gov/pubmed/22889796

Abstract

OBJECTIVES:
Lyme disease is an infectious disease that frequently involves the central nervous system, leading to cognitive and/or mood dysfunction. The basis for these symptoms remains to be defined but may be the result of a vasculitis or metabolic abnormality secondary to the infection. SPECT scans of the brain might provide an objective measure of abnormalities present in patients with otherwise difficult to objectify clinical findings. The objective of this study was to determine the frequency, location, and severity of abnormalities in SPECT scans of the brain of patients with chronic Lyme disease.

METHODS:
A total of 183 individuals who met the clinical definition of chronic Lyme disease underwent SPECT scanning of the brain using Tc and standard nuclear imagine techniques. Abnormalities of perfusion to affected areas of the brain were defined as mild, moderate, or severe.

RESULTS:
Of all patients, 75% demonstrated abnormalities in perfusion to various areas of the brain, most notably the frontal, temporal, and parietal lobes. Patients considered to be seropositive and those considered seronegative had similar rates, types, and severity of perfusion defects. Abnormalities of MRI of the brain were seen in 14% of patients. Treatment with antibiotics, especially those with intracellular-penetrating activity, resulted in resolution or improvement of abnormalities in 70% of patients over a 1- to 2-year period.

CONCLUSIONS:
Brain SPECT scans are abnormal in most patients with chronic Lyme disease, and these scans can be used to provide objective evidence in support of the clinical diagnosis. The use of certain antibiotic regimens seems to provide improvement in both clinical status and SPECT scans.

Mielenkintoista on se, etää bakteeritulehdus aiheuttaa verenkiertohäiriöitä aivoissa, joita normaalissa magneettikuvauksessa näkyi 14%:lla potilaista .. Ja 70% paranee kokonaan tai osittain 1-2 vuoden antibioottikuurilla.  Pitäisi saada koko artikkeli, jotta näkisi mitä antibiootteja käytettiin korjaamaan vaurioita.

Koska minulle ei ollut SPECT skannaus tuttu, katsoin wikin selityksen siitä:

SPECT scan: Single-photon emission computed tomography (SPECT, or less commonly, SPET) is a nuclear medicine tomographic[1] imaging technique using gamma rays. It is very similar to conventional nuclear medicine planar imaging using a gamma camera. However, it is able to provide true 3D information. This information is typically presented as cross-sectional slices through the patient, but can be freely reformatted or manipulated as required.
Usually, the gamma-emitting tracer used in functional brain imaging is 99mTc-HMPAO (hexamethylpropylene amine oxime). 99mTc is a metastable nuclear isomer that emits gamma rays that can be detected by a gamma camera. Attaching it to HMPAO allows 99mTc to be taken up by brain tissue in a manner proportional to brain blood flow, in turn allowing cerebral blood flow to be assessed with the nuclear gamma camera.

Because blood flow in the brain is tightly coupled to local brain metabolism and energy use, the 99mTc-HMPAO tracer (as well as the similar 99mTc-EC tracer) is used to assess brain metabolism regionally, in an attempt to diagnose and differentiate the different causal pathologies of dementia. Meta-analysis of many reported studies suggests that SPECT with this tracer is about 74% sensitive at diagnosing Alzheimer's disease vs. 81% sensitivity for clinical exam (cognitive testing, etc.). More recent studies have shown the accuracy of SPECT in Alzheimer's diagnosis may be as high as 88%.[3] In meta analysis, SPECT was superior to clinical exam and clinical criteria (91% vs. 70%) in being able to differentiate Alzheimer's disease from vascular dementias.[4] This latter ability relates to SPECT's imaging of local metabolism of the brain, in which the patchy loss of cortical metabolism seen in multiple strokes differs clearly from the more even or "smooth" loss of non-occipital cortical brain function typical of Alzheimer's disease.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja kilpikonnax Pvm 04.10.2012 - 11:13:03

tuli vastaan duodecimin juttu vuodelta 2009

http://www.duodecimlehti.fi/web/guest/arkisto?p_p_id=dlehtihaku_view_article_WAR_dlehtihaku&p_p_action=1&p_p_state=maximized&p_p_mode=view&_dlehtihaku_view_article_WAR_dlehtihaku__spage=%2Fportlet_action%2Fdlehtihakuartikkeli%2Fviewarticle%2Faction&_dlehtihaku_view_article_WAR_dlehtihaku_tunnus=duo97777&_dlehtihaku_view_article_WAR_dlehtihaku_p_frompage=uusinnumero

siinä Perttu J. Lindsberg, Jari Koistinaho ja Pentti Tienari
spekuloivat minosykliinillä ja MS:llä ihan mielenkiintoisella tavalla, myös hintanäkökulma tulee mukaan..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja kilpikonnax Pvm 04.10.2012 - 11:16:05

mielenkiintoista on kaivaa myös vuotta 2005 parlamentista, että eihän tämä minosykliini mitenkään uusi asia ole, mutta päästiinkö silloin minnekään asti sen kanssa? http://mscrossroads.org/cgibin/YaBB.cgi?num=1132843627/0

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 05.10.2012 - 21:33:41

Kun tarpeeksi kauan odottaa, asiat tulevat uudelleen muotiin. Ja samoista asioista keksustellaan näköjään edelleen. Sääli, ettei lupaava lääke saa rahoitusta lisätutkimuksiin. CCSVI Facebookissa on myös keskustelua minosykliinistä.  Näköjään kannattaa ostaa ulkomailta ja tuoda mukanaan. Näin lomailu saa uuden ulottuvuuden..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja kilpikonnax Pvm 06.10.2012 - 21:29:16

en halua mennä facebookin ryhmään koska en julkisesti taudistani puhu kun se ei mitenkään näykään. sen verran mitä olen puhunut, niin eipä kannustanut kyllä jakamaan tietoa edelleen. sanotaan nyt että siinäpä ystävät punnitaan..
niin piti kysyä että millä keinoin ihmiset ulkomailta (tallinna, kauempaa?) tätä hakevat? menevät siellä lääkäriin ja sanovat että saiskos minosykliiniä mäsään? tai jotain muuta keinoa? jenkeissähän lääkkeet ainakin lie tosi edullisia. (ja norwegian alkaa lentää halvalla sinnekin pian...) että ei tämä ihan hullu vaihtoehto olisi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja erekki Pvm 06.10.2012 - 21:58:59

Kilpikonnax, tuon facebookin kanssa no problem - teet vain feikki identiteetin ja haet sillä jäsenyyttä. Siellä on käsittääkseni muutamia mäsiä feikkinimillä ja ihan ok. Minosykliinistä ja muutamasta muusta antibiootista on siellä käyty keskusteluja ja ihmiset ovat niitä hankkineet joko ulkomailta tai erityislupahakemuksen myötä Suomesta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.10.2012 - 17:28:59

Association between multiple sclerosis and cystic structures in cerebrospinal fluid.

http://www.ncbi.nlm.nih.gov/pubmed/11787831?dopt=Abstract

Abstract

BACKGROUND:
The aim of the study was to search for infectious agents in the cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS).

PATIENTS AND METHODS:
CSF from ten patients with the diagnosis relapsing remitting MS and from five controls without MS were examined by transmission electron microscopy (TEM), dark field microscopy (DF), interference contrast microscopy (ICM) and UV-microscopic examination of acridine orange staining (AO). All CSF samples from patients and controls were cultured.

RESULTS:
Cystic structures were observed in CSF of all ten patients by AO and TEM. DF revealed eight cyst-positive patients out of nine. One of five control persons had such structures in the CSF; this person had suffered from erythema migrans. Spirochete or rod-like structures emerged after culturing two of the MS patient CSF samples and these structures could be propagated.

CONCLUSION:
A significant association of CSF cysts and MS was identified in this small study among residents in a coastal area of southern Norway. The cysts could be of spirochetal origin. Our study may encourage other researchers to study larger patient groups.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.10.2012 - 17:47:16

Lisää edelliseen:

http://www.lymenet.de/literatur/brorson2001.htm

...Cysts were significantly associated with MS patients using each of the three different methods. This multi-method approach strengthens the association between CSF cysts and MS in a well-defined coastal area of southern Norway.  There are two possible explanations for the association between MS and CSF cysts: the cystic structures are either the agents causing MS or they have appeared in the CSF as a consequence of MS.

  The positive reaction with antispirochetal antiserum, the similarity of the cystic structures with cystic forms of spirochetes and the similarities between the cysts in the erythema migrans patient and the MS patients suggest that the patients were infected with a spirochete.  The  appearance of rod-like,slightly curved bacteria and spirochetes after culturing two of the CSF samples in BSK-H medium suggests the same.  Spirochetes may vary in appearance and may sometimes emerge as rod-like structures [18].  The fact that only two spinal fluids gave rise to  spirochete-like structures after culturing may be caused by the fact that cystic forms of spirochetes may often be difficult to convert to normal bacteria {11) and the BSK-H medium is not necessarily optimal for this possible unknown spirochete.

  It could be argued that the damage which MS caused in the brains of the patients had made them more vulnerable to spirochetal infection. But this does not seem a probable explanation. since all the MS patients had these cystic structures in their CFS. Other researchers have proposed that spirochetes could be the agents responsible for MS [5, 6, 8, 9]. For instance. Steiner [6] found spirochetes and granular bodies in brain autopsies of MS patients. These were proposed to belong to the genus BorreIia and were named Spirochaeta myelophthora [6].

  We previously studied spirochetes (B. burgdorferi) that have converted from spirochetes to cystic forms in CSF in vitro using the same methods as mentioned above [11].  With all these methods used in this study (TEM, AO, DF), the cystic structures observed in the CSF of the MS patients are morphologically similar to cystic forms of spirochetes. We found that cysts which are produced by inoculating  B. burgdorferi in CSF at 37  C can be PCR negative using conventional DNA extraction and OspA primers (unpublished observation). This is either because the cyst wall inhibits the entrance to the genome or because the genomes of spirochetes have been changed. We have also to keep in mind that PCR detection of B. burgdorferi spirochetes often may give false-negative  results [19).

  The positive IgG index associated with MS in our patient cohort proves that the patients had an active inflammatory process in the CNS (Table 1).  Inflammatory processes in the b~ and spinal cord of virtually any cause are usually less intense than inflammation in peripheral tissues and some microbiological agents, including spirochetes, provoke a very gentle inflammatory response [20, 21 ]. Considering the nature of MS, this disease could very well be a chronic infection and the clinical picture of MS has repeatedly been confused with neuroborreliosis [22-26). Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS.


1930-luvulta aina toiseen maailmasotaan tutkittiin spirokeetta-teoriaa, mutta se lopahti tutkijoiden kuoltua. Vain Steiner jatkoi ja löysi borrelia- sukuun kuuluvan spirokeetan, jonka nimesi Spirochaeta myelophthoraksi. Kun muut eivät onnistuneet löytämään samaa bakteeria, tutkimus lopahti. Sanottakoon sen verran, että vaikka borrelioosin oireet on kirjattu jo 1880-luvulla, sen aiheuttava bakteeri löydettiin vasta 1970-luvulla.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.10.2012 - 13:59:44

Inflammation and central nervous system Lyme disease

http://www.lymenet.de/literatur/Fallon_Inflammation-and-central-nervous-system-Lyme-disease_2009.pdf

Abstract:
Lyme disease, caused by the bacterium Borrelia burgdorferi, can cause multi-systemic signs and symptoms,  including peripheral and central nervous system disease. This review examines the evidence for and mechanisms of inflammation in neurologic Lyme disease, with a specific focus on the central nervous system, drawing upon human studies and controlled research with experimentally infected rhesus monkeys.
Directions for future human research are suggested that may help to clarify the role of inflammation as a mediator of the chronic persistent symptoms experienced by some patients despite antibiotic treatment for neurologic Lyme disease.


...When Lyme disease affects the brain and spinal cord, it can look like multiple sclerosis (MS) (Ackermann et al., 1985). In 1988, Pachner described two patients with Lyme disease whose MS-like neurologic symptoms responded well to antibiotic therapy for Lyme disease (Pachner, 1988). The brain MRI among patients with Lyme disease may at times be suggestive of a demyelinating disease. A recent review (Hildenbrand et al., 2009) described two patients with Lyme disease who had neuroimaging findings partially suggestive of MS. The first patient, whose illness started with an EM rash and developed into meningitis, had a MRI which revealed callososeptal interface involvement remarkably similar to that in MS. Arcuate and confluent subcortical white matter involvement was also present, but without periventricular white matter disease. The patient's symptoms improved after IV ceftriaxone. The second patient was an elderly man with 2 years of cognitive decline, positive serologic and CSF titers with evidence of intrathecally produced B.b.-specific antibodies, and MRI findings suggestive of a demyelinating disease—a dot–dash appearance of the callososeptal interface as well as a periventricular distribution of involvement; this patient improved with iv ceftriaxone therapy. Resolving MS signs and symptoms however in the context of Lyme disease may simply reflect the waxing and waning course of relapsing remitting MS and be unrelated to Lyme disease or it may reflect the improvement that would be expected after antibiotic therapy for Lyme disease. That B.b. may exacerbate MS or be a trigger for a MS-like inflammatory demyelinating disease of the CNS is not a surprising hypothesis, as infections with foreign agents are thought to either activate myelin-specific T cells by molecular mimicry, via crossrecognition of a bacterial and a myelin peptide, or by bystander activation, via inflammatory cytokines (Martinet al., 2001). As a result of B.b. infection, autoreactive antibodies may develop to myelin and myelin components (Suchanek et al., 1986; Garcia-Monco et al., 1988; Martin et al., 1988). Sequence homology has been noted between myelin basic protein and B.b. spirochetal flagellin (Weigelt et al.,1992) and there are studies demonstrating cross-reactive polyclonal and monoclonal antibodies which recognize flagellar antigenic determinants as well as epitopes on neural cells (Sigal and Tatum, 1988; Aberer et al., 1989; Fikrig et al., 1993). Such cross-reactivity could contribute to a chronic, relapsing-remitting, B. burgdorferi triggered, immune-mediated neurological disorder similar to MS.


....This study demonstrated that the deficits primarily reflect abnormalities in cerebral metabolism, although there was evidence for a component of vascular compromise as well. The patients with Lyme encephalopathy had a diminished ability to increase cerebral blood flow in response to a hypercapnic challenge compared to age-, sex-, and education matched controls, a finding that would suggest vascular compromise (as perhaps from inflammation) as part of the disease process.  The precise cause of these objective vascular and metabolic deficits however is unclear. While some of these patients do respond to repeated antibiotic therapy, the antibiotic responsiveness itself need not indicate persistent infection as antibiotics are also known to have roles in modulating glutamate (Rumbaugh et al., 2007) and in reducing inflammation (Bernardino et al., 2009).


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 24.10.2012 - 14:00:41

Kirjoitin heinäkuussa Dr Stephen Fryn löytämästä alkueläimestä, ja hän on yksi luennoitsiva CCSVI:n erikoistuneen International Society for Neurovascular Disease (ISNVD):n 2013 vuosikokouksessa Krakovassa, Puolassa. Hänen aiheensa:  Infection by intracellular protozoan Protomyxzoa rheumatica and its potential link with MS. S. Fry (USA).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.10.2012 - 21:21:30

'Autoantibodies' may be created in response to bacterial DNA
Published: Monday, April 27, 2009 in Biology & Nature

http://esciencenews.com/articles/2009/04/27/autoantibodies.may.be.created.response.bacterial.dna

Autoimmune diseases have long been regarded as illnesses in which the immune system creates autoantibodies to attack the body itself. But, researchers at the California non-profit Autoimmunity Research Foundation (ARF) explain that the antibodies observed in autoimmune disease actually result from alteration of human genes and gene products by hidden bacteria. Not long ago, scientists believed they had located all bacteria capable of causing human disease, But DNA discoveries in the last decade have led the NIH Human Microbiome Project to now estimate that as many as 90% of cells in the body are bacterial in origin. Many of these bacteria, which have yet to be named and characterized, have been implicated in the progression of autoimmune disease.

In a paper published in Autoimmunity Reviews, the ARF team, under the guidance of Professor Trevor Marshall of Murdoch University, Western Australia, has explained how Homo sapiens must now be viewed as a superorganism in which a plethora of bacterial genomes – a metagenome – work in concert with our own. Marshall and team contend that the human genome can no longer be studied in isolation.

"When analyzing a genetic pathway, we must study how bacterial and human genes interact, in order to fully understand any process related to the human superorganism," states Marshall. "Especially since some of these pathways contribute to the pathogenesis of autoimmune disease."

For example, the team notes that the single gene ACE has an impact on myocardial infarction, renal tubular dysgenesis, Alzheimer's, the progression of SARS, diabetes mellitus, and sarcoidosis, yet recently ACE has been shown to be affected by the common species Lactobacillus and Bifidobacteria. Found in yogurt, these species are often considered to be innocuous or "friendly."

"No one would argue that these species aren't present in the human body, yet there has been inadequate study of how these 'friendly' species affect disease," states Amy Proal, the paper's lead author.

"What we thought were autoantibodies generated against the body itself can now be understood as antibodies directed against the hidden bacteria," states Marshall. "In autoimmune disease, the immune system is not attacking itself. It is protecting the body from pathogens."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 29.10.2012 - 18:07:11

Kävin tarkastamassa laskimot Varsovassa ja radiologien mukaan takaisinvirtausta esiintyy toisessa kaulalaskimossa. Sen jälkeen juttelin verisuonikirurgin kanssa ja kuultuaan bakteeri-infektioista, suositteli, että tulen takaisin kolme kuukautta sen jälkeen kun olen parantunut infektioista ja lopettanut antibioottikuurin ja sitten tutkitaan IVUS:lla mikä on suonten tilanne. Hänen mukaansa bakteeri-infektiot lisäävät muuttujia ja epävarmuutta, joten on parempi odottaa mikä tilanne on sen jälkeen kun infektiot on parannettu. Mutta hän painotti sitä, että laskimolaajennus ei välttämättä poista oireita ja asiassa on paljon mitä ei vielä tiedetä. Koska Puolassa esiintyy paljon borrelioosia, hän tiesi aika paljon sairaudesta ja jopa senkin että likvorin borrelioositesti on melkein aina negatiivinen, mikä ei kerro totuutta. En tiedä yhtään CCSVI:iin erikoistunutta klinikkaa, joka tarkastaisi mahdolliset krooniset bakteeri-infektiot potilaasta ennen laskimolaajennusta. Eli se jää potilaan tehtäväksi. Puolassa ainakin testejä on saatavilla ja ne maksavat puolet Saksan hinnoista. Suomessa testit eivät ole luotettavia, eivätkä lääkärit pidä niitä tarpeellisina. Minullekin neurologit väittivät moneen otteeseen, ettei minulla ole borrelioosia, koska minulla on MS. Ikään kuin MS olisi suojellut minua punkin puremilta. (Hyi olkoon, MS-potilas, enpä ime sen verta, sanoi punkki)

Oli todella miellyttävä tavata asian osaava ja potilasta ymmärtävä lääkäri. Ja vaikka hän työskenteli yksityisessä sairaalassa, ei millään tavalla painostanut toimenpiteisiin, päinvastoin. Hän sanoikin, että potilas tietää oireensa ja sairautensa ja myös sen, mikä sopii hänelle ja mikä ei. Lääkäri on vain parantumisen väline. Tämä sama asenne on Borreliose Centrum Augsburgin lääkäreillä, jotka myös kuuntelevat potilasta tuntikaupalla, jos niin on tarpeen. On vain sääli, että täytyy lähteä ulkomaille, jotta joku kuuntelisi ja auttaisi. Mutta onneksi potilasdirektiivi astuu voimaan 2013 loppuun mennessä ja siinä hyväksytään myös hoidot, joita ei saa kotimaassa, ja ulkomailla aloitetun hoidon jatkaminen kotimaassa (ellei eduskunta sitä vesitä täydellisesti).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.11.2012 - 14:41:44

Cpnhelp.org-sivuilla törmäsiin Karlin tarinaan:
Karl's Treatment of MS via Combined Antibiotic Protocol (CAP), http://www.cpnhelp.org/karls_treatment_of_ms_via

Hänellä todettiin MS, krooninen keuhkoklamydia, babesioosi ja mahdollisesti borrelioosi. Yhdestoista lääkäri arvio tilanteen seuraavalla tavalla: He stated that the suspicious titers in my Lyme tests were low, but he determined I had Lyme disease, particularly because my CD-57 test count for killer immune cells was low (21). He was aware of the research on the connection between CPN and MS, and he stated that he believes that the combination of Lyme and CPN can lead to progressive MS, which was what he feels I have.
Kahdestoista lääkäri: Interestingly enough, this doctor was aware that MS could be treated with antibiotics as several of his patients were diagnosed with Lyme induced MS, and had gotten much better from antibiotics.

Jossain on siis lääkäri, joka tunnistaa borrelioosin aiheuttaman MS-taudin ja määrää hoidoksi antibiootteja. Mietin onko itselläni sama boorelioosin aiheuttama MS, koska borrelioosi ja lisäinfektiot sain kaksi vuotta ennen MS-diagnoosia.. Karlin hoito oli rankka: suonensisäisen antibiootin lisäksi kolmea muuta antibioottia. Koko kuuri kesti ilmeisesti ainakin vuoden, mutta potilas oli kirjoittamisen aikaan paranemassa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 25.11.2012 - 15:22:28

Geo-Statistical Analysis of Possible Spirochetal Involvement in Multiple Sclerosis

http://proceedings.esri.com/library/userconf/proc06/papers/papers/pap_1358.pdf

Valittuja paloja tutkimuksesta:

.. In certain cases, patients are misdiagnosed with Lyme several times before receiving a diagnosis of MS. Both diseases can produce MRI's marked by sclerotic plaques, and both manifest similar symptoms such as memory lapses, fatigue, and joint pain. Both diseases involve vascular inflammation wihin the CNS caused in part by inflammatory cytokines and chemokines.

.. If, in fact, the T-cells and the body's immune cells are "incorrectly" attacking the healthy Myelin Basic Protein (MBP) or some other feather of fatty sheath surrounding the axons and not an invader, then one would not expect the disease the remit when there is still myelin left to be digested - as have been observed. For the autoimmune theory to be plausible, there would have to be some mechanism by which the immune system switches from the misidentification of healthy tissue as the invader to correct identification, and a ceasing of the attack in mid-attack.

... Both Lyme and MS can follow a relapse-remitting progression which, in Lyme, is thought to result from  the many different forms that spirochetes such as Borrelia Burgdorferi are known to take. When the environment is positive for  the spirochetal activity, the bacteria remain in fully elongated form, but in the presence of antibiotics many spirochetes defensively curl up in a granular form. While in granular form, the spirochetes are virtually undetectable even by electronic microscopy, and the disease appears to be latent for some time. This latency period, though, is perhaps the most deleterious stage of disease. While in the highly minimized forms, the spirochetes are able to traverse many of the body's pores and enter into cells and organs. When no longer threatened, they expand again into their elongated form.

.. The steroids could be paying additional roles in MS is in fact influenced by spirochetes. Although spirochetes thrive in the presence of steroids, the steroids could bring about the bacteria's destruction. Acting as a sort of bait, often steroids cause spirochetes to expand into their elongated forms, though in this form the bacteria are more susceptible to T-cells attack. This could explain the success of steroids as a medication and provide some insight for developing a more permanent solutions.

...The results of statistical analyses support geographically the proposed connection between MS, Lyme and related diseases... The correlation and regression analyses also show a clear geographic co-occurence of MS and Lyme... Nevertheless, sufficient similarities exist in this study to suggest, but not confirm, a common spirochetal basis for MS and Lyme.

Minulle oli aina epäselvää autoimmuuni teoriassa se, miten myeliini tuhoutuu vähitellen - hermoimpulssit toimii joskus, joskus taas ei. Luulisi, että kun myeliini alkaisi tuhoutua, se vaan jatkuisi.  Ja kuten tässäkin tutkijat huomauttavat, että ollakseen uskottava autoimmuuniteoria tarvitsee mekanismin mikä säätelee immuunijärjestelmää siten, että tunnustettuaan  terveen kudoksen väärin se aloittaa hyökkäyksen, sitten kesken hyökkäyksen tunnistaakin kudoksen terveeksi ja lopettaa hyökkäyksen. Eli olisi oltava olemassa mekanismi, joka säätelee autoimmuunihyökkäystä.  Tietenkin tälläisen mekanismin olemassaolo tekisi hoidonkin mahdolliseksi. Eli autoimmuuniteoria ei pysty selittämään myeliinikatoa uskottavasti.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.11.2012 - 18:10:52

Kroonisesta mykoplasma infektiosta

http://www.drgregemerson.com/fact-file/mycoplasma

They (mycoplasmas) are the smallest free living organisms. Like viruses, they are intracellular organisms but unlike viruses, they can reproduce outside cells. They lack a cell wall which makes them resistant to many antibiotics. They enter the body through skin, lungs or digestive system. They then spread through the bloodstream to infect vascular endothelium. They multiply within cells until numbers are so great that the cells burst. This then damages blood flow to multiple organs, hence the multitude of symptoms which may occur.

Most of us have an immune system which can eradicate these organisms. In people without an optimal immune system, mycoplasma can cause both acute and chronic infections. Acute mycoplasma infections can present as atypical pneumonia or a severe flu like illness which frequently involves joint pains and headaches. Symptoms can persist of months. Chronic mycoplasma infections have been implicated in:

   Rheumatoid arthritis and psoriatic arthritis
   Chronic Fatigue Syndrome
   Fibromyalgia and Polymyalgia Rheumatica
   Gulf War Syndrome
   Autoimmune diseases such as lupus, scleroderma, vasculitis, multiple sclerosis and Sjogren’s.

Research by Dr Cecile Jardin (a French surgeon now based in South Africa and specialising in the treatment of chronic fatigue) has shown that the most common symptoms of chronic mycoplasma type infections include:

   Sweats 28%
   Chest pain and palpitations 47%
   Bruising 48%
   Visual disturbances 58%
   Depression 62%
   Recurrent sore throat 69%
   Sleep disturbances 71%
   Muscle and joint pain 73%
   Memory and concentration impairment 80%
   Headaches 80%
   Fatigue 87%

Symptoms are caused by the release of 3 types of toxins into the blood:

   Endocytokines that cause inflammation and pain.
   Neurocytokines that produce neurological symptoms including the demyelinisation found in multiple sclerosis and psychiatric symptoms such as depression and anxiety.
   Allergens causing allergies.

Mycoplasma infections can be occult. That means they can be asymptomatic and lie dormant until another bacteria, virus, parasite, stress or toxin activates it and causes the symptomatic phase.

Often these chronic conditions improve dramatically and even completely recover once the infection is identified and appropriately treated. In my opinion, everyone with the above conditions should be screened for chronic mycoplasma infection.

Treatment of an acute respiratory mycoplasma infection usually involves a 3 week course of an antibiotic such as doxycycline, rulide or a 5 day course of azithromycin. Eradication of a chronic mycoplasma infection requires long term antibiotic treatment. This can range from 3-24 months but averages around 9 months. The course has to be so long because:

   the organisms being intracellular are hard to kill.
   the infection has been present for a long time
   the organisms are present in multiple organs
   dormant organisms can be protected against antibiotics and can only be killed once they become active

Aivan samoin kuin kroonisen keuhkoklamydian testaamisessa, krooninen mykoplasma voidaan havaita PCR-testillä.  En tiedä mikä labra Suomessa tekee PCR-testejä tai paljonko se maksaa, mutta tälläinen "kävelevä keuhkokuume", jota voi sairastaa tietämättään, olisi hoidettava pitkällä antibioottikuurilla.



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 10.12.2012 - 19:19:17

The Biotoxin Pathway

http://www.publichealthalert.org/Articles/scottforsgren/biotoxin%20pathway.html

Chronic illnesses often seem like complex puzzles where it quickly becomes evident that many of the pieces are missing. No matter how hard we try to understand exactly what is causing us to be ill, a full understanding seems to often be evasive. The work of Ritchie C. Shoemaker, MD provides us many more pieces of that puzzle and sheds brighter light on understanding the complex nature of chronic illness.
....
If a person is genetically susceptible to a biotoxin-associated illness, it is likely the case that the biotoxins themselves, rather than Lyme infection or mold exposure, are causing many of the symptoms being experienced. Even further, it is plausible to suggest that infection could be cleared, or the exposure entirely removed, and yet the remaining symptoms may be almost entirely due to circulating biotoxins. It comes down to a genetic predisposition which results in the body’s inability to remove these biotoxins...

There are many sources of biotoxins that may be encountered including Borrelia spirochetes and Babesia infections found in Lyme disease, fungi and mold (Aspergillus, Penicillium, Stachybotrys, and others), ciguatera toxins from seafood, dinoflagellates such as Pfiesteria, some algaes, various types of bacteria, and recluse spiders. With each of these sources of biotoxins, there is one thing in common. People that are impacted by these toxins, regardless of their origin, have the same or very similar symptom presentations. The similarities, which are confirmed by sophisticated statistical analysis, are compelling.
....
There are specific genotypes associated with specific susceptibility to biotoxins. For patients with Lyme disease or mold exposure, approximately 25% of the population has a genetic predisposition which results in an inability to clear biotoxins naturally. Understanding whether or not one is in this population can provide key insight into the cause of illness. Though the result may suggest a genetic make-up which cannot itself be corrected, once known, specific interventions can be put into play that may significantly improve the outcome.

The test is called HLA DR and it is commonly known as a test which provides insight into possible organ rejection after a transplant operation. Human Leukocyte Antigen (HLA) is a grouping of genes that lie on chromosome 6. In the case of biotoxins, HLA codes for whether or not a person is capable of clearing biotoxic substances following an exposure. For these people that are genetically incapable of clearing these toxic substances, biotoxins will continue to circulate within the body indefinitely and may reduce one’s chances of recovery. There is generally no “selfhealing” in these cases without appropriate interventions.
....

In the world of biotoxins, it is the biotoxin itself that continuously signals the body to produce more cytokines. It is this excess cytokine production that makes us feel unwell. Excess cytokines result in flu-like symptoms, body aches, temperature fluctuations, cognitive difficulties and other symptoms. This increase in cytokines has further downstream effects.

VEGF (vascular endothelial growth factor) is often reduced which leads to fatigue and reduced blood flow. Hypoperfusion, this resulting reduction in blood flow, results in a starving of cells for nutrients and oxygen. There is also an increase in MMP9 (matrix metalloproteinase) as the cytokine itself causes the white blood cells to release MMP9. MMP9 is a superb marker for the presence of excess cytokines.

MMP9 may be responsible for delivering inflammatory compounds out of the blood and into the brain which causes plaque formations similar to those seen in MS. In Lyme disease, MMP9 levels may skyrocket as the result of treatment with antibiotics and the resulting bacterial die-off in what is commonly referred to as a Herxheimer reaction. Taking this even further, if you give a Lyme-infected person antibiotics and they are not HLA-susceptible, they generally have an uneventful recovery.

An increase in cytokines may also trigger auto-immunity. There are three key types of antibodies observed in those with biotoxin-associated illnesses. These are myelin (the protective sheath around nerve cells) antibodies, gliadin (a protein found in gluten) antibodies, and cardiolipin antibodies which impact circulation in the small blood vessels.

MSH, which is made in the hypothalamus, is the most potent anti-inflammatory compound we have. It is responsible for regulating innate immune response and is involved in numerous hormone pathways. Reduced MSH is at the heart of the “Biotoxin Pathway” in that many negative downstream effects result when MSH is low. Of interest here is that in Lyme disease, chronic fatigue syndrome, mold illness and any other biotoxin illness regardless of the source of the biotoxin, MSH is low in about 95-98% of patients.

When MSH levels are low, people become sleep disturbed; they have chronic pain; they experience leaky gut syndrome; their recovery from illness is delayed; they develop multiple antibiotic resistant coagulase negative staph colonization (MARCoNS); they have frequent thirst as a result of lowered anti-diuretic hormone (ADH); they have a loss of libido due to a lowering of sex hormones and more.
....
To summarize, in susceptible individuals, biotoxins lead to increased leptin, increased cytokines, increased MMP9, increased C4a, reduced VEGF, reduced MSH, reduced ADH, reduced sex hormones, changes in cortisol and ACTH, prolonged illness, resistant staphylococci colonizations, gastrointestinal problems, chronic pain, and sleep disturbances. All of these are downstream effects of the “Biotoxin Pathway” in an HLAsusceptible individual.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 31.12.2012 - 13:53:56


The differential diagnosis of multiple sclerosis: classification and clinical features of relapsing and progressive neurological syndromes.

Neurol Sci. 2001 Nov;22 Suppl 2:S98-102. Trojano M, Paolicelli D.
Department of Neurological and Psychiatric Sciences, University of Bari, Italy.
Abstract

In the absence of pathognomonic clinical features or a definitive laboratory test, multiple sclerosis (MS) remains ultimately a diagnosis of exclusion. Accurate diagnosis is increasingly important with available disease modifying therapy. Unfortunately the rate of misdiagnosis remains around 5%-10%, indicating that 1 in 20 patients thought to have MS has, instead, a condition resembling MS. In this review we describe conditions that may be confused with MS because they can present as lesions disseminated in time, space, or both. Conditions often confused with MS may be inflammatory (systemic lupus erythematosus, Sjögren's syndrome, vasculitis, sarcoidosis, Behçet's disease), infectious (Lyme disease, syphilis, progressive multifocal leukoencephalopathy, HTLV-1 infection, herpes zoster), genetic (lysosomal disorders, adrenoleukodystrophy, mitochondrial disorders, CADASIL), metabolic (vitamin B12 deficiency), neoplastic (CNS lymphoma) and spinal (degenerative and vascular malformations) diseases. The key to the accurate diagnosis of MS is vigilance for atypical features, suggesting the possibility of an alternative diagnosis.

Eli MS-diagnoosin saaneista 5-10%:lla  on virheellinen diagnoosi, ainakin Italiassa, missä otetaan enemmän testejä ja seurataan potilaita aktiivisesti. Niitäkin, jotka eivät käytä MS-taudin lääkkeitä.  Kokemuksesta voin sanoa, etteivät suomalaiset lääkärit ole italialaisia parempia, joten ehkä prosenttiyksiköt pätevät myös Suomeen.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.01.2013 - 15:08:55

Lisää MMP9:stä, joka on siis MS-, infektio- ja CCSVI-potilailla kohonnut:

Gelatinase B/matrix metalloproteinase‐9 cleaves interferon‐β and is a target for immunotherapy
, 2003


Summary
Parenteral administration of interferon (IFN)‐β is one of the currently approved therapies for multiple sclerosis. One characteristic of this disease is the increased production of gelatinase B, also called matrix metalloproteinase (MMP) 9. Gelatinase B is capable of destroying the blood–brain barrier, and of cleaving myelin basic protein into immunodominant and encephalitogenic fragments, thus playing a functional role and being a therapeutic target in multiple sclerosis. Here we demonstrate that gelatinase B proteolytically cleaves IFN‐β, kills its activity, and hence counteracts this cytokine as an antiviral and immunotherapeutic agent. This proteolysis is more pronounced with IFN‐β‐1b than with IFN‐β‐1a. Furthermore, the tetracycline minocycline, which has a known blocking effect in experimental autoimmune encephalomyelitis, an in vivo model of acute inflammation in multiple sclerosis, and other MMP inhibitors prevent the in vitro degradation of IFN‐β by gelatinase B. These data provide a novel mechanism and rationale for the inhibition of gelatinase B in diseases in which IFN‐β has a beneficial effect. The combination of gelatinase B inhibitors with better and lower pharmacological formulations of IFN‐β may reduce the side‐effects of treatment with IFN‐β, and is therefore proposed for multiple sclerosis therapy and the immunotherapy of viral infections.


MMP9 toimintaa pienentää edellä mainittu minosykliini, mutta myös seuraavat:
VIT D3
RESVERATROL (Grape Skin Extract)
GREEN TEA EXTRACT(EGCGs)
QUERCETIN..........................
ALPHA LIPOIC ACID (R-lipoic/ R-Dihdro-LipoicAcid)
NAC N-Acetyl-L-Cysteine .......
STATIN DRUGS (i.e Zocor) .....
Omega-3s (ie Fish oil) ...........
Minocycline/Doxycycline.........
Curcumin
Pycnogenol (Pine bark extract)..
Chondroitin sulfate (CS) and CS plus glucosamine sulfate (GS) ..


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.01.2013 - 21:58:39

Asiasta toiseen.. Bakteerit pääsevät aivoveriesteen läpi, mutta pääsevätkö lääkkeet? Minosykliini pääsee aivoihin, ja suonensisäiset antibiootit.  Tässä tutkimuksessa yritetään saada lääkkeet aivoihin. Lisäksi josain päin tutkitaan, miten estää aivoveriesteen läpäisy MS-taudissa, jotteivät vahingolliset immuunisolut pääse aivoihin.  Toisaalta, jos immuunisolut menevät aivoihin korjaamaan kuolleita soluja, eivätkä aiheuttamaan vahinkoa, niin mitenkäs sitten käy..

Breaching the blood-brain barrier: Researchers may have solved 100-year-old puzzle
September 13, 2011 in Neuroscience

Cornell University researchers may have solved a 100-year puzzle: How to safely open and close the blood-brain barrier so that therapies to treat Alzheimer's disease, multiple sclerosis and cancers of the central nervous system might effectively be delivered. (Journal of Neuroscience, Sept. 14, 2011.)

The researchers found that adenosine, a molecule produced by the body, can modulate the entry of large molecules into the brain. For the first time, the researchers discovered that when adenosine receptors are activated on cells that comprise the blood-brain barrier, a gateway into the blood-brain barrier can be established. Although the study was done on mice, the researchers have also found adenosine receptors on these same cells in humans. They also discovered that an existing FDA-approved drug called Lexiscan, an adenosine-based drug used in heart imaging in very ill patients, can also briefly open the gateway across the blood-brain barrier. The blood-brain barrier is composed of the specialized cells that make up the brain's blood vessels. It selectively prevents substances from entering the blood and brain, only allowing such essential molecules as amino acids, oxygen, glucose and water through. The barrier is so restrictive that researchers couldn't find a way to deliver drugs to the brain – until now. "The biggest hurdle for every neurological disease is that we are unable to treat these diseases because we cannot deliver drugs into the brain," said Margaret Bynoe, associate professor of immunology at Cornell's College of Veterinary Medicine and senior author of a paper appearing Sept. 14 in the Journal of Neuroscience. Aaron Carman, a former postdoctoral associate in Bynoe's lab, is the paper's lead author. The study was funded by the National Institutes of Health. "Big pharmaceutical companies have been trying for 100 years to find out how to traverse the blood-brain barrier and still keep patients alive," said Bynoe, who with colleagues have patented the findings and have started a company, Adenios Inc., which will be involved in drug testing and preclinical trials.

Researchers have tried to deliver drugs to the brain by modifying them so they would bind to receptors and "piggyback" onto other molecules to get across the barrier, but so far, this modification process leads to lost drug efficacy, Bynoe said. "Utilizing adenosine receptors seems to be a more generalized gateway across the barrier," she added. "We are capitalizing on that mechanism to open and close the gateway when we want to." In the paper, the researchers describe successfully transporting such macromolecules as large dextrans and antibodies into the brain. "We wanted to see the extent to which we could get large molecules in and whether there was a restriction on size," Bynoe said. The researchers also successfully delivered an anti-beta amyloid antibody across the blood-brain barrier and observed it binding to beta-amyloid plaques that cause Alzheimer's in a transgenic mouse model. Similar work has been initiated for treating multiple sclerosis, where researchers hope to tighten the barrier rather than open it, to prevent destructive immune cells from entering and causing disease. Although there are many known antagonists (drugs or proteins that specifically block signaling) for adenosine receptors in mice, future work will try to identify such drugs for humans. The researchers also plan to explore delivering brain cancer drugs and better understand the physiology behind how adenosine receptors modulate the blood-brain barrier.

Read more at: http://medicalxpress.com/news/2011-09-breaching-blood-brain-barrier-year-old-puzzle.html#jCp

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.02.2013 - 22:37:35

Dr Richard Horowitz on perehtynyt borrelioosin ja lisäinfektioiden hoitoon ja tutkimukseen. Hän puhuu MCIDS:stä, Multiple Chronic Infectious Disease Syndromasta.

http://www.infectiologie.com/site/medias/JNI/JNI11/CT/JNI2011-Lyme-horowitz.pdf

Potilailla on yleensä moninaisia vaivoja:
1. Infections:
a)Bacterial: Lyme disease, Ehrlichiosis, Bartonella, Mycoplasma, Chlamydia, Rickettsia, Typhus, Tularemia, Q-Fever, Tick paralysis
b) Parasites: Babesiosis and other piroplasms, filiariasis, amebiasis, giardiasis…
c) Viruses: EBV, HHV-6, HHV-8, CMV, St Louis Encephalitis, W Nile, Powassan encephalitis and other viral
encephalopathies, ?XMRV virus
d) Candida and other fungi
2. Immune dysfunction: ANA+, RF+ ↑ HLA DR-4
3. Inflammation: ↑ IL-1, IL-6, TNF-α→ “Sickness syndrome”
4. Toxicity: Heavy Metals, Mold, and Neurotoxins
5. Allergies
6. Nutritional & Metabolic abnormalities
7. Mitochondrial dysfunction
8. Psychological disorders
9. Endocrine disorders (and nutritional deficiencies)
10. Sleep disorders
11. Autonomic nervous system dysfunction
12 Gastrointestinal disorders
13. Elevated LFT’s
14. Drug Use/Addiction
15. Need for Physical Therapy

http://www.youtube.com/watch?v=dQnlnbbON_8

Babesioosista ja muista bakteeri-infektioista: http://www.poughkeepsiejournal.com/VideoNetwork/2020635580001/FULL-VIDEO-Babesiosis-discussion-with-Dr-Horowitz?nclick_check=1

Suomessa babesioosia ei tutkita, joten sitä ei esiinny, ja koska sitä ei esiinny, sitä ei tutkita. Babesioosia esiintyy muualla Euroopassa ja tunnen useita babesioota sairastavia Suomessa (tutkittu ja diagnosoitu ulkomailla).



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.02.2013 - 21:00:21

Lisää MMP-9:stä ja MMP-8:sta suomalaisessa tutkimuksessa kroonisesta borrelioosista. Tutkimuksessa käytetään inhibiittorina doksisykliiniä, joskin minosykliini käy myös, korkeiden MMP-arvojen laskemiseen:

Serum Matrix Metalloproteinase-8 and -9 Levels in Disseminated Lyme Borreliosis with Special Reference to Arthritis

http://ccaasmag.org/bio_2012/vol2/Sorsa_DLB.pdf

We demonstrated that serum MMP-8 and MMP-9 levels were significantly higher at study entry than at 1 year follow-up among disseminated LB patients (n= 110). In contrast, serum MPO and HNE levels of the disseminated LB patients at study entry when compared to those at 1 year follow-up showed no statistical significant differences. These findings suggest that excessive upregulation of both MMP-8 and MMP-9 in serum of disseminated LB patients before antibiotic therapy contributes to host inflammatory response indicating their important role in the pathogenesis of disseminated LB. We further found that among LA patients serum MMP-8 levels decreased significantly when compared the serum MMP-8 level of the patients at study entry to those at 1 year follow-up. Additionally serum MMP-8 levels were significantly higher after antibiotic treatment at 1 year follow-up among those patients who had poor response to given betalactam antibiotic treatment than among those patients who had good response and were totally recovered at 1 year follow-up. The present findings demonstrating the upregulation of serum MMP-8 levels among betalactam antibiotic resistant patients is in agreement with and further extend previous results by Lin and co-workers[7] demonstrating that in antibiotic treatment resistant LA patients the synovial fluid MMP-8 levels were significantly higher than among patients with good response. We also found that serum MMP-9 levels of LA patients decreased, but not statistically significantly when compared the levels at study entry to those at 1 year follow-up. The results of this work showing that up-regulation of MMP-8 is associated with poor outcome, suggest that inflammation persists in disseminated LB patients who are not fully recovered after betalactam antibiotics.
There is no internationally accepted way to treat those disseminated LB patients, who have persisting symptoms after antibiotic treatment[8-10]. In a Finnish multicenter, prospective study regarding the treatment of disseminated LB it was found that by using betalactam antibiotics, the cure rate was quite high, but there still were patients, who were not totally recovered at 1 year follow-up[12]. The results of the present work showing that among these patients suffering from persistent joint symptoms after betalactam antibiotic treatment high serum MMP-8 was associated with poor outcome suggest that the treatment of the patients having persisting symptoms after betalactam antibiotics should include doxycycline as an MMP-8 inhibitor. It is likely that due to rebound effect a short one week course will not be sufficient[21], but instead a longer treatment with doxycycline would be needed[15,18,19]. In addition, the results of this work suggest that serum MMP-8 assessment could possibly be useful in the monitoring of the effectiveness of the therapy[22]. One possibility could also be that by using MMP-8 measurement, the subgroup of the patients, who need for prolonged doxycycline therapy after, for example intravenous ceftriaxone, could be found. However, more studies concerning this topic are needed. Chlamydia arthritis, one form of reactive arthritis, is like Lyme arthritis an infectious associated arthritis, where some patients suffer from chronic sequelae. In a study by Lauhio and co-workers[23]it was shown that three month lymecycline has afavorable effect in acute chlamydia arthritis and recently it was demonstrated that six months combination therapy of two antibiotics is efficient in chronic chlamydia arthritis[24]. Single antibiotic therapy with doxycycline in disseminated LB has shown relatively low cure rates, as has been shown in studies by Borg and colleagues[25], Orgnic and co-workers[26]as well as by Ljøstad and co-workers[27].Thus, one possibility to achieve better cure rates could be to use a combination therapy of doxycycline and intravenous ceftriaxone, at least to the subgroup of patients with persistent symptoms after ceftriaxone treatment. One possibility to improve the outcome of disseminated LB could be to use combination therapy for those patients, who are not fully recovered after ceftriaxone treatment. In the future, instead of doxycycline, chemically modified tetracyclines (CMTs) with MMP-8 inhibitory capacity could also be one possibility in combination with ceftriaxone[22]. More clinical studies concerning the combination therapy including MMP-8 inhibitor are needed to get better treatment strategies for disseminated LB. In addition, Yrjänäinen and co-workers [28]has shown that Borrelia burgdorferi-infected and ceftriaxone-treated mice have viable spirochetes in their body, since immunosuppressive treatment allows B. burgdorferi to be detected by culture. In a subsequent study the niche of persisting B. burgdorferi in ceftriaxone-treated mice was obviously the joint or a tissue adjacent to the joint[29]. Also these recent animal model studies supports the view that a combination therapy could possibly lead to better outcome than single antibiotic therapy, at least to some subgroup of patients with disseminated LB.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.03.2013 - 11:33:07

Wrong immune response aids TB

http://www.bbc.co.uk/news/health-21619594

Some bacteria, including tuberculosis, are able to invade because the body launches the 'wrong' immune response, say researchers.

Instead of fighting off tuberculosis, people with a severe infection produce a protein which attacks viruses, the journal Science reports.

About 8.7 million people are infected with tuberculosis every year.

The findings may explain why viruses can make people more susceptible to bacterial infections.

*******
Further work showed the genes for interferon-beta - the virus-fighting protein - were more frequently expressed in the blood of tuberculosis patients with more severe disease.

In disguise

The researchers said in those with severe disease, the body was responding as if it was attacking a virus, enabling the bacteria to remain hidden and replicate unchallenged within cells.

Not only is interferon-beta an ineffective weapon against bacteria, it can block the action of interferon gamma - which is when bacteria can gain a foothold, the researchers said.

In the face of a real viral infection it may mean that the attention of the immune system is diverted letting a bacterial infection in.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.03.2013 - 23:01:20

Vanha tutkimus neurologeilta miten aivojen vähentynyt verenkierto parannettu borrelioosipotilailla:

Reversible cerebral hypoperfusion in Lyme encephalopathy.

http://www.ncbi.nlm.nih.gov/pubmed/9409364

Logigian EL, Johnson KA, Kijewski MF, Kaplan RF, Becker JA, Jones KJ, Garada BM, Holman BL, Steere AC.
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Cambridge, MA, USA.

Lyme encephalopathy (LE) presents with subtle neuropsychiatric symptoms months to years after onset of infection with Borrelia burgdorferi. Brain magnetic resonance images are usually normal. We asked whether quantitative single photon emission computed tomography (SPECT) is a useful method to diagnose LE, to measure the response to antibiotic therapy, and to determine its neuroanatomic basis. In 13 patients with objective evidence of LE, SPECT demonstrated reduced cerebral perfusion (mean perfusion defect index [PDI] = 255), particularly in frontal subcortical and cortical regions. Six months after treatment with 1 month of intravenous ceftriaxone, perfusion significantly improved in all 13 patients (mean PDI = 188). In nine patients with neuropsychiatric symptoms following Lyme disease, but without objective abnormalities (e.g., possible LE), perfusion was similar to that of the treated LE group (mean PDI = 198); six possible LE patients (67%) had already received ceftriaxone prior to our evaluation. Perfusion was significantly lower in patients with LE and possible LE than in 26 normal subjects (mean PDI = 136), but 4 normal subjects (15%) had low perfusion in the LE range. We conclude that LE patients have hypoperfusion of frontal subcortical and cortical structures that is partially reversed after ceftriaxone therapy. However, SPECT cannot be used alone to diagnose LE or determine the presence of active CNS infection.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.03.2013 - 11:03:27

Tri Garth Nicholsonin haastattelu koskien MS, FM, CFS tauteja:

http://www.youtube.com/watch?v=jpvLjJ4O7T8&feature=youtu.be

Published on Feb 23, 2013

Meet Kate, a 30 year old Physiotherapist and currently full time mother of two from Brisbane Qld Australia. Kate has M.S, CFS and Fibromyalgia amongst various other viral, fungal and infectious imbalances.

During this clip Kate chats to Californian Chief Research Officer and Founder of the Institute for Molecular Medicine, Prof. Garth Nicolson about multiple sclerosis, chronic fatigue, fibromyalgia, rheumatoid arthritis, autism and birth defects, diet, heavy metals and ways to recoup her depressed immune system.

Late 2011, Kate travelled with her 6 month year old together with her mum and Beyond the Bandaid founder Bec Mills to attend the Fibromyalgia Treatment and Learning Centre, Sacramento, California where she would consult with Rheumatologist Dr Michael Powell, for treatment planning.

During this 12 day trip, Kate was amongst the action, well placed and eager to chat to Prof. Garth Nicolson who drove 2 hours from Huntington Beach, California to meet with Bec for a 2 hour interview in their L.A hotel room. Kate and Prof Garth Nicolson explore a number of questions related to infections ideology, MS medications, how to recoup a depressed immune system, how to protect her children from becoming sick with the same illnesses, and what she can do herself to restore mitochondrial damage and other symptoms.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.03.2013 - 11:44:59

Antibiootit ja MS-lääkkeet:
http://www.mymsaa.org/drugs/summer-fall10/Tetracycline.php

Tetracycline Antibiotics

-    The tetracycline antibiotics, including minocycline and doxycycline, have immunomodulatory and neuroprotective activities. They appear to decrease the passage of leukocytes across the blood-brain barrier. An earlier trial of Copaxone plus minocycline showed favorable MRI data.

-    In a small trial in patients with RRMS, minocycline decreased gadolinium-enhancing activity by 50 percent over a period of six months. A subsequent 24-month trial showed a significant decrease in lesion activity and clinical status.

-   A Phase III trial that began in 2008 is studying the effect of 100 mg of oral minocycline twice daily on the conversion of CIS to a diagnosis of MS at six and 24 months.

-    A small Phase IIa study with 45 patients will study minocycline in acute optic neuritis (ON). It began in February 2010, and is scheduled for completion in February 2013. The primary aim of this open-label pilot trial is to estimate the treatment effect of 100 mg of oral minocycline twice daily for 90 days, initiated within 30 days of onset of ON. The study will evaluate the effects on functional and structural optic nerve recovery compared to no treatment. The primary outcome measure will be the degree of optic nerve recovery, as measured by the retinal nerve fiber thickness.

-   A small Phase IV study combining doxycycline with Avonex demonstrated a statistically significant reduction of gadolinium-enhancing lesions compared with Avonex alone. A larger trial is needed to confirm these results.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.03.2013 - 12:16:51

FMT (Fecal Microbiota Transplantation) parantanut kolme MS potilasta:

http://www.cdd.com.au/pdf/publications/All%20Publications/2011-Fecal%20microbiota%20transplantation%20%28FMT%29%20in%20Multiple%20Sclerosis%20%28MS%29,%20TJ%20Borody,%20SM%20Leis,%20JL%20Campbell,%20M%20Torres,%20A%20Nowak,%20American%20College%20of%20Gastroenterology%20p111.pdf

TITLE: Fecal Microbiota Transplantation (FMT) in Multiple Sclerosis (MS)
AUTHORS/INSTITUTIONS:  T.J. Borody, S.M. Leis, J.L. Campbell, M. Torres, A. Nowak, , Centre for Digestive Diseases, Five Dock, New South Wales, AUSTRALIA;
ABSTRACT BODY:
Purpose: Recent evidence implicates the GI microbiota in the progression of neurological diseases such as
Parkinsons Disease 1, Multiple Sclerosis and Myasthenia Gravis
2. We report three patients with MS diagnoses who achieved durable symptom reversal with FMT for constipation.
Methods: Case study observations on three MS cases

Results: Case 1: A 30 yr old male with constipation, vertigo and impaired concentration and a concomitant
history of MS and trigeminal neuralgia. Neurologica l symptoms included severe leg weakness and he
required a wheelchair and an indwelling urinary catheter. Previous failed treatments included Mexiletine,
Tryptanol and β-interferon. The patient underwent 5 FMT infusions for his constipation, with its complete
resolution. Interestingly his MS also progressively improved, regaining the ability to walk and facilitating the removal of his catheter. Initially seen as a ‘remission’, the patient remains well 15 yrs post-FMT without relapse.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.03.2013 - 20:56:53

Kirjoitin aikaisemmin Dr Horowitzista ja multiple Chronic Infectious Disease Syndromasta. Tässä on käytännöllisiä ohjeita eri kohtien parantamiseen:

http://www.dailystrength.org/c/Lyme_Disease/forum/10947611-dr-richard-horowitz-md

"Dr. Richard Horowitz, MD, in Hyde Park, New York, has treated over 10,000 Lyme disease patients.
I listened to Dr. Horowitz speak at a LIA webinar on April 18th and if you read my blog post from that day, you'll notice that I briefly mention Dr. Horowitz' approach to Lyme disease, which includes addressing what he calls the "three I's" of illness: Infections, Immune Issues and Inflammation.

...

First, it is important to treat for infections,and not just the commonly known co-infections of Lyme disease, such as babesia, borrelia, and bartonella. Think categories and think big here! A multi-bug protocol involves treating: 1) Bacteria, from such diverse agents such as Q-fever (yup, I bet you didn't think of that one, did you?), 2) Parasites, including multiple strains of babesia.  As another rabbit trail (because I just can't help but hop from subject to subject), babesia patients, according to Horowitz, are four times sicker than those with just a borrelia infection. Not that I know of any lucky Joe Shmoe who has nothing more than a simple borrelia infection! 3). Viruses. Herpes-6 is a popular one found in Lyme patients, and anti-virals are not very effective against it. It is found to cause chronic fatigue; hence, treating it is vital for resolution of symptoms. 4) Candida. Take it for granted that if you have immune dysfunction, candida is going to be an issue. 5) Mold and fungus. These pernicious infections can be a big deal. Mycotoxins (from mold) can cause just as many symptoms as borrelia and other co-infections. Getting rid of them is important.

According to Dr. Horowitz, the most problematic, or most difficult, infections to eradicate include: bartonella, mycoplasma, chlamydia, rocky mountain spotted fever, typhus, tularema, and q-fever. (And, as Lyme disease sufferers, we are likely to have an assortment of these, as well as others). The difficulty in their eradication lies in the fact that all of the aforementioned are intracellular organisms; that is, they hide inside of human cells. I infer from this information that one of two things then happens; either the body attacks its own cells in an attempt to get the bugs, thereby creating auto-immunity in the body, or/and the bugs remain protected from certain treatments because the cell acts as a safe, comfy fortress for them to hide from the big, bad immune system. Also, not all antibiotics can reach organisms inside the cells, therefore multiple interventions are required to get rid of the ones that find refuge here.

For treatment of infections, Dr. Horowitz combines antibiotics with herbal protocol. I won't mention specifics of these protocol in this post for the sake of space and your sanity, but suffice it to say he believes that incorporating herbs such as smilax (sasaparilla), andrographis, stephania root and japanese knotweed into an antibiotic protocol can decrease a patient's possibilities for relapse. Not only do herbs fight infection, they also decrease inflammation and increase immune function.

Which brings me to the second "I": Inflammation, which, according to Horowitz, causes free radicals and oxidative stress that damage cell membranes, mitochondria, and nerve cells. Pro-inflammatory cytokines also create symptoms through other mechanisms. In addition to antioxidants, such as fruits and vegetables, magnesium, zinc, omega-3 fatty acids and CO-Q10 (see my post on April 18th), Dr. Horowitz advocates low dose Naltrexone (one of the new buzz drugs of 2008) to modulate cytokine response, and glutathione for "pulling" cytokines out. Glutathione, by itself and when taken daily, improves Dr. Horowitz's patients' symptoms by an average of 20%. That is significant.

Treating the third "I", Immune Issues, is just as important as dealing with inflammation and infections. It is, remember, your body that heals you; the drugs don't do it. They can only help. Thus, strengthening the immune system is paramount for healing. This is accomplished through multiple interventions, which also overlap and assist with the second aspect of healing--treating inflammation, (as inflammation is part of immune system response).

We all know that the infectious agents of Lyme disease are masters at making a mess of the immune system. Borrelia suppresses NK cell production; neurotoxins damage nerve and other types of cells; auto-immunity results from antibodies that are produced to infections that cross-react with our own tissue antigens, and the cumulative effects of environmental toxins and infections results in the destruction of cells, including those of the immune system. ..

A multi-faceted approach to strengthening the immune system includes:

1)Detoxifying the body, which includes the following components:
a) Ensuring that the body is well-hydrated
b) Loading up on antioxidants, through a healthy diet and with the help of alpha-lipoic acid
c) Supporting the liver with glutathione and glutathione precursors such as N-acetyl-cysteine, as well as B-vitamins (There are a multitude of ways to support the liver; however, I am mentioning only a few that Dr. Horowitz noted in his presentation)
d) Optimizing mitochondrial function (Where energy is made in the cell) with products such as CO-Q10, NT Factor, and NADH)
e) Minimizing toxic exposures by eating a "clean" diet, high in organic protein and vegetables; living in a clean-air environment, and so on.
f) Optimizing bowel health, with probiotics, fiber, and colon cleanses
g) Assisting and balancing bio-transformation with NAC, glycinate and B-vitamins

Dealing with heavy metal toxicity is likewise important. For this, Dr. Horowitz uses 100-200 mg of DMSA and a product called Algas (10 drops), along with split-cell chlorella and 600 mg NAC. Also DMPS, EDTA, and Med Caps DPO (which contains B-vitamins, NAC and alpha-lipoic acid)
..


2) Healing allergies, by avoiding common food allergens such as wheat, dairy, corn, nuts, and shellfish. (Indeed, you are lucky if you are able to incorporate even one of the above into your diet. Many Lyme disease sufferers cannot have ANY of these. And that is my opinion, not that of Dr. Horowitz). Also, allergies are often related to candida and leaky gut syndrome, so healing the gut can often alleviate allergy problems. Enzyme therapy and NAET (an allergy technique) are likewise beneficial.

3) Treating nutritional and enzyme deficiencies, with essential vitamins, minerals, fatty and amino acids. In my humble opinion, nutrient deficiencies in Lyme disease sufferers are so severe that taking supplements is necessary, in addition to eating a balanced, healthy diet which includes protein, fats and plenty of low-glycemic vegetables.

4) As mitochondrial membranes are particularly susceptible to free radical damage, supporting energy production with CO-Q10, NADH and L-carnitine can also give power to the immune system.

5)Dealing with the psychological factors of Lyme disease. Dr. Horowitz notes that many patients with chronic Lyme disease have a history of depression, anxiety, OCD, post-traumatic stress syndrome and abuse. What's more (and how lovely), Lyme can cause previous psychological patterns to intensify, or cause new ones to emerge. I definitely found this to be true in my own experience with Lyme disease. Dr. Horowitz suggests medication, stress reduction techniques such as Tai Chi or yoga, calming herbs and Journey work (Brandon Bays) as protocol for treating this aspect of illness.

6)Treating endocrine abnormalities. Lyme affects the HPA, or hypothalamus-pituitary-adrenal axis in profound ways, and supporting it with hormones and nutrients is vital for recovery. I was not surprised when Dr. Horowitz confirmed a suspicion that I have always held; that healing from Lyme disease cannot happen if you have adrenal insufficiency. According to Horowitz (and I concur with his opinion) adrenal insufficiency in Lyme can be caused by any form of chronic stress, whether physical, emotional, psychological, environmental or as a result of infectious agents. Getting a saliva cortisol test through Aeron, Metametrix, Genova or Diagnostek is one reliable way to ascertain adrenal fatigue. A complete thyroid panel is also necessary, as the thyroid and adrenals work in concert with one another, and Lyme affects thyroid function as well. Blood tests are acceptable for thyroid testing, although Dr. Horowitz notes that the "normal" ranges for results on blood tests may not be valid indicators of thyroid function. As with adrenal cortisol tests, often, patients must have hormone levels that fall within the higher range of "normal" in order to see clinical improvement.

7) Fixing sleep disorders. If you don't sleep, your body won't re-generate and heal. Plain and simple. There's no way out of the Lyme labyrinth if you don't get restorative sleep, because a lack thereof correlates directly with impaired immune function. Dr. Horowitz suggests Lyrica, trazodone, gabitril, seroquel and Xyrem as medications that will encourage deeper stages of sleep.  In any case, medications can help when all else fails. Dr. Horowitz also advocates balancing neurotransmitters with 5-HTP and other interventions to aid with sleep.

8) Healing autonomic nervous system dysfunction. This also relates to treating endocrine abnormalities. Taking salt (particularly sea salt), at a minimum of 3-4 grams per day is important. Taking Florinef (for aldosterone deficiency) and Cortef (for cortisol deficiency) may also be necessary.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.03.2013 - 21:01:18

Jatkuu:

9) Healing Gastrointestinal disorders. You want to know if you have leaky gut? Avoid gluten products, and see how you feel. When your gut "leaks", gliadin, the protein found in gluten, gets into the bloodstream, causing inflammation. You don't feel good, and this is a great indication that it's time to throw that croissant out the window. Other indications of leaky gut and hence malabsorption, according to Horowitz, include lab results that show low levels of calcium, magnesium, B-12, iron, potassium, and albumin. Other tests such as Anti-gliadin AB and TTG can also be helpful.



10) Dealing with elevated liver enzymes.
Most Lyme patients, at some stage during illness, have elevated liver enzymes. Well, are you surprised? The liver has a lot of work to do getting borrelia and associated gunk out of the body, and thanks to Leaky Gut, it doesn't have the tools it needs to do its job properly. Dr. Horowitz recommends milk thistle, Hepa #2 (a traditional chinese medicine remedy) NAC, (n-acetyl cysteine) and alpha lipoic acid for improving liver function.


11) Conditioning the body with exercise.
According to Dr. Horowitz, patients need to be on a regular exercise program, as soon as their physical condition permits. But start slow!



12)Dealing with issues of drug use and addiction.

No, the doc isn't talking about crack here, but rather the fact that narcotics, while they may help patients who have severe pain, when taken too often, also interfere with regenerative sleep. Rebound pain and headaches often result which then become part of a chronic symptom complex that becomes difficult to treat. He advises patients trapped in this cycle to consider a pain management specialist and detoxification program.


Vaikka ohjeet ovat borrelioosipotilaalle, on huomattavaa miten paljon asioita liittyy myös MS epävirallisiin, luonnonlääke, vitamiini ja hivenaine hoitoihin. Samat ympyrät...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.03.2013 - 22:12:25

Kirjoitin aikaisemmin veriaivonesteen läpäisevistä antibiooteista. Tässä enemmän mahdollisuuksia, kirjoittajana borrelioosiin perehtynyt lääkäri:

http://lymemd.blogspot.fi/search?updated-min=2013-01-01T00:00:00-08:00&updated-max=2014-01-01T00:00:00-08:00&max-results=11

Blood brain barrier

A lot of patients are concerned about the blood brain barrier (BBB). They want to know which antibiotics pass through it and/or if only intravenous antibiotics are able to traverse it.

Well then, what is the BBB? It is a diffusion barrier created by special features of small blood vessels leading to the brain. The lining of these vessels, the endothelium, contains unique cellular elements. Tight junctions in the endothelium (inside walls of blood vessels) are made up of a number of factors including "astrocyte end-feet." Astrocytes are supporting cells found in the brain. Most importantly, the BBB keeps out most blood borne substances including antibodies. Antibiotics that cross the BBB tend to have certain physical characteristics including: small molecular size, being lipophilic, binding to fatty molecules on cell membranes, low plasma protein binding and other specialized characteristics.

One of the best drugs is the original, used to syphilis, penicillin. Penicillin derivatives like amoxicillin are also effective. Cephalosporins do not do as good a job; there is some penetration. Then for brain penetration amoxicillin is a better choice than the popular Ceftin and Omnicef. Quinolones do an excellent job crossing the BBB (Levaquin, Cipro and others). Tetracylines are at the top of the list, especially doxycycline. Macrolides, (Biaxin, Zithromax) do a poor job because of their size. Flagyl and Tindamax,which are small and lipophilic, do a great job of passing through the BBB.  Rifamycins (Rifampin) are large and penetrates poorly into the brain. Sulfonomides and Trimethoprim, the ingredients in Bactrim, fulfil the right criteria and pass well through the BBB. This is by no means a comprehensive list of all antibiotics which has been used for Lyme disease.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.04.2013 - 15:35:12

Dr Richie Shoemaker puhuu biomyrkyistä, ennen kaikkea homeesta, vähän samaan tyyliin kuin Dr Horowitz:

http://www.survivingmold.com/diagnosis

What Is Mold Illness?

Biotoxin Illness - World Health Organization
Mold illness is not an allergy.  It is inflammation within the body which is caused by an immune system that has gone haywire.  The term "mold illness" is a subcategory of biotoxin illness, called Chronic Inflammatory Response Syndrome (CIRS).  The proper definition of CIRS is:

an acute and chronic, systemic inflammatory response syndrome acquired following exposure to the interior environment of a water-damaged building with resident toxigenic organisms, including, but not limited to fungi, bacteria, actinomycetes and mycobacteria as well as inflammagens such as endotoxins, beta glucans, hemolysins, proteinases, mannans, c-type lectins and possibly spirocyclic drimanes, plus volatile organic compounds.

Symptoms

If you are experiencing several of these symptoms, you could be suffering from mold illness.  Take the Online Screening Test to determine your probability of having this illness.

♦Fatigue ♦Weakness ♦Aches ♦Muscle Cramps ♦Unusual Pain ♦Ice Pick Pain ♦Headache ♦Light Sensitivity ♦Red Eyes ♦Blurred Vision ♦Tearing ♦Sinus Problems ♦Cough ♦Shortness of Breath ♦Abdominal Pain ♦Diarrhea ♦Joint Pain ♦Morning Stiffness ♦Memory Issues ♦Focus/Concentration Issues ♦Word Recollection Issues ♦Decreased Learning of New Knowledge ♦Confusion ♦Disorientation ♦Skin Sensitivity ♦Mood Swings ♦Appetite Swings ♦Sweats (especially night sweats) ♦Temperature Regulation or Dysregulation Problems ♦Excessive Thirst ♦Increased Urination ♦Static Shocks ♦Numbness ♦Tingling ♦Vertigo ♦Metallic Taste ♦Tremors

This illness affects multiple systems in the body, which causes the patient to exhibit multiple symptoms.

Shoemakerin mukaan kaikista maailman ihmisistä 24% on sellaisia, jotka eivät pysty käsittelemääm tai tuhoamaan myrkkyjä ja niin eivät parane infektioista tai ympäristömyrkyistä, kuten homeesta. Sivuilla oleva video on melkein 1,5 tuntia, mutta mielenkiintoinen.

Sivuilla on myös ohjeet miten poistaa kertyneitä myrkkyjä kehosta. http://www.survivingmold.com/treatment


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.04.2013 - 17:02:04

Henkilökohtainen tilannetiedoitus: vuoden antibioottikuurin jälkeen yksi kolmesta infektiosta kukistettu. Saksassa tutkitusta verinäytteestä käy ilmi, että mykoplasma pneumoniaen vasta-aineet ovat normaalit. Seuraava testi taas kolmen kuukauden kuluttua, ja katsotaan sitten miten borrelioosi ja ehrlichioosi voivat.
Liikkumisvaikeudet jatkuvat, mutta fatiikki ja aivosumu ovat väistyneet. Energiataso on parempi, muttei vielä normaalilla tasolla. Että näin eteenpäin..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.04.2013 - 20:36:16

En ymmärrä geeneistä mitään, mutta luin uudelleen Dr Shoemakerin nettisivuja,
http://www.survivingmold.com/diagnosis/lab-tests, jossa on geenitaulukko:


HLA DR - Your Genes

Human Leukocyte Antigens (HLAs), are found on the surface of nearly every cell in the human body.  They help the immune system tell the difference between body tissue and foreign substances.

The immune response genes are found on chromosome six.  Patients could have two alleles, copies of genes (for each gene, one allele is inherited from a person's father, and the other is inherited from a person's mother), out of approximately 10 possible, as part of their genotype.  Based on Dr. Shoemaker's data, in normal populations compared to international registries of gene frequencies of HLA DR, we know the frequency of mold illness-susceptible patients approximates 24% of the normally distributed population.  Almost a quarter of the normal population is genetically susceptible to chronic mold illness.  Three quarters isn't.

                              DRB1       DQ       DRB3       DRB4       DRB5
Multisusceptible       4                3                         53      
                             11/12       3          52B              
                               14                5          53B              
Mold Susceptible       7              2/3                          53      
                               13                6           52A, B, C              
                                17                2            52A              
                                18*       4            52A              
                                       
Borrelia                   15                6                                        51
                                16                5                                         51
Dinoflagellates       4              7/8                             53      
MARCoNS               11                7              52B              
No rec.significance       8              3, 4, 6                      
Low-risk Mold                 7               9                               53      
                                12                 7                52B              
                                 9                 9                               53      

Rivit meni sekaisin, mutta tärkein on borrelioosin geenit, HLA DR ja DQ,  chromosomi numero 6, MHC , luokka II proteiinin HLA DRB1 15 ja HLA DQ6. En ole löytänyt samanlaista taulukkoa MS- taudin geeneistä, mutta http://www.ndcn.ox.ac.uk/publications/34025 mukaan HLA DRB1 15 lisää MS-riskiä pohjois eurooppalaisissa. Wikipedian mukaan toinen MS-taudin riskiä lisäävistä geeneistä on HLA DQ6. Eli samat geenit näyttävät kokemattoman silmiin lisäävän MS taudin ja kroonisen borrelioosin riskiä.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.05.2013 - 11:53:30

Dr Garth Nicholson tutkii neurogeneratiivisia sairauksia ja niihin liittyviä infektioita. Tässä hän puhuu lipid replacement terapiasta ja mitokondrioista:

http://www.youtube.com/watch?v=IKp4xCbNhag (osa 1)

Origin of chronic neurogenerative diseases  noin 2:00 minuutin kohdalla, chronic diseases 3:45 kohdalla, chronic infections in neurogenerative diseases 4:55 kohdalla (MS-taudissa mycoplasma, borrelia, HHV-6 virus, keuhkoklamydia ja muut).  Kaikille kroonisille sairauksille on yhteistä krooniset infektiot. Mielenkiintoista on sekin, että hänen tutkimuksissaan CFS (Chronic Fatigue Syndrome)  potilaat olivat borrelia potilaita, eli hänen mielestään CFS on borrelioosi.

http://www.youtube.com/watch?v=BhdcR0VptWs (osa 2 puhuu NT Factorin kliinisestä tutkimuksesta)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.06.2013 - 18:04:21

What Could Be a Primary Cause of Multiple Sclerosis: Is It an Autoimmunity Triggered by Chronic Protozoan Infection?
Marian Simka

http://www.ashdin.com/journals/JND/235688.aspx

Abstract

The generally accepted paradigm of multiple sclerosis is the autoimmune one; still, a body of evidence suggests that this disease may actually be triggered by an infectious factor. In this paper, it is hypothesized that multiple sclerosis may actually be a rare complication of a protozoan infection, which is usually asymptomatic but in some susceptible individuals is accompanied by autoimmune attack against the nervous tissue. If multiple sclerosis were actually caused by such an infection, then a microorganism responsible should exhibit several properties: it (i) is transmitted by an arthropod vector; (ii) is characterized by specific metabolism of the lipids; (iii) should be dependent on iron; (iv) should be associated with an autoimmune response of the host; and (v) should be susceptible to pharmaceutical agents used for the treatment of multiple sclerosis but not to the degree that would allow its eradication. A combination of these properties suggests a role of a blood-residing protozoan.

Kiitokset FB:n ryhmälle tästä artikkelista. Ilmoitin prof. Simkalle viime vuonna, että minulta oli todettu useita infektioita, joten laskimolaajennuksen osittainen epäonnistuminen ei ollut ihme.  Enkä siten ollut menossa jälkitarkastuksiin Puolaan. Artikkeli on mielenkiintoinen, ennen kaikkea siksi että hänen mielestään babesioosi saattaa olla MS:ää aiheuttava tekijä. Enemmän babesioosista helmikuussa liittämästäni Dr Horowitzin luennosta. Babesioosi pahentaa borrelioosia, ja on usein syynä siihen, ettei borrelioosista parane helposti. Babesioosi on vaikea todeta verikokeista, ja sitä on kymmeniä eri lajeja. Itsellänikin tulokset olivat rajalla, mutta minulla esiintyi kuumeilua, johon sain malarialääkityksen.  Se auttoi: ainakaan kuurin jälkeen ei ole esiintynyt selittämätöntä matalaa kuumeilua. Knock on wood..  Monet käyttävät myös luonnonlääkkeitä babesioosin hoidossa.
Babesioosi on paha alkueläin (protozoa), kuten Dr Horowitz kertoo, mutta en jaksa uskoa sen olevan ainut tekijä MS:n oireiden synnyssä. Ja vaikka Suomessa lääkärit väittävät toista, esiintyy sitä Suomessakin. Tunnen monia babesioosipotilaita, joilla on myös borrelioosi. Kuten minulla,  joillakin saataa olla myös MS-diagnoosi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.06.2013 - 20:58:04

Prof. Paul Ewaldin, University of Louisville, haastattelu:

http://www.peoplespharmacy.com/PP-906Germs.mp3


Prof. Ewald puhuu kroonisista sairauksista, jotka ovat  infektioiden aiheuttamia. Haastattelu kestää noin tunnin, ja on kuunneltavissa neljän viikon ajan eli heinäkuun alkupuolelle.  Jos ei jaksa kuunnella kaikkea, sitten ehkä seuravat kohdat: 6:50, 12:50, 15:50, 20:00 keuhkoklamydiasta, 43:40 MS:stä, jonka synnyssä keuhkoklamydia näyttelee jotain roolia, 51:00 EBV virus erilaisissa syövissä, kuten rintasyövässä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 08.07.2013 - 10:52:44

Huomaan, että olet käynyt paljon tutkimustietoa läpi. Itsestäni voin sanoa, että olen saanut ppms-diagnoosin vuonna 2007, jolloin testattiin borrelioosin mahdollisuus (kotoisilla testeillä). Sairaus eteni nopeasti ja tartuin ensimmäisenä LDN:ään, jota olen nyt syönyt n. kolme vuotta. Olen myös siihen tyytyväinen, joskin se on MS-taudin autoimmuuniteorian vastainen. Kuten varmaan tiedät se pyrkii normalisoimaan immuunijäjestemää. LDN:stä on tehty myös MS-potilailla ainakin kolme pientä tutkimusta, joista uusimpien absraktit löytyvät täältä.

Sharafaddinzadeh N, Moghtaderi A, Kashipazha D ym. The effect of low-dose naltrexone on quality of life of patients with multiple sclerosis: a randomized placebo-controlled trial. Mult Scler. 2010 Aug;16(8):964-9. PMID: 20534644

Cree BA, Kornyeyeva E, Goodin DS. Pilot trial of low-dose naltrexone and quality of life in multiple sclerosis. Ann Neurol. 2010 Aug;68(2):145-50.  PMID: 20695007

Tässä on myös lyhyt uutispätkä (vanha) LDN:stä

http://www.youtube.com/watch?feature=player_embedded&v=Kz52KK5IhOc

Olen myös käynyt läpi ns. Wheldonin antibioottikuurin (n. vuosi) ja yritin rikkoa ns. biofilmiä Boswellia kapseleilla ja viherminttutipoilla kuurin ajan, nyt syön jälkihoitoa kahden kuukauden välein. Miksikö? Koska kuten varsin hyvin tiedät testit eivät ole kovin aukottomia. Olen ikäni asunut ja työskennellyt etelä-suomen rannikolla. Borrelioosista ei puhuttu 60-, 70- 80-, 90-luvuilla, vasta 2000-luvulla alettiin puhua taudin mahdollisuudesta, vaikka bakteereja on punkeissa ollut jo dinosaurusten aikaan.

Tilanteeni on kuitenkin huomaavasti parempi, kuin noin kaksi vuotta sitten ja aion parantua kiusallanikin tästä "parantumattomasta" sairaudesta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.07.2013 - 18:54:15

Hei Äijä,

Kiva löytää "sukulaissielu", joka on haastanut diagnoosin ja lähtenyt etsimään parantumista tästä "parantumattomasta" sairaudesta. Olen myös ollut kiinnostunut LDN:sta, mutta lähdin antibioottien suuntaan, koska se nyt tuli ensin diagnoosien kautta. Ehkä myöhemmin, jos immuunijärjestelmä ei kohennu. Totuus on se, etten olisi näin hyvässä kunnossa, jos olisin totellut lääkäreitä ja ottanut erilaisia syöpälääkkeitä, jotka ehkä, mahdollisesti, epävarmasti voisivat hidastaa taudin kulkua. Matkaa on vielä, ja kerron kyllä miten tämä kokeiluni sujuu.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 16.07.2013 - 13:30:19

Tervehdys taas!
Syöpälääkkeitä, toisin sonoen solunsalpaajia on minullekin suositeltu, olotilaa kohentamaan. Olen kylläkin aina kieltäytynyt niistä, koska uskon niistä olevan pitkässä juoksussa enemmän haittaa, kuin hyötyä. LDN:stä sen verran vielä, että sain reseptin naltreksoniin tämän pienen tutkimuksen perusteella.
Gironi M, Martinelli-Boneschi F ym. A pilot trial of low-dose naltrexone in primary progressive multiple sclerosis. Mult Scler. 2008 Sep;14(8):1076-83. PMID: 18728058

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.07.2013 - 11:55:44

Aivoverenkierrosta ja borrelioosista:
Tämän 2003 julkaistun tutkimuksen mukaan kroonista borrelioosia sairastavat kärsivät heikentyneestä verenkierrosta aivoissa, joka vaikuttaa kognitiivisiin toimintoihin, jotka palautuvat antibiootti hoidolla.Selittäisikö tämä omat parantuneet kognitiiviset ongelmat...

Regional Cerebral Blood Flow and Cognitive Deficits in Chronic Lyme Disease

http://neuro.psychiatryonline.org/article.aspx?articleid=101812

This study examined brain functioning in patients with Lyme encephalopathy. Eleven patients underwent neuropsychological tests and Xenon133-regional cerebral blood flow (rCBF) studies, using an external detector system. Each rCBF scan was age- and sex-matched to two archival, normal controls. While few differences were noted on gray-matter flow indices (ISI, fg), Lyme patients demonstrated significant flow reductions in white matter index (k2) (p=.004), particularly in the posterior temporal and parietal lobes bilaterally (p=.003). Flow reductions in white matter areas were significantly associated with deficits in memory (r=.66, p=.027) and visuospatial organization (r=.62, p=.041). Results suggest that Lyme encephalopathy may be a disease primarily affecting the cerebral white matter.

................



What is striking in this study is the finding that there is an alteration of presumed white matter blood flow in the brains of patients who have chronic Lyme Disease and complain of cognitive deficits. Each of the 11 patients in our sample reported ongoing mild to severe cognitive problems that were confirmed on objective neuropsychological testing. As a group, when compared to published norms, the Lyme patients had significant deficits in verbal memory, which was demonstrated using both the Wechsler Memory Scale and the Buschke Selective Reminding Test. Memory deficits such as these are typically seen in samples of patients with Lyme encephalopathy.2,29

Lyme patients did not differ from controls on the standard, gray matter-weighted rCBF index, which is the ISI. However, when CBF was separated into faster-clearing and slower-clearing components, the patients showed abnormalities that were restricted to slower-clearing flows, reflecting diminished white matter perfusion.18 Therefore, Lyme-related perfusion deficits, which were evident in a large portion of posterior cortex, are more likely to affect white matter. This is one of the first studies to find differences that are restricted to slow-clearing flows. Compartment modeling has generally been used to characterize decrements in fast-clearing flow associated with gray matter degeneration.10,24 The k2 index can be unstable in low flow conditions,18 but findings with k2 were confirmed by results obtained with both fg and the wg ratio. If k2 were reduced by artifact, the fg would more than likely have been reduced as well; and the wg ratio would not have differed from that of controls. A noteworthy observation is that differences in wg in this small sample of Lyme patients appear to be more widespread than differences in k2. The k2 index tends to be less sensitive than other flow indices because it varies across a smaller range of values and may actually understate the level of deficit in white-matter flows that is suggested by the wg ratio. Further studies using three-dimensional tomographic imaging techniques are clearly needed in order to resolve this discrepancy, particularly because the resolution of these techniques is less than half that of the method used here.

Global reductions in k2 were significantly correlated with the magnitude of cognitive deficits in Lyme patients, specifically in memory (Buschke Total Recall and CLTR) and visuospatial organization (Block Design). An association was also found between left-sided temporal-parietal white matter flow and poorer Digit Symbol performance. These correlational analyses were limited by the small size of the patient sample and the unusual distribution of premorbid intelligence in this sample (highest estimated premorbid intelligence in those with worst perfusion measures). Further studies with larger samples are needed in order to delineate the association between perfusion abnormalities and cognitive impairment. Because our sample size was small, the likelihood of finding statistically significant group differences was reduced (a Type II error), the possibility that the sample was unusual increased (Type I error), and the generalizability of our findings is limited.

We are well aware of the complexity of the wg and k2 findings and the difficulty of their interpretation. While some k2 results may be due to "slippage" or other artifacts, constructing an artifactual explanation that would affect the patients and not the controls is difficult. The face validity of our results is supported by two additional factors. First, as reviewed below, the literature is consistent with a neuropathological process affecting predominantly white matter. Second, the significant correlations of k2 reductions with neuropsychological test performance indicate that our physiological observations are meaningfully related to disease severity.

A similar impression regarding white matter involvement was reached in the Logigian et al SPECT study.7 In their study, hypoperfusion of the subcortical basal ganglia and white matter was a common feature in 13 patients with Lyme encephalopathy. Given that B burgdorferi has been found to preferentially injure oligodendrocytes when rat brain has been cultured in vitro, white matter hypoperfusion might reflect injury to the oligodendrocyte resulting in a secondary deafferentation of the cortical structures. A postmortem case report of a man with rapidly progressive dementia after well-documented Lyme disease is consistent with a primarily subcortical localization for the damage that may occur in patients with Lyme encephalopathy. In this case report, neuropathology revealed severe subcortical neuronal loss, neuronophagia, and gliosis, primarily in the substantia nigra and the thalalmus; but only mild cortical pathology was observed.30

Myelinated tracts comprise nearly half of the volume of adult cerebral hemispheres, and they connect gray matter structures throughout the brain.31 Diffuse white matter pathology can disrupt these ubiquitous gray matter connections and could account for deficits in neurobehavioral functions that rely upon multiple networks of interconnected neurons. Such functions would include attention, memory, visuospatial ability, complex cognition, and emotional status. A variety of primarily cerebral white matter disorders are associated with neuropsychiatric disturbances, including multiple sclerosis, Binswanger’s disease, traumatic brain injury, acquired immune deficiency syndrome (AIDS) dementia complex, and normal pressure hydrocephalus. Impaired retrieval but preserved procedural memory and encoding are most characteristic of the dementia associated with white matter disease.31 Most studies that involve larger groups of patients with Lyme encephalopathy have identified deficits in consistent, long-term retrieval but not in actual storage or in procedural memory32—findings consistent with white matter involvement. White matter disease may have a greater potential for recovery than gray matter disease, perhaps because neuronal loss is less common. Spontaneous remission can occur in Multiple Sclerosis, and resolution of MRI white matter hyperintensities, after antibiotic treatment, has been observed in Lyme disease.33

In conclusion, this cerebral blood flow study using Xenon133 demonstrated that patients with persistent Lyme encephalopathy have areas of decreased perfusion that appear to affect primarily the cerebral white matter. This decreased perfusion is associated with cognitive impairment. Future functional imaging studies that use more sophisticated tools (such as PET and/or fMRI) to examine biological and behavioral challenges need to focus on delineating white matter abnormalities in order to better characterize the pathophysiology of Lyme encephalopathy.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 25.07.2013 - 10:11:18

Hei, oletko nähnyt tämän uutispätkän? Tämä antaa bakteeriteorialle MS-taudin aiheuttajana lisää vahvistusta. Tiesithän, että Wheldonin kuurin pitäisi tehota useihin mahdollisiin taudinaiheuttajiin. Neurologit tosin eivät hyväksy teoriaa. Video on tosin vanha ja Wheldonin teoria on sinulle jo ennestään tuttu, mutta kuitenkin!!!

http://www.youtube.com/watch?feature=player_detailpage&v=NjfVygIdnds

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Eikka Pvm 25.07.2013 - 11:18:06

Moi Käyn täällä harvoin mielipiteeni edellisestä videosta se on järkeen sopiva olen katsellut tuon viimmevuoden lopulla. Ja etsin lääkäriä jolla olisi rohkeutta määrätä antibiootia kyllä se sitten löytyikin (neljäs) Tiennari kauppasi azamun aloittamista uudeleeen olen käyttänyt 7 vuotta lopetin parivuotta sitten neuron toivomuksesta se oli hyvä rauohoitti tilanteen kun repiffit ja copat kokeiltu todettu kohdallani tehottomaksi :P  Olen syönyt antibioottia helmikuusta lähtien olen tyytyväinen lopetin kannapiksenkäytön parikk sitten kun säryt loppui Aloitin minocyslinen käytöllä lisäsin kk kulutua azithromycin ja kk kuluttua viikon kuureina metronidazol kolmen viikon tauolla. Olen tosi tyytyväinen omaan ratkaisuuni kokeilu jatkuu vielä vuoden silloin tiedän enemmän  8-) Kiitos ja hyväää kesää  ;)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 27.07.2013 - 10:53:37

Kuuri kannattaa ottaa, mitään ole menetettävänä. Minäkin olen syönyt ns. Wheldonin kuurin, enkä kadu. Lisäksi yritin rikkoa bakteerien suojakuorekseen muodostamia ns. biofilmejä mm. boswelliaöljy-kapseleilla. Niiden käyttöä perustelisin esim. liittenä olevan tutkimuksen absraktilla.

Lett Appl Microbiol. 2008 Nov;47(5):433-8. doi: 10.1111/j.1472-765X.2008.02469.x.

In vitro anti-biofilm activity of Boswellia spp. oleogum resin essential oils.

Schillaci D, Arizza V, Dayton T, Camarda L, Di Stefano V.


Source

Dipartimento di Chimica e Tecnologie Farmaceutiche, Università degli Studi di Palermo, Via Archirafi 32, Palermo, Italy. dschill@unipa.it


Abstract


AIMS:

To evaluate the anti-biofilm activity of the commercially available essential oils from two Boswellia species.

METHODS AND RESULTS:

The susceptibility of staphylococcal and Candida albicans biofilms was determined by methyltiazotetrazolium (MTT) staining. At concentrations ranging from 217.3 microg ml(-1) (25% v/v) to 6.8 microg ml(-1) (0.75% v/v), the essential oil of Boswellia papyrifera showed considerable activity against both Staphylococcus epidermidis DSM 3269 and Staphylococcus aureus ATCC 29213 biofilms. The anti-microbial efficacy of this oil against S. epidermidis RP62A biofilms was also tested using live/dead staining in combination with fluorescence microscopy, and we observed that the essential oil of B. papyrifera showed an evident anti-biofilm effect and a prevention of adhesion at sub-MIC concentrations. Boswellia rivae essential oil was very active against preformed C. albicans ATCC 10231 biofilms and inhibited the formation of C. albicans biofilms at a sub-MIC concentration.

CONCLUSIONS:

Essential oils of Boswellia spp. could effectively inhibit the growth of biofilms of medical relevance.

SIGNIFICANCE AND IMPACT OF THE STUDY:

Boswellia spp. essential oils represent an interesting source of anti-microbial agents in the development of new strategies to prevent and treat biofilms.


PMID: 19146534  [PubMed - indexed for MEDLINE]

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 28.07.2013 - 10:20:23

Tuli mieleen myös tällaiset tutkimukset, jotka liittyvät Borrelia burgdorferin aiheuttamaan kroonistuneeseen borrelioosiin (Lymen tauti) ja bakteerin karkotukseen. Cistus creticus L. (Cistaceae) tunnetaan myös nimeltä Rock rose, tutkimusten mukaan sen eteeriset öljyt auttavat bakteerin häädössä ja helpottavat kipuja. Täältä löytyy parin tutkimuksen abstraktit:

http://www.ncbi.nlm.nih.gov/pubmed/19542332

http://www.ncbi.nlm.nih.gov/pubmed/20432627

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.08.2013 - 15:07:55



Inflammation and central nervous system Lyme disease


http://www.lymenet.de/literatur/Fallon_Inflammation-and-central-nervous-system-Lyme-disease_2009.pdf

Tässä borrelioositutkimuksessa on paljon asiaa ja se puhuu myös MS:stä ja näiden kahden taudin samanlaisista oireista, mutta tässä valittuja paloja:

Encephalopathy refers to the mild to moderate cognitive deficits that the patients with neurologic Lyme disease may experience. Typically, patients experience problems with verbal fluency, short-term memory, and slower processing speed, often referring to their experience as one of brain fog (Kaplan and Jones-Woodward, 1997;Keilp et al., 2006
); these cognitive deficits may be accompanied by peripheral sensory findings on neurologic examination in up to 70% of patients and systemic symptoms such as fatigue, sleep disturbance, emotional lability, and depressed mood (Fallon et al., 2008)...
Myelitis, a less common manifestation of neuroborreliosis, refers to the inflammation of the parenchyma of the spinal cord that usually results in weakness, dysautonomia, and sensory loss(Hansen andLebech, 1992). Rarely, the parenchyma of the brain may be affected by vasculitic changes, resulting in seizures or stroke, or white matter inflammation, resulting in subacute MS-like manifestations. When the brain is involved, patients may experience a wide array of neurologic and neuropsychiatric symptoms...
In peripheral nervous system Lyme disease, patchy multifocal axon loss has been associated with epineural  perivascular inflammatory  infiltrates (Camponovo and Meier, 1986; Kindstrand et al., 2000).
Perivascular and vascular inflammatory processes may also be involved in CNS Lyme disease, with several case reports of stroke attributed to neurologic Lyme disease (Oksi et al., 1996; Keil et al.,1997; Topakian et al., 2007). CNS involvement from vascular or perivascular inflammation is understandable given that adherence of the spirochete to the endothelium lining of blood vessel walls leads other release of inflammatory mediators which in turn recruit leukocytes to the perivascular tissue; damage to the blood–brain barrier may then ensue with penetration of B.b. into the CNS(Garcia-Moncoet al.,1990;Sellati et al., 1995). The perivascular mononuclear cell infiltrates observed incerebral cortex infected with B.b. consist predominantly of T-helper cells (Meurersetal.,1990). The infiltrates are associated with mild, spongiform changes, a focal increase in microglial cells, as well as an infiltration of lymphocytes and plasma cells in the leptomeninges (Duray, 1989) .B.b .spirochetes are usually present in very low numbers in the CNS, and thus infection by itself does not likely cause much direct dysfunction or damage. However, B.b .may cause disease indirectly via the induction of inflammatory mediators, such as cytokines and chemokines. ....

The course of illness in many of these cases has been insidious, demonstrating vascular deficits months after initial infectious symptoms. ... Treatment with appropriate antibiotics invariably halted the disease progression with no recurrence of cerebral infarcts and most often led to a recuperation from deficits.
When Lyme disease affects the brain and spinal cord, it can look like multiple sclerosis (MS) (Ackermann et al., 1985). In 1988, Pachner described two patients with Lyme disease whose MS-like neurologic symptoms responded well to antibiotic therapy for Lyme disease (Pachner, 1988). The brain MRI among patients with Lyme disease may at times be suggestive of a demyelinating disease. A recent review (Hildenbrand et al., 2009) described two patients with Lyme disease who had neuroimaging findings partially suggestive of MS. The first patient, whose illness started with an EM rash and developed into meningitis, had a MRI which revealed callososeptal interface involvement remarkably similar to that in MS. Arcuate and confluent subcortical white matter involvement was also present, but without periventricular white matter disease. The patient's symptoms improved after IV ceftriaxone. The second patient was an elderly man with 2 years of cognitive decline, positive serologic and CSF titers with evidence of intrathecally produced B.b.- specific antibodies, and MRI-findings suggestive of a demyelinating disease —a dot –dash appearance of the callososeptal interface as well as a periventricular distribution of  involvement; this patient improved with iv ceftriaxone therapy. Resolving MS signs and symptoms however in the context of Lyme disease may simply reflect the waxing and waning course of
relapsing remitting MS and be unrelated to Lyme disease or it may reflect the improvement that would be expected after antibiotic therapy for Lyme disease. That B.b.may exacerbate MS or be a trigger for a MS-like inflammatory demyelinating disease of the CNS is not a surprising hypothesis, as infections with foreign agents are thought to either activate myelin-specific T cells by molecular mimicry, via cross-recognition of a bacterial and a myelin peptide, or by bystander
activation, via inflammatory cytokines (Martinet al., 2001).
As a result of B.b. infection, autoreactive antibodies may develop to myelin and myelin components (Suchanek et al., 1986; Garcia-Monco et al., 1988; Martin et al., 1988). Sequence homology has been noted between myelin basic protein and B.b. spirochetal flagellin (Weigelt et al.,1992) and there are studies demonstrating cross-reactive polyclonal and monoclonal antibodies which recognize flagellar antigenic determinants as well as epitopes on neural cells (Sigal and Tatum, 1988; Aberer et al., 1989; Fikrig et al., 1993). Such cross-reactivity could contribute to a chronic, relapsing-remitting, B. burgdorferi-triggered, immune-mediated neurological disorder similar to MS.....

Adherence of B.b. to brain capillaries would lead to focal inflammation at the interface of the basement membrane of the capillary endothelium and the adjacent astroglial membrane, resulting in capillary permeability changes. The spirochete may then cause direct damage to oligodendroglial cells, possibly resulting in demyelination (Baig et al., 1991).....Functional imaging studies, however, of patients with later stage neurologic Lyme disease using either Positron Emission Tomography (PET) or Single Photon Emission Computed Tomography (SPECT) scans have consistently demonstrated abnormalities suggestive of impaired blood flow and/or  metabolism, which may improve after antibiotic treatment (Fallon et al., 1997; Logigian et al., 1997).






Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 14.08.2013 - 08:48:29

Mielenkiintoista! Minulla alkoi sairaus yleisenä heikentymisenä, mihin liittyi myös lähimuistin heikentyminen. Toimintakyky myös heikkeni nopeasti, vaikka aivojen magneettikuvissa ei näkynyt ns. tulehduspesäkkeitä. Selkäytimessäkään ei ollut tulehduspesäkkeitä, "vain" joitain muutoksia selkäytimen poikkiprofiilissa ja likvor-näytteen arvo oli normaalin rajalla.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.09.2013 - 11:05:38

Rickettsia, bakteerin ja viruksen välimuoto, joka elää verisuonissa ja pystyy läpäisemään aivoveriesteen, on mahdollisesti  myös Chronic Fatigue Syndroman aiheuttaja. Dr Jadin mainitsee myös pararickettsiat, mykoplasmat ja klamydiat, jotka on nykyisin luokiteltu erilleen muista rickettsioista.

http://chronicfatiguesyndrome.co.za/what-is-csf

Sivulla on linkki Rickettsia Patients Bookletsiin, jossa enemmän tietoa, esim:

Rickettsiae are found in ticks, lice, fleas, mites, meat, milk, stools and dust. From the entry into the skin, the lungs, conjunctives, and the digestive mucosa, Rickettsiae spread via the bloodstream to infect vascular endothelium. These organisms grow and multiply by binary fission in and only in the cytoplasm of the host cell until the number of Rickettsiae is so great that the cell bursts, releasing hundreds of them. This invasion will impair or paralyse the vascular function, acting like a sponge between blood and organs and this vascular sponge will be the cause of memory loss, and/or muscular weakness and pain, and/or palpitations, and/or ulcers, depending on its localisation. These organisms will enlarge the endothelial cells of small vessels with partial or complete occlusion of the vascular lumen. They are known for long survival in various organs and lymphatic tissue.

****
According to which vessel they invade, they might display a constellation of symptoms; amazingly similar to those presented by the CFS group of patients that may be the origin of a flock of diseases such as:

-      CFS, Fibromyalgia, where they cause a cellular Anoxemia.
-      Cardio-vascular diseases, (valve replacements, infarctus, high blood pressure).
-      Neurological diseases (from acute encephalitis to Multiple Sclerosis (MS), epilepsy etc).
-      Abdominal diseases (appendicitis, cœliac disease and others).
-      Ocular diseases (uveitis, retinal angiopathy, optic nevritis sometimes a long time after a general infection).
-      Auto-Immune diseases (such as Rheumatoid Arthritis, Psoriatic Arthritis, Lupus, Sclerodermia, Sjögren Disease).

****
Rickettsiae release into the bloodstream 3 types of endotoxins, which have different effects. All or some of these endotoxins may produce symptoms. First, endocytokines that will cause inflammation and pain; second, neurocytokines that would be the origin of neurological symptoms such as demyelinisation found in MS patients, and psychological symptoms, such as depression, anxiety, troubled behaviour, sometime even causing attempted suicide and third, allergens producing allergies.

****
Furthermore, In the presence of CFS, Fibromyalgia, Auto-immune diseases, Heart diseases, MS, Depression, the screening for Rickettsial-like infections might be a valuable tool for treatment.

Sivuilla on myös Case Study, jossa mahdolliseksi MS-potilaaksi diagnosoitu pyörätuolissa oleva potilas sairastikin rickettsiaa ja alkoi parantua antibiooteilla.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 10.09.2013 - 21:16:11

Uusi tilannetiedotus: viimeisimpien Saksassa otettujen verikokeiden mukaan on myös borrelioosi kukistettu 1,5 vuoden antibioottikuurin jälkeen, mutta nyt tarkistettiin uudelleen myös ne infektiot, joiden tulokset olivat aiemmin rajalla.  Ja voittaja on keuhkoklamydia - se on nyt selvästi positiivinen, joten uudet antibiootit ja uusi kamppailu edessä. (En ole muuten sairastanut flunssaa tai muuta hengitysteiden tulehdusta ensimmäisten kokeiden jälkeen). Joulukuussa tarkistetaan kaikki uudelleen, myös ne infektiot jotka ovat jo ns. parantuneet..

Omituista on se, että immuunijärjestelmäni ei ole toiminut CD 57- testien mukaan ollenkaan, eli bakteeri-infektioiden ansiosta se on ollut toimintakyvytön. Ja silti minulle määrättiin immunosuppresiivisia lääkkeitä MS-tautiin. Ei niitä tarvita: krooninen borrelioosi (tai muu krooninen infektio) ajaa saman asian: T-solut ovat alhaisella tasolla ilman kallista lääkitystä..  Ongelmani on nyt se, miten saan immuunijärjestelmäni taas toimimaan normaalisti ilman antibiootteja, ja mitä seurauksia siitä olisi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.09.2013 - 15:58:45


Doctor, Do I have Lyme or MS

http://lymemd.blogspot.fi/2009/01/doctor-do-i-have-lyme-or-ms.html

Many patients are diagnosed with multiple sclerosis because they present to a neurologist with a variety of neurological symptoms and an abnormal MRI of the brain showing white matter lesions. A diagnosis cannot be made on the basis of an abnormal MRI. The findings in Lyme disease and MS can be identical. Medical diagnoses, including MS must be based on a history and clinical examination of the patient.

Most of the "MS" patients I see have a collection of symptoms which are not typically associated with MS. For example, MS patients do not have generalized muscle and joint pains. The two groups of patients usually have different histories and different physical.

MS is a disease of the brain, central nervous system and optic nerve. Neurological disease found in other areas is not compatible with MS. Many of the symptoms of MS and Lyme are the same: Optic neuritis, motor and sensory loss, vertigo, weakness, cognitive changes and many others. The history tends to be different however. Classically, MS is associated with discrete neurological events which tend to improve over time which is/are followed by additional discrete events involving different aspects of the central nervous system. Traditionally, MS is considered a relapsing and remitting disorder. Lyme tends to be a progressive disorder associated with a bewildering array of symptoms which tend to evolve in a progressive manner over time, without the relapsing and remitting feature.

With MS the neurological abnormalities are specifically associated with disease of the central nervous system. Lyme disease, on the other hand, tends to attack a wide spectrum of the nervous system. These diffuse, seemingly unrelated lesions are bewildering to neurologists, but par for the course for physicians accustomed to treating Lyme disease.

Lyme patients frequently have cranial nerve abnormalities of the type not seen in MS.
Lyme patients have upper motor neuron disease- as seen in MS, but may also have lower motor neuron disease, as seen with nerve entrapment syndromes or less frequently ALS. Lyme patients almost invariably have findings of sensory peripheral neuropathy, as seen with diabetes, hypothyroidism, Lyme disease and others. Sometimes neurologists perform EMG/NCV electrical studies to exclude the presence of peripheral neuropathy. These tests are relatively insensitive and are only revealing when the neuropathy is profound.

Despite proclamations made on the TV show House, there is no definitive diagnostic test for MS. It is a clinical diagnosis.

MS is an autoimmune disease. The neurological manifestations of Lyme disease are also for the most part mediated by autoimmune effects. The cause of MS is felt to be unknown. There are clear geographical differences in its prevalence. Many have felt that infections may be the root cause of the autoimmune process causing MS.

Dr. David Weldon in England, building on the work of Dr. Charles Stratton at Vanderbilt, has promoted the hypothesis that MS is causally related to infection with Chlamydia pneumonia. He has reported that his experimental therapy with antimicrobial therapy has shown benefits to patients with early MS.

The patient I refer to has had a protracted disabling illness. She has suffered with a progressive illness. She has had optic neuritis, vertigo, numbness and tingling, weakness, speech difficulties and progressive cognitive effects. She also lives in a wooded, Lyme endemic area and has suffered with severe muscle and joint pain. Her pain has required the use of narcotic pain killers. She had been treated for MS for several years, without much benefit. Her physical exam was not characteristic of MS. She has multiple neurological abnormalities which do not occur in MS. Recently, lab tests for Lyme and Babesia were positive. After several months of intensive antibiotic therapy she is now showing a great deal of improvement.

When I saw her last she was quite confused: "What do I have- is it Lyme or MS- I don't know what to tell my family?"

I stammered- and gave her a convoluted answer. I was soon clear that the technical details were contributing nothing to her understanding. Finally I said: "Just tell them that you have both."

Both Lyme and MS are associated with autoreactive T cells and autoantibodies directed against the lipoprotein coat of neurons called myelin. Both are Th1 mediated processes. Both are exacerbated by inter-current infections. MS therapies, like beta interferons, have anti-viral effects. They also may down regulate MHC molecules on antigen presenting cells and inhibit pro-inflammatory cytokines and T cell proliferation. These effects should benefit neuroborrelios patients. If a neurologists prescribes such drugs for MS they should dovetail nicely with antibiotic therapy prescribed by LLMDS (Lyme Literate Medical Doctors).

Of course, LLMDS are concerned about the routine use of high dose intravenous steroids prescribed by many neurologists for MS exacerbations when "MS" co-exists with Lyme and neuroborreliosis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 22.09.2013 - 14:49:04

Diagnosis and Treatment of Chronic Chlamydia Pneumoniae

http://www.vanderbilt.edu/cttc/technology/diagnosis-and-treatment-chronic-chlamydia-pneumoniae

Clinical Background
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that affects 2.5 million people worldwide. Current treatments for MS have adverse effects and are poorly tolerated. The cause of MS is not known, but there is considerable evidence that suggests infectious agents play a role in the debilitating disease.
It has been shown that the presence of one such infectious agent, Chlamydia, indicates the presence of MS and that treatment of Chlamydia improves or sustains neurological function. Present treatment of Chlamydia includes a short course of a single antibiotic. Such treatment often results in relapse as Chlamydia is often present as a latent species that will later re-infect cells.

Sivun alaosasa on useita patentteja, esim. seuraava:

Methods and reagents for the treatment of multiple sclerosis

http://www.google.com/patents/us7094397

Abstract
The invention features methods and reagents for the diagnosis, monitoring, and treatment of multiple sclerosis. The invention is based in part on the discovery that Chlamydia is present in patients with multiple sclerosis, and that anti-chlamydial agents improve or sustain neurological function in these patients.

********
Therapy
In addition to demonstrating that C. pneumoniae infection correlates with MS, we have also found that patients with MS that were treated with anti-chlamydial agents showed improved Expanded Disability Status Scale (EDSS; Kurtzke, Neurology 33:1444–1152, 1983) scores. Thus, it is highly likely that chlamydial infection causes or exacerbates MS. We have also identified combination therapy regimens that, because of the phase of Chlamydia targeted by each drug, are particularly suited for the treatment of MS.
********
It is also believed that persistance of chlamydial infections may be due in part to the presence of cryptic forms of Chlamydia within the cells. This cryptic intracellular chlamydial form apparently can be activated by certain host factors such as cortisone (Yang et al., Infect. and Immun., 39:655–658, 1983; Malinvemi et al., J. Infect. Dis., 172:593–594, 1995). Anti-chlamydial therapy for chronic Chlamydia infections must be continued until any intracellular EBs or other intracellular cryptic forms have been activated and extracellular EBs have infected host cells. This reactivation/reinfection by chlamydial EBs clearly is undesirable as it prolongs the therapy of chlamydial infections, as well as increases the opportunity for antimicrobial resistance to occur.

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For the treatment of MS, the combinations of anti-chlamydial agents shown in Table 2 are preferred.
TABLE 2

Combination      Drug Class      Preferred
           
1      Rifamycin                               Rifampin
     Azalide                                Azithromycin
     Macrolide      
     Ketolide      
     Streptogramin      
2      Rifamycin                               Rifampin
     Ampicillin or Amoxicillin      
     Probenecid      
3      Rifamycin                                Rifampin
     Azalide      
     Macrolide      
     Ketolide      
     Ampicillin or Amoxicillin         Azithromycin                      
     Probenecid      
4      Rifamycin                                 Rifampin
     Azalide                                 Azithromycin
     Macrolide      
     Ketolide      
     Streptogramin      
     Ampicillin or Amoxicillin      
     Probenecid      
     Nitroimidazole                          Metronidazole
5      Fluoroquinolone                  Ofloxacin
           Levoflozacin
     Rifamycin                                  Rifampin
6      Sulfonamide                          Sulfamethoxazole/
                                                Trimethoprim
     Rifamycin                                   Rifampin
     Isonicotinic congener           INH
7      Rifamycin                                    Rifampin
     Tetracycline                            Minocycline
           

To any of the drug combinations, any or all of the following compounds can also be added: probenecid, disulfide reducing agents (e.g., penicillamine), statins (e.g., dantolene), type-1 interferons (e.g., α-IFN or β-IFN), and activators of iNOS activity.

B) Compounds that Increase iNOS Expression or Activity
Nitric oxide (NO) is a relatively unstable free radical synthesized from L-arginine by inducible nitric oxide synthase (iNOS) and is considered to play a role in containing and/or eradicating intracellular pathogens. NO is implicated in a number of in vitro and in vivo models of host resistance to intracellular pathogens such as Leishmania major, Toxoplasma gondii, Listeria monocytogenes, and Mycobacterium tuberculosis. iNOS may also play a role in inhibiting replication of C. trachomatis in epithelial cells. Moreover, disruption of the iNOS gene in mice leads to dissemination of C. trachomatis-infected macrophages and delays the clearance of C. pneumoniae infections.
*******

Patient Population
The study evaluated 17 patients with relapsing remitting MS (4M/13F, mean age 31 years) at the time of diagnosis of clinically definite disease (Table 3) and 20 patients with progressive MS (10M/10F, mean age 40 years) (Table 4). Among the 17 relapsing remitting MS patients, two patients were on β-IFN that was instituted four weeks and 16 weeks, respectively, prior to the enlistment of these patients for the lumbar puncture. Both patients (#5 and #14) were also recovering from a recent clinical worsening. The remaining 15 patients were not on any immunosuppressive or immunomodulatory drugs. All except three of these 17 MS patients had oligoclonal bands in the CSF (Table 3). Among the patients with progressive disease, two had primary progressive disease, four had relapses with sequelae (relapsing progressive disease), and the remaining 14 had secondary progressive disease.

********
Among patients with newly diagnosed relapsing remitting MS, 47% of patients (8/17) had C. pneumoniae isolated from CSF cultures (Table 3). Among patients with progressive MS, 80% of patients (16/20) were culture positive (Table 4).

********
These results suggest that the majority of oligoclonal bands in CSF of MS patients represent antibodies to C. pneumoniae antigens. Non-specific adsorption of antibodies to C. pneumoniae antigens in MS patients was an unlikely explanation, since antibodies present in the anodal region did not bind to C. pneumoniae antigens. Also, no decrease in the oligoclonal bands was seen among nine OND controls following incubation with C. pneumoniae antigens.

*********
TABLE9

Patient      Case History
     
BL      First symptoms began with numbness of the left arm and leg which rapidly progressed to a partial
     Brown-Sequard syndrome (i.e. cord myelitis) with an associated urinary retention. Despite therapy with
     corticosteroids, and β-IFN, he rapidly progressed over the next three months with an EDSS = 8.0
     (triplegic plus speech and swallowing impairments). A positive CSF PCR and culture for C.
     pneumoniae led to treatment with combination antibiotics. The patient improved in all aspects of
     neurologic function over the following six months. His EDSS score nine months later was 3.0 with
     return to work and routine athletic activities. His neurological status remains stable and he continues on
     an anti-chlamydial combination regimen.
MC      This patient had a ten year history of MS with evidence of progressive ataxia and weakness in the legs.
     Over five months his EDSS score worsened from a 7.0 to 8.0. His CFS was positive by PCR for C.
     pneumoniae and he was placed on combination antibiotics. Over the next six months he gradually
     improved in his balance, coordination and lower extremity strength. His most recent EDSS score was
     6.5.
JM      Initially seen with rapidly progressive paraparesis secondary to MS. He failed to response to
     corticosteroids on two successive occasions. Five months later, his EDSS score was 7.5. Following a
     positive C. pneumoniae PCR, he was placed on combination antibiotics. He has gradually gain strength
     in his lower extremities and five months later was able to walk with a walker (EDSS = 6.5) while
     maintaining on combination antibiotics.
LL      Patient with a long history (14 years) of secondary progressive MS with recent progressive bulbar
     symptoms, axtaxia, and paraplegia (EDSS = 8.5). PCR for the MOMP gene of C. pneumoniae in the
     CSF was positive. She was placed on combination antibiotics with no further progression of symptoms
     for the last six months.
AN      Long history of MS and wheel chair bound for approximately ten years. She has received continuous
     physical therapy to retain leg muscle tone. Following approximately six months of combination
     antibiotics, she was able to stand unaided and take several unaided steps. She reports significant
     decrease in fatigue and cognitive dysfunction. She remains on combination antibiotics and other
     supportive medications.
FO      Wheel chair bound with a long history of MS with a two-three year progression of severe dysarthriae and
     incontinence. On combination antibiotics (14 months) he has had improvement of speech and
     incontinence. Speech, ability to open mouth for dentist, stamina all improved. He can stand better on
     his own mid-transfer, but remains wheelchair-bound.
JC      Diagnosis of MS with development of a foot drop approximately one year prior to therapy requiring the
     use of a cane in walking. Approximately four months after initiation of combination antibiotic therapy,
     patient reports reversal of foot drop and no longer requires a cane. She continues on antibiotic therapy.
FW      Male with a 15 year history of MS. Used a cane for a rolling, unstable gait. Easily fatigued. After 12
     months of combination antibiotics, was able to walk without cane or excessive fatigue, although his gait
     can still wander. Can easily make it across the parking lot, which had previously been a challenge.
     Stopped antibiotics even though was still PCR positive; plans to restart therapy if he has another flare-
     up.



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 24.09.2013 - 09:53:45

Itse olen yrittänyt parantaa immuunipuolustustani LDN:n avulla. Tässä suora lainaus LDN- sivustoilta:
Miten LDN toimii?
LDN-hoidossa (pieniannoksinen naltreksoni/matala-annoksinen naltreksoni), annos on sen sijaan vain muutamia milligrammoja. Se salpaa reseptorit vain lyhyeksi aikaa, mikä stimuloi kehoa erittämään enemmän endorfiineja ja muita endogeenisiä opioidipeptidejä. Koska naltreksonia on Suomessa ja useimmissa muissa maissa tarjolla vain 50 mg tabletteina (Revia), täytyy apteekin valmistaa naltreksoni sopivan kokoisiksi kerta-annoksiksi.

Endorfiineilla on monia erilaisia vaikutuksia elimistössä, muitakin kuin yleisesti tunnetut kivunlievitys ja mielialan kohottaminen. Ne ovat erittäin tärkeitä immuunijärjestelmän ylläpitäjiä. On havaittu, että esimerkiksi autoimmuunisairauksissa, syövissä ja AIDSissa kehon beetaendorfiinitaso on hyvin alhainen. LDN nostaa endorfiinitasoja jopa 2-3-kertaisiksi, mikä normalisoi (käytännössä stimuloi) immuunijärjestelmää. Monissa syöpäkasvaimissa on opioidireseptoreita, minkä ansiosta LDN:stä on apua myös joihinkin syöpiin. Hoidon vaikutusmekanismia kuvataan tarkemmin ja tieteellisemmin Tiede-sivulla.

Opioidiantagonismin lisäksi naltreksoni myös salpaa TLR-4-reseptoria (toll-like receptor 4), mikä vähentää inflammaatiota (tulehdusta) ja lievittää kipua. Aiemmin uskottiin LDN:n koko vaikutuksen johtuvan endogeenisten opioidien erityksen lisäämisestä, mutta todennäköisesti TLR-4-salpauksella (ja kenties muillakin, vielä tuntemattomilla mekanismeilla) on huomattava osuus.

Asiasta toiseen, kuten varmaan olet lukenut, että esim. David Wheldonin mukaan Chlamydia pneumonia-bakteeri tarttuu pisaratartuntana hengitysteihin, eikä ole siis yleisesti luultu pelkkä sukupuolitauti.

Keskustelin erään tutkimuksista kiinnostuneen neurologin kanssa ja kysyin MS-taudin syntyjä syviä. Onko kyse immuunipuolustuksen heikkoudesta tai "laiskuudesta" vai kuten pidetään yleisenä totuutena, yliaktiivisuudesta, josta seuraa ns. auto-immuunisairaus. No, kunnon vastausta en saanut, mutta se selvisi, ettei nykyisillä havaitomenetelmillä voida seurata myeliinin tuhoutumista reaaliaikaisesti. Eli, kun ei tiedetä arvataan loput, immuunipuolustusjärjestelmässä on vika.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Caroline80 Pvm 24.09.2013 - 10:40:47

Pieniannoksinen naltreksoni (low dose naltrexone eli LDN): tästä olen lukenut jo aikaisemminkin, mutta voiko lääkäri määrätä sitä potilaalleen. :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 24.09.2013 - 13:30:19

Kyllä lääkäri kirjoittaa Revia reseptin, mutta itse pieniannoksinen naltreksoni on viisainta teettää esim. yliopiston apteekissa. LDN on tutkimuksin todettu vaarattomaksi, tosin sen käyttö yhdessä opiaattien kanssa ei ole järkevää, sillä ne kumoavat toistensa vaikutuksen.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 24.09.2013 - 20:35:57

Äijä,

Olen ajatellut LDN:n käytön aloittamista sitten kun infektiot on taltutettu (tällä hetkellä antibiootit riittävät).  Olen kuullut, että reseptin saisi myös joltakin Fibromyalgia/CFS lääkäriltä, joolloin LDN:ää käytetään väsymyksen ehkäisemiseen. Minulla oli ennen MS-diagnoosia noin kolmen vuoden ajan toistuvat "flunssat", jotka kestivät kuukausia kerrallaan. Myöhemmin keuhkojen röntgenkuvista yksi lääkäri totesi, ettei ole kuin keuhkokuumeen jättämiä arpia. Se oli pienoinen yllätys. Siinä vaiheessa en ollut siis tietoisesti sairastanut keuhkokuumetta, enkä kuullutkaan "kävelevästä keuhkokuumeesta" eli keuhkoklamydiasta. Minulla todettiin myöskin mykoplasma pneumoniae, mikä on samanlainen bakteeri - alkaa hengitysteistä ja kroonistuu joka puolelle kroppaa. Mutta mykoplasma on nyt ilmeisesti kukistettu, joten keuhkoklamydia on näistä kaksosista jäljellä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 25.09.2013 - 07:53:51

Keuhkoklamydiaan pitäisi sopivan antibiootti-koktailin tehota, ainakin pitkässä juoksussa, mikäli uskoo David Wheldonia. Ongelma tuli,ainakin minulle jatkuvasta vatsan löysyydestä, jota helpotti huomattavasti erilaiset probiootit, koska otin antibiootit suun kautta. Apteekista nykyisin saatavat antibioottiripuliin auttavat ovat kylläkin aika tehokkaasti. Asia on varmaan toisin, jos antibiootit otetaan suonen sisäisesti. Kuten olen jo aiemminkin kertonut otan antibiootteja ns. jälkihoitona kahden kuukauden välein kaksi viikkoa, jolloin syön myös paljon lisä/suojaravinteita ja erilaisia propiootteja. Olen ottanut myös iltaisin 4,5 mg LDN:ää jo useamman vuoden ajan.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja muju62 Pvm 26.09.2013 - 19:59:08


Caroline80 24.09.2013 - 10:40:47:
Pieniannoksinen naltreksoni (low dose naltrexone eli LDN): tästä olen lukenut jo aikaisemminkin, mutta voiko lääkäri määrätä sitä potilaalleen. :)


Kyllä voi  :)
LDN-resepti lähetetään Helsinkiin Yliopiston apteekkiin ja he valmistavat kapselit sekä lähettävät ne ohjeineen potilaalle. Resepti jää sinne ja sen jälkeen riittää soitto, he lähettävät lisää. Siis jos on määrätty esim. vuodeksi lääkkeet. Hinta postikuluineen noin 40 e/ 3kk satsi.
Voi sen varmaan muullakin tavalla hoitaa, mutta tuo on aika näppärä tapa. Se on auttanut monia CFS-potilaita, kunhan löytää itselleen sopivan annoksen ja lääkkeen "ottamisajankohdan" .

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 27.09.2013 - 08:14:41

Sen verran vielä LDN:n teettämisestä, tärkeää on varmistaa täyteaineen sopivuus. Mikrokiteinen selluloosa on sopiva, jos halutaan lääkkeen imeytyvän nopeasti, kuten tässä tapauksessa halutaan. Kalsiumkarbonaatti tekee lääkeaineen imeytymisen hitaammaksi, eikä se ole tässä tapauksessa suotavaa, lääkeaineen vaikutusmekanismi muuttuu. Vuosia sitten täytyi jopa yliopiston apteekkiin lähettää valmistusohjeet, nykyisin luulisin asian hoituvan kivuttomammin, muista apteekeista en tiedä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Caroline80 Pvm 27.09.2013 - 16:34:49

Lääkärini ei tiennyt LDN:n "hankkimisesta" mitään, joten annoin hänelle tämän sivun teksteistä kopion. Kiitän nyt siitä. - Karoliina L. :)


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 28.09.2013 - 07:48:22

LDN:stä on hyvät "kotisivut", perehdy niihin ja aloita LDN:n käyttö pienin annoksin, asteittain nostaen. Itse teetän LDN:ää 1,5 mg voimakkuisina kapseleina, jolloin lääkkeen portattainen nosto on helpompaa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja VPS358 Pvm 28.09.2013 - 10:38:26


Äijä 28.09.2013 - 07:48:22:
LDN:stä on hyvät "kotisivut",


Linkki?

T: Vesku

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 28.09.2013 - 11:59:16

LDN:n "Kotisivut" löytyvät täältä:
http://ldn.gehennom.org/

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.09.2013 - 12:50:26

Asia, joka sivuaa MS:ää ja bakteeri-infektioita:

Thickened Blood

http://digitalnaturopath.com/cond/C546009.html
     

Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.

David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn’s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.

Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
*****
There are at least three possible causes or contributing factors:

   Viruses, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits.
   Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it.
   Chemical exposure can result in changes that trigger the coagulation process.

The results of this thickened blood are:

   When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised.
   The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment.
   Thicker blood is harder to pump.
   By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly.
   The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin.
****
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.

Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
********

http://www.anapsid.org/cnd/diffdx/hypercoagulation.html

Treatment
In 1998, 16 patients started on taking heparin injections daily...
To improve the outcome, Berg now recommends testing for bacterial infections such as Mycoplasma and Chlamydia pneumonia, as well as for active virus infections, such as Humanherpes virus 6 (HHV6), Cytomegalyvirus (CMV), and Epstein-Barr virus (EBV).
The heparin (two subcutaneous injections per day) is taken for six months. One month or so into the heparin, antibiotic and/or antiviral treatment is started to combat the bacteria and viruses exposed by the reduction in the fibrin coating the vessel walls; this treatment lasts three months. At this same time as the antibiotic/antiviral treatment is started, Transfer Factor is also started; it is continued for four months. For those who test high in lipoprotein (a) (Lp(a)) or high plasminogen activator inhibitor-1 (PAI-1), 500-1000 mg/day of bromelain is started at the same time as the heparin and is continued for four months. The heparin is continued after the antibiotic and transfer factor therapies have stopped to prevent any organisms remaining from starting the hypercoagulation process all over again.




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 28.09.2013 - 13:41:24

Erittäin mielenkiintoista, olen murrosiästä lähtien mittaessa saanut hemoglobiini-mittauksissa yli 170 arvoja, pari vuotta sitten mitattiin yli 180. Lääkärini suositteli verenluovutusta, mutta sairaanverta ei voi kellekään antaa vaan heittää pois. No, se jäi silloin pelkäksi puheeksi. Täytyy tutkia asiaa tarkemmin ja lähettää tutkimusartikkelit lääkärilleni. Kiitos tiedoista!!!

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja kaizas Pvm 28.09.2013 - 20:04:06

En todellakaan lukenut koko ketjua..

Mul on ollu keuhkoklamydiaa usein ja crp silloin toti koholla

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 29.09.2013 - 12:20:28

Lisää hepariinista: Mieleen tulee Prof. Simkan hypoteesi babesiasta MS-taudin aiheuttajana. Jos näin olisi, voisiko laskimolaajennuksen jälkeinen hyöty perustua joillakin operoiduilla hepariinin, jota piikitetään pari viikkoa operaation jälkeen.. Jossittelun puolelle menee, mutta tietoa löytyy täältä:

Growth-Inhibitory Effect of Heparin on Babesia Parasites


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC310193/

Abstract

We examined the inhibitory effects of three heparins on the growth of Babesia parasites. The multiplication of Babesia bovis, B. bigemina, B. equi, and B. caballi in in vitro cultures and that of B. microti in vivo were significantly inhibited in the presence of heparins, as determined by light microscopy. Treatment with various concentrations of heparin showed complete clearance of the intracellular parasites. Interestingly, a higher percentage of abnormally multidividing B. bovis parasites was observed in the presence of low concentrations of heparin. Furthermore, fluorescein isothiocyanate-labeled heparin was preferably found on the surfaces of extracellular merozoites, as detected by confocal laser scanning microscopy. These findings indicate that the heparin covers the surfaces of babesial merozoites and inhibits their subsequent invasion of erythrocytes.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.09.2013 - 12:56:10

Berberiiniä on käytetty itämailla tuhansia vuosia kaikenlaisiin vaivoihin. Tämän tutkimuksen mukaan tehoaa myös keuhkoklamydiaan.

Zhang LJ, Zhang LJ, Quan W, et al. Berberine inhibits HEp-2 cell invasion induced by Chlamydophila pneumoniae infection. Journal of Microbiology. 2011 Oct;49(5):834-40. Epub 2011 Nov 9.


Abstract


This study investigated the inhibitory effects of berberine on Chlamydophila (Chlamydia) pneumoniae infection-induced HEp-2 cell invasion and explored the possible mechanisms involved in this process. C. pneumoniae infection resulted in a significant increase in HEp-2 cell invasion when compared with the control cells (P<0.01) in a Matrigel invasion assay. This enhanced cell invasion was strongly suppressed by berberine (50 μM) (P<0.01). In a cell adhesion assay, the infection-induced HEp-2 cell adhesion to Matrigel was also significantly inhibited by berberine (P<0.01). C. pneumoniae infection was found to promote HEp-2 cell migration remarkably (P<0.01), which was markedly suppressed by berberine (P<0.01) in the cell migration assays. There were no statistically significant differences in the expression of matrix metalloproteinase-1 (MMP-1) and MMP-9 in the infected cells and berberine did not change the expression of MMP-1 and MMP-9. These data suggest that berberine inhibits C. pneumoniae infection-induced HEp-2 cell invasion through suppressing HEp-2 cell adhesion and migration, but not through changing the expression of MMP-1 and MMP-9.


Hiirikokeissa sen on myös havaittu hillitsevän MS-tautia.

Ma X, Jiang Y, Wu A, et al. Berberine Attenuates Experimental Autoimmune Encephalomyelitis in C57 BL/6 Mice. PLoS One. 2010 Oct 19;5(10):e13489.

Abstract

Background

Berberine, an isoquinoline derivative alkaloid, has a wide range of pharmacological properties and is considered to have anti-inflammatory and neuroprotective effects. However, there are no reports about the effects and mechanisms of berberine in experimental autoimmune encephalomyelitis (EAE), an established model of multiple sclerosis (MS).

Methodology/Principal Findings

Female C57 BL/6 mice immunized with myelin oligodendrocyte glycoprotein 35–55 amino acid peptide were treated with berberine at the day of disease onset and medication was administered daily until mice were sacrificed. Blood–brain barrier (BBB) permeability and the alteration of matrix metalloproteinase-2 (MMP-2, 72 kDa) and matrix metalloproteinase-9 (MMP-9, 92 kDa) in the brain and cerebrospinal fluid (CSF) of EAE mice were detected by quantitative measurement for Evan's blue (EB) content, Western blot and gelatin zymography respectively. The results showed that berberine attenuated clinical and pathological parameters of EAE, reduced the permeability of BBB, inhibited the activity and expression of MMP-9 but not MMP-2 in the CSF and brain of EAE mice.

Conclusions/Significance

These findings suggest that berberine is effective to attenuate the clinical severity of EAE in C57 BL/6 mice by reducing the permeability of BBB, decreasing the expression and activity of MMP-9, and decreasing the inflammatory infiltration. We think that berberine might be a potential therapeutic agent for MS.





Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.09.2013 - 13:34:29

Epäilevä Tuomas kun olen, niin tulee kaiken tämän tutkimustiedon jälkeen sellainen "fiilis", että neurologienkin täytyy tietää MS-taudin synnystä ja kulusta enemmän, kuin annetaan ymmärtää. On esimerkiksi monta bakteeriehdokasta, jotka kroonistuessaan tai sanottaisiinko pesiytyessään elimistöön sen eri kudoksiin voivat aiheuttaa MS-taudin. Ne voivat tunkeutua esim. spirokeetta-muotoisina syvälle eri elimiin ja vaipua lepotilaan muodostaen ympärilleen suojakuoren tai suojautua ns. biofilmin alle muiden bakteerien kanssa vaihtamaan informaatiota, sekä ollen tällöin turvassa esim. antibiooteilta.
     
Yleinen virallinen hoito on heikentää immuunijärjestelmää, joka on "liian" innokas ja tuhoaa myelliiniä hermosoluista sekopäisenä, onhan kyseessä autoimmuunisairaus. Kukaan ei ole esittänyt sitä vaihtoehtoa, että immuunijärjestelmä on MS-potilailla liian heikko puolustautumaan eri taudinaiheuttajia vastaan.

Mielestäni kyse voisi olla siitä, ettei sopivaa "lääkekoktailia" ole löydetty tai jos onkin, sen käyttäminen tulee liian kalliiksi tai on muuten epäsovinnaista niin kauan kun pidetään kiinni autoimmuuniteoriasta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 03.10.2013 - 20:17:31

Meinasin selostaa erilaisia tutkimuksia ja niihin sisältyviä "suden kuoppia", mutta Tri Tolonen on mielestäni kiteyttänyt aika hyvin seuraavassa osittain lainatussa tekstissä :


Mitä tieteellinen tutkimus tarkoittaa?

Tieteellinen menetelmä on tapa yrittää ratkaista jokin ongelma luotettavasti. Menetelmä sisältää tietynlaisen muodon lähestyä ongelmaa ja luo kehyksen, jonka puitteissa edetään. Se on prosessi, jonka avulla tutkija(ryhmä) pyrkii selvittämään ympäröivää maailmaa ja sen ilmiöitä, ja siinä pyritään havaitsemaan, tiedostamaan ja tunnistamaan omat, ympäristöön ja kulttuuriin liittyyvät uskomukset, jotka vaikuttavat tiedon keräämiseen, tulkintaan ja johtopäätöksiin sekä minimoimaan näiden vaikutuksia. Tutkimuksella tulee olla päämäärä, tavoite ja selkeä käsitys siitä, mitä ollaan tekemässä. Siksi tarvitaan aina hyvä tutkimussuunnitelma, josta käy ilmi paitsi hypoteesi myös se, miten edetään ja mitä keinoja käytetään tiedon hankkimiseen. Tutkijoilla pitää myös olla hallussa entuudestaan olemassaoleva tieto tutkittavasta ongelmasta.

Hypoteesi tarkoittaa olettamusta syy- ja seuraussuhteista, joita halutaan testata. Siis sitä, pitääkö oletus paikkaansa ja missä määrin se pitää paikaansa, vai eikö se pidä paikkaansa ko. ympäristössä (eli valitussa aineistossa). Tutkimus selvittää sitten valittua menetelmää käyttäen asian todellista laitaa valitussa ympäristössä (aineistossa). Tutkimuksen tulisi vastata myös kysymykseen, "ellei asia ole näin, niin miten se siten on?" Yleinen ongelma ravintolisätutkimuksissa on ei-positiivisista tuloksista (nollatutkimuksista) tehdyt virheelliset yleistykset tutkitun aineiston ulkopuolelle eli väestöön yleensä tai sen erikoisryhmiin (katso jäljempänä).


Miten lääkevaikutuksia nykyään tutkitaan?

Lääketieteessä, varsinkin farmakologiassa, vaaditaan nykyisin, että uusi hypoteesi todennetaan ns. satunnaistetun kaksoissokkotutkimuksen avulla. Tieteen filosofiassa tätä menetelmään kutsutaan hypoteettis-deduktiivisiksi. Siinä testataan tilastotieteen menetelmiä hyväksi käyttäen, pitääkö uusi hypoteesi paikkansa. Itse asiassa uutta hypoteesia (H1) testataan "nollahypoteesia" (H0) vastaan.

Nollahypoteesin (H0) mukaan uusi käsitys ei pidä paikkaansa. Jos vastoin tätä oletusta uusi käsitys (H1) osoittautuukin oikeaksi, se muuttaa tiedeyhteisön käsitystä tutkimuksen kohteena olevasta ilmiöstä, esimerkiksi jonkin lääkkeen tai vaikkapa vitamiinin vaikutuksesta johonkin vaivaan tai tautiin.

Kaksoissokkotutkimuksessa koehenkilöt saavat joko tutkittavaa hoitoa (tai ainetta) tai ennestään hyväksyttyä lääkettä taikka plaseboa eli lumehoitoa.

Satunnaistettu kaksoissokkotutkimus

Termi "satunnaistettu kaksoissokko" tarkoittaa sitä, että tutkittavat jaetaan sattumanvaraisesti hoito- ja verokkiryhmiin. Lisäksi tutkimuksen kestäessä sen enempää tutkittavat koehenkilöt kuin tutkijatkaan eivät tiedä, ketkä tutkituista saavat oikeaa ainetta ja ketkä lume- tai parasta nykyisin tunnettua hoitoa. Molemmat osapuolet on siis "sokkoutettu" tutkimuksen ajaksi. Tämä on tärkeää siksi, että tutkijat vaikuttavat aina joko tietoisesti tai tietämättään tutkittavien paranemistaipumukseen. Tutkijat itse ja tutkimuksen rahoittajat uskovat usein vahvasti H1-hypoteesiin ja voivat siirtää uskonsa koehenkilöihin. Kaksoissokkoasetelman pyrkimys on eliminoida suggestion vaikutus tuloksista.

Perinteisesti tutkimustieto on perustunut induktioon: On ajateltu, että jos esimerkiksi nitro auttaa kymmentä peräkkäistä angina pectoris -potilasta, niin se auttaa kaikkia muitakin samaa tautia sairastavia. Itse asiassa juuri näin tutkittuna nitro tuli yleiseen käyttöön sepelvaltimotaudin hoidossa. Nykyään tällaista "avointa" tutkimusta (jossa ei ole yhtä tai useampaa vertailuryhmää) ei juuri arvosteta, koska tulos voi perustua suggestioon.

Englanniksi "oikeaa" eli tutkittavaa hoitoa saavaa ryhmää kutsutaan usein nimellä "verum-" tai propositae-" ryhmäksi, ja verrokkeja plaseboryhmäksi.

Tutkittavat valmisteet ("verum" ja "plasebo") valmistetaan samannäköisiksi, samanmakuisiksi ja -hajuisiksi (jos vain mahdollista), ja ne varustetaan koodinumeroilla ja annetaan tutkittaville täsmälleen saman näköisistä purkeista. Koodi säilytetään tutkimuksen ajan kassakaapissa, eivätkä tutkijat enempää kuin tutkittavatkaan pääse siihen käsiksi. Vasta tutkimuksen päätyttyä koodi avataan, jolloin selviää, kuka sai mitäkin valmistetta.

Verrokkirymän merkitys

Vertailuryhmän tarkoituksena on kertoa tutkijoille ja muillekin, mitä verum-ryhmälle olisi tapahtunut, elleivät he olisi saaneet tutkittavaa hoitoa (vaan olisivat jääneet kokonaan hoidotta tai saaneet vertailun kohteena olevaa perinteitä hoitoa). Uutta testattavaa hoitoa voidaan verrata myös johonkin käytössä olevaan hoitomuotoon, jolloin sitä saavat toimivat verrokkeina. Joskus tarvitaan useampia kuin yksi verrokkiryhmä. Verrokeille annetaan ennen tutkittavaan tautiin hyväksyttyä lääkettä tai plaseboa eli lumevalmistetta. Esimerkiksi Pohjois-Karjala-projektissa oli se vika, ettei ollut kahta, kolmea vertailuväestöä. Nyt ei voida tietää, johtuiko sydäntautien väheneminen Pohjois-Karjalassa projektista, vai olisiko se tapahtunut muutoinkin, kuten muualla Suomessa on tapahtunut.

Plasebo ja nocebo

Latinan sana "plasebo" tarkoittaa "minä miellytän". Plasebona annetaan vaikuttamatonta ainetta, joka on saatettu saman näköiseksi, makuiseksi ja hajuiseksi kuin tutkittava "verum"-aine. Plasebohoidosta puhutaan joskus vähättelevään sävyyn, kun halutaan väittää, että hoitovaikutus perustuu pelkkään uskoon.

Lääketieteessä on 1950-luvulta alkaen uskottu, että pelkän plasebohoidon vaikutus on noin 35%. Tämä käsitys perustui bostonilaisen lääkärin Henry Beecherin tekemiin analyyseihin noin tusinasta eri tutkimuksesta, joiden mukaan plasebolla oli tautia tai sen oireita lievittävää tai parantavaa vaikutusta.

Tuokokuussa 2001 julkaistun tanskalaisen meta-analyysin mukaan plasebon teho vaihtelee eri ihmisillä ja eri taudeissa. Asbjorn Hjorbatsson ja Peter Götzsche analysoivat 114 tutkimusta plasebon vaikutuksista. Niihin oli osallistunut 7500 potilasta, jotka kärsivät 40 eri oireesta. Tulosten mukaan paraneminen onkin usein "lumetta", joka ei välttämättä perustu itse pillerin tehoon, vaan siihen, että potilas haluaa kertoa lääkärilleen voivansa tänään hiukan paremmin kuin ennen hoitoa. Vain kipuilevien potilaiden kohdalla pelkkä plasebo auttoi hiukan. Tutkijat päättelevät, ettei plasebolla ole lääketieteessä muuta perusteltua käyttöä kuin kliinisissä tutkimuksissa vertailuryhmän valelääkityksenä (kuten edellä on selostettu).
(Hjorbatsson A, Götzsche P: Is the placebo powerless? An analysis of clinical trials comparing placebo with no treattment. New England Journal of Medicine 2001;344(21):1594-15602, Abstract)

Plasebon vastakohta on "nocebo". Nocebovaikutuksella tarkoitetaan sitä, että tutkittava aine saa aikaan epämiellyttäviä tuntemuksia. Plaseboryhmässä ilmenee usein joillakin yksilöillä sivuvaikutuksia, joille ei ole mitään farmakologisia eikä biokemiallisia perusteita. Ne ovat silloin psyykkisiä (kuviteltuja) nocebovaikutuksia.


Aineiston suuruus

Lääketieteellisten tutkimusten suunnittelussa on usein vaikeaa päättää, montako koehenkilöä tarvitaan tutkittavan aineen vaikutuksen osoittamiseksi. Se riippuu kokonaan sitä, miten voimakas vaikutus tutkittavalla hoidolla on. Jos se on hyvin suuri, riittää muutama koehenkilö.

Esimerkki arkielämästä: tarvitaan vain muutama henkilö sen seikan osoittamiseksi, että pullollisesta viinaa tulee humalaan. Mutta jos vaikutus on lievä ja se ilmenee vain esimerkiksi joka viidennellä potilaalla, tarvitaan jo huomattavan suuret verum- ja plaseboryhmät, jotta ero olisi tilastollisesti osoitettavissa. Siksi tutkimuksen suunnittelijalla tulee olla ennakkoon jonkinlainen käsitys siitä, kuinka monessa prosentissa koehenkilöitä hoito vaikuttaa. Käytännössä moni tutkimus on tuottanut nollatuloksen (eli ei-positiivisen) siksi, että tutkimusryhmät ovat liian pienet tai muutoin väärin valittuja.

Viime vuosina on julkaistu hyvin suuriin väestöryhmiin perustuvia tutkimuksia, joissa on ollut tuhansia, jopa kymmeniä tuhansia koehenkilöitä. Niistä saadaan tilastollisesti luotettavat tulokset, mikäli verrokkiryhmä(t) on valittu oikein.

Tulosten tulkinta

Jos verum-ryhmän tulokset osoittautuvat tilastollisesti paremmiksi kuin verrokkiryhmän, on tutkimuksen tulos positiivinen eli H1-hypoteesi saa siitä tukea. Yksi tutkimus ei tietenkään aina takaa sitä, että tiedeyhteisö uskoisi H1-hypoteesiin. Niinpä tutkimusraporttien lopussa tutkijat usein nöyrästi toteavat, että vaikka tulokset osoittavat "näin ja näin", tarvitaan lisää tutkimuksia havainnon varmistamiseksi.

Tutkimuksella on sisäinen ja ulkoinen validiteetti. Sisäisellä tarkoitetaan, että tulos pätee tutkitussa aineistossa (edellyttäen että tutkimus on oikein tehty). Useimmiten tuloksia halutaan kuitenkin yleistää muihinkin ihmisiin, jolloin tulee arvioida, ovatko tulokset ulkoisesti päteviä (valideja). Näin ei suinkaan aina ole asianlaita.

Nollatutkimus, ei-positiivinen tutkimus

Nollatutkimuksia on pääasiassa kahdenlaisia. Toiset ovat itsestään selvyyksiä, kuten tutkimus, jossa todettiin että käsien pesun jälkeen käsissä on vähemmän bakteereja kuin ennen pesua. Mutta on myös toisenlaisia nollatutkimuksia, joissa ei saadakaan toivottua tulosta. Tulos tulkitaan kuitenkin usein väärin sanomalla, että tutkimus osoitti, ettei aine X vaikuta väitetyllä tavalla. Esimerkiksi Helsingin Sanomat julkaisi SETTI-tutkimuksen perusteella ison artikkelin, jossa väitettiin, ettei E-vitamiini vaikuta myönteisesti verisuonitauteihin. Toimittaja tulkitsi tietämättään tai tahallaan tutkimusta väärin tai tarkoitushakuisesti.

Lääketieteessä julkaistaan edelleen valitettavan paljon nollatutkimuksia. Voisimme verrata niitä arkipäivän tilanteeseen: Poliisi puhalluttaa tiellä 50 perättäistä autoilijaa, eikä kenelläkään heistä todeta liikaa promilleja. Siitä ei pidä suinkaan päätellä, etteikö Suomessa olisi rattijuoppoja.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.10.2013 - 08:44:02

Tässä on muutama kohta pitkästä artikkelista näiltä sivuilta:

http://owndoc.com/lyme/multiple-sclerosis-is-lyme-disease-anatomy-of-a-cover-up/


Multiple sclerosis is Lyme disease: Anatomy of a cover-up


Perhaps the biggest ongoing medical scandal of the past hundred years is the fact that it has been known since 1911 that Multiple Sclerosis is caused by a bacterium, and that the Big-Pharma-controlled medical-industrial complex covered this up in order to make money selling symptom relievers to MS patients. At the lower levels there is no cover-up at all, but simply human nature at work, as we wrote about here, to dispel the notion that we are “conspiracy theorists”. Since 1911, overwhelmingly much medical research has been conducted where living Borrelia bacteria were found in the brains of people who were diagnosed with MS.

Time and time again. By at least a dozen medical researchers. In at least ten countries. Since 1911 – the past one hundred years. Several older but also recent autopsy findings linked to in this article found that all deceased MS patients’ brains harbored living Lyme spirochetes. Even when tests, notorious for their large percentage of false negatives were used on living MS patients, staggeringly many tested positive for active Lyme borreliosis.



1. Multiple Sclerosis Societies.

Every Western country has at least one MS Society. Each of those tax-exempt societies typically receives tens of millions of dollars in funding from various sources, year after year. The people running those societies usually award themselves CEO-level salaries and run them as one would run a highly commercial corporation. Advertising is used to solicit funds but if you don’t read ads then you’ll bump into them, one day, begging you for money on the street. For all those billions that have been pumped over the decades in those hundreds of MS societies worldwide, not a single one has ever done anything really useful for MS patients. The worst that could possibly happen for the bosses of those setups is that the cause of MS would become known. A known cause would either mean the development of either a cure or at least better symptom relievers, and that would rapidly result in the obsoleteness of their money making machine – the chicken that lays the golden eggs if you will. Such MS societies are working in concert with MS “researchers” employed by Big Pharma.

The painful truth is: There is no such thing as Multiple Sclerosis. It’s the name of a symptom. A symptom of a disease of “unknown” cause. But the real cause has been known for a hundred years: The spirochete Bb s.l., Borrelia burgdorferi, the bacterium that causes Lyme neuroborreliosis, Lyme disease. MS doesn’t exist. MS is Lyme neuroborreliosis. MS is Lyme disease. It’s a bacterial infection you can get from a tick bite, amongst many other suspected infectious pathways.

But were those 15 researchers who said they found living Lyme bacteria (spirochetes) in the brains of a great majority of Multiple sclerosis patients all lying?

1911 Buzzard E F Spirochetes in M.S. Lancet 11:98 1911
1913 Bullock W E (now Gye) MS agent in Rabbits  Lancet 1185 1913
1917 Steiner Spirochetes The Cause of MS. Med Kiln
1918 Simmering Spirochetes in MS by Darkfield Micro
1918 Steiner G. Guinea Pig Inoculation with MS infectious agent from Human
1919 Steiner MS Agent Inoculation into Monkeys
1921 Gye F. MS Agent In Rabbits Brain 14:213
1922 Kaberlah MS Agent In Rabbits. Deutch Med Works
1922 Sicard MS Spirochetes in Animal Model. Rev Neurol
1922 Stepanopoulo Spirochetes in the CSF of MS Patients
1923 Schlossman MS Agent in Animal Model. Rev Neuro
1924 Blacklock MS Agent in Animals. Journal of Path and Bac
1927 Wilson The Rat as A Carrier of MS. British Med Journal
1927 Steiner G Understanding the Pathogenesis of MS
1928 Steiner Spirochetes in the Human Brain of MS Patients
1932 Rogers, Helen J. The question of silver cells as proof of the spirochetal theory of disseminated sclerosis. J. Neurol and Psychopathol. 13:50, 1932
1933 Simons Spirochetes in the CSF of MS Patients
1939 Hassin Spirochete-like formations in MS
1948 Adams Spirochetes within the Ventricle Fluid of Monkeys Inoculated from Human MS
1952 Steiner Acute Plaques in MS and The Pathogenic Role of Spirochetes as the Etiological Factor. Journal of Neuropathology Exp Med 11: No 4:343
1954 Steiner Morphology of Spirochaeta Myelophthora (Myelin Loving). MS Journal of Neuropathology and Exp Neurol 11:4 343
1954 Steiner G. Acute plaques in M.S., their pathogenetic significance and the role of spirochetes as the etiological factor. J. Neuropath. and Exp. Neur. 11:no 4:343, 1954
1957 Ichelson R. Cultivation of Spirochetes from Spinal Fluids of MS Cases with Negative Controls. Procl. Soc. Exp. Biol Med 70:411
1986 Gay D  thingy G Is multiple sclerosis caused by an oral spirochaete?  Lancet (1986 Jul 12) 2(8498):75-7
1988 Marshall V Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent. Med Hypotheses (1988 Feb) 25(2):89-92
1986 (USA): Relapsing fever/Lyme disease – Multiple sclerosis. Medical Hypotheses, volume 21, issue 3,  pages 335-343
2000 (Poland): Lyme borreliosis and Multiple sclerosis: Any Connection? A Seroepidemic study. Ann Agric Environ Med. issue 7, 141-143
2001 (Norway): Association between Multiple sclerosis and Cystic Structures in Cerebrospinal Fluid. Infect 29:315
2004 (Switzerland): Chronic Lyme borreliosis at the root of Multiple sclerosis – is a cure with antibiotics attainable?
2009 (Romania): Controversies in late Neuroborreliosis and Multiple sclerosis – case series

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.10.2013 - 16:58:00

Kroonisten sairauksien taustalla useita bakteeri-infektioita, viruksia ja sieniä. Antiobiootteja rajoittavat biofilmit:

Dr Wilmore Webley on Cpn (Chlamydia pneumoniae) & Biofilms:


http://www.youtube.com/watch?v=68zYTzTlTlk

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 21.10.2013 - 07:50:55

Niinpä! Biofilmit ja niiden tuhoaminen, ennenkuin antibiootit voivat tehota. Siihen kun löytyisi yksinkertainen ratkaisu. Seuraavassa hieman lisää tietoa biofilmeistä:

http://www.youtube.com/watch?list=PLMz9Cxv17J018ixKazyUvumZtI8kcWb12&v=lpI4WCM_9pM&feature=player_detailpage

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 26.10.2013 - 14:41:10


Tulevaisuuden biofilmien hallintaa:

Genetically engineered bacteria can be used to attack other bacterial species

http://www.economist.com/news/science-and-technology/21587769-genetically-engineered-bacteria-can-be-used-attack-other-bacterial-species-set



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.10.2013 - 12:24:40

Valacyclovir in the treatment of post viral fatigue syndrome

http://www.drmyhill.co.uk/wiki/Valacyclovir_in_the_treatment_of_post_viral_fatigue_syndrome

Artikkelista lyhyesti:

Chronic Epstein-Barr virus and other human herpes viruses may be a cause of long term symptoms in chronic fatigue syndrome. Treatment with anti-virals is effective in restoring sufferers to health.

Martin Lerner has been working since 1993 on the idea that many cases of chronic fatigue syndrome result from longstanding infection with herpes viruses. The most important of these is Epstein-Barr virus (glandular fever or “mono”), but he has also identified two other herpes viruses as a particular problem in CFS* sufferers, namely cytomegalovirus and human herpes virus 6 (HHV-6). He demonstrates that in CFS/MEs there is non-permissive replication of virus. By this he means that there is sufficient viral replication going on in cells to disrupt cellular metabolism and cause cell death, but not sufficient to result in a positive DNA polymerase test, or antigenemia with antibody response. This means that such chronic infection will not be picked up by standard virology tests including antibodies and PCR. This very much echoes the ideas of Dr John Chia, who believes that many patients with chronic fatigue syndrome have ongoing viral infection which he describes as being “under the radar”, i.e. the immune system does not seem to see it. This is a little bit like HIV infection, where the virus tucks itself away inside cells, again so the immune system cannot “see” it.

Four studies showing that long term antivirals work

Lerner looked at 106 consecutive cases of CFS* and found the presence of Epstein-Barr virus alone in 28% of these cases, in a further 53% of cases there was Epstein-Barr virus combined with cytomegalovirus, or HHV-6, which means that Epstein-Barr virus was involved in a total of 81% of patients with CFS/ME.

Most importantly, he went on to show that the Epstein-Barr virus could be treated effectively with an anti-viral valacyclovir and if there is co-infection with HCMV or HH-V-6 then some trials used valganciclovir in addition to the valacyclovir. He reported good responses to treatment. Indeed, he reviewed four studies involving several hundred patients with CFS using this combination of drugs and reported long term patient recovery. This recovery was determined in terms of clinical improvement, improvement in serum EBV titres (with regard to EBV virus, early antigen (diffuse), EBV viral capsid antigen and immoglobulin-M), together with improvements in 24 hour ECG and improvement in cardiac dynamic studies.

**********
Lähes kaikilla on EBV, mutta kuinka monella se on jäänyt "päälle", kroonistunut..  Saksan kokeiden perusteella saan EBV:hen hoitona Delimmun-lääkettä, jota ei ole saatavilla Suomessa. Ehkä minulla on MSDIS, eli Multiple Systemic Infectious Disease Syndrome, jonka nimitti  Dr Horowitz (katso aiemmat sivut).

Toinen EBV tutkimus, josta ei abstraktia:

Babesiosis mimicking Epstein Barr Virus (EBV) infectious mononucleosis: another cause of false positive monospot tests.

http://www.ncbi.nlm.nih.gov/pubmed/22266386

Ja juuri kun kuvittelit, että testituloksiin voisi luottaa..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.11.2013 - 12:49:11

Enemmän tietoa keuhkoklamydiasta, Dr Wheldonin esitelmä 2010:

The Pathogenesis of Chlamydia pneumoniae in Multiple Sclerosis: Current Thoughts and Future Directions


http://beyondthebandaid.com.au/wp-content/uploads/2012/07/The-Pathogenesis-of-Chlamydia-pneumonia-in-Multiple-Sclerosis_Current-Thoughts-and-Future-Directions.pdf

Tutkituista 37:stä MS-potilaasta 97% löydettiin PCR-testeissä keuhkoklamydia bakteeri. Esitelmässä myös useita piirroksia, jotka havainnollistavat bakteerin tunkeutumista keskushermostoon, demyelinisaatiota jne. Ilman ääntä kuvat eivät kerro aivan niin helposti tarinoitaan.




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.11.2013 - 13:23:58

Human Babesiosis

http://dermatologycentral.typepad.com/files/nejmra1202018.pdf

Tämä on yhteenveto babesioosista ihmisissä. Levinnyt pohjoiselle pallanpuoliskolle. Euroopassa lähinnä kahta kantaa. Mutta artikkelissa ei mainita tapauksia, joissa potilaat sairastavat useampia infektioita samanaikaisesti.

Toinen yhteenveto:

Babesiosis Review


http://www.nslc.wustl.edu/courses/Bio348/thach/2011/Babesiosis%20review.pdf

Norjassa on tutkittu babesioosia punkeista, ja sitä esiintyy noin 1%:lla. Mitenkähän Suomessa.. Babesia venatorum taitaa olla se kanta, josta prof. Simka kirjoitti MS-tautiin liittyen, vaikka hän ei mainitse sitä.

Prevalence and diversity of Babesia spp. in questing Ixodes ricinus ticks from Norway

http://www.parasitesandvectors.com/content/pdf/1756-3305-5-156.pdf

Abstract

Background:
Ixodes ricinus ticks transmit Babesia species to vertebrate hosts. Using molecular tools we were able to
detect the presence of this piroplasmid in its vector. The aims of this study were to investigate the prevalence and
identity of Babesia species in questing ticks collected in various areas of Norway.

Methods:
DNA from questing l. ricinus ticks were examined with a realtime PCR for the presence of Babesia.
Positive samples of tick DNA were identified to species using PCR, and sequence analysis.

Results:
From a total of 1908 questing l. ricinus ticks, 17 (0.9%) indicated the presence of Babesia spp. after realtime-
PCR screening. Ixodes ricinus harbouring Babesia spp. was detected in 9 out of 22 localities. Further molecular
analyses of DNA from these positive ticks indicate the presence of Babesia venatorum, B. divergens, B. capreoli
and a currently undescribed Babesia in Norwegian ticks. The most prevalent was B. venatorum found in 71% of the
positive ticks.

Conclusions:
A total of 17 out of 1908 (0.9%) ticks were positive for Babesia. Our data confirm that there are several
Babesia species in ticks in Norway.

Babesia venatorum
was the most prevalent. This species has a zoonotic potential
and may cause human babesiosis following a tick bite.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 06.11.2013 - 08:44:24

Niinpä, virallisten tietojen mukaan babesia bakteeri-infektiot ovat erittäin harvinaisia Suomessa. Ne oletetaan liittyvän karjatalouteen ja ovat harvinaistuneet viimeisten 20 vuoden aikana Suomessa. Seuraavassa linkissä on yhden suomalaismiehen tarina.
http://wwwnc.cdc.gov/eid/article/16/7/09-1905_article.htm

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.11.2013 - 13:10:36

Antimicrobial implications of vitamin D

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3256336/

Evidence exists that vitamin D has a potential antimicrobial activity and its deficiency has deleterious effects on general well-being and longevity. Vitamin D may reduce the risk of infection through multiple mechanisms. Vitamin D boosts innate immunity by modulating production of anti-microbial peptides (AMPs) and cytokine response. Vitamin D and its analogues via these mechanisms are playing an increasing role in the management of atopic dermatitis, psoriasis, vitiligo, acne and rosacea. Vitamin D may reduce susceptibility to infection in patients with atopic dermatitis and the ability to regulate local immune and inflammatory responses offers exciting potential for understanding and treating chronic inflammatory dermatitides. Moreover, B and T cell activation as well as boosting the activity of monocytes and macrophages also contribute to a potent systemic anti-microbial effect. The direct invasion by pathogenic organisms may be minimized at sites such as the respiratory tract by enhancing clearance of invading organisms. A vitamin D replete state appears to benefit most infections, with the possible noteworthy exception of Leishmaniasis. Antibiotics remain an expensive option and misuse of these agents results in significant antibiotic resistance and contributes to escalating health care costs. Vitamin D constitutes an inexpensive prophylactic option and possibly therapeutic product either by itself or as a synergistic agent to traditional antimicrobial agents. This review outlines the specific antimicrobial properties of vitamin D in combating a wide range of organisms. We discuss the possible mechanisms by which vitamin D may have a therapeutic role in managing a variety of infections.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Sirunen Pvm 08.11.2013 - 14:24:26

Wow!
Pää pyörällä tästä kaikesta tiedosta. Tutustumista riittää! Kiitos tästä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.11.2013 - 09:58:35

Tässä on Sarahin tarina suomenkielisenä:

Sarah Longlands - toissijaisesti etenevä MS-tauti
Alkuperäinen teksti http://www.davidwheldon.co.uk/ms-treatment1.html
Wheldonin protokolla
Tämä tieto on laitettu julkiseksi Sarahin pyynnöstä. On sanottava, että kaikista tutkimuksista huolimatta, joita on julkaistu tieteellisissä julkaisuissa, lääketiede tuskin ymmärtää kroonisen C. pneumoniae (keuhkoklamydia) infektion olemassaolon, ja *varsinkaan* miten sitä tulisi hoitaa.
- Tri. David Wheldon

Sarah, vaimoni, taitava taiteilija, sai MS-diagnoosin heinäkuussa 2003. Hänen sairautensa itseasiassa ulottuu takaisin vuoteen 1989, kun hänen oikea kätensä tuli äkkiä heikoksi. Yön jälkeen hänen kätensä toimintakyky palautui täysin. Muutama vuosi myöhemmin, hän koki vähäistä näön harmaantumista yhdessä silmässään; tämä parani muutamassa viikossa. Relapseja tuli joskus uudelleen, mutta kaikki paranivat täysin. Vuonna 1999 remissiot tulivat vähemmän täydellisiksi. Oikean jalan riippunilkka alkoi salakavalasti, eikä parantunut. Sitten vuonna 2001, lyhyen ajan jälkeen pitkittyneen ylähengitystieinfektion jälkeen, joka johti lievän astman puhkeamiseen, Sarah alkoi edetä sairauden uuteen ja nopeasti etenevään muotoon. Kahden vuoden sisällä hän ei enää pystynyt seisomaan ilman apua, hänen piti ottaa tukea huonekaluista, eikä pystynyt pitämään tai käyttämään kynää tai pensseliä oikealla kädellään, ja hän tunsi itsensä huteraksi. Hän sanoi että vaikutti elävänsä henkisessä sumussa: todellakin, iltoina hän oli puoli-unessa, joka ei tehnyt levänneeksi. Hänen puheensa tuli sammaltavaksi. Oli jatkuvaa tunnetta aistien välkkymisestä ja neurologisten oireiden pahenemista. Hän kärsi tinnituksesta, kuuli jatkuvaa ääntä kaukaisesta koneistosta. Hänelle myös kehittyi L'hermitte, joka ilmeni sähköshokkimaisella kivulla selässä, kun päätä taivutti eteenpäin, ja joka ilmaisi vaurioita kaularangan ytimessä.

MRI kuva näytti monta tyypillistä aktiivista leesiota, jotka näkyivät erikokoisina helmimäisinä hyperintensiteetteinä valkeassa aineessa aivoissa. Neurologi sanoi Sarahille että hänellä on MS-tauti; sairaus oli edennyt sekundaaris-progressiiviseen muotoonsa, jolle ei ole olemassa mitään hoitoa, ja sairauden on oletettava etenevän. Olen paljon enemmän interventionaalisempi kuin hän, ja tämä johtuu siitä että olen mikrobiologi, ja suosittelen seuraava anti-klamydiaalista kuuria:

doksisykliini 200 mg kerran päivässä
roksitromysiini 300 mg kerran päivässä (atsitromysiini 250 mg kolme päivää viikossa vaihtoehtona).
Lyhyet kuurit metronidatsolia lisätään myöhemmin tähän kuuriin.

Aloitimme doksisykliinin ensimmäiseksi, koska se oli heti saatavilla. Tulokset olivat hämmästyttäviä. Viisi päivää hän kärsi pahenevista oireista; tähän liittyi flunssankaltaiset oireet, päänsärkyä silmien ympärillä, ja yölliset hikoilut. Tämä on tyypillinen Herxheimer-reaktio; se aiheutuu siitä kun iso bakteerijoukko hajoaa antibiooteilla, tai muilla aineilla. Viiden päivän kuluttua aivosumu hävisi; todellakin, hän sanoi tunteneensa olonsa selkeämmäksi kuin pariin vuoteen. Roksitromysiini lisättiin kolme viikkoa myöhemmin, kun se tuli saataville.

1. syyskuuta 2003
Nyt, vain kuukausi hoidon aloittamisen jälkeen, Sarah paranee. Kuten voisi odottaa, viimeisimmät oireet paranevat ensin. Hänen puheensa ei enää sammalla, mutta on selkeä. Hän voi seistä ilman apua. Kognitiiviset puutteet ovat suurilta osin poissa. Hänellä ei enää ole L'hermitten ilmiötä. Tietysti, matkaa on vielä paljon jäljellä, mutta tämä on alku. Sanotaan usein että MS on relapsoiva sairaus, mutta kun tauti on vakiintunut etenevässä muodossaan, niin sitä pidetään hellitsemättömänä: globaali paraneminen on harvinaista.

25. syyskuuta 2003
Käveleminen on hieman sekavampaa. Toipuminen ei ole vain yksinkertaisesti sitä että jokin toiminto palautuu. Korjaus tapahtuu solutasolla, eikä ole keskitetysti hallittua. Kun korjausta tapahtuu, voi olla monta kummallista tuntemusta - Sarah sanoo että ne ovat aika vaikeasti kuvattavissa - mitkä, kunnes järjestäytyvät, itseasiassa haittaavat toimintoja. Toiminnot on opittava uudelleen. Hän huomauttaa että "on helpompaa kävellä tunnottomilla jaloilla, kuin jaloilla joilla epäjärjestynyt tunne palaa". On olemassa motorisia vastineita tähän - sormien nytkiminen ja pienet raajojen hallitsemattomat liikkeet - mutta nämä ovat vähäisiä. Sarah huomasi että nämä tapahtumat ennustivat isoa toiminnan paranemista. Toipuminen tapahtuu askel askeleelta, kun toiminta opitaan uudelleen.

15. lokakuuta 2003
Iso paraneminen kävelemisessä; 1 km kävelysauvojen kanssa, ja välillä lepäilyä. Vain yli kolme kuukautta doksisykliinin ja roksitromysiinin aloittamisen jälkeen, ja 12:ta B12 injektion jälkeen, ja lisäravinteiden jälkeen, Sarah tunsi itsensä tarpeeksi hyväksi aloittaakseen lyhyen (5 päivää) metronidatsoli kuurin, 400 mg kolme kertaa päivässä. Tämä on pääasiallinen bakteerien tappava antibiootti tässä kuurissa. Reaktio bakteerien jäänteisiin on odotettavissa, ja se tosiaan tapahtui. Se alkoi kolmantena päivänä, ja ilmeni epävakaisuutena, ajattelun vaikeudella, ja epätodellisuuden tunteena; se jatkui kolme päivää sen jälkeen kun metronidatsoli lopetettiin, ja sitten asteittain hävisi ilman täsmällistä loppua. Prochlorperazine, 10 mg suun kautta, oli erittäin tehokas hajoittamaan oireita jotka tulivat tästä reaktioista. Paljon nestettä, verensokeritason pitäminen tasaisena juomalla paljon glukoosia joka oli liuotettu veteen tai mehuun, ja lääkehiilikapselit viimeisinä iltaisin auttoivat kaikki. Jos lääkehiiltä käytetään, on parasta ottaa se veden kanssa tyhjään vatsaan, kaukana siitä hetkestä kun on syönyt, ottanut lääkkeitä tai lisäravinteita. Älä välitä valmistajan ohjeesta, joka suosittelee ruuan jälkeen ottamista. 6-8 260 mg kapselia vaikuttaa sopivalta. Se on vaaratonta.

Toisin kuin ensimmäinen reaktio (doksisykliinin aloittamisen jälkeen), ei ollut mitään hetkellistä neurologisten toimintojen menettämistä; tosiaan, hyvä edistyminen jatkui viiden päivän metronidatsoli hoidon jälkeen.

28. lokakuuta 2003
Ensimmäistä kertaa lähes 18 kuukauteen, Sarah pystyi ajelemaan polkupyörällä, vaikka hän sanoi ettei ole vielä valmis pyöräilemään sännöllisesti, kaatumisriskin vuoksi. Kaatumiset ovat todellinen vaara kaikille joilla on MS-tauti.

Toinen kuuri metronidatsolia aloitettiin; jälkeenpäin ajateltuna, se alkoi liian aikaisin. Reaktio ensimmäiseen kuuriin ei ollut vielä aivan hävinnyt, ja reaktio toiseen oli siksi kumulatiivinen, ja erittäin napakka. Toinen kuuri annettiin vain kolmena päivänä. Reaktio aiheutti epävakaisuutta, vähän tunnottomuutta jaloissa, ja kihelmöintiä käsissä ja jaloissa. Neljän päivän jälkeen tämä oli suurelta osiltaan poissa.

Kun hän maalasi, Sarah huomasi että hän pystyi käyttämään oikeata kättään kauemmin, ja että välttämättömät lepohetket olivat lyhyempiä. Hänen työnsä sai lisää varmuutta.

3. tammikuuta 2004
Myrkkyreaktio jatkuu, tullen ja mennen epäsännöllisesti, mikä vihjaa että toinen metronidatsolikuuri oli jollakin tapaa tuonut esiin bakteerin solunsisäisen muodon immuunipuolustukselle. Hänen virtsansa sisälsi epänormaalin paljon porfobilinogeenia, ja tämä vaikka hän oli anti-porfyriakuurilla (paljon nestettä, paljon hiilihydraatteja, punaisen lihan ja alkoholin välttäminen, ja lääkehiiltä kaksi kertaa päivässä); tämä on näyttöä siitä että reaktiolla oli ainakin joitain sekundaariporfyrian tunnusmerkkejä. Myrkkyreaktio on epämiellyttävä, muttei sietämätön. Se osoittaa että patogeeneja kuolee. Se näyttäytyy pienenä tunnottomuutena jaloissa, jalkojen ja käsien kihelmöintinä, ja epävakaisuudella jota voidaan kuvata "kuin olisi laivan kannella". Olen nähnyt identtisiä myrkkyreaktioita muilla (ei MS-taudista kärsivillä), kun raskas krooninen keuhkoklamydia infektio hoidetaan tappavilla antibioottiyhdistelmillä. Vaikka tämä on epämiellyttävää, se todentaa että kyseessä on infektio.

Tämän reaktion oireiden alla, keskushermoston paraneminen jatkuu. Spastisuuden ja klonuksen merkit, jotka ovat tyypillisiä MS-taudille, ovat lähes poissa. Epänormaalit plantaarirefleksit (todiste vaurioista pitkille keskushermostopäätteille) ovat nyt lähes normaaleja vasemmalla ja vähemmän intensiivisiä oikealla.

Sarah pystyy käyttämään oikeata kättään enemmän voimallisemmin, ja pidemmän ajan. Hän pystyy käsittelemään painavampia esineitä. Hänen käsialansa on parantunut.

Tarina jatkuu...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.11.2013 - 10:03:51

Jatkoa Sarahin tarinaan:

28. helmikuuta 2004
Toinen MRI aivokuva 26 viikkoa ensimmäisen jälkeen, näytti suurta paranemista. Yhtäkään uutta leesiota aivojen valkoisessa aineessa ei ole näkyvissä, ja monet leesioista, jotka näkyivät ensimmäisessä kuvassa olivat pienempiä, olivat menettäneet ääriviivansa, ja olivat vähemmän tiheitä (johtuen filmien eri tiheyksistä). Isoimmat (ja oletettavasti viimeisemmät) leesiot, jotka olivat valkoisen aineen periferiassa olivat erityisen heikentyneitä. Ei ollut paljon muutosta joukossa pienissä aivokammioiden viereisissä leesioissa; nämä olivat oletettavasti aikaisia leesioita jotka ovat tehneet glioosin (arpeutumisen); paljon muutosta näissä ei olisi odotettavissa. Konsulttiradiologi, joka tutki ne kaksi kuvaa minuuttien kuluessa kun toinen otettiin, oli haltioissaan.

Muuten, porfyriareaktiot jatkuvat. Olen nähnyt näitä eräissä potilaissa nyt; oireet tyypillisesti tulevat ja menevät päivän aikana. Niille on tunnusomaista symmetrinen mutta epätäydellinen tunnottomuus ja kihelmöinti käsissä ja jaloissa; vähän heikkoutta käsissä ja jaloissa; tasapainoelinten häiriöitä (huimausta kun liikuttaa päätä, mutta ei kun päätä pidetään paikallaan) ja suhiseva ääni korvissa, usein matala-taajuisella komponentilla. Vaikka ne kuulostavat hälyttäviltä, ne eivät ole oikeastaan ongelmallisia. Tunnottomuus on enemmän näennäistä kuin oikeaa; kosketuksen tunne on tuskin heikentynyt. On tärkeää korostaa että nämä oireet ovat ei-keskushermoston neuropatiaa, eikä niillä ole siten mitään tekemistä MS-taudin kanssa. Niitä voivat kokea myös ne potilaat joilla ei ole aktiivista kroonista keuhkoklamydia infektiota keskushermostossa, jopa ennen kuin hoito aloitetaan, ja niillä on taipumusta pahentua, kun sairautta hoidetaan, ja patogeenit kuolevat. Usein on myös olemassa flunssankaltainen komponentti näissä reaktioissa.

13. kesäkuuta 2004
Sarah jatkaa edistymistään. Ote ja ketteryys hänen oikeassa kädessään, heikkous joka oli ensimmäinen tapahtuma hänen taudissaan - ovat nyt lähes normaaleja. Porfyria-oireet jatkuvat, ja ovat ärsyttäviä eivätkä niinkään ongelmallisia.

10. syyskuuta 2004
Sarah on nyt ollut hoidolla 13 kuukautta. Sinä aikana ei ole ollut mitään epäsuotuisia keskushermosto-oireita. Kolmannessa MRI-kuvassa, joka otettiin radiologin pyynnöstä, ei ole mitään uusia leesioita; vanhat leesiot jatkavat kutistumistaan. Jotkut isot leesiot ovat hävinneet kokonaan. Radiologisti sanoi että hän ei ole nähnyt mitään tällaista ennen MS-taudissa, ja aikoo keskustella kuvista spesialisti neuroradiologien kanssa.

Edistymistä tapahtuu sekä motorisella ja sensorisella rintamalla. Ote on samanlainen molemmilla puolilla; tunne on normaali molemmissa jaloissa.

Sarahilla on vielä pientä perifeeristä neuropatiaa, mikä vaikuttaa tapahtuvan silloin kun kroonista keuhkoklamydia infektioita hoidetaan, ja joka johtuu, osittain, hemi-esiasteista joita vapautuu systemaattisesti ohjelmoitujen solukuolemien jälkeen (keuhkoklamydia estää ohjelmoitua solukuolemaa kroonisissa sairauksissa, ja kun se tapetaan, tapahtuu massiivista uudellenorganisointia kudoksissa). Se on päivittäinen kuvio, joka pahenee päivällä, häviten yöksi. Tätä nähdään usein kun hoidetaan potilaita, joilla on serologisesti todettu krooninen keuhkoklamydiainfektio; sen intensiteetti vaikuttaa olevan verrannollinen alkuperäiseen bakteerikuormaan. Tätä voidaan myös nähdä potilaissa, joilla on hyvin raskas infektio ennen kuin hoidon edes aloittaa.

Sekä krooninen solunsisäinen infektio ja jatkuvat bakteerien rippeet, jotka vapautuvat antibioottihoidon kuluessa, ja sen jälkeen, voivat aiheuttaa "sytokiinimyrskyjä". (Sytokiinit ovat solunsisäisiä viestittäjä-molekyylejä jotka toimivat monimutkaisessa tapahtumasarjassa). Korostunut sytokiinitoiminta voi tuntua alkavalta influenssalta; (todellakin, influenssan oireet johtuvat sytokiini turbulenssista).

Krooninen solunsisäinen tulehdus voi aiheuttaa epätasapainon solujen ja humoraalisen immuunijärjestelmän välille, tuoden esille jälkimmäisen (mahdollisesti bakteerien vapauttamien proteiinien seurauksesta), mikä tukahduttaa edellisen. Tämä ei vain johda immuunipuolustuksen kyvyttömyyteen selviytyä infektioista, mutta myös vääränlaiseen vasteeseen muille vieraille proteiineille. Sama prosessi voi saada aikaan allergiaa. Infektion hoito näyttää korjaavan tätä epätasapainoa. Tämä vaikuttaa tapahtuneen Sarahille. Monena vuotena hyönteispistot olivat aiheuttaneet suurta epämukavuutta; kissankirput ja hyttysten pistot aiheuttivat valtavia vesirakkuloita (4 cm tai enemmän halkaisijaltaan), ja sai hänet tuntemaan itsensä huonovointiseksi useiksi päiviksi, jopa viikoiksi. Hoidon aloittamisen jälkeen hyönteispuremat ovat lakanneet olemasta ongelma.

18. joulukuuta 2004
Sarah lopetti jatkuvan antibioottihoidon kaksi kuukautta sitten. Paranemista tapahtui niitten lopettamisen jälkeen. Me päätimme antaa epäjatkuvan ylläpitoterapian johon kuului 14 päivää doksisykliiniä 200 mg päivittäin, ja roksitromysiiniä 300 mg päivittäin*. Metronidatsoli, 400 mg kolme kertaa päivässä, annetaan viimeiset viisi päivää. Tämä ylläpitoaikataulu toistetaan kahden kuukauden välein.

Muuten, Sarah saa vielä etuja - hänen hienokontrollinsa sormissa ja yleinen ketteryys on lisääntynyt huomattavasti. Hienovaraiset, mutkikkaat tehtävät (kuten korvarenkaiden "perhos" kiinnikkeiden laittaminen) ovat nyt helppoja. Hänellä on myös lisääntynyttä sinnikkyyttä toistuvissa tehtävissä kuten käsinkirjoittamisessa. Hän pystyy myös kävelemään 2 km.

Kun katsastelen hänen edistymistään, pitää sanoa että kestävät spontaanit globaalit remissiot ovat hyvin epätavallisia MS-taudissa, kun etenevä vaihe on kestänyt kauemmin kuin vuoden [Kremenchutzky M., et al. 1999 Brain Oct;122 (Pt 10):1941-50].

*Jos roksitromysiini ei ole saatavilla, atsitromysiiniä voi käyttää. Rifampisiini ei ole sopiva ajoittaiseen käyttämiseen.

31. maaliskuuta 2005
Ajoittainen terapia menee hyvin. Sarah maalaa monimutkaista akvarellia, kun kirjoitan tätä. Toipuminen jatkuu, erityisesti hienomotoriikassa ja ketteryydessä; myös kestävyydessä.

Neuroradiologi spesialisti kävi läpi MRI kuvat, ja sanoi että hän ei ole koskaan nähnyt tällaista paranemista kaikissa uusissa leesioissa vakiintuneessa etenevässä MS-taudissa.

On mielenkiintoista todeta, että missään vaiheessa hiiva ei ollut ongelma. Tämä voi olla koska antibiootit pyyhkivät C. pneumoniaen pois immuunijärjestelmän soluista, jolloin niistä tulee tehokkaampia (Hiiva on aika tavallista niillä, joilla on krooninen väsymysoireyhtymä, joka voi johtua kroonisesta C. pneumoniae infektiosta joissain tapauksissa; paradoksaalisesti sillä on taipumusta poistua spontaanisti antibioottihoidolla).

8. huhtikuuta 2005
Sarahin reaktiot näkö-ärsykkeisiin (dominantti käsi), jotka mittasimme muutama päivä sitten, ovat nyt normaalissa rajoissa, kestäen 245 millisekuntia (vertailun vuoksi normaali aikuisten reaktio-aika on 200-250 millisekuntia, joka kasvaa iän myötä; teinitietokonepelaajat voivat kehittää erittäin nopeat reaktioajat).

Reaktioajat visuaalisiin ärsykkeisiin ovat usein paljon kohonneita MS-taudissa, erityisesti kun on fatiikkia ja "aivosumua"; ne ovat usein luokkaa 1500 - 2000 ms. Luonteenomaisesti, ne kohoavat jopa pidemmiksi toistoilla, mikä tarkoittaa väsyttävää prosessia, ja luultavasti epänormaalia kortikaalista toimintaa (ja sellaista mitä ei voi selittää demyelinaatiolla yksin).

7. kesäkuuta 2005
Tällä viikolla vaimoni ratkaisi London Timesin lauantain shakkiprobleeman paljon nopeammin kuin minä itse (pahimpina aikoina hän ei voinut muistaa nappuloiden nimiä, tai miten niitä siirretään).


7. elokuuta 2005
Nyt on kulunut kaksi vuotta siitä kun Sarah aloitti antibiootit; sinä aikana on tapahtunut valtavaa paranemista. Katsaus noihin kahteen vuoteen on henkisesti raskasta; varhaiset paranemiset tapahtuivat askel askeleelta, ja olivat aika epäsäännöllisiä. Yhtenä aikana käveleminen itseasiassa vaikeutui, kun tunto palasi. Äskettäiset paranemiset - mitkä vielä tapahtuvat - ovat enemmän hienoisia, ja tapahtuvat sujuvasti. Näinä kahtena vuotena, Sarah ei ole kokenut mitään uutta keskushermostovajetta. Matalimmassa kohdassaan, Sarah meni nopeasti alaspäin vammaisuus (EDSS) asteikolla, mennen 6:en läpi kohti 8:aa. Hän on nyt palanut tasolle 2 tällä asteikolla.

Tämän mikro-organismin tunnetaan aiheuttavan kroonista jatkuvaa infektiota koko elimistössä; sen tiedetään myös haittaavan solujen toimintaa. Epäilen että suuri osa paranemisesta tulee vähentyneestä oksidatiivisesta solunsisäisistä vaurioista ja jonkin asteisista palautumisesta mitokondrioiden stressistä: tämä on hyvä syy ottaa laaja valikoima anti-oksidantteja.

27. elokuuta 2005
Neljäs MRI aivokuva oli suhteellisen muuttumaton kolmannesta, joka otettiin vuosi sitten. Uusia leesioita ei ole tullut antibioottien aloittamisen jälkeen, ja paljon kutistumista on tapahtunut jo olemassa olevissa leesioissa.

23. lokakuuta 2005
On vähän sanottavaa, mutta kaikki on positiivista. Ehkä paras asia on heinovarainen Sarahin kasvonilmeiden palautuminen. Fatiikki on ollut kauan poissa, paitsi luonnollinen väsymys joka seuraa pitkän työpäivän jälkeen.

Sarahilla on nyt kestävyyttä maalata koko päivän, jotain mikä ei olisi ollut mahdollista vain muutama kuukausi sitten; edut vaikuttavat olevan lujittuneita. Kunto on myöskin parempi kävellessä. Sarah on työskennellyt sellaisen asian parissa mitä hän on halunnut tehdä jo kauan: neljä vesiväritutkimusta kukista jotka ovat kasvaneet aitamme alla.

9. tammikuuta 2006
Taas jaksaminen ja kestävyys ovat parantuneet. Sarah suunnittelee joitain isoja maalauksia, ja on ojentanut kaksi isoa maalauspohjaa. Tämä vaatii huomattavaa voimaa käsissä, kuten kuka tahansa joka on tehnyt tämän voi kertoa sinulle.

Jatkuu vielä vähän..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.11.2013 - 10:11:36

Viimeistely Sarahin tarinaan:

18. maaliskuuta 2006
Kaikki jatkuu hyvin, monilla hienovaraisilla parannuksilla. Edellinen päivitys näyttää maalauspohjan valmistautumista taiteilijalta; se ja sen kaveri ovat nyt valmiita maalauksia. Päivitykset tulevat nyt todennäköisesti harvemmin, kun Sarah on saanut niin paljon vanhaa itseään takaisin.

13. elokuuta 2006
Nyt on kolme vuotta siitä kun Sarah aloitti hoidon; sinä aikana nopeasti etenevä toissijaisesti etenevä MS-tauti ei ollut vain pysäytetty, vaan ajettu suoraan taaksepäin. Tämä on hyvin harvinaista sairauden luonnollisessa historiassa, kun eteneminen on ollut paikallaan yli vuoden. Hienovaraiset paranemiset jatkuvat. On kliininen truisimi että, jopa yksittäisissä tapauksissa, kuten vauriot onnettomuudesta, tai aivohalvaukset, huomattava paraneminen on epätodennäköistä vammoissa jotka ovat olleet olemassa yli kuusi kuukautta tai pitempään. Se tosiasia että Sarah vielä paranee kolmen vuoden jälkeen, johtuu todennäköisesti hänen lisäravinteistaan, joiden tavoitteena on vähentää hapetusstressiä, tukien hermojen korjausta metyylikobalamiinilla, mitokondriatuki ja tulehduksen vähentäminen. Joku voisi kuvitella että paraneminen johtuu meneillään olevasta uusien vaihtoehtoisten reittien löytämisestä, mutta tämä ei voi selittää tasaista paranemista Babinskin heijasteessa oikeassa jalassa. Antibioottien aloittamisen aikaan, riitti että koski isovarpaseen joka sai aikaiseksi rajun ojennusvasteen; tämä on tasaisesti parantunut, ja, vaikka on vielä lievästi ekstensorinen, siinä että varvas menee ylöspäin vähän, kaikki klonuksen merkit ovat poissa. Tätä samaa pitkä-aikaista paranemista nähdään Sarahin oikeassa kädessä, mikä on ollut heikko vuoden verran, ja halvaantunut kuusi kuukautta. Voima on palanut asteittain, mutta vain viimeisinä kuukausina Sarah on huomannut että se on saanut edeltävän dominanssinsa kun se suorittaa refleksiliikkeitä.

24. marraskuuta 2007
Hienovaraiset paranemiset jatkuvat. Viimeinen on motorisen fatiikin häviäminen oikeassa kädessä; tämä on havaittu voiman laskemisena kun sormia venytetään: venytystä ei voitu ylläpitää. Mitään fatiikkia ei ole nähtävissä (motorinen fatiikki on tavallista etenevässä MS-taudissa, ja sairauden luonnollisessa historiassa, toipuminen on harvinaista).

15. tammikuuta 2008
Taas hienovaraista paranemista on havaittavissa. Vuonna 2003 Sarahilla oli vähän epätaipuisa katse. Tämä ilmiö, mikä on hyvin tavallista MS-taudissa tarkoittaa silmän liikkeen häiriötä kun katse liikkuu sivusuunnassa, ja toinen silmämuna seuraa toista, kestää vähän aikaa että toinen silmä ehtii perässä. Tämä ei nyt näy selvästi Sarahissa, varsinkaan jos et ole tiennyt sen olemassaolosta aikaisemmin.

Paraneminen ei rajoitu keskushermostoon. Krooninen C. pneumoniae infektio tunnetaan siitä että se voi olla loisena pehmytkudoksen soluissa, missä se stimuloi solujen jakaantumista. Tämä voi selittää - niin epätodennäköiseltä kuin se kuulostaakin - pehmytkudoksen ja rasvakudoksen lisääntymisen, jota voidaan havaita keski-iässä. Olen havainnut vuosien kuluessa asianmukaisen kroonisen keuhkoklamydia infektion hoidon jälkeen, että paino, painoindeksi, ja ulkonäkö voivat kaikki normalisoitua. Sarah läpikäy tätä ruumiillista "remonttia". Hän näyttää nuorekkaammalta.

6. kesäkuuta 2009
On vähän raportoitavaa. Mitään kielteistä ei ole tapahtunut kuuden vuoden aikana hoidon aloittamisesta. Tätä ei ole lähes koskaan aikaisemmin tapahtunut sekundaaris-progressiivisessa MS-taudissa, joka on mennyt aggressiiviseen vaiheeseen. (The natural history of multiple sclerosis: a geographically based study. 7. Progressive-relapsing and relapsing-progressive multiple sclerosis: a re-evaluation. Kremenchutzky M, Cottrell D, Rice G, Hader W, Baskerville J, Koopman W, Ebers GC. Brain. 1999 Oct;122 (Pt 10):1941-50.)

Sarahin tarina on tehty julkiseksi muiden auttamiseksi, hänen pyynnöstään.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.11.2013 - 13:26:52

Äijä,

Sarahin tarinan kääntäminen on ollut melkoinen homma - kiitokset!
Tässä 2012 tehty tutkimus, jossa lista tuttuja ja tuntemattomia viruksia ja bakteereita.


Emerging viral and bacterial infections of the central nervous system

http://www.dovepress.com/emerging-viral-and-bacterial-infections-of-the-central-nervous-system-peer-reviewed-article-NBHIV

Ote keuhkoklamydiasta:

Chlamydia pneumoniae
Chlamydia pneumoniae (Cpn), an obligate intracellular
bacterium in the family Chlamydiaceae, typically infects
the human respiratory tract often resulting in a chronic
cough, little sputum production, and a low-grade fever. The
organism has been shown to enter the systemic circulation
following infection of monocytes surveilling lung tissues.
The ability to spread systemically may be one reason this
bacterium has been identified in nonrespiratory conditions,
including AD (Alzheimer's disease) and multiple sclerosis (MS). Associations
of Cpn with AD and MS were first reported in 1998.

Over the last several years, other reports have strengthened
these associations, but more evidence is required
to demonstrate proof of causality.
In this regard, studies
have addressed and continue to address Cpn infection in
vivo in diseased populations and in animal models, and in
vitro in infected tissue cultures. What is becoming clearer
is that Cpn can enter and remain in the CNS as a chronic/
persistent infection, and may be a major stimulus for
neuroinflammation. Furthermore, infection of the brain
may involve not only monocyte delivery but also infection
of the olfactory cranial nerve following exposure in the nose.
Evidence for this pathway follows from analysis of olfactory
tissues from patients with AD, as well as animal models.
Molecular analyses following Cpn infection in cell culture
are addressing specific pathways known to be disrupted or
modified in AD. For example, modification of apoptosis
and autophagy pathways as well as inflammatory pathways
following infection are being studied to better understand
the molecular pathogenesis of infection-mediated disease. In
effect, continued correlation of CNS infection with Cpn and
AD and MS may reflect the relatively newly recognized emergence
of chronic infection with major neurological diseases.
Treatment for community-acquired pneumonias, including
those caused by Cpn, typically involves antibiotics such as
doxycycline, azithromycin, and/or fluoroquinolones.
One clinical trial with some positive results has been performed
using the anti-Cpn antibiotics doxycycline and rifampin in
treating patients with AD.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.11.2013 - 15:26:03

HopeSpringsin kiitokset kuuluvat jolle kuule muulle suomennoksesta, eivät minulle. Minä hiukan vain editoin tekstiä, en asiasisältöä kuitenkaan!

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Sirunen Pvm 09.11.2013 - 16:34:31

Siis ihan kaikille tästä viesti(mikä se nyt on-en muista sanaa) no koko jutusta, että ollaan kaivettu tietoa. Tähän menee aikaa tutustua, mutta ainakin erilaisia hoitomuotoja ON OLEMASSA.
Vaikka itse nyt miettii just nyt mikä tulee olemaan dg, niin siis paljon on vielä kaikkea mitä toisten lääkäreiden mielestä- pätkii...niinku eri tapoja hoitaa.
Ja siis kiitos myös tietty vinkistä tulla katsomaan tänne =)
Anteeksi kun pätkii kirjoittaminen...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.11.2013 - 19:13:13

Jos lääketieteen edistysaskeleista huolimatta MS-tautia ei ole pystytty hoitamaan, jossain mättää. Eli ehkä asiaan tarvitaan uusia katsontakantoja.. En näe mitään syytä iskeä päätä seinään, jos siitä ei ole apua.

Tässä uutinen lokakuulta 2013:

Soil-based bacteria discovered in humans 'may trigger MS'


http://www.medicalnewstoday.com/articles/267676.php

Scientists have discovered a soil-based bacteria in humans for the first time, and they believe it may be a trigger of multiple sclerosis. This is according to a study published in the journal PLOS ONE.

Researchers from Weill Cornell Medical College and Rockefeller University discovered the bacterium Clostridium C. perfringens type B in a 21-year-old patient suffering from multiple sclerosis (MS).

The researchers say although their study is small, their findings are so "intriguing" that it has caused them to start work on new treatments for the debilitating disorder.

The researchers explain that Clostrodium perfringens - found in soil - is one of the most common bacteria worldwide. The bacterium is divided into five types, A to E.

Type A is a common form found in the human gastrointestinal tract that is thought to be harmless. However, the researchers say that type B and D carry a gene (epsilon toxin) that emits a protoxin, which develops into a potent epsilon toxin in the intestines of grazing animals.

The epsilon toxin then goes through the blood stream to the brain, causing damage to brain blood vessels and myelin - insulation protecting neurons - resulting in symptoms similar to that of MS in humans.

The researchers say that only two humans have been found with type D bacterium, while type B had never been found. But they wanted to determine whether both types B and D did exist in humans, and whether these bacterium are linked to MS.
C. perfringen type B in humans 'truly significant'

After blood and spinal fluid samples were taken from patients with MS, these were tested for antibody reactivity to epsilon toxin and compared with samples from patients without MS.

Stool samples were also taken from both MS patients enrolled in the Harboring the Initial Trigger for MS (HITMS) trial, and those without the disease.

Results showed that patients with MS had levels of epsilon toxin antibodies ten times higher than those without MS. Furthermore, the stool samples showed that only 23% of MS patients carried the type A bacterium, compared with 52% of healthy patients.

"This is important because it is believed that the type A bacterium competes with the other subtypes for resources, so that makes it potentially protective against being colonized by epsilon toxin secreting subtypes and developing MS," the researchers note.

But most importantly, the researchers discovered the type B bacterium in one patient who they say was experiencing a "flare-up" of MS.

The researchers explain that this discovery is of vital importance:

   "This bacterium produces a toxin that we normally think humans never encounter.

   That we identified this bacterium in a human is important enough, but the fact that it is present in MS patients is truly significant because the toxin targets the exact tissues damaged during the acute MS disease process."

Bacterium 'may send toxin to the brain'

The researchers hypothesize that after a human is infected with C. perfringens B or D, the bacterium can reside in the gut as an endospore, defined as a "seed-like structure" allowing certain bacteria to stay dormant for long periods.

"The human gastrointestinal tract is host to approximately 1,000 different bacterial species, but is not a hospitable environment for C. perfringens type B or D, so it does not grow well there," explains Dr. Timothy Vartanian, professor of neurology and neuroscience at Weill Cornell Medical College and senior study author.

"It hibernates in a protective spore. When it does grow, we anticipate it generates a small quantity of epsilon toxin, which travels through the blood into the brain."

He adds that they believe the bacterium's growth is always present, but "rears its ugly head from time to time."
Potential for 'probiotic cocktail' that destroys bacteria

From these findings, the research team have already begun looking at various treatments that could help to block or destroy C. perfringens B and D.

They note that there are already vaccines available for farm animals that target these pathogens, so a human vaccine is possible. The team are also looking at the creation of small-molecule drugs that would work by stopping the epsilon toxin from binding to the receptor.

But Dr. Vartanian says he is particularly excited about the possibility of a "probiotic cocktail" that can kill the pathogens:

"One of my favorite approaches is development of a probiotic cocktail that delivers bacteria that compete with, and destroy, C. perfringens types B and D. It would be such a beautiful and natural way to treat the gastrointestinal system and solve the problem."

Although the researchers are unaware of how humans can become infected with C. perfringens B or D, Dr. Vartanian says future studies will analyze the potential routes of exposure for MS patients:

   "While it is clear that new MS disease activity requires an environmental trigger, the identity of this trigger has eluded the MS scientific community for decades.

   Work is underway to test our hypothesis that the environmental trigger for MS lays within the microbiome, the ecosystem of bacteria that populates the gastrointestinal tract and other body habitats of MS patients."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 10.11.2013 - 10:01:52

Kuten olen jo varmaan aiemminkin tehnyt selväksi sen tosiseikan, että kun globaalisti on "sovittu" MS-taudin olevan autoimmuunisairaus. On todella vaikeaa saada suurta koneistoa muuttamaan suuntaa. Vaikka tutkimuksia tehdään vaihtoehdoista, niin vastassa on miljardiluokan bisnes ja lähes koko neurologien "virkakoneisto". Vaaditaan paljon aikaa, tutkimustietoa ja empiirisiä tuloksia, ennen kuin käsitykset voivat muuttua. Mutta aina löytyy yksittäisiä lääkäreitä, ei välttämättä neurologeja, jotka ovat valmiita kokeilemaan jotain vaihtoehtoista hoitoa. Usein vaaditaan kärsivällisyyttä, tutkimustuloksia, verikokeita (esim. ulkomailla) tms., että voidaan kokeilla jotain vaihtoehtoa. Ja on oleellisen tärkeää ymmärtää mikä on autoimmuunisairauden hoidon ja infektiosairauksien hoitojen ero.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 10.11.2013 - 10:36:08

Tästä linkistä pääsee sivustolle, jossa on taas paljon eri tutkimuksiin johtavia linkkejä sprokeetasta ja MS-tautia sairastavan hermosoluista (aivoista).
http://molecularsolution.wordpress.com/2011/02/20/spirochetes-found-in-multiple-sclerosis-patients/

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.11.2013 - 20:40:21

Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells

http://www.ncbi.nlm.nih.gov/pubmed/12630667

Abstract

Since the possibility of interruption of latent EBV infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. We have observed EBV replication in lymphoblastoid cells after superinfection with B. garinii and B. afzelii strains after 1 and 4 h of their interaction. We found that viral and borrelial antigens persisted in the lymphoblasts for 3 and 4 days. Morphological and functional transformation of both agents facilitate their transfer to daughter cells. Association with lymphoblasts and internalization of B. garinii by tube phagocytosis increased replication of viruses more successfully than B. afzelii and chemical inductors. Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.11.2013 - 20:45:54

Kombinaatio antibiootteja keuhkoklamydian aiheuttaman  reuman hoidossa:

Combination Antibiotics as a Treatment for Chronic Chlamydia-Induced Reactive Arthritis

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2907099/

Background

Chlamydia trachomatis (Ct) and Chlamydophila (Chlamydia) pneumoniae (Cpn) are known triggers of reactive arthritis (ReA). These chlamydial species exist in a persistent metabolically active infection state in the synovium suggesting that persistent chlamydiae may be susceptible to antimicrobial agents. The goal of this study was to investigate whether a six-month course of combination antibiotics is an effective therapy for patients with chronic Chlamydia-induced ReA.
****
Conclusion

These data suggest that a 6-month course of combination antibiotics is an effective therapy for chronic Chlamydia-induced ReA.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.11.2013 - 13:17:41

Long-term impact of systemic bacterial infection on the cerebral vasculature and microglia

http://www.jneuroinflammation.com/content/9/1/146

Background

Systemic infection leads to generation of inflammatory mediators that result in metabolic and behavioural changes. Repeated or chronic systemic inflammation leads to a state of innate immune tolerance: a protective mechanism against overactivity of the immune system. In this study, we investigated the immune adaptation of microglia and brain vascular endothelial cells in response to systemic inflammation or bacterial infection.

Methods

Mice were given repeated doses of lipopolysaccharide (LPS) or a single injection of live Salmonella typhimurium. Inflammatory cytokines were measured in serum, spleen and brain, and microglial phenotype studied by immunohistochemistry. To assess priming of the innate immune response in the brain, mice were infected with Salmonella typhimurium and subsequently challenged with a focal unilateral intracerebral injection of LPS.

Results

Repeated systemic LPS challenges resulted in increased brain IL-1β, TNF-α and IL-12 levels, despite attenuated systemic cytokine production. Each LPS challenge induced significant changes in burrowing behaviour. In contrast, brain IL-1β and IL-12 levels in Salmonella typhimurium-infected mice increased over three weeks, with high interferon-γ levels in the circulation. Behavioural changes were only observed during the acute phase of the infection. Microglia and cerebral vasculature display an activated phenotype, and focal intracerebral injection of LPS four weeks after infection results in an exaggerated local inflammatory response when compared to non-infected mice.

Conclusions

These studies reveal that the innate immune cells in the brain do not become tolerant to systemic infection, but are primed instead. This may lead to prolonged and damaging cytokine production that may have a profound effect on the onset and/or progression of pre-existing neurodegenerative disease.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.11.2013 - 13:25:50


INNATE IMMUNITY: THE MISSING LINK IN NEUROPROTECTION AND NEURODEGENERATION?


http://people.ucalgary.ca/~mdnguyen/pdf/20025.pdf

Innate immunity was previously thought to be a nonspecific immunological programme that was
engaged by peripheral organs to maintain homeostasis after stress and injury. Emerging
evidence indicates that this highly organized response also takes place in the central nervous
system. Through the recognition of neuronal fingerprints, the long-term induction of the innate
immune response and its transition to an adaptive form might be central to the pathophysiology
and aetiology of neurodegenerative disorders. Paradoxically, this response also protects neurons
by favouring remyelination and trophic support afforded by glial cells.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.11.2013 - 15:30:41

Lääkäri, joka parani ALS:sta. Itse asiassa hänellä olikin borrelioosi ja babesioosi:

Motor neuron disease recovery associated with IV ceftriaxone and anti-Babesia therapy

http://owndoc.com/pdf/4g-day-ceftriaxone-als-bb.pdf

This report summarizes what we believe to be the first verifiable case of a significant and progressive motor neuron disease (MND) consistent with amyotrophic lateral sclerosis that resolved during treatment with
i.v. ceftriaxone plus oral atovaquone and mefloquine. The rationale for use of these antibiotics was (i) positive testing for Borrelia burgdorferi and (ii) red blood cell ring forms consistent with Babesia species infection. The patient has continued to be free of MND signs and symptoms for 15 months, although some symptoms consistent with disseminated Borreliosis remain.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 16.11.2013 - 14:28:34

Borrelioosi lääkärin vertailu:

MS vs Lyme Disease

http://www.drsusanmarra.com/services/patient-resources/ms-vs-lyme-disease

....Alan MacDonald, MD, a pathologist in Long Island, New York suggested that we rule out Lyme disease as a causal agent of Multiple Sclerosis.  In a scientific study authored by Alban, P, Johnson, P, and Nelson, D, , in the Journal of Microbiology (2000),  it was demonstrated in the laboratory that spirochetes are unable to manufacture their own fatty acids and therefore gravitate to places of high density fatty acids exhibiting “neurotropic behavior”. This would make sense in light of the fact that, Neuroborreliosis (neurological Lyme disease) is often characterized by white matter lesions in the brain resembling those found in MS patients.  Additionally, MS and Lyme disease can both be relapsing diseases.  I am not suggesting that ALL MS patients have Lyme disease, but rather, that Lyme disease should be considered in the differential diagnosis.  White matter lesions on an MRI look the same whether the etiology is MS or Lyme disease.  However, lesions due to MS do not recede with antibiotic use, whereas lesions due to the bacteria that cause Lyme disease may simply decrease in size or disappear with antibiotics.

To date there is no known cure for MS, and treatments including interferon may help to halt progression of the disease.  However, if an underlying tick-borne infection is present, antibiotics that cross the blood brain barrier can be used.  Follow up MRI tests can reveal that if infection is present, a receding of the white matter lesions occurs, and healing can take place.  Return of total function may or may not occur depending on many factors including: genetic propensity, environmental influences, diet, length of time of infection, status of the immune system, and virulence of the strain of spirochete(s) present.

Western Blot IgM and IgG testing for Lyme disease should be considered in patients with a diagnosis of Multiple Sclerosis who have known previous tick bites or who live in endemic areas where the exposure rate to ticks is high.    

A diet rich in fats known as the “Swank Diet” has been reported to aid in slowing the progression of MS symptoms.  This makes sense in light of the fact that if the disease in question is caused by the spirochetal bacteria, providing fatty acid nutrients which these bacteria require to live and replicate, may decrease symptoms and neural inflammation by keeping the bacteria well fed and “happy”.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 16.11.2013 - 15:53:57

Niinpä, Tämän tutkijan mukaan Lymen tauti lähtee antibiooteilla ja MS-tauti ei. Mutta miksi ppms (kuten minulla) luokitellaan MS-taudiksi, vaikka ei tulehduspesäkkeitä ole ollenkaan? Ihmettelen suuresti suomalaista julkista terveydenhoitoa, joka ei ota Lymen taudin mahdollisuutta tosissaan. Kyllä ainoa mahdollisuus on turvautua ulkomailla tehtäviin veren bakteerimäärityksiin, kotimaiset alkavat tuntua lähinnä vitseiltä. "Swank Diet" on ruokavaliona varmaan hyvä, olen itsekin vähentänyt varsinkin rasvojen käyttöä jo pitkään.
Tässä linkki Tri Swankin sivuille:
http://swankmsdiet.charityfinders.org/About%20Dr%20Swank/#top

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 16.11.2013 - 21:18:52

Jep. Minun neurologini sanoi, että minulla on näivetystauti, johon ei ole lääkitystä tai hoitoa. Virallisesti papereissa lukee PPMS-tauti. Ensimmäisenä vuonna minulla oli RRMS, toisena epätyypillinen MS, ja kolmantena edellä mainittu näivetystauti. Niin se kehittyy neurologien mielestä. Diagnoosista masentuneena ja myöhemmin kiukustuneena päätin etsiä muita vaihtoehtoja, ennen kaikkea mahdollista borrelioosia, joka oli ollut pari vuotta diagnoosin jälkeen tehdyissä kokeissa positiivinen. Tietysti Suomessa se oli vanhan infektion serologinen arpi, eikä sille tarvinnut tehdä mitään. Että semmoista.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Caroline80 Pvm 17.11.2013 - 10:33:31

Jos RRMS etenee, siitä saattaa tulla SPMS, mutta kaikilla se ei etene koskaan. Joidenkin MS-tauti on benign. PPMS ei ole RRMS.:).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 17.11.2013 - 14:02:30

Vaikkei aihe kuulukaan tälle palstalle, selvyyden vuoksi kerrataan:
MS-tauti jaetaan karkeasti neljään pääryhmään:
1. Aaltomaisesti etenevä MS-tauti (relapsoiva-remitoiva) eli RRMS
2. Toisisijaisesti etenevä MS-tauti (sekundaarisesti-etenevä) eli SPMS, SPMS kehittyy RRMS:stä ei kuitenkaan kaikille.
3. Ensisijaisesti etenevä MS-tauti (ensijaisesti-etenevä) eli PPMS, jossa ei ole "pahiksia", se etenee tasaisesti alusta alkaen.
4. Ns. hyvälaatuinen MS-tauti, jonka alussa 1-2 "pahista", mutta joista potilas toipuu lähes täysin.
Näiden virallisten luokitusten jälkeen alkavat vaikeudet. On paljon potilaita, joiden oireet muistuttavat tänä vuonna tätä ja ensi vuonna tota. Sitten on lisäksi potilaita, joita ei voida laittaa mihinkään katekoriaan, heidät armollisesti vain todetaan sairastavan MS-tautia ja annetaan joku diagnoosi (parempi kuin ei mitään).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Tuikku-80 Pvm 17.11.2013 - 22:01:39

Kiitos Äijä yhteenvedosta!
Armollisesti MS-diagnoosin pari kuukautta sitten saaneella on edessä vielä paljon asiaan perehtymistä...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 18.11.2013 - 11:47:31


HopeSprings 16.11.2013 - 21:18:52:
Minun neurologini sanoi, että minulla on näivetystauti, johon ei ole lääkitystä tai hoitoa. Virallisesti papereissa lukee PPMS-tauti. Ensimmäisenä vuonna minulla oli RRMS, toisena epätyypillinen MS, ja kolmantena edellä mainittu näivetystauti. Niin se kehittyy neurologien mielestä.

Näivetystautiko? http://fi.wikipedia.org/wiki/Hevosen_n%C3%A4ivetystautivirus "Hevosen näivetystautivirus eli hevosen lentivirus (lyh. EIAV) on hevosilla esiintyvä retroviruksiin kuuluva lentivirus, joka infektoi hevosen makrofageja ja lymfosyyttejä ja aiheuttaa hevoselle näivetystaudin"

Sinulla on mielestäni outo neurologi. Mä vaihtaisin lääkäriä heti.:)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 18.11.2013 - 12:36:06

Joopa joo, ei pidä laskea leikkiä toisen sairaudella! Kyllä ihmiselläkin voi olla näivetystauti. Tässä pari linkkiä asiaan:
http://www.saunalahti.fi/arnoldus/cobalami.htm
http://www.ojrd.com/content/pdf/1750-1172-1-17.pdf

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.11.2013 - 12:53:03

Lisää tutkimusta kaivataan:

Chronic Lyme borreliosis at the root of multiple sclerosis--is a cure with antibiotics attainable?

http://www.ncbi.nlm.nih.gov/pubmed/15617845


Abstract

Apart from its devastating impact on individuals and their families, multiple sclerosis (MS) creates a huge economic burden for society by mainly afflicting young adults in their most productive years. Although effective strategies for symptom management and disease modifying therapies have evolved, there exists no curative treatment yet. Worldwide, MS prevalence parallels the distribution of the Lyme disease pathogen Borrelia (B.) burgdorferi, and in America and Europe, the birth excesses of those individuals who later in life develop MS exactly mirror the seasonal distributions of Borrelia transmitting Ixodes ticks. In addition to known acute infections, no other disease exhibits equally marked epidemiological clusters by season and locality, nurturing the hope that prevention might ultimately be attainable. As minocycline, tinidazole and hydroxychloroquine are reportedly capable of destroying both the spirochaetal and cystic L-form of B. burgdorferi found in MS brains, there emerges also new hope for those already afflicted. The immunomodulating anti-inflammatory potential of minocycline and hydroxychloroquine may furthermore reduce the Jarisch Herxheimer reaction triggered by decaying Borrelia at treatment initiation. Even in those cases unrelated to B. burgdorferi, minocycline is known for its beneficial effect on several factors considered to be detrimental in MS. Patients receiving a combination of these pharmaceuticals are thus expected to be cured or to have a longer period of remission compared to untreated controls. Although the goal of this rational, cost-effective and potentially curative treatment seems simple enough, the importance of a scientifically sound approach cannot be overemphasised. A randomised, prospective, double blinded trial is necessary in patients from B. burgdorferi endemic areas with established MS and/or Borrelia L-forms in their cerebrospinal fluid, and to yield reasonable significance within due time, the groups must be large enough and preferably taken together in a multi-centre study.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.11.2013 - 13:01:50

Anti-Malaria Drug Chloroquine Finding May Lead to Treatments for Arthritis, Cancer and Other Diseases

http://www.sciencedaily.com/releases/2011/07/110718155616.htm

July 22, 2011 — In a study published recently in the journal Science Signaling, Van Andel Research Institute (VARI) scientists demonstrate on the molecular level how the anti-malaria drug chloroquine represses inflammation, which may provide a blueprint for new strategies for treating inflammation and a multitude of autoimmune diseases such as arthritis, multiple sclerosis, and certain cancers.



Chloroquine is a widely used anti-malaria drug that inhibits the growth of parasites. For decades, chloroquine and its derivative amodiaquine have also been used as anti-inflammation drugs to treat diseases such as rheumatoid arthritis, though the exact mechanism of how chloroquine affects the immune system has remained unclear.

By providing an understanding of these basic functions, researchers may now have the necessary tools to develop improved treatments for a myriad of common autoimmune disorders.

"The implications of this study are significant," said Henry F. McFarland, Ph.D., former Chief of the Neuroimmunology Branch of the National Institute of Neurological Disorders and Stroke (NINDS). "These results provide a mechanistic basis for therapeutic strategies for treating inflammation and autoimmune diseases and should provide exciting new approaches which can be tested in clinical trials."

Autoimmune diseases arise when the body's immune system mistakes otherwise healthy cells, tissues, and organs for pathogens and attacks them. These diseases can afflict any part of the body, but one symptom common to most autoimmune diseases is that of inflammation.

The National Institutes of Health (NIH) lists more than 80 common autoimmune diseases including asthma, Crohn's disease, Guillain-Barré syndrome, multiple sclerosis, myasthenia gravis, psoriasis, rheumatoid arthritis, and some types of cancers among many others.

Dr. H. Eric Xu, Head of the VARI Center for Structural Biology and Drug Discovery, and his colleagues showed that chloroquine represses inflammation through synergistic activation of glucocorticoid signaling. Glucocorticoids are a class of steroid hormones that bind to the glucocorticoid receptor present in almost every vertebrate animal cell. They are among the most potent and effective agents for treating inflammation and autoimmune diseases.

Synthetic glucocorticoids are used for treating asthma, allergies, and rheumatoid arthritis. Since glucocorticoids also interfere with some of the abnormal mechanisms in cancer cells, they are also used in high doses to treat certain cancers such as leukemia and lymphoma. However, at therapeutic dosages, glucocorticoids can cause a range of debilitating side effects including diabetes, osteoporosis, skin atrophy, and growth retardation.

"The discovery and development of novel uses of glucocorticoids that retain their beneficial therapeutic effects but reduce undesired adverse side effects remains a major medical challenge," said VARI Research Scientist Yuanzheng He, Ph.D., lead author of the study.

The VARI research revealed an unexpected regulation of glucocorticoid signaling by lysosomal functioning. Lysosomes are organelles found in animal cells that use enzymes to break down waste materials and cellular debris.

Researchers found that they could mimic the effect of chloroquine by inhibiting lysosomes in the cell. They believe that the development of new therapies for treating inflammation and autoimmune disease will involve strategies that combine both glucocorticoid and lysosomal inhibitors.

"We have known for some time that both steroids and lysosomes affect the immune system, but we didn't know that they worked together," said VARI President and Research Director Jeffrey Trent, Ph.D. "Researchers now have a clear path forward for undertaking projects to develop glucocorticoid and lysosomal inhibitors, and to improve the efficacy and potency of chloroquine as a therapeutic agent."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 19.11.2013 - 08:32:00

Kyllä MS-taudin syytä yritetään löytää usealla rintamalla, itse pidän bakteeritulehduksia usealla "MS-potilaalla" tärkeänä syynä oireisiin, mutta ne biofilmit. Onneksi asiaa tutkitaan koko ajan, kuten tämä tanskalainen:

The role of bacterial biofilms in chronic infections.
Bjarnsholt T.
Source
Københavns Universitet, København N, Denmark. tbjarnsholt@sund.ku.dk

Abstract

Acute infections caused by pathogenic bacteria have been studied extensively for well over 100 years. These infections killed millions of people in previous centuries, but they have been combated effectively by the development of modern vaccines, antibiotics and infection control measures. Most research into bacterial pathogenesis has focused on acute infections, but these diseases have now been supplemented by a new category of chronic infections caused by bacteria growing in slime-enclosed aggregates known as biofilms. Biofilm infections, such as pneumonia in cystic fibrosis patients, chronic wounds, chronic otitis media and implant- and catheter-associated infections, affect millions of people in the developed world each year and many deaths occur as a consequence. In general, bacteria have two life forms during growth and proliferation. In one form, the bacteria exist as single, independent cells (planktonic) whereas in the other form, bacteria are organized into sessile aggregates. The latter form is commonly referred to as the biofilm growth phenotype. Acute infections are assumed to involve planktonic bacteria, which are generally treatable with antibiotics, although successful treatment depends on accurate and fast diagnosis. However, in cases where the bacteria succeed in forming a biofilm within the human host, the infection often turns out to be untreatable and will develop into a chronic state. The important hallmarks of chronic biofilm-based infections are extreme resistance to antibiotics and many other conventional antimicrobial agents, and an extreme capacity for evading the host defences. In this thesis, I will assemble the current knowledge on biofilms with an emphasis on chronic infections, guidelines for diagnosis and treatment of these infections, before relating this to my previous research into the area of biofilms. I will present evidence to support a view that the biofilm lifestyle dominates chronic bacterial infections, where bacterial aggregation is the default mode, and that subsequent biofilm development progresses by adaptation to nutritional and environmental conditions. I will make a series of correlations to highlight the most important aspects of biofilms from my perspective, and to determine what can be deduced from the past decades of biofilm research. I will try to bridge in vitro and in vivo research and propose methods for studying biofilms based on this knowledge. I will compare how bacterial biofilms exist in stable ecological habitats and opportunistically in unstable ecological habitats, such as infections. Bacteria have a similar lifestyle (the biofilm) in both habitats, but the fight for survival and supremacy is different. On the basis of this comparison, I will hypothesize how chronic biofilm infections are initiated and how bacteria live together in these infections. Finally, I will discuss different aspects of biofilm infection diagnosis. Hopefully, this survey of current knowledge and my proposed guidelines will provide the basis and inspiration for more research, improved diagnostics, and treatments for well-known biofilm infections and any that may be identified in the future.

© 2013 APMIS Published by Blackwell Publishing Ltd.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 19.11.2013 - 09:04:20

Lisää tutkimusta biofilmeistä,koko tutkimus löytyy linkistä, alla on abtracti:

http://perspectivesinmedicine.cshlp.org/content/3/4/a010306.full.pdf+html

Bacterial Biofilms: Development, Dispersal, and Therapeutic Strategies in the Dawn of the Postantibiotic Era


Abstract

Biofilm formation constitutes an alternative lifestyle in which microorganisms adopt a multicellular behavior that facilitates and/or prolongs survival in diverse environmental niches. Biofilms form on biotic and abiotic surfaces both in the environment and in the healthcare setting. In hospital wards, the formation of biofilms on vents and medical equipment enables pathogens to persist as reservoirs that can readily spread to patients. Inside the host, biofilms allow pathogens to subvert innate immune defenses and are thus associated with long-term persistence. Here we provide a general review of the steps leading to biofilm formation on surfaces and within eukaryotic cells, highlighting several medically important pathogens, and discuss recent advances on novel strategies aimed at biofilm prevention and/or dissolution.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Annelis Pvm 19.11.2013 - 21:52:09

Voi rähmä, luin Äijän linkistä http://www.saunalahti.fi/arnoldus/cobalami.htm: "Verenheikkous eli anemia näkyy ihon ja limakalvojen kalpeutena, ja lisäksi iho ja silmänvalkuaiset ovat heikosti kellertäviä. Hitaasti kehittyvänä verenheikkous saattaa olla varsin voimakas taudin tullessa ilmi. Anemiaan liittyy sen vaikeusasteesta riippuen yleistä heikkoutta, voimattomuutta, huimausta, sydämentykytystä, hengenahdistusta, rasitusrintakipuja ja erityisesti alaraajojen turvotuksia. Kielen limakalvo muuttuu ohueksi ja sileäksi. Lisäksi pernisiöösissä anemiassa esiintyy usein raajojen kärkiosista alkaen lisääntyvää puutumista, värinätunnon heikkenemistä, pistelyä ja heikkoutta, toisinaan myös lihasten velttoutta tai jäykkyyttä. Erilaiset vatsaoireet ovat yleisiä. Virtsarakon ja peräsuolen sulkijalihakset saattavat heikentyä. Sukukypsässä iässä olevilla hedelmällisyys voi alentua. Myös masennusta ja tylsistymistä on esiintynyt toisinaan" ja totesin monet asiat liiankin tutuiksi. Enpä tiedä haluaisinko edes kuulla omia B12 veriarvojani...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 20.11.2013 - 10:31:27

"Itse ei saa tehdä uutta diagnoosia": näin sanoo neurologi mulle. Kiusaus on kyllä usein suuri. :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.11.2013 - 20:39:57

Biofilmiä on kaikkialla, hampaiden plakkikin on biofilmiä, ja se on myös bakteereiden suojamekanismi. Kaikki mitä olet halunnut tietää biofilmeistä:

http://www.biofilmcommunity.org/

On myös antibiootteja, jotka pystyvät hajoittamaan biofilmiä:

Evaluation of in-vitro antibiotic susceptibility of different morphological forms of Borrelia burgdorferi

https://www.dovepress.com/evaluation-of-in-vitro-antibiotic-susceptibility-of-different-morpholo-peer-reviewed-article-IDR-MVP

Ja eri lähteistä poimittuja biofimiin enemmän tai vähemmän tehoavia hoitokeinoja:

- Lumbrokinaasi, nattokinaasi, serrapeptaasi
- Entsyymivalmiste Biofilm defense
- Tri Ettingerin protokolla:
1. Kookos: Monolaurin (lauriinihappo) 600mg. 2 kapselia x 2/vrk ja/tai Nutiva Extra Virgin Coconut Oil (kylmäpuristettu kookosöljy) 1-3 ruokalusikallista/vrk
2. Nattokinaasi (fibrinolyyttinen entsyymi) 100mg 1 -3 x vrk
3. InterFasePlus (laajakirjoinen entsyymivalmiste jossa on EDTA:ta) 2 kapselia 3 x vrk tyhjän vatsaan.
4. Serrapeptaasi 20 000 yksikköä 2 x vrk.
+ Vältä lisäravinteita joissa on magnesiumia, rautaa tai kalsiumia sillä ne ruokkivat biofilmejä.
+ Käytä pro-ja prebiootteja

-  Rife/EMF/Biofilmi-bakteerit
- Hunaja
- Otsoni
- N-Asetyylikysteiini (NAC)
- ACS200ppm silver, ACZnano Zeolite, BioEnergy-C, Wobenzyme


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 21.11.2013 - 10:07:01

Mielenkiintoista, mutta minkään antibiootin ei yksinään käytettynä luvata läheskään 100 % tehoa. Tässä varmaan perussyy, miksi esim. tri. David Wheldon on käyttänyt kolmen antibiootin yhdistelmää kuurissaan.
Tässä linkki biofilmien yleiseen muodostumiseen:
http://www.youtube.com/watch?feature=player_detailpage&v=FfY19rpnbew
Tästä pääsee katsomaan borrelioosin (Lymen tauti) aiheuttajan, spirokeetan suojautumista biofilmiin.
http://lookingatlyme.blogspot.fi/2013/10/borrelia-burgdorferi-lyme-disease.html
Hammaslääketiede ja sen mukana suuhygienia on pisimmällä biofilmien torjunnassa. Hyvällä suuhygienialla (harjaus ja erilaiset huuhteet) on saatu hyviä tuloksia biofilmin poistossa. Suomessakin on tehty useita opinnäytetöitä (AMK) ja jopa opetuspelejä. Tässä yksi:
http://publications.theseus.fi/bitstream/handle/10024/34376/Biofilmipeli%20-%20virtuaalipelin%20kehittaminen%20suun%20terveydenhuoltoalan%20opiskelijoille.pdf?sequence=1

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 22.11.2013 - 11:35:11

Ettei asia menisi liian helpoksi spirokeetan (borrelia burgdorferi) torjunnassa, biofilmi on vain yksi bakteerin suojautumismenetelmä. Yleinen tapa on siirtyä ns. lepotilaan, kysta-muotoon. Kysta muodon voi tämä bakteeri ottaa nopeasti tunkeuduttua uhriinsa ja myös kohdatessaan antibiootteja, jolloin ne eivät tehoa. Tutkijoiden mukaan se voi verisoluihin tunkeutuneena levitä veren mukana ympäri elimistöä, myös aivoihin, eikä näy siksi julkisen terveyden hoidon testeissä. Asiaan liittyviä tutkimuslinkkejä:
http://droopyyoupi.blogspot.fi/2013/05/bacteria-change-to-cystic-forms-in-just.html
http://lookingatlyme.blogspot.fi/2009/11/brorson-research-translated.html

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 22.11.2013 - 20:50:20

Borrelia bakteerilla on hyvinkin erilaisia muotoja ja niihin kaikkiin löytyy soveltuvia antibiootteja ja kombinaatioita:
Katso Dr Horowitzin esitelmä ILADSin konferenssissa, Treatment of Lyme Disease and Associated Tick-Borne Co-Infections, sivu 14:
cystic forms. (L-forms, spheroplasts, CDW forms) Plaquenil (hydroxychloroquinine), GSE, Flagyl, Tindamax

http://www.ilads.org/lyme_programs/ilads-live/scheduleeur.php




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 22.11.2013 - 21:07:22

Borrelioosin yksi lisäinfektioista on vähän tunnettu babesioosi, joka on kohtalokas henkilöille joilta puuttuu perna, mutta voi kroonistua muiden infektioiden ohella. Babesioosihan on Prof. Simkan mukaan mahdollinen MS-taudin aiheuttaja.

Babesia, re-visited


http://lymemd.blogspot.fi/2011/09/babesia-re-visited.html

Valittuja paloja:

Babesia in humans is an infection of red blood cells. The protozoa invade and reproduces within red blood cells. When the cells rupture Babesia forms quickly attach to other red blood cells. Babesia has two hosts: mouse and tick, both of which are required for the parasite's normal life cycle. The tick is considered the definitive host because this is where sexual reproduction of the organism occurs. Humans are considered an unintended, bystander host, unlucky enough to have been bitten by the wrong tick. In humans Babesia is seen as any of three forms: sporozoites which microscopically have a spherical form, trophozoites which have a ring appearance and merozoites which may have the "Maltese cross" (tetrad) appearance.

*****

The authors report that multifocal coagulative necrosis has been shown to occur with B. duncani at least in Syrian hamsters. This means that Babesial infection within narrow blood vessels likely caused blood clotting associated with multi-organ damage.

In May 2011, The CDC reports a study of Babesia sp. EU1 (of reindeer) which found hemosiderin laden macrophages in multiple tissues, meaning that infected red blood cells were ingested by macrophages. Babesia DNA was found in: bone marrow, brain, heart, kidney, liver, lung, lymph nodes, small intestinal wall and spleen. Perhaps Babesia can sequester itself with organs.

In summary: Babesia can likely cause blood clotting with localized tissue damage. It may persist only within tiny blood vessels or it may be able to exist within tissues. There are many species of Babesia. They may exhibit different biological behavior. Little is known here.

The evolving science may help us uncover a better narrative by which we may describe patho-anatomic-physiological mechanisms supporting the notion of chronic Babesiosis.

In the meantime, our clinical experience and our supporting laboratory data cannot and should not be ignored.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 23.11.2013 - 07:16:37

Niinpä niin, dr. Richard Horowitz on periamerikkalaiseen tapaan ratkaissut Lymen taudin arvoituksen ja keksinyt parannuksen siihen. Hän tietää myös, miten spirokeetta eri lepomuodoissaan voidaan tuhota. Häneltä voi ostaa myös Lymen taudin hoitoa koskevan kirjan.

Toiset tutkijat ympäri maailmaa ovat vasta lähtökuopissaan, kun amerikkalaiset ovat jo myymässä kirjoja? Horowitz ei ole ainoa jenkki, joka vetää mutkat suoriksi (Lymen taudin kohdalla) ja toteuttaa amerikkalaista unelmaa. Jos joku kuulostaa liian hyvältä ollakseen totta, siihen on suhtauduttava erittäin kriittisesti!!!

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.11.2013 - 16:08:22

Erilaisista borrelioosin ja lisäinfektioiden hoitomuodoista voi lukea Suomen Lyme Borrelioosiyhdistyksen sivuilta. Borrelioosia ja lisäinfektioita voi hoitaa IDSA:n ohjeiden mukaan, kuten Suomessa, ILADS:in mukaan, tai Saksan Borrelioosiyhdistyksen mukaan, kuten BCA:ssa.  
Monet borrelioosipotilaat valitsevat  antibioottien sijasta luonnonlääkkeet, joita ovat esim. Dr Comdenin protokolla http://www.nutramedix.ec/ns/lyme-protocol, BCA:n luonnonlääkkeet tai Dr Berweilerin protokolla http://www.dieter-berweiler.de/fileadmin/pdfs/HP/Therapieplan_Borreliose.pdf. Itselleen sopivasta hoidosta voi päätää hoitavan lääkärin kanssa (ainakin Saksassa).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.11.2013 - 16:18:46

Potilaalla oli diagnosoitu MS, mutta olikin neuroborrelioosi:

CO-EXISTANCE OF TOXOPLASMOSIS AND NEUROBORRELIOSIS - A CASE REPORT

http://www.aaem.pl/pdf/12305.pdf

Abstract:
The 53-year-old woman was initially diagnosed with multiple sclerosis, despite the fact that she did not really meet the clinical criteria. Her only symptoms were clumsiness and weakness of the right extremities. Being a veterinary research worker she had been exposed to infectious material. In 1995, she was diagnosed with ELISA as having toxoplasmosis and treated as such. In 2002, after the infectious, flu-like disease, she revealed arthritis and drowsiness, also with memory and language impairment. The patient continued to have symptoms consistent with previously examined clumsiness. She was diagnosed with Lyme via ELISA and PCR, and treated.
She made a full recovery from acute symptoms. After a few months, neurological and neuropsychological examinations were performed. On the background of mild cognitive decline apraxia and difficulties of attention were noted as the main problems. A apraxia [the inability to execute learned purposeful movement] of the right hand complicated the patient’s life and depreciated her quality of life. The patient underwent MRI examination. FSE, FAST and FLAIR sequences were made. The MRI demonstrated the appearance of several small hyperintense lesions in the  white matter of the left and right frontal and left parietal lobe. These lesions were
typical of the post-inflammatory leucoencephalopathy. Additionally, a ring-shaped, low-intensity lesion in the posterior part of the left parietal lobe was noticed. The lesion was 8 mm in diameter and described to be an old toxoplasmosis lesion. The patient had been treated and the symptoms consistent with Lyme disease resolved. Patient continues to have symptoms consistent with focal destruction of the parietal lobe. Over the past
six months, she has not progressed and relapsed in a manner that is consistent with MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.11.2013 - 20:57:02

Kirjoitin aikaisemmin: "Itselleen sopivasta hoidosta voi päätää hoitavan lääkärin kanssa (ainakin Saksassa)"

Tarkoitin, että voi päättää lääkärin kanssa haluaako antibioottihoidon vai luonnonlääkkeet. Verikokeiden perusteella lääkäri pystyy päättämään sopivan hoitomuodon.  Kaikille eivät antibiootit käy, tai he eivät halua pitkää antibioottikuuria.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.11.2013 - 21:04:18

Role of bacterial infection in exacerbation of multiple sclerosis

http://www.ncbi.nlm.nih.gov/pubmed/8534384
Am J Phys Med Rehabil. 1995 Nov-Dec;74(6):415-8

Abstract

One hundred consecutive patients admitted to the hospital with a diagnosis of exacerbation of multiple sclerosis were evaluated for an infectious process. All patients received a complete blood count, urinalysis, urine culture with susceptibility studies, blood cultures, and a chest x-ray at the time of admission. A control group of 55 patients carrying the diagnosis of multiple sclerosis but without symptoms of neurologic decline were also studied. Thirty-five percent of patients experiencing exacerbation of their disease were identified as having a significant bacterial infection compared with 11% in the control group with quiescent disease. These results were significant with a P value of < 0.001. [b]When presumptive viral and bacterial infections diagnosed before admission were included, almost 50% of patients could have had an exacerbation of their disease in response to an infectious process.[/b] Bacterial infection might well play a role in precipitating relapse in multiple sclerosis as well as influencing treatment.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 24.11.2013 - 08:58:53

Vielä kerran borreliosista. Borrelioosi on sikäli ikävä sairaus, että se pitkälle kehittyessään ts. spirokeettojen "asetuttua" ns. taloksi ihmiskehon eri osiin (eri kudoksiin, aivoihin ym.), ja on vaikea parantaa. Sen parantaminen esim. antibiooteilla on vaikeaa, tiedän lähipiirissäni kanssaihmisen, joka on taistellut bakteeria vastaan eri antibiooteilla jo yli 8 vuoden ajan. Antibioottihoitojen tukena voi tietysti kokeilla vaikka mitä, esim. S.H.Buhner on kirjoittanut paksun teoksen "Healing Lyme Disease Coinfections", jossa on paljon antibioottihoitoa tukevaa asiaa.
Lisäksi eri ihmisten immuunipuolustusjärjestelmät ovat teholtaan erilaisia, tästä johtuen mikä lääke tai luontaistuote sopii toiselle ei välttämättä sovi, eikä tehoa toiselle. Vielä ei ole keksitty yhtä ainoaa tehokasta hoitoa, joka sopisi kaikille.
No niin, olen kirjoitellut mielestäni tästä asiasta jo tarpeeksi, joten lopetan tähän. Hyvää alkutalvea kaikille!

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 24.11.2013 - 10:47:16

Mulla oli lapsena punainen kohta jalassa, ja lääkäri epäili punkkia. Sain antibioottikuurin. :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.11.2013 - 13:00:15

Use of penicillin and other antibiotics and risk of multiple sclerosis: a population-based case-control study.

http://www.ncbi.nlm.nih.gov/pubmed/21920946

Abstract

A 2006 study from the United Kingdom found that penicillin use may decrease the risk of multiple sclerosis (MS). To confirm this finding, the authors conducted a nationwide case-control study in Denmark, using the Danish Multiple Sclerosis Registry to identify 3,259 patients with MS onset from 1996 to 2008, and selected 10 population controls per case (n = 32,590), matched on sex and age. Through the National Prescription Database, prescriptions for antibiotics redeemed from 1995 to 2008 and before the date of first MS symptom/index date were identified. Conditional logistic regression analysis was used to compute odds ratios associating antibiotic use with MS occurrence. In total, 1,922 patients (59%) redeemed penicillin prescriptions before the index date and 2,292 (70%) redeemed any type of antibiotic prescription. Penicillin use was associated with an increased risk of MS (odds ratio = 1.21, 95% confidence interval: 1.10, 1.27). Use of any type of antibiotic was similarly associated with an increased risk of MS (odds ratio = 1.41, 95% confidence interval: 1.29, 1.53). The odds ratios for different types of antibiotics ranged between 1.08 and 1.83. Thus, this study found that penicillin use and use of other antibiotics were similarly associated with increased risk of MS, suggesting that the underlying infections may be causally associated with MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.12.2013 - 16:02:58

Tutkimus vuodelta 2000 siitä miten Cpn aiheuttaa ateroskleroosia ja vaikuttaa verenkiertoon.

Growth in Vascular Cells and Cytokine Production by Chlamydia pneumoniae

http://jid.oxfordjournals.org/content/181/Supplement_3/S473.full

Abstract

The proposed pathogenesis of Chlamydia pneumoniae in atherosclerosis is supported by the finding that C. pneumoniae can initiate and sustain growth in human vascular cells. In vitro growth of C. pneumoniae is found in macrophages, peripheral blood monocyte (PBMC)—derived macrophages, endothelial cells, and aortic artery smooth muscle cells. U-937 macrophages infected with C. pneumoniae are capable of transmitting the infection to human coronary artery endothelial cells (CAEC) with direct cellular contact. Production of cytokines by cells infected with C. pneumoniae indicates that the organism can stimulate the immune system. CAEC infected with C. pneumoniae produce more interleukin-8 than cells sham inoculated with negative control cells. When interferon-γ is used to stimulate HEp-2 cells, U-937 cells, and PBMC (before infection with C. pneumoniae), inhibition of a productive growth cycle occurs in a dose-related response. Studies are needed to learn the relationship between productive infection and persistence, the ability of C. pneumoniae to affect the immune response, and the potential for C. pneumoniae to influence atheromatous lesions.

****
The in vitro ability of C. pneumoniae to infect human macrophages, vascular endothelial cells, and aortic smooth muscle cells in vitro provides support for the hypothesis that C. pneumoniae can infect such cells in vivo.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 05.12.2013 - 09:13:53

TB vaccine 'could help prevent MS

http://www.bbc.co.uk/news/health-25207033

An anti-tuberculosis vaccine could prevent multiple sclerosis, early research suggests.

A small-scale study by researchers at the Sapienza University of Rome has raised hopes that the disease can be warded off when early symptoms appear.

More research is needed before the BCG vaccine can be trialled on MS patients.

The MS Society said the chance to take a safe and effective preventative treatment after a first MS-like attack would be a huge step forward.

MS is a disease affecting nerves in the brain and spinal cord, causing problems with muscle movement, balance and vision.

Early signs include numbness, vision difficulties or problems with balance.
     
About half of people with a first episode of symptoms go on to develop MS within two years, while 10% have no more problems.

In the study, published in the journal Neurology, Italian researchers gave 33 people who had early signs of MS an injection of BCG vaccine.

The other 40 individuals in the study were given a placebo.

After five years, 30% of those who received the placebo had not developed MS, compared with 58% of those vaccinated.

"These results are promising, but much more research needs to be done to learn more about the safety and long-term effects of this live vaccine," said study leader Dr Giovanni Ristori.

"Doctors should not start using this vaccine to treat MS or clinically isolated syndrome."

Dr Susan Kohlhaas, head of biomedical research at the MS Society, said it was a small but interesting study.

"It's really encouraging to see positive results from this small trial, but they'll need validating in larger and longer-term studies before we know if the BCG vaccination can reduce the risk of someone developing MS.

"Ultimately, the chance to take a safe and effective preventative treatment after a first MS-like attack would be a huge step forward."

The findings add weight to a theory that exposure to infections early in life might reduce the risk of diseases such as MS by stimulating the body's immune system.

Dr Dennis Bourdette, of Oregon Health and Science University in Portland, US, said the research suggested "BCG could prove to be a 'safe, inexpensive, and handy' treatment for MS".

He wrote in an accompanying editorial in Neurology: "The theory is that exposure to certain infections early in life might reduce the risk of these diseases by inducing the body to develop a protective immunity."

BCG vaccine

   Bacillus Calmette-Guerin (BCG) is a live vaccine made up of a weakened strain of Mycobacterium bovis, a bacterium that causes tuberculosis (TB) in cattle
   The bacteria are altered so that they do not cause a TB infection, but stimulate the body's immune system to make it resistant to the disease
   The vaccine has existed for 80 years and is one of the most widely used of all current vaccines, reaching more than 80% of newborns and infants in countries where it is part of the national childhood immunisation programme.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.12.2013 - 17:50:25

Borrelioosista hieman lisää. Tässä 27 erilaista syytä miksi testi voi olla negatiivinen: http://www.mentalhealthandillness.com/seronegativelymedisease.html

Yksi syistä on se, ettei testata kaikkia lajeja. Huslabin ohjekirjan mukaan http://huslab.fi/ohjekirja/3552.html siellä on käytössä Entsyymi-immunomenetelmä (EIA) ja immunokemiluminometrinen menetelmä. Akkreditoitu menetelmä. IgG- ja IgM-vasta- aineiden seulontavaiheen mittaus EIA-menetelmällä (antigeenina Borrelia afzelii -kanta, johon on IgG-vasta- ainemittauksessa lisätty myös Borrelia burgdorferi ryhmän bakteerien VlsE- antigeenia).


Prevalence, Diversity, and Load of Borrelia species in Ticks That Have Fed on Humans in Regions of Sweden and Åland Islands, Finland with Different Lyme Borreliosis Incidences

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836827/

Abstract

The incidence of Lyme borreliosis (LB) in a region may reflect the prevalence of Borrelia in the tick population. Our aim was to investigate if regions with different LB incidences can be distinguished by studying the prevalence and diversity of Borrelia species in their respective tick populations. The Borrelia load in a feeding tick increases with the duration of feeding, which may facilitate a transmission of Borrelia Spirochetes from tick to host. Therefore, we also wanted to investigate how the Borrelia load in ticks that have fed on humans varies with the duration of tick feeding. During 2008 and 2009, ticks that had bitten humans were collected from four regions of Sweden and Finland, regions with expected differences in LB incidence. The duration of tick feeding was estimated and Borrelia were detected and quantified by a quantitative PCR assay followed by species determination. Out of the 2,154 Ixodes ricinus ticks analyzed, 26% were infected with Borrelia and seven species were identified. B. spielmanii was detected for the first time in the regions. The tick populations collected from the four regions exhibited only minor differences in both prevalence and diversity of Borrelia species, indicating that these variables alone cannot explain the regions’ different LB incidences. The number of Borrelia cells in the infected ticks ranged from fewer than ten to more than a million. We also found a lower number of Borrelia cells in adult female ticks that had fed for more than 36 hours, compared to the number of Borrelia cells found in adult female ticks that had fed for less than 36 hours.

*****
In Europe, 8 species of this complex have been reported: B. afzelii, B. garinii, B. burgdorferi sensu stricto (ss), B. valaisiana, B. lusitaniae, B. spielmanii, B. bavariensis and B. bissettii. Among them, B. afzelii, B. garinii, and B. burgdorferi ss are the most frequently reported in human clinical specimens.
*****
Overall, 26% of the collected ticks (556 of 2,154) contained Borrelia (Table 1). Adult female ticks had a higher Borrelia prevalence (36%) compared to nymphs (25%, p < 0.001).
*****
Seven different Borrelia species were identified by sequence analysis of the 5S-23S and 16S-23S IGS (Table 1). B. afzelii was the predominant species and was detected in 50% of all ticks containing Borrelia, followed by B. garinii (19%), B. valaisiana (7%), B. burgdorferi ss (4%), B. miyamotoi (2%), B. spielmanii (1%), B. lusitaniae (1%), mixed infection of Borrelia species (1%), and 15% were untypeable.
*****
Even though no significant differences in prevalence of Borrelia species between the different regions were noticed, higher proportions of B. garinii infected adult ticks and nymphs were found in Åland Islands, compared to the regions in Sweden (Table 1). Further, 80% (5 of 6) of the ticks infected with B. spielmanii were collected from the Åland Islands.
*****

Detection and Genetic Characterization of Relapsing Fever Spirochete Borrelia miyamotoi in Estonian Ticks

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3522604/

Abstract

During the years 2008–2010 I. ricinus and I. persulcatus ticks were collected from 64 sites in mainland Estonia and on the island Saaremaa. Presence of B. miyamotoi was found in 0.9% (23/2622) of ticks. The prevalence in I. persulcatus and I. ricinus ticks differed significantly, 2.7% (15/561) and 0.4% (8/2061), respectively. The highest prevalence rates were in found South-Eastern Estonia in an area of I. persulcatus and I. ricinus sympatry and varied from 1.4% (1/73) to 2.8% (5/178). Co-infections with B. burgdorferi s.l. group spirochetes and tick-borne encephalitis virus were also revealed. Genetic characterization of partial 16S rRNA, p66 and glpQ genes demonstrated that Estonian sequences belong to two types of B. miyamotoi and cluster with sequences from Europe and the European part of Russia, as well as with sequences from Siberia, Asia and Japan, here designated as European and Asian types, respectively. Estonian sequences of the European type were obtained from I. ricinus ticks only, whereas the Asian type of B. miyamotoi was shown for both tick species in the sympatric regions.



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 14.12.2013 - 19:33:36

Miten löytää keuhkoklamydia selkäydinnesteestä:

PCR in Diagnosis of Infection: Detection of Bacteria in Cerebrospinal Fluids
(PCR = polymerase chain reaction, polymeraasiketjureaktio)

http://cvi.asm.org/content/9/3/508.full

The PCR is the most sensitive of the existing rapid methods to detect microbial pathogens in clinical specimens. In particular, when specific pathogens that are difficult to culture in vitro or require a long cultivation period are expected to be present in specimens, the diagnostic value of PCR is known to be significant. However, the application of PCR to clinical specimens has many potential pitfalls due to the susceptibility of PCR to inhibitors, contamination and experimental conditions. For instance, it is known that the sensitivity and specificity of a PCR assay is dependent on target genes, primer sequences, PCR techniques, DNA extraction procedures, and PCR product detection methods. Even though there are many publications concerning basic protocols of a PCR assay, including DNA extraction and preparation as well as the amplification and detection of amplicons, PCR detection of bacteria in clinical specimens such as cerebrospinal fluid (CSF) has not yet been reviewed. Since a variety of clinical specimens, such as blood, urine, sputum, CSF and others, vary in regard to the nature of the content and amount available, careful design of the PCR assay for each specific specimen before a PCR application is conducted is essential. In particular, a diagnosis based on detection of a few bacteria in clinical specimens by using PCR must be carefully evaluated technically as well as microbiologically. In this regard, current studies concerning detection of Chlamydia pneumoniae in CSF obtained from patients with multiple sclerosis (MS) by using PCR provide a good example for discussion of use of the PCR assay in diagnosis. Because C. pneumoniae is difficult to culture in vitro, often low numbers of bacteria may be detected in the CSF of patients with chronic neurological diseases by PCR. Therefore, in this review general PCR protocols for detection of bacteria in clinical specimens, as well as a specific example of using PCR for detection of C. pneumoniae in CSF, will be discussed.
*******

MS is a chronic demyelinating disease of the CNS characterized by focal areas of demyelination. Although the exact etiology of MS is unknown, it is generally accepted that autoimmunity is involved and that the autoantigen(s) probably resides in CNS myelin, the target of the immune response (1). In this regard, current studies argue for an infectious agent as an initiating or enhancing factor for MS with any immunological mechanisms (24). To identify a specific causative agent for MS, many groups have attempted to detect microbes in CSF as well as lesions of CNS obtained from MS patients. However, there have been no consistent results with specific pathogens. Recent studies by Sriram et al. (56) highlighted a possible involvement of a bacterium in MS with the finding of C. pneumoniae in the CSF of nearly all patients with MS but in only a small proportion of CSF samples from control subjects without MS by utilizing PCR and culture methods. That study has shown the highest association with MS of any organism to date. However, other research groups were not successful in detecting this bacterium or found only a low rate of detection of C. pneumoniae in CSF from MS patients (Table 2).

Detection of C. pneumoniae DNA in CSF by PCR

To date, there have been 10 reports concerning detection of C. pneumoniae in CSF from MS patients by PCR (Table 2). The results of studies concerning the presence of C. pneumoniae in CSF of MS patients as determined by PCR have shown a very wide variation in the positive rate, ranging from 0% to almost 100%. Such variation of the C. pneumoniae positive rate in CSF may be dependent on the source of CSF and/or the PCR protocol utilized. Since there is no standard PCR protocol for C. pneumoniae detection and no consistent pattern of positive results among the various laboratories determined by a multicenter comparison trial of PCR assays for detection of C. pneumoniae (2), each step of the PCR protocol utilized in each study should be carefully reviewed.

******

Detection of C. pneumoniae in CSF.
Controversy surrounds the detection of C. pneumoniae in CSF obtained from MS patients, primarily because of the lack of a definitive test for detecting the small numbers of C. pneumoniae present. Culture is always considered the “gold standard” in microbiology but is difficult to perform for certain fastidious bacteria such as C. pneumoniae in specific clinical specimens. For instance, this bacterium has not been successfully cultured from blood samples, although its DNA can be detected in blood and the organism has been recovered in limited numbers from vascular tissue specimens (18). Even though PCR enables the detection of low concentrations of bacteria in clinical specimens, great variability of detection is usually found in CSF from MS patients (Table 2), atherosclerotic tissue samples, and peripheral blood mononuclear cells, ranging from a 0 to 100% detection rate between studies (5, 6, 64). In this regard, a recent study conducted by Smieja et al. (55) demonstrated the relationship between target concentrations and PCR detection rate; that is, lower concentrations of C. pneumoniae were only intermittently PCR positive, and this relationship was predictable from a statistical viewpoint. From this point of view, theoretically a larger number of replicates of a PCR assay may result in a better chance for detecting low numbers of bacteria. In other words, the negative PCR results obtained from a single PCR test may not be a true negative due to the low validity of detection with a lower concentration of target. Since none of the papers reporting results of C. pneumoniae detection by PCR in CSF from MS patients provided any replicate number of PCR tests, the negative results reported may possibly not be true negatives but could indicate that there were few bacteria, if any, present.

CONCLUSIONS

It has been well documented that specific infectious agents may be involved in autoimmune diseases, such as Trypanosoma cruzi as the causative agent of Chagas' disease and Streptococcus pyogenes and measles virus for encephalomyelitis (51). Some chronic inflammatory diseases which are not yet definitely classified as an autoimmune diseases are also considered to be linked to some microbial infections. However, in contrast to infectious diseases, causative or contributing microbes for such chronic inflammatory diseases, including autoimmune diseases, may not be readily detected in specimens obtained from the specific lesion. Since chronic inflammatory diseases as well as autoimmune diseases, including atherosclerosis and MS, may be attributed to the immune response through molecular mimicry and/or the possible adjuvant effect of infectious agents (50), the presence of microbes in a lesion may not always be necessary. Even under such circumstances, a consistent detection of bacteria in specimens should be critical in diagnosis and future therapy. In this regard, PCR is the most reliable assay for detection of microbes in clinical specimens. Careful design and protocol for a PCR assay to detect, measure, and identify microbes in clinical specimens are essential. Analysis of PCR results is also a critical issue in diagnosis, particularly for chronic inflammatory diseases. Application of a clinically relevant PCR assay to these issues in monitoring bacterial presence in CSF may reveal a role for bacteria, such as C. pneumoniae, in chronic inflammatory or autoimmune diseases, such as MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.12.2013 - 14:33:21

Hypoteesi vuodelta 1986:

Relapsing fever/Lyme disease. Multiple sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/3642202

Abstract

Lyme Disease and Relapsing Fever caused by Borrelia burdorferi and Borrelia hermsii, respectively, have been generally considered curable if diagnosed early. However, it is becoming apparent that when these diseases are left undiagnosed and untreated they may cause severe problems for some people. They, in fact, may be one of the major causes of Multiple Sclerosis. These two Borrelia infections, when left untreated, are now known to be capable of causing neurological problems, cardiac problems, relapses as much as ten years later, increased IgG/albumin ratio and increased lymphocytes. These same things hold true for Multiple Sclerosis patients. This paper discusses the Borrelia spirochetes which cause Lyme Disease and Relapsing Fever and what correlation that may have with Multiple Sclerosis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.12.2013 - 14:37:16


Lyme borreliosis: from infection to autoimmunity.

http://www.ncbi.nlm.nih.gov/pubmed/15214872

Abstract

Lyme borreliosis in humans is an inflammatory disease affecting multiple organ systems, including the nervous system, cardiovascular system, joints and muscles. The causative agent, the spirochaete Borrelia burgdorferi, is transmitted to the host by a tick bite. The pathogenesis of the disease in its early stages is associated largely with the presence of viable bacteria at the site of inflammation, whereas in the later stages of disease, autoimmune features seem to contribute significantly. In addition, it has been suggested that chronic persistence of B. burgdorferi in affected tissues is of pathogenic relevance. Long-term exposure of the host immune system to spirochaetes and/or borrelial compounds may induce chronic autoimmune disease. The study of bacterium-host interactions has revealed a variety of proinflammatory and also immunomodulatory-immunosuppressive features caused by the pathogen. Therapeutic strategies using antibiotics are generally successful, but chronic disease may require immunosuppressive treatment. Effective and safe vaccines using recombinant outer surface protein A have been developed, but have not been propagated because of fears that autoimmunity might be induced. Nevertheless, new insights into the modes of transmission of B. burgdorferi to the warm-blooded host have been generated by studying the action of these vaccines.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.12.2013 - 22:25:45

The differential diagnosis of multiple sclerosis: classification and clinical features of relapsing and progressive neurological syndromes
Neurological Sciences, November 2001, Volume 22, Issue 2 Supplement, pp S98-S102

http://link.springer.com/article/10.1007/s100720100044

Abstract.

In the absence of pathognomonic clinical features or a definitive laboratory test, multiple sclerosis (MS) remains ultimately a diagnosis of exclusion. Accurate diagnosis is increasingly important with available disease modifying therapy. Unfortunately the rate of misdiagnosis remains around 5%–10%, indicating that 1 in 20 patients thought to have MS has, instead, a condition resembling MS. In this review we describe conditions that may be confused with MS because they can present as lesions disseminated in time, space, or both. Conditions often confused with MS may be inflammatory (systemic lupus erythematosus, Sjögren's syndrome, vasculitis, sarcoidosis, Behçet's disease), infectious (Lyme disease, syphilis, progressive multifocal leukoencephalopathy, HTLV-1 infection, herpes zoster), genetic (lysosomal disorders, adrenoleukodystrophy, mitochondrial disorders, CADASIL), metabolic (vitamin B12 deficiency), neoplastic (CNS lymphoma) and spinal (degenerative and vascular malformations) diseases. The key to the accurate diagnosis of MS is vigilance for atypical features, suggesting the possibility of an alternative diagnosis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 31.12.2013 - 10:02:45

Niinpä, puhuin kerran erään neurologin kanssa asiasta ja kysyin, että jos minulla ei olekaan MS-tauti (autoimmuunisairaus) vaan jotain muuta samoja oireita aiheuttavaa esim. kroonistunut borrelioosi. Neurologi vastasi, että virhediagnooseja tehdään ja se on aivan normaalia. Kysymys ei aiheuttanut mitään yllätyksiä neurologille, eikä myöskään johtanut mihinkään jatkotutkimuksiin. Että näin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 07.01.2014 - 10:30:33

BORRELIOOSIN HOITO

Borrelioosia hoidetaan ensisijaisesti antibiooteilla. Kaikki ovat yleensä yhtä mieltä siitä, että parhaat hoitotulokset saadaan silloin, kun hoito päästään aloittamaan varhaisessa vaiheessa. Sen sijaan lääkkeen annostuksesta, hoitoajan pituudesta ja kroonisen borrelioosin hoidosta esiintyy kirjallisuudessa tällä hetkellä toisistaan poikkeavia näkemyksiä. Yleiset hoitosuositukset esim. EUCALBin (=European Union Concerted Action on Lyme Borreliosis) suosittelee käyttämään antibiootteja, sairauden vaiheesta ja antibiootista riippuen, viikosta neljään viikkoon. Esimerkiksi Doksisykliinin annostus on heidän ohjeidensa mukaan 10-30 vrk 2x100mg. Useiden potilasjärjestöjen ja Borrelioosiin erikoistuneiden amerikkalaisten lääkäreiden (LLMD) mielestä yleiset hoitosuositukset eivät aina ole riittäviä. Syinä on mainittu mm. taudin monimuotoisuus, bakteerin hidas kehittyminen (20-24h), bakteerin kyky paeta immuunijärjestelmää ja antibiootteja esimerkiksi muuntumalla kystamuotoon sekä bakteerin nopea siirtyminen verenkierrosta kudoksiin, esimerkiksi keskushermostoon, lihaksiin, sydämeen ja jänteisiin, joista sitä on vaikea tavoittaa. (esim. Liegner 1993, Burrascano 2002, Donta 2002, MacDonald ym. 1990, Vukadinov ym. 2002.)

Kroonisen borrelioosin hoito vaatii Burrascanon (2002) mukaan useimmiten suonensisäistä antibioottihoitoa, korkeita annoksia, pulssihoitoa ja yhdistelmäantibiootteja esim. metronidatsolin/tinidatzolin kanssa. Hoitoa jatketaan useiden kuukausien ajan ja antibiootteja vaihdetaan silloin, kun hoidossa on saavutettu taso, jolloin paraneminen ei enää edisty. Hoidossa kiinnitetään huomiota myös esim. mahdolliseen hiivan liikakasvuun, kuntoutukseen, dieettiin (vähän hiilihydraatteja, paljon kuituja, ei alkoholia eikä kahvia). Mikäli oireet palaavat pian antibiootin lopettamisen jälkeen, voidaan joutua tilanteeseen, jossa antibioottihoitoja on jatkettava määräämättömäksi ajaksi.

Seuraavassa on kertomus borrelioosiin sairastuneesta lääkäristä. Hän on ollut jatkuvalla antibiootihoidolla jo vuosia ja on sen avulla kyennyt jatkamaan työtään (Sherr 2000. The Physician as a Patient, Prac Gastroent 24; 1:28). " Sairastuin äkillisesti vilunväreisiin, rytmihäiriöihin, tuntohäiriöihin, lihaskipuihin, hikoiluun, tinnitukseen, kuumeiluun jne. Minulla oli ollut aiemmin rengasmainen ihimuutos. Soitin J. Burrascanolle ja hänen suosituksestaan aloitin antibioottihoidot.http://www.ilads.org/outcomes.htm

Dontan (2002) mukaan useat antibiootit (esim. tetrasykliini, doksisykliini ja amoksisilliini) ovat useimmiten tehokkaita silloin, kun potilaalla ei ole vielä muita oireita kuin ihomuutos (EM). Hoidon pituus tulee hänen mukaansa olla näissä tapauksissa kuukauden pituinen. Mikäli potilaalla esiintyy muita kuin iho-oireita, hoidon tulisi kestää 3 kuukautta ja mikäli potilaan oireet ovat kestäneet kauemmin kuin kuusi kuukautta, hoidon pituuden tulisi olla vieläkin pitempi. Silloin kun oireita on kestänyt yli vuoden, saatetaan tarvita vuodesta puoleentoista vuotta kestävä antibioottihoito. Dontan mukaan pitkät antibioottihoidot ovat borrelioosin hoidossa perusteltuja, aivan samoin kuin ne ovat esim. tuberkuloosin, Q - kuumeen ja lepran kohdalla. Hoito-ohjeista voi lukea lisää esim Dontan (2002) artikkelista tai Burrascanon (2002) ohjeista: Advanced topics in lyme disease: Diagnostic hints and treatment guidelines for lyme and other tick borne illnesses: http://www.ilads.org/burrascano_1102.htm Burrascano suosittelee esim. Doksisykliinin annostukseksi 400mg tavanomaisen 200mg:n sijaan. Hän suosittelee tarkistamaan doksisykliinin määrän veressä jokaisen potilaan kohdalta ja määräämään annostuksen sen perusteella. Yleisimmin annostus on alussa 400mg.. "My recommendations on the dose of Doxy are based on objective measure of doxycycline blood levels. Based on hundreds of measurements, it is clear that 400 mg daily is the best choice for a starting dose. .. NEVER seen a chronic Lyme patient fully recover on a 200 mg daily dose. Please feel free to share this information with your friends and certainly with your physicians. I am always willing and happy to speak to other physicians, to answer any questions they have regarding care of the Lyme patient."

Hoidon aloittaminen varhaisessa vaiheessa ei välttämättä takaa, että bakteeri saadaan kiinni riittävän aikaisin, sillä esim. Patmasin ja Remorcan (1994) tutkimuksessa esitellään potilastapaus, jossa borreliabakteeri oli levinnyt kudoksiin jo noin kuuden tunnin kuluttua punkin puremasta. Tutkimuksissa on myös havaittu, että Bb on säilynyt kudoksissa elinvoimaisena riittäväksi katsotuista antibioottihoidoista huolimatta (esim. Preac-Mursic ym. 1989, Straubinger ym. 1997, Strle ym. 1996). Fried (2001) havaitsi, että B burgdorferi-bakteeria esiintyi suolistossa lukuisten antibiootihoitojenkin jälkeen. On myös huomattu, että bakteeri kykenee heikentämään elimistön omaa immuunijärjestelmää ja sitä kautta estämään immuunijärjestelmän omat yritykset tuhota se (esim Diterich ym. 2001, 2003).

Onko antibiooteilla ylipäätään mahdollista hävittää Bb bakteeri kokonaisuudessaan elimistöstä varsinkaan sen jälkeen, kun tauti on levinnyt pidemmälle? Asiasta ei ole vielä varmaa tietoa, mutta joidenkin tutkijoiden mielestä se ei ole mahdollista. Joidenkin mielestä antibiooteilla kyetään ainoastaan kontrolloimaan bakteerin kasvua, mutta sitä ei kyetä poistamaan kokonaan ja se saattaa aktivoitua uudelleen milloin tahansa (Adams 2003). Horowitz (2000) tutki 80 kroonista borrelioosia sairastavaa PCR positiivista henkilöä. Henkilöille annettiin 1-53 kuukautta kestavät antibioottihoidot (keskimäärin 13 kk). Tutkimuksessa käytettiin erilaisia antibioottiyhdistelmiä (esim. doksisykliini, minosykliini, tetrasykliini, makrolidit, penisilliini, kefalosporiini, metronidatsoli, hydroksiklorokiini). Tutkimuksessa todettiin, että jatkuva antibioottilääkitys auttoi potilaita merkittävästi, mutta ei kyennyt poistamaan infektiota kokonaan. http://www.ilads.org/chronic.htm

Borreliabakteeri on erittäin selviytymiskykyinen ja siksi se kykenee selviytymään hyvin esim. silloin, kun ravintoa on niukasti, kylmyydessä, elimistön immuunijärjestelmän tai antibioottien uhatessa sitä. Pitkään tunnettu selviytymiskeino on bakteerin kyky muuntautua kystamuotoon. Asiasta on ollut saatavana tietoa noin sadan vuoden ajan. Jo vuonna 1905 Schaudinn & Hoffmann havaitsivat että spiraalimuoto ei ole spirokeettojen ainoa muoto. Asiasta on tehty vuosien aikana lukuisia tutkimuksia. Viimeisimmissä tutkimuksissa esim.Gruntar ym. (2001) havaitsivat, että B. garinii kykeni muuntumaan kystamuodosta takaisin liikkuvaksi spirokeetaksi senkin jälkeen, kun se oli ensin jäädytetty. Brorson & Brorson (1999a) huomasivat, että spirokeetat muuntuivat kystamuotoon minuutissa sen jälkeen, kun ne oli laitettu tislattuun veteen. Neljän tunnin kuluttua liuoksessa ei ollut havaittavissa yhtään normaalia liikkuvaa spirokeettaa. Vuorokauden kuluttua siitä, kun bakteerit laitettiin ravintoliuokseen, ne alkoivat jälleen vähitellen muuntua takaisin liikkuviksi spirokeetoiksi.

Mursic ym. (1996) huomasivat, että bakteerit muuntuivat antibiootihoidon aikana niin, että niillä ei ollut solun seinämää. Bakteerien ja niiden kystamuotojen on havaittu kestävän hyvin erilaisia borrelioosin hoidossa yleisesti käytettyjä antibiootteja, kuten keftriaksoni, doksisykliini ja penisilliini. (esim. Brorson & Brorson 2000, Kersten ym. 1995.) Joidenkin tutkimusten mukaan (Brorson & Brorson 1999) kystamuotoiset bakteerit olivat herkkiä Metronidazolelle ja sen vuoksi jotkut lääkärit ja potilaat (lähinnä USA:ssa ja jonkin verran myös Englannissa) ovat kokeilleet lääkettä tavallisten antibioottien rinnalla. Lääkkeen tehosta kroonisen borrelioosin hoidossa ei ole vielä tutkimuksellista näyttöä.

Kystamuotoisista bakteeereista on kerrottu lisää esim. seuraavalla sivulla:

http://www.lymeinfo.net/medical/LDCysts.pdf Tutkimuksia + kuvia bakteerin kystamuodosta

http://www.lymenet.de/literatur/cystsl.htm

Tietoa erilaisten antibioottien käytöstä Borrelioosin hoidossa, voi lukea esim. seuraavalta sivulta: http://www.geocities.com/HotSprings/Oasis/6455/antibiotics-links.html Sivulla on runsaasti linkkejä tutkimuksiin ja artikkeleihin.

Borrelioosin hoidosta löytyy paljon tutkimuksia seuraavilta sivuilta: http://www.geocities.com/HotSprings/Oasis/6455/treatment-links.html

Hoitojen vaikutuksesta voi lukea esimerkiksi seuraavilta sivuilta:

http://www.geocities.com/HotSprings/Oasis/6455/outcomes-links.html

Borrelioosin hoitoon käytettävistä antibiooteista on tietoa myös seuraavalla sivulla. Sieltä löytyy tietoa mm. metronidazolesta/tinidatzolesta, jotka ovat joidenkin tutkimusten mukaan osoittautuneet tehokkaiksi kystamuotoisiin bakteereihin.

http://www.geocities.com/HotSprings/Oasis/6455/adverse-links.html http://www.postgradmed.com/issues/1997/04_97/cunha_1.htm Sivulla kerrotaan doksisykliinistä. minosykliinistä ja metronidazolesta. Artikkelin mukaan minosykliini läpäisee kudokset (esim keskushermosto) doksisykliiniä paremmin.

Suomen Lyme Borrelioosi ry
 

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.01.2014 - 15:07:05

Chlamydophila pneumoniae Infection and Its Role in Neurological Disorders

http://www.hindawi.com/journals/ipid/2010/273573/

Abstract

Chlamydophila pneumoniae is an intracellular pathogen responsible for a number of different acute and chronic infections. The recent deepening of knowledge on the biology and the use of increasingly more sensitive and specific molecular techniques has allowed demonstration of C. pneumoniae in a large number of persons suffering from different diseases including cardiovascular (atherosclerosis and stroke) and central nervous system (CNS) disorders. Despite this, many important issues remain unanswered with regard to the role that C. pneumoniae may play in initiating atheroma or in the progression of the disease. A growing body of evidence concerns the involvement of this pathogen in chronic neurological disorders and particularly in Alzheimer's disease (AD) and Multiple Sclerosis (MS). Monocytes may traffic C. pneumoniae across the blood-brain-barrier, shed the organism in the CNS and induce neuroinflammation. The demonstration of C. pneumoniae by histopathological, molecular and culture techniques in the late-onset AD dementia has suggested a relationship between CNS infection with C. pneumoniae and the AD neuropathogenesis. In particular subsets of MS patients, C. pneumoniae could induce a chronic persistent brain infection acting as a cofactor in the development of the disease. The role of Chlamydia in the pathogenesis of mental or neurobehavioral disorders including schizophrenia and autism is uncertain and fragmentary and will require further confirmation.

***************
The continuous breakdown and regeneration of myelin has been demonstrated within the progressive MS plaque [99]. Toll-like receptors (TLR) are intimately involved in several neurodegenerative and demyelinating disorders including MS as demonstrated with the finding of a marked increase in TLR expression in MS lesions. PCR studies have shown that microglial cells from MS patients express TLRs 1–8 [100]. Moreover, while healthy white matter from MS patients does not contain TLRs, active lesions are associated with high expression of TLR3 and TLR4 on microglia and astrocytes. In contrast, late active lesions also contain astrocytes bearing surface TLR3 and TLR4 [100]. This suggests that early lesions are characterized by microglia infiltration, while astrocytes are also active in later MS lesions. However, the precise role of TLR3 and TLR4 activation in these lesions is yet unknown. TLRs have been shown to recognize highly conserved regions in various microorganisms (Pathogen-Associated Molecular Patterns) including C. pneumoniae and thus stimulate a potent inflammatory response contributing to the clearance of the pathogen [101]. Unpublished our findings have detected the major expression of mRNA TLR-2 and TLR-4 in peripheral blood but not in CSF from SM patients with RR forms, indicating that their combined activity might be crucial to modulate and activate the cellular-mediated immune response during chronic infections by C. pneumoniae. Based on epidemiological observations, it has been proposed that exposure to an environmental factor, such as an infectious agent, in combination with genetic predisposition could be implicated in MS pathogenesis [103]. The risk of MS is enhanced by the presence of specific genes on chromosome 6 in the area of MHC, Human Leukocyte Antigens (HLA) in humans. In particular, HLA-DR and HLA-DQ genes, which are involved in antigen presentation, are strongly associated to the development of the disease.

*************
After this innovative publication, a number of studies have suggested that C. pneumoniae infection may be associated with MS, while other studies have found no association [108, 109]. During recent years, there have been many evidences of a possible role of C. pneumoniae involvement in MS disease supported in part by seroepidemiological, cultural, molecular, immunological and therapeutic studies. However, it is also true that there are not many studies that argue for a role of organism in MS. First, while some reports have documented that C. pneumoniae seropositivity was related to the risk of MS progressive forms (SP and PP), but only moderately linked to the risk of developing MS [110], others have not found association between serum titers of anti-C. pneumoniae antibodies and the risk for MS or, by contrast, a higher risk to develop MS in a subgroup of older patients after than before disease onset [111]. Second, the organism was found in course of MS relapses in the throat together with a rising serology [112]. Third, relapses of MS have long been noted to follow respiratory infections, including sore throat, or pneumonia with a clinical pattern typical of respiratory infection caused by C. pneumoniae. The isolation of the pathogen, as assessed by culture assay in CSF and brain tissue failed repeatedly in MS patients [113–115] or was positive only in a small proportion of MS patients [81, 116].

*************

Thus, it cannot be excluded that, in a particular subgroup of RR active MS patients, C. pneumoniae may enter into brain early in the course of the disease via transendothelial migration across the blood/brain barrier of activated infected blood-borne monocytes, resulting in ongoing inflammatory immune activation that takes place within the CNS. Alternatively, the presence of elevated rates of C. pneumoniae DNA in CSF in this subset of MS patients could merely reflect the selective infiltration of monocytes which traffic into the brain after activation, thus suggesting a role for C. pneumoniae only as a silent passenger. In attempting to recover C. pneumoniae from cultured CSF and PBMC compartments with a PCR targeting multiple genes, a positivity for C. pneumoniae DNA and mRNA was recently detected in 64% of cocultured CSF and PBMCs of RR MS patients with evidence of disease activity, whereas only 3 controls were positive for Chlamydial DNA, suggesting that C. pneumoniae may occur in a persistent and metabolically active state at both peripheral and intrathecal levels in MS, but not in controls.

************
From the data presented, there is strong evidence that C. pneumoniae has not a causal role in MS disease. Thus, the actual involvement of C. pneumoniae in MS still remains a matter of debate and requires further understanding through standardized cultural, molecular and ultrastructural protocols for C. pneumoniae in biological samples coming from MS patients and controls. While some studies suggest a role of C. pneumoniae only as a CNS innocent bystander epiphenomenon due to ongoing MS inflammation which favours a selective infiltration of infected-mononuclear cells within the CNS, others indicate a role of C. pneumoniae as a cofactor in development and progression of the disease by enhancing a pre-existing autoimmune response in a subset of MS patients, as supported by recent immunological and molecular findings [95, 109, 136]. Recent our findings have demonstrated a possible association between Parachlamydiae Like Organisms and MS suggesting that these can act alone or together with C. pneumoniae as a cofactor in the development and progression of MS [137]. Although these data needs further assessment, their possible involvement in MS could be of great importance in public health.

Finally, we cannot exclude that other pathogens may be potentially involved in the development of MS disease. Virus have often been considered as potential candidates because they are known to cause demyelinating disease in experimental animals and man, and often cause disease with long periods of latency that presents clinically with relapsing, remitting symptoms [138]. To date, however, studies have failed to identify any single virus as playing a major role in MS. Among the virus suggested as MS cofactors, there are ubiquitous members of the family Herpesviridae, Human herpesvirus 6 (HHV-6), Epstein-Barr virus (EBV) [139–146]. As Chlamydia, these viruses can undergo an alternative infection cycle, entering a quiescent state (latency), with low grade viral infection that does not cause cell lysis, from which they subsequently can be reactivated. However, the cell type in which this occurs is usually not the same cell type in which the productive, cytocidal infection occurs. The human MS-associated retrovirus (MSRV) belonging to endogenous retrovirus family, has been also described as potential pathogen in MS [147].

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 14.01.2014 - 09:48:58

Uusimmissa tutkimuksissa on löydetty yhteys MS-taudin ja bakteerin välillä.
http://weill.cornell.edu/news/releases/wcmc/wcmc_2013/10_16_13.shtml
Abstrakti:

Toxin-Emitting Bacteria Being Evaluated as a Potential Multiple Sclerosis Trigger
Variant of Common Soil-Based Pathogen Found for the First Time in a Patient With MS
Researchers Find Evidence of Similar Infection in Other MS Patients

NEW YORK (October 16, 2013) — A research team from Weill Cornell Medical College and The Rockefeller University has identified a bacterium it believes may trigger multiple sclerosis (MS), a chronic, debilitating disorder that damages myelin forming cells in the brain and spinal cord.

Their study, published in PLoS ONE, is the first to identify the bacterium, Clostridium (C.) perfringens type B, in humans.

The scientists say their study is small and must be expanded before a definitive connection between the pathogen and MS can be made, but they also say their findings are so intriguing that they have already begun to work on new treatments for the disease.

"This bacterium produces a toxin that we normally think humans never encounter. That we identified this bacterium in a human is important enough, but the fact that it is present in MS patients is truly significant because the toxin targets the exact tissues damaged during the acute MS disease process," say the study's first author, K. Rashid Rumah, an MD/PhD student at Weill Cornell Medical College, and the study's senior investigator, Dr. Timothy Vartanian, professor of neurology and neuroscience at Weill Cornell Medical College and director of the Judith Jaffe Multiple Sclerosis Center at New York-Presbyterian Hospital/Weill Cornell Medical Center.

"While it is clear that new MS disease activity requires an environmental trigger, the identity of this trigger has eluded the MS scientific community for decades," Dr. Vartanian says. "Work is underway to test our hypothesis that the environmental trigger for MS lays within the microbiome, the ecosystem of bacteria that populates the gastrointestinal tract and other body habitats of MS patients."

Connection to MS in grazing animals

The study describes discovery of C. perfringens type B in a 21-year-old woman who was experiencing a flare-up of her MS.

The woman was part of the Harboring the Initial Trigger for MS (HITMS) observational trial launched by Dr. Vartanian and K. Rashid Rumah, who works both with Dr. Vartanian and with co-author Dr. Vincent Fischetti at The Rockefeller University.

C. perfringens, found in soil, is one of the most common bacteria in the world. It is divided into five types. C. perfringens type A is commonly found in the human gastrointestinal tract and is believed to be largely harmless.

C. perfringens types B and D carry a gene (epsilon toxin) that emits a protoxin — a non-active precursor form of the toxin — which is turned into the potent "epsilon" toxin within the intestines of grazing animals. The epsilon toxin travels through the blood to the brain, where it damages brain blood vessels and myelin, the insulation protecting neurons, resulting in MS-like symptoms in the animals. While the D subtype has only been found in two people, based on prior studies by other investigators, the B subtype had never been found in humans.

Nevertheless, Rumah and the research team set out to see if subtypes B or D exist in humans and if they are associated with MS. They tested banked blood and spinal fluid from both MS patients and healthy controls for antibody reactivity to the epsilon toxin. Investigators found that levels of epsilon toxin antibodies in MS patients were 10 times higher than in the healthy controls — the blood of only one out of 100 control participants showed an immune reaction to the toxin.

The team also examined stool samples from both MS patients and healthy controls enrolled in the HITMS clinical study, and found that 52 percent of healthy controls carried the A subtype compared to 23 percent of MS patients. "This is important because it is believed that the type A bacterium competes with the other subtypes for resources, so that makes it potentially protective against being colonized by epsilon toxin secreting subtypes and developing MS," say Rumah and Vartanian.

The search by investigators for evidence of C. perfringens type B paid off in the case of a young MS patient. Co-author Dr. Jennifer Linden, a microbiologist at Weill Cornell Medical College, isolated the actual bacterium from the patient's stool.

A choice of approaches for treatment

The authors suspect that once a human is infected with C. perfringens type B or D, the pathogen usually lives in the gut as an endospore, a seed-like structure that allows some bacteria to remain dormant for long periods. "The human gastrointestinal tract is host to approximately 1,000 different bacterial species, but is not a hospitable environment for C. perfringens type B or D, so it does not grow well there. It hibernates in a protective spore. When it does grow, we anticipate it generates a small quantity of epsilon toxin, which travels through the blood into the brain," Dr. Vartanian says. "We believe the bacterium's growth is episodic, meaning the environmental trigger is always present, and it rears its ugly head from time to time."

He says researchers do not know how humans are infected with C. perfringens type B or D, but they are studying potential routes of exposure. The scientists are also in the first stages of investigating potential treatments against the pathogen.

"There are a variety of approaches we can take. A vaccine for humans is possible — there is already a vaccine available for farm animals, but it requires repeat immunizations," say Vartanian and Rumah. "We are also investigating the possibility of developing small-molecule drugs that prevent the toxin from binding to its receptor.

"But one of my favorite approaches is development of a probiotic cocktail that delivers bacteria that compete with, and destroy, C. perfringens types B and D," Vartanian says. "It would be such a beautiful and natural way to treat the gastrointestinal system and solve the problem. We are also starting to work on this approach."

This work was generously supported in part by The Laurence Tisch Family Research Fund, The Dr. Mortimer D. Sackler Family Fund for Neuroregenerative Research, The Widgeon Point Charitable Foundation, and the Rockefeller University Funds to the Laboratory of Bacterial Pathogenesis and Immunology.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.01.2014 - 13:00:57

Lisää hypoteeseja vuodelta 2001:

Is multiple sclerosis caused by a silent infection with malarial parasites? A historico-epidemiological approach: part I.

http://www.ncbi.nlm.nih.gov/pubmed/11516218

Abstract

Though many details are known about the epidemiology of multiple sclerosis (MS), its aetiology has remained an enigma. To find a solution to this problem, the concept of so called 'anophelism without malaria' was put on trial. 'Anophelism without malaria' is a basic assumption of the epidemiology of malaria. It means that there is no transmission of malaria in the temperate zone, although the insect vector (the different species of anopheles) can be found nearly everywhere. Starting with the results from blood tests of five patients suffering from MS which indicate an infection with plasmodia, the old hypothesis of the malarial aetiology of MS (Mannaberg 1899) is reappraised and compared with today's pathological findings. A comparison of the old map of malaria with the later distribution of MS in the USA has been made, supporting the assumption that an infection with plasmodia in early childhood prevents a later disease, while a silent infection at the time of adolescence or later is its cause.


Is multiple sclerosis caused by a silent infection with malarial parasites? A historico-epidemiological approach: part II.

http://www.ncbi.nlm.nih.gov/pubmed/11516219

Abstract

The comparison between the old map of malaria and the later distribution of multiple sclerosis (MS) first carried out in the USA (Part I) is continued in Europe. The Italian 'dilemma' (Kurtzke), meaning the disappearance of the north-south gradient in Italy by recent surveys, can be solved when considering the dependence of malaria transmission in relation to the altitude. Further, the high prevalence of MS in earlier times in Mississippi, Louisiana and in the former province of Lucania in Italy can be explained by preceding epidemics of malaria. Brickner's therapeutic trial with quinine in cases of MS patients is reevaluated, and by this the Jarisch-Herxheimer reaction is shown to exist in MS too. The possible significance of the old and rather forgotten provocative methods for the diagnosis of latent malaria is discussed.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 20.01.2014 - 21:24:55

Joopa joo, täytyykin pyytää lääkäriä testaamaan Malaria. Sen on oletettu hävinneen jo 1940-luvulla Suomen etelärannikolta, jossa se oli Malarian pohjoisin paikka maailmassa saada tauti kotoperäisesti. Mutta teoria on hyvä, sillä meikäpoika on viettänyt kesäpäivät ja illat Suomenlahden rannikolla ja saaristossa aina 60-luvulta asti (tosin en enää). Täytyykin perehtyä asiaan tarkemmin.
http://fi.wikipedia.org/wiki/Malaria#Malaria_Suomessa

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.01.2014 - 13:20:29

Tämä hypoteesi vuodelta 2008:

Hygiene hypothesis: innate immunity, malaria and multiple sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/17889443

Abstract

The establishment of new hygienic conditions plays a role in the appearance of autoimmunity in "westernalised" countries. Consistently, but still unconvincingly, several epidemiological and immunogenetic evidences link the disappearance of malaria with the increase of multiple sclerosis (MS) in Sardinia, insular Italy. To this purpose, we have made an attempt to build a relationship between malaria disappearance and MS under the light of the hygiene hypothesis. This relationship has taken into account the MS frequency increase soon after malaria eradication in Sardinia, the present malaria endemism in Africa, the innate immune system activity here represented by Chitotriosidase (Chit), an hydrolytic enzyme produced by macrophages, and an unproductive polymorphism of Chit gene (CHIT1) as a measure of the genetic weight of Plasmodium-related immunity in these populations. Data were derived from both experimental results specifically designed for this study and other data obtained from the available literature. The experimental and the hystorical-epidemiological findings concur to indicate that whilst in Africa CHIT1 mutation is rare and MS incidence is very low due to unmodified parasitic influence and hygienic conditions, in Sardinia a relationships between CHIT1 mutation, plasma Chit activity and MS prevalence rate is detected, even to a higher extent compared to Sicily, area at former lower rate of malaria endemy. Upon such a basis, we have found convincing argumentations that, at least in part, MS has increased over the last four decades in Sardinia also because of the eradication of malaria, 50 years ago. This infectious disease that run for centuries in Sardinia, besides well documented enzyme deficiencies and red cell pathologies, have left an abnormal macrophage reactivity against Plasmodium falciparum. As a result, some Sardinian individuals secrete abnormally high levels of mediators of the innate immunity, relics of former protective anti-malaria infection, in response to new environmental factors. Therefore, MS, an immune-conditioned pathology of the central nervous system has been subject to an unexplained epidemiological increase in the last few decades in Sardinia because cells of the innate immune system, immuno-genetically selected over the centuries in response to widespread P. falciparum malaria, have kept the tendency to over-respond to triggering factors even after the disappearance of malaria. This hypothesis may have an influence in re-directing clinicians toward a innate immunity-based rather than an antigen specific-based new MS therapies.


Multiple sclerosis and anti-Plasmodium falciparum innate immune response, 2007

http://www.ncbi.nlm.nih.gov/pubmed/17336397

Abstract

Several epidemiological investigations conducted in Sardinia, insular Italy, indicate that the strong selective pressure of malaria along the centuries may have concurred to the elevated genetic MS-risk in this region. To test such hypothesis in an experimental setting, we have compared the immune response to P. falciparum (the causative agent of malaria) in Sardinian MS patients relative to their ethnic healthy controls and control MS patients of different ethnicity. To this purpose, the P. falciparum-driven peripheral mononuclear cell proliferation, the production of pro-inflammatory cytokines of the innate immunity such as TNF-alpha, IL-6 and IL-12 and the ability to inhibit the parasite growth have been tested in relation to HLA-DR alleles and TNF promoter polymorphisms known of being associated to MS. We found that P. falciparum-induced proliferation, cytokine production and parasite killing are significantly augmented in Sardinian MS patients as compared to controls (p<0.01). Additionally, a correlation is found with genes associated to Sardinian MS, namely the TNF(-376A) promoter polymorphism and the class II HLA-DRB1*0405 allele. In conclusion, we have found evidences that some genetic traits formerly selected to confer a protective responses to P. falciparum now partially contribute to the elevated MS susceptibility amongst Sardinians.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 21.01.2014 - 13:34:30

Amerikkalaiset tutkijat ovat mielestään löytäneet syy ja seuraussuhteen malarian ja MS-taudin välille. Esimerkiksi on otettu Italia (sardinia), josta malaria on hävinnyt, mutta tilalle on ilmestynyt MS-tauti.
Tässä linkissä näkyy nykyinen Malarian levinneisyys maailmalla.
http://www.terveyskirjasto.fi/kotisivut/tk.koti?p_artikkeli=mat00108
Jos haluat lisää tietoa Malariasta katso täältä:
http://www.medicina.fi/fato/58.pdf

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Caroline80 Pvm 21.01.2014 - 15:44:04

Moikka Äijä! Luettuani tuota tekstiä ajattelin kuten sinä. - Karoliina L.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 22.01.2014 - 00:45:49

Moro Caroline, kyllä tässä on naurussa pitelemistä kun ajattelee, kuinka paljon on tehty tutkimusta MS-tautiin liittyen. Taudin syntyyn on liitetty vaikka mitä ja kaikki tutkimukset loppuvat ikään kuin asia olisi sillä selvä!!! Eikä mitään valmista saada aikaan, kaikkihan arvaavat sen, ettei kyse ole yhdestä totuudesta MS-taudissakaan. Toivoisi, että jossain osa-alueessa päästäisiin niin pitkälle, jotta voitaisiin testata potilaita ja löytää ne, joille kyseinen hoito toisi parannuksen. Mutta ei, pelkkiä teorioita ja keskeneräisiä tutkimuslinjoja, tässä kohtaa tulee mieleeni erinäisiä ikäviä vaihtoehtoja, jotka jääköön jokaisen omaan mietintään. Ehkä sitä on tullut "leipäpappeutta" harrastettua itsekin aikanaan. No tässä sitä vaan kärsitään jalkasätkyistä ja odotetaan, että ne loppuisivat ja tulisi niin "väsy" että pääsisi nukkumaan.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.01.2014 - 09:06:13

Vielä lisää teorioita! Tiedetään yleisesti, että mm. nielurisat ovat ihmisen ensimmäisiä puolustusvarustuksia mm. bakteereja vastaan.
http://fi.wikipedia.org/wiki/Nielurisa
Niiden poistaminen nuorena lisää tutkijoiden mukaan mm. autoimmuunisairauksien puhkeamisen riskiä (esim. MS-tauti). tässä yksi linkki.
http://www.medscape.com/viewarticle/806905

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Murhonen Pvm 30.01.2014 - 13:15:37

Tätä ketjua ja lukuisia tutkimuksia lukiessa heräsi suuren suuri epäilys siitä, että olikohan ne seerumista löydetyt Borrealia-vasta-aineet sittenkään mitään epäspesifistä reaktiota! Ensimmäisessä tuloksessa olivat "koholla" ja kun otettiin uudestaan niin selitys oli tuo epäspesifinen reaktio. Olen kuitenkin suurimman osan elämästäni asunut seudulla, jossa niitä punkkeja on omalla pihanurmellakin. Ja muistanpa kerran lapsena käyneeni hoitajan luona näyttämässä erästäkin punkin puremaa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.02.2014 - 17:16:42

Taas tutkimus, joka tarvitsee lisää tutkimista. Bakteerien leviäminen nenästä selkäydinnesteeseen...

Staphylococcal immune complexes and myelinolytic toxin in early acute multiple sclerosis lesions—An immunohistological study supported by multifactorial cluster analysis and antigen-imprint isoelectric focusing

http://www.msard-journal.com/article/S2211-0348%2813%2900005-9/abstract

Abstract

Highly significant clinical, epidemiological and pathogenetic similarities between multiple sclerosis (MS) and nasopharyngeal sinusitis has led to the hypothesis that MS is caused by the inadvertent incorporation of the lymphatic drainage of the nasopharynx into the extracellular fluid circulation of the CNS. It has been postulated that, in response to antigenic and toxic products generated by the mucosal nasopharygeal flora, the leptomeninges and CNS parenchyma acquire the characteristics of a persistently stimulated lymphoid organ. Using an extensive panel of bacterial antibodies, tissues from exceptionally early cases, identified and classified using multifactorial cluster analysis, were screened for bacterial antigens using immunohistological methods. Anti-staphylococcal antibodies detected antigen co-locating with IgG/C3d immune complexes in pre-demyelinating and in primary lesions. The distribution of the antigen in relation to the morphogenesis of early acute MS lesions is detailed. Evidence for the intrathecal processing of staphylococcal antigen was obtained using isoelectric focusing and antigen imprinting to identify antigen-specific oligoclonal bands. Employing a combination of isoelectric focusing, western blotting and mass spectrometric analysis, evidence for the intrathecal processing of staphylococcal β-haemolysin (sphingomyelinase) was obtained using CSF from MS cases. While a myelinolytic transportable toxin may be an important component in the pathogenesis of demyelination, in oligodendrocyte apoptosis, and in deviant immune responses within the CNS, the detection of other as yet unidentified staphylococcal-positive and negative oligoclonal bands points to the involvement of a cocktail of transportable antigens leaking in a similar manner into the CNS from the paranasal sinus mucosal tissues where these molecules are conserved by the resident flora to manipulate and subvert the normal processes of local and systemic immunity. Evidence for the access of other bacterial transportables to the CNS in MS should now be sought. The presence of ‘high-output’ toxigenic bacterial strains within the nasopharyngeal flora of MS patients should also be explored. The use of tracer molecules to detect and quantify nose-to-brain transport in MS patients is clearly apposite.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 04.02.2014 - 10:02:28

Ettei asia menisi liian yksinkertaiseksi, niin seuraavasta linkin kautta voi tutustua ihmisen puolustusjärjestelmään:

http://tuomiopaivantytto.wordpress.com/2012/08/24/veri-ja-verisolut/

Ja, että pysyttäisiin itse asiassa, voi vaarattomaltakin tuntuva bakteerin aiheuttama niveltulehdus hoitamattomana aiheuttaa vaikka mitä:

Septic arthritis is an infection in a joint. Symptoms include pain and tenderness over a joint, pain on moving the joint, and feeling unwell. It is an uncommon infection, but serious. Urgent treatment is needed. This includes antibiotic medicines, and drainage of infected fluid from the joint to prevent permanent joint damage.


What is septic arthritis?

Septic arthritis is an infection in a joint. Many different types of germs (bacteria) can cause septic arthritis. Infection with a bacterium called Staphylococcus aureus is the most common cause.



Related articles Medicines and drug information
Calcium Pyrophosphate Deposition - including Pseudogout

How do you get septic arthritis?

If some germs (bacteria) settle on a small section of a joint, they can multiply and cause infection. Bacteria can get to a joint:
•Via the bloodstream. This is the most common cause, particularly in children. Bacteria may get into the blood from an infection in another part of the body and travel to a bone. Even if you are healthy, bacteria sometimes get into the blood from the nose or gut.
•From an injury. Bacteria can get into a joint if you have a wound that cuts into a joint.
•During surgery. Infection is an uncommon complication if you have joint surgery or joint investigations (such as arthroscopy).

Who is at risk of developing septic arthritis?

Anyone at any age can develop septic arthritis. However, you have an increased risk if you:
•Have certain types of arthritis such as rheumatoid arthritis. If the joints are already inflamed, they are at greater risk of becoming infected. It can be difficult to tell the difference between a flare-up of non-infective arthritis and infective (septic) arthritis. As a rule, if you already have arthritis and symptoms suddenly get worse, and you feel unwell, septic arthritis is a possibility. Tests can confirm, or rule out, an infection.
•Have recently had an injury to a joint.
•Have a joint prosthesis (such as an artificial hip or knee).
•Have recently had surgery to a joint.
•Have a poor immune system. For example, if you have AIDS, if you are taking chemotherapy, if you are seriously ill with another disease, etc.
•Inject street drugs which can be contaminated with germs (bacteria).
•Have gonorrhoea. This is a sexually transmitted disease. If untreated, the gonococcus bacteria can spread in the bloodstream and may cause a septic arthritis.
•Have an infection of bone (osteomyelitis) near to a joint.

Which joints can be affected?

The knee is the site of infection in more than half of cases. The hip is affected in about 1 in 5 cases. The rest are usually the shoulder, wrist, elbow and ankle. Other joints are rarely affected. In most cases, just one joint is affected. However, in about 1 in 5 cases the germs (bacteria) from one joint spread in the blood to another, and two or more joints may be affected at the same time.

What are the symptoms of septic arthritis?
•Pain from the affected joint. The pain tends to be severe and develops quite quickly. Any movement of the joint can be very painful.
•Swelling usually develops over the affected joint which is usually very tender.
•Redness of the overlying skin is typical if the joint is near to the skin surface.
•Feeling generally unwell with high temperature (fever) is common.

In most cases of septic arthritis the symptoms develop quickly, within a few days. However, with an infection in an artificial joint, the symptoms may not be so dramatic. Pain and fever may be mild at first before gradually becoming worse. Also, in cases caused by the tuberculosis (TB) germ (bacterium), the symptoms may develop more slowly.

Are any tests needed?

Tests to confirm the diagnosis

If you have typical symptoms coming from a joint near to the skin surface then the diagnosis may be fairly clear. However, pain coming from deeper joints such as the hip may be due to a number of causes. Certain blood tests can help to confirm that you have severe inflammation 'somewhere' in the body, which may be septic arthritis.

A plain X-ray is not so useful to diagnose the early stages of septic arthritis. However, it may be a useful test to rule out other causes of joint pain. A scan of the joint may help to confirm the diagnosis.

Tests to find which germ (bacterium) is causing the infection

The blood often contains some bacteria from the infected joint. Samples of blood are sent to the laboratory to identify which type of bacterium is causing the infection. This is important, as it will help to decide which is the best treatment. (Some bacteria are resistant to some antibiotic medicines.) Also, if septic arthritis is suspected, a sample of fluid from the joint is taken by a fine needle. Tests on the fluid can usually confirm the diagnosis, and identify the bacterium which is causing the infection.

What is the treatment for septic arthritis?

Antibiotic medicines

Antibiotics are started as soon as possible. At first, high doses are given straight into a vein. The antibiotics chosen are ones that are likely to kill the germs (bacteria) which commonly cause septic arthritis. However, the antibiotics are sometimes changed to different ones when the results of the tests confirm which bacterium is causing the infection. (Some bacteria are resistant to some antibiotics.) The symptoms often settle quite quickly after starting antibiotics. However, you need to continue taking the antibiotics for several weeks. This is to make sure all infection has gone from the joint.

Draining the joint fluid

Infected fluid is drained from the affected joint. This helps to stop damage to the joint while the antibiotics clear the infection. With an infection in a knee, elbow or shoulder joint the drainage may be relatively easy to do with a needle. However, deeper joints such as a hip joint are more difficult and may need a small operation to drain the infected fluid. The joint may need to be drained several times until infected fluid stops building up.

Splinting

The affected joint may need to be splinted, as movement can be very painful at first.

Physiotherapy

Once the infection has been treated and when symptoms begin to settle it is important to get the affected joint moving again. This may help to prevent long-term stiffness in the affected joint.

If the infection is in an artificial joint

The most common artificial joints to get infected are elbow, shoulder and ankle joints, followed by knee and hip joints. The joint often has to be removed to treat the infection properly. However, in many cases a new joint can be inserted with a good chance of success.

What is the outlook (prognosis)?

If the infection is treated promptly, there is a good chance of complete cure with no long-term problems.

If there is delay in treatment, the infection can quickly destroy parts of the joint. This may lead to long-term pain, reduced movement of the joint, and some disability. In some cases the infection becomes severe and leads to blood poisoning (septicaemia). This is a serious complication which can be fatal, but is now rare in the UK since antibiotic medicines became available.

References & Disclaimer | Provide Feedback


Original Author: Dr Tim Kenny  Current Version: Dr Colin Tidy  Peer Reviewer: Dr John Cox  
Last Checked: 30/08/2013  Document ID: 4646  Version: 39 © EMIS




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.02.2014 - 21:15:17

Multiple sclerosis onset: Could mycobacteria play a role?

http://www.sciencedaily.com/releases/2010/02/100226084007.htm

A non-pathogenic bacterium is capable to trigger an autoimmune disease similar to the multiple sclerosis in the mouse, the model animal which helps to explain how human diseases work. This is what a group of researchers from the Catholic University of Rome, led by Francesco Ria (Institute of General Pathology) and Giovanni Delogu (Institute of Microbiology), have explained for the first time in a recently published article on the Journal of Immunology.

Multiple sclerosis is a disease due to an inflammatory reaction provoked by the immune system. It causes the disruption of the coating of the nerve fibres in the central nervous system.

"We do not know what causes multiple sclerosis," explains Francesco Ria, immunologist of the Catholic University. "We know that there exist a genetic factor and an environmental factor, but we do not yet posses a satisfactory theory which can explain how exactly this environmental factor works."

Currently, there are two competing theories on the field: according to the first hypothesis, a virus hides within the brain and what causes the disease is the immunologic antiviral reaction. The second hypothesis states that a viral or bacterial pathogen similar to specific molecules of the central nervous system causes an inflammation which provokes a reaction of the immune system. This reaction ends up destroying the brain cells. The latter is called the autoimmune hypothesis.

This is the hypothesis that the researchers coming from the Institutes of General Pathology, Microbiology and Anatomy of the Catholic University of Rome have been testing with their two-year long project. To demonstrate the viability of this idea, scientists have fooled the mouse immune system, modifying subtly a bacterium of the common family of mycobacteria (the same family to which also the bacterium causing tuberculosis belongs) to make it look like to myelin, the protein coating nerve cells. This modified mycobacterium is completely innocuous. As all external agents, though, it is capable to trigger the reaction of the T-cells of the immune systems. They intervene to destroy it. Since they are innocuous bacteria, although very common in the environment, and since they induce an immune reaction, they are the ideal bacteria scientists can use to study the environmental factor contributing, together with the genetic factor, to cause multiple sclerosis.

"Normally, T-cells cannot penetrate into the central nervous system," adds Rea, "because the hematoencephalic barrier prevents them from doing so. But the bacterium modifies the characteristics of the T-cells and allows them to overcome the barrier. In 15 days the bacterium disappears completely from the body."

Yet these T-cells can now enter into the brain. They begin to attack the myelin of the nerve cells, and this is how the immune disease starts up.

"We basically demonstrate -- explains Rea -- that in an animal model it is possible to be infected with something not carrying any disease, and later on develop a purely autoimmune disease."

There is another element in this complex research, sponsored by the Italian Association of Multiple Sclerosis (AISM). "Normally -- clarifies Rea -- to understand which diseases we have encountered, we measure the antibodies produced by that specific pathogen. But there is a whole world of infectious agents which do not induce the production of antibodies, as is the case in our research: mycobacteria and many other bacteria produce a very low and variable number of antibodies. It is thus very hard to establish whether a population has encountered that specific infectious agent. So, we demonstrate that those infectious agents which are more likely to produce an autoimmune reaction are just those which do not induce antibody production."

Obviously, this is only the first step to better understand the way this very complex and devastating disease works. Ria and Delogu are not stopping here: "We want to try to understand the exact characteristics which this infectious agent should have," they explain. "Might it truly be a good experimental model for multiple sclerosis? If we had prolonged the action of the bacteria, would we have favoured or hampered the development of the disease? And what about the myelin-like bacterium protein: where should it lie? On the surface, or inside? These are all questions -- conclude the two researchers -- which we will be trying to answer in the next years, in the hope to defeat this terrible illness. We could even imagine to develop a vaccine by which we could prevent the immune response associated to multiple sclerosis."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 09.02.2014 - 10:19:37

Katolisen kirkonkin rahoittama tutkimus on lähtenyt MS-taudin jäljille, hyvä niin, mutta pyörä on jo keksitty. Seuraavasta linkistä löytyy yhteenvetoa eri tutkimuksista kroonistuneista bakteerien ja virusten aiheuttamista neurologisista sairauksista.
Alempana teoriaa MS-taudin todennäköisistä aiheuttajista artikkelista, joka sekin on jo keväältä 2008.

http://www.intmed.us/html_frame_pages/dis_htmls/Chronic%20Bacterial%20and%20Viral%20Infections%20in%20Neurodegenerative%20and%20Neurobehavioral%20Diseases.indd%20copy.pdf

Neurodegenerative and Neurobehavioral Diseases
Garth L. Nicolson, PhD
(Department of Molecular Pathology, The Institute for Molecular Medicine, Huntington Beach, CA)

Multiple Sclerosis
Multiple sclerosis (MS) is the most common demyelinating
disease of the CNS, and it can occur in young as well as
older people. In MS, inflammation and the presence of autoimmune
antibodies against myelin and other nerve cell antigens
are thought to cause the myelin sheath to break down, resulting
in decrease or loss of electrical impulses along the nerves.38,39 In
the progressive subset of MS, neurological damage occurs additionally
by the deposition of plaques on the nerve cells to the
point where nerve cell death occurs. In addition, breakdown of
the blood-brain barrier in MS is associated with local inflammation
caused by glial cells.38,39 The clinical manifestations
of demyelinization, plaque damage, and blood-brain barrier
disruptions are variable but usually include impaired vision,
alterations in motor, sensory, and coordination systems, and
cognitive dysfunction. Often these are cyclic (relapsing-remitting
subset) over time, but a substantial MS subset progresses
without remitting.39
There is strong evidence for a genetic component in
MS.40,41 Although it has been established that there is a genetic
susceptibility component to MS, epidemiological and twin
studies suggest that MS is an acquired, rather than an inherited,
disease.42
The possibility that MS is linked to chronic infections
has attracted attention.43,44 In fact, MS patients show immunological
and cytokine elevations consistent with chronic
infections.44-46 A possible infectious cause for MS has been
under investigation for approximately the last decade, and
patients have been examined for various viral and bacterial
infections.44,47 One of the most common findings in MS patients
is the presence of antibodies and DNA of C. pneumoniae
in their CSF.47-49 For example, Sriram and colleagues48 examined
relapsing-remitting (N=17) and progressive (N=20) MS
patients for the presence of C. pneumoniae in CSF by culture,
PCR, and immunoglobulin reactivity with C. pneumoniae
elementary body antigens. They were able to isolate C. pneumoniae
from 64% of MS patients’ CSF versus 11% of patients
with other neurological diseases. High rates of PCR-positive
(MOMP gene) patients (97% MS-positive versus 18% with
other neurological diseases) as well as serology-positive patients
(86% MS-positive, confirmed by enzyme-linked immunosorbant
assays [ELISA] and Western blot analysis) were found
in MS.48 Further examination of MS patients for oligoclonal
antibodies against C. pneumoniae revealed that 14 of 17 patients
were positive, whereas none of the control non-MS patients had
antibodies that were absorbed by C. pneumoniae elemental body
antigens.49
Other studies have also found evidence for the presence of
C. pneumoniae in MS patients but at lower incidence. Fainardi
and colleagues50 used ELISA techniques and found that highaffinity
antibodies against C. pneumoniae were present in the
CSF of 17% of 71 MS cases compared with 2% of 52 patients
with noninflammatory neurological disorders. They found that
the majority of the progressive forms of MS were positive compared
with patients with remitting-relapsing MS. The presence
of C. pneumoniae antibodies were also found in other inflammatory
neurological disorders (N=51), and thus it was not specific
to MS.50 Using immunohistochemistry, Sriram and colleagues51
performed a study of formalin-fixed CNS tissue from MS and
non-MS neurological disease controls and found that in a subset
(7 of 20) of MS patients, chlamydial antigens were localized to
ependymal surfaces and pariventricular regions. Staining was
not found in 17 CNS tissue samples from other neurological
diseases. Frozen tissues were available in some of these MS
cases, and PCR amplification of C. pneumoniae genes was accomplished
in 5 of 8 CNS tissue samples from MS patients but
none in 17 frozen CNS tissues from other neurological diseases.
In addition, they examined CSF sediment by immuno-goldlabeled
staining for chlamydial antigens and found by electron
microscopy that the electron-dense bodies resembling bacterial
structures correlated with PCR-positive results in 10 of 11 MS
cases.51 The same group also used different nested PCR methods
to examine additional C. pneumoniae gene sequences in the CSF
of 72 MS patients and linked these results to MRI evidence of
MS-associated lesions.52 Similarly, Grimaldi and colleagues53
linked the presence of C. pneumoniae infection with abnormal
MRI results in 23 of 107 MS patients with more progressive
disease. In addition, a higher rate of C. pneumoniae transcription
was found by Dong-Si and colleagues54 in the CSF of 84 MS
patients. The above, among other data,55-57 support the presence
of C. pneumoniae in the CNS of MS patients, at least in a subset
of more progressed patients that are most likely the progressive
forms of MS.
Not all studies have obtained evidence, however, for the
presence of C. pneumoniae58,59 or other bacteria60 in the CNS
of MS patients. Hammerschlag and colleagues61 used nested
PCR and culture to examine 12 frozen brain samples from MS
patients but could not find C. pneumoniae in any of the tissue
samples. Alternatively, in one study, C. pneumoniae was found
at similar incidence in MS and other neurological diseases, but
only MS patients had C. pneumoniae in their CSF.59 Swanborg
and colleagues62 have reviewed the evidence linking C. pneumoniae
infection with MS and have concluded that they are
equivocal due to negative reports, and they also speculated that
specific genetic changes may be necessary to fulfill the role of
such infections in the etiology of MS.
Another possible reason for the equivocal evidence linking
MS etiology with infection, such as C. pneumoniae, is that
multiple coinfections could be involved. In addition to C.
pneumoniae found in most studies, MS patients could also have
Mycoplasma species, B. burgdorferi, and other bacterial infections
as well as viral infections.63 When multiple infections are considered,
it is likely that >80% of MS patients have obligate intracellular
bacterial infections caused by Chlamydia (Chlamydophila)
or other bacteria that can be intracellular, such as Mycoplasma,
Borrelia, and other infections. These infections were found only
singly and at very low incidence in age-matched subjects.63 In
spite of these findings, others did not find evidence of Mycoplasma
species in brain tissue (N=30), CSF, or peripheral blood
(N=57) of MS patients.64
Viruses have also been associated with MS. Certain viruses
have been found in MS patients, such as HHV6, but these
viruses have also been found at lower incidence in control samples.
62 Sanders and colleagues65 used PCR to examine postmortem
brain tissue (N=37) and controls (N=61) for the presence
of neurotrophic viruses. They found that 57% of MS cases and
43% of non-MS neurological disease controls were positive for
HHV6, whereas 37% and 28%, respectively, were positive for
herpes simplex virus (HSV1 and HSV2) and 43% and 32%,
respectively, were positive for varicella zoster virus; however,
these differences did not achieve significance, and the authors
concluded that “an etiologic association to the MS disease process
[is] uncertain.” They also found that 32% of the MS active
plaques and 17% of the inactive plaque areas were positive for
HHV6.65 Challoner and colleagues66 used sequence difference
analysis to search for pathogens in 86 MS brain specimens.
Using PCR, they found that >70% of the MS specimens were
positive. They also used immunocytochemistry and found staining
around MS plaques more frequently than around white
matter; nuclear staining of oligodendrocytes was also seen in MS
samples but not in controls.66 Using immunofluorescent and
PCR methods, HHV6 DNA has also been found in peripheral
leukocytes in the systemic circulation of MS patients.67,68 However,
using PCR methods, others did not find herpesviruses in
the peripheral blood or CSF of MS patients.69,70
Although significant information (reviewed in43,44,70) points
to an infectious process in MS, this remains a controversial concept.
As evidence emerges of new possible pathogens in MS, such
as a new putative retrovirus,71 these reports must be intensively
examined and further studies initiated. Since most studies have
found that the progressive form of MS, rather than relapsingremitting
forms of MS, were associated with chronic infections,
infections might be more important in MS progression than in
its inception. Various infections may also nonspecifically stimulate
the immune system.43 As in other neurodegenerative diseases,
multiple factors appear to be involved in the pathogenesis of MS.
Thus, like ALS, MS progression may turn out to be more likely
linked to chronic infections, rather than its inception.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 10.02.2014 - 12:29:00

Uusi hoitomuoto progressiivista tautia sairastaville. Itse käytin viime vuoden lopussa viruslääkkeitä EBV-virukseen, joka on pysynyt itsepäisesti korkealla tasolla. Suomessa MS-diagnoosia tehdessä ei edes testattu EBV, eli HHV-4 virusta, vaikka muut herpesvirukset ja jopa HIV testattiin:

Queensland researchers make major breakthrough with promise for treatment of progressive MS


http://www.msra.org.au/QLD-breakthrough-progressive-ms

NEW Queensland research suggests that controlling Epstein-Barr virus (EBV) infection – the most common cause of glandular fever – may be beneficial in treating multiple sclerosis (MS), a chronic inflammatory demyelinating disease of the brain and spinal cord affecting more than 23,000 Australians.

The study led by Professor Michael Pender with collaborators at the QIMR Berghofer Medical Research Institute, The University of Queensland School of Medicine, and the Royal Brisbane and Women’s Hospital describes a the use of a new treatment that boosts CD8 T cell immunity to EBV using a technique known as 'adoptive immunotherapy'.

While the treatment was conducted in a single person with secondary progressive MS, the promising results suggest that it could potentially be a useful treatment for progressive forms of MS and other chronic autoimmune diseases. There are currently no disease-modifying treatments available for progressive MS patients.

The researchers administered a six week treatment course to a 42 year old man with secondary progressive MS. The treatment had no adverse effects and within two weeks of commencing treatment the patient began to experience clinical improvement. These improvements were sustained up to the most recent follow-up 21 weeks later.

Results of the study were published today in the international Multiple Sclerosis Journal.

The treatment involves collecting immune cells known as T cells from the patient’s blood, growing them in the laboratory with an EBV vaccine and then transferring the cells back to the patient by intravenous infusion. The treatment was developed by Professor Rajiv Khanna of the QIMR Berghofer Medical Research Institute to treat patients with EBV-related malignancy and does not require the use of any drugs.

This is the first use of this treatment, known as EBV-specific adoptive immunotherapy, to treat progressive MS.

Professor Pender said: “The beneficial effect of boosting immunity to EBV by this treatment highlights the importance of impaired immunity to EBV in the development of MS. We believe the treatment corrects the impaired CD8 T cell immunity that allowed EBV infection to cause MS.”

The Brisbane patient, Mr Gary Allen, suffered what he now knows was his first MS attack in 1994 which led to a clinical diagnosis of relapsing-remitting MS in 2000 and later progressed into secondary progressive MS. Since 2008 Gary has been unable to walk or transfer himself without assistance, but has remained working full-time from home.

Following the treatment, Gary experienced a significant reduction in fatigue and painful spasms, an improvement in thinking, memory, attention and hand function, and increased productivity at work. There was also reduced disease activity on his MRI brain scan. At the latest follow-up Gary also had improvement in leg movement.

Gary said the treatment enabled him to perform everyday tasks more easily such as actively assisting with showering, dressing and shopping, and spending more time with his son.

“It’s impossible to overstate the significance of the improvements I’ve enjoyed – whether you look at my work at Griffith University, time with family or resurgent social life, it’s been an amazing change for the better,” he said.

Professor Pender said that the symptom improvement was backed up by other evidence such as the reduction in disease activity on brain scans and reduction in antibodies in the cerebrospinal fluid.

Professor Pender receives funding from MS Research Australia. “Treatments for progressive MS are one of the greatest needs,” commented Dr Matthew Miles, Chief Executive of MS Research Australia. “We are delighted with the results of Professor Pender’s research and congratulate him on this outcome.”

This breakthrough study has profound implications globally for understanding the cause of MS and for the treatment of MS, particularly in its progressive phase, for which currently there is no effective disease-modifying therapy.

A clinical trial is now needed to determine safety and therapeutic efficacy across the clinical spectrum of MS.

The full study can be viewed online at Multiple Sclerosis Journal.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 11.02.2014 - 09:07:30

Mielenkiintoista, kyseessähän on ilmeisesti lähes meillä kaikilla oleva (EBV) ns. pusutautivirus. Miten sitä voi lääkkeillä karkottaa? M.Pender käytti uutta "adoptive immunotherapy"-menetelmää hoitokokeiluissaan MS-potilailla, jossa ilmeisesti manipuloidaan immuunipuolustusjärjestelmää joltain osin, vai olenko väärillä jäljillä?
Tässä lisää asiaan liittyvää tutkimusta:
http://msj.sagepub.com/content/early/2014/02/03/1352458514521888

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.02.2014 - 14:27:23

Activation of MSRV-Type Endogenous Retroviruses during Infectious Mononucleosis and Epstein-Barr Virus Latency: The Missing Link with Multiple Sclerosis?

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078474

Abstract
The etiology of multiple sclerosis (MS) is still unclear. The immuno-pathogenic phenomena leading to neurodegeneration are thought to be triggered by environmental (viral?) factors operating on predisposing genetic backgrounds. Among the proposed co-factors are the Epstein Barr virus (EBV), and the potentially neuropathogenic HERV-W/MSRV/Syncytin-1 endogenous retroviruses. The ascertained links between EBV and MS are history of late primary infection, possibly leading to infectious mononucleosis (IM), and high titers of pre-onset IgG against EBV nuclear antigens (anti-EBNA IgG). During MS, there is no evidence of MS-specific EBV expression, while a continuous expression of HERV-Ws occurs, paralleling disease behaviour. We found repeatedly extracellular HERV-W/MSRV and MSRV-specific mRNA sequences in MS patients (in blood, spinal fluid, and brain samples), and MRSV presence/load strikingly paralleled MS stages and active/remission phases. Aim of the study was to verify whether HERV-W might be activated in vivo, in hospitalized young adults with IM symptoms, that were analyzed with respect to expression of HERV-W/MSRV transcripts and proteins. Healthy controls were either EBV-negative or latently EBV-infected with/without high titers of anti-EBNA-1 IgG. The results show that activation of HERV-W/MSRV occurs in blood mononuclear cells of IM patients (2Log10 increase of MSRV-type env mRNA accumulation with respect to EBV-negative controls). When healthy controls are stratified for previous EBV infection (high and low, or no anti-EBNA-1 IgG titers), a direct correlation occurs with MSRV mRNA accumulation. Flow cytometry data show increased percentages of cells exposing surface HERV-Wenv protein, that occur differently in specific cell subsets, and in acute disease and past infection. Thus, the data indicate that the two main links between EBV and MS (IM and high anti-EBNA-1-IgG titers) are paralleled by activation of the potentially neuropathogenic HERV-W/MSRV. These novel findings suggest HERV-W/MSRV activation as the missing link between EBV and MS, and may open new avenues of intervention.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 13.02.2014 - 08:18:24

Monimutkaiseksi menee, mutta helppoa ja yksinkertaista ratkaisua tuskin onkaan. Aikanaan tehtiin tutkimus EVB-viruksen ja MS-taudin yhteydestä, joka oli mielestäni puhdas 0-tutkimus. Jos tämä uusi teoria ja tutkimuslinja tuottaa jotain tulosta, hyvä niin, vaikka ei ehkä kuulukaan tähän aihepiiriin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 16.02.2014 - 13:30:04

Tämä artikkeli ei mainitse MS:ää, mutta esimerkiksi borrelioosin hoidossa jotkut vannovat ruokavalion merkitykseen ja ennen kaikkea sellaisten metallien vähentämiseen, jotka ruokkivat bakteereita.


Research shows iron's importance in infection, suggests new therapies


http://www.sciencedaily.com/releases/2012/12/121203131700.htm

A Kansas State University research team has resolved a 40-year-old debate on the role of iron acquisition in bacterial invasion of animal tissues.

The collaborative research -- led by Phillip Klebba, professor and head of the department of biochemistry -- clarifies how microorganisms colonize animal hosts and how scientists may block them from doing so. The findings suggest new approaches against bacterial disease and new strategies for antibiotic development.

The study -- in collaboration with Tyrrell Conway, director of the Microarray and Bioinformatics Core Facilities at the University of Oklahoma, and Salete M. Newton, Kansas State University research professor of biochemistry -- recently appeared in PLOS ONE. It shows how iron acquisition affects the ability of bacteria to colonize animals, which is the first stage of microbial disease.

"This paper establishes that iron uptake in the host is a crucial parameter in bacterial infection of animals," said Klebba, the senior author on the publication. "The paper explains why discrepancies exist about the role of iron, and it resolves them."

Iron plays a key role in metabolism, leading bacteria and animals to battle each other to obtain it. Klebba's team found that E. coli must acquire iron from the host to establish a foothold and colonize the gut -- a concept that was often debated by scientists.

"For years it was theorized that iron is a focal point of bacterial pathogenesis and infectious disease because animals constantly defend the iron in their bodies," Klebba said. "Animal proteins bind iron and prevent microorganisms from obtaining it. This is called nutritional immunity, and it's a strategy of the host defense system to minimize bacterial growth. But successful pathogens overcome nutritional immunity and get the iron."

Little was known about what forms of iron enteric bacteria -- which are bacteria of the intestines -- use when growing in the host, but this study shows that the native Gram-negative bacterial iron uptake systems are highly effective. Scientists questioned whether prevention of iron uptake could block bacterial pathogenesis. This article leaves no doubt about the importance of iron when E. coli colonizes animals because bacteria that were systematically deprived of iron became 10,000-fold less able to grow in host tissues, Klebba said.

"This is the first time our experiments unambiguously verified the indispensability of iron in infection, because here we created the correct combination of mutations to study the problem," Klebba said.

Enteric bacteria have so many iron transport systems that it's difficult to eliminate them all. For example, E. coli has at least eight iron acquisition systems.

"These transporters are redundant because iron is essential," Klebba said. "Bacteria are resilient. If one system is blocked, then another one takes over."

These findings suggest strategies to block microorganisms from creating diseases in animals and humans, including the potential for antibiotic development and for therapeutic antibodies.

"It gives us insight," Klebba said. "Now we know that iron deprivation protects against disease, but we must be comprehensive and inhibit multiple systems to completely shut down the microorganisms' ability to obtain the metal."

The researchers are using their findings to isolate antibodies that block bacterial iron uptake. This may help animals and humans defend themselves against microbial diseases.

"We would like to apply this research and protect people from bacterial infection," Klebba said. "That's one of the focal points of our laboratory."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Rami Pvm 16.02.2014 - 17:31:54


HopeSprings 16.02.2014 - 13:30:04:
Tämä artikkeli ei mainitse MS:ää, mutta esimerkiksi borrelioosin hoidossa jotkut vannovat ruokavalion merkitykseen ja ennen kaikkea sellaisten metallien vähentämiseen, jotka ruokkivat bakteereita.


Josko parsakaali kelpaisi? Olisko tehokas ja parantaisko?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 16.02.2014 - 19:41:01

Rami, ehdotit parsakaalia jo sivulla 2 ja vaikka itse pidän parsakaalista, olin hieman skeptinen. Mutta olit oikeassa - parsakaali voi  kukistaa bakteerit.

Bacterial growth is inhibited by broccoli

http://www.rsc.org/chemistryworld/2012/10/broccoli-inhibits-bacterial-growth

Chemists from Israel say that the isothiocyanates sulforaphane and erucin, found in brassicaceae vegetables such as broccoli, Brussels sprouts, cabbage and cauliflower, inhibit growth of the disease-causing bacteria Pseudomonas aeruginosa.

Bacterial quorum sensing (QS) is the method by which bacteria communicate. Instead of language, they release signalling molecules into the environment and a single cell can sense the number of other local bacteria. By using QS, bacteria can coordinate their behaviour through gene expression and adapt to changing environmental conditions. With bacteria such as MRSA and Pseudomonas aeruginosa developing antibiotic resistance, alternative strategies to inhibit bacterial growth are necessary and QS inhibition has been suggested as a new strategy to prevent bacterial growth.

The team, led by Michael Meijler from Ben-Gurion University of the Negev, Be’er-Sheva, found that isothiocyanates from broccoli inhibit quorum sensing. ‘This might signal to the bacteria that conditions for colonisation are not optimal,’ he explains. ‘The benefits of eating vegetables to human health in general have been known for quite some time now. At the molecular level, not a great deal is known yet, providing a fertile ground for fundamental research.’

The work by Meijler supports research from the group of Michael Givskov and co-workers at the University of Copenhagen, Denmark. ‘They made several important discoveries in the area of quorum sensing and discovered that similar isothiocyanates (from horseradish) also inhibit quorum sensing in Pseudomonas aeruginosa,’ explains Meijler.

‘[Meijler’s] work largely confirms the data from the Givskov lab and both groups offer a development within the field as a whole,’ says Paul Williams, professor of molecular microbiology at the University of Nottingham, UK. ‘Clearly there is a lot of interest in potential therapeutic agents which attenuate virulence rather than kill the infecting organism and quorum sensing has emerged as a “popular” potential target. Ajoene [an unsaturated disulfide] from garlic is another interesting QS inhibitor lead.’

However, further research and testing is required. ‘As interesting as our findings are, they do not prove that these isothiocyanates have this activity in vivo. So that would be an obvious avenue to study further,’ says Meijler.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 22.02.2014 - 19:49:14

Olen lueskellut Dr Horowitzin kirjaa "Why Can't I get Better? Solving the Mystery of Lyme & Chronic Disease" ja koska hän on hoitanut myös MS- potilaita, tässä osia yhdestä luvusta:

Is it MS or Lyme?

After rheumatoid arthritis, the most frequent autoimmune disease that may be confused with Lyme is MS.
There are at least 5 reasons for the hypothesis that Lyme is the basis for some cases of MS:
1. Spirochetes have been documented in MS pathology specimens.
2. Spirochetal flagellin (the tail of Borrelia burgdorferi that allow it to move through the body) is immunologically very similar to human myelin.
3. The demyelination process in MS and Lyme is also similar: they both can cause inflammation of the eye and in the spinal cord, leading to a loss of vision and difficulty walking, making it difficult to differentiate between the two diseases clinically.
4. If a physician  were to do a spinal tap trying to differentiate MS from neurological Lyme disease, they would find extremely similar results. As with MS, central nervous system infection with B. burgdorferi can cause an increased protein synthesis with IgG antibodies, lymphocytic pleocytosis (increased lymphocytes in spinal fluid), increased protein, increased plasma cells, and oligoclonal bands. Lyme that affects the central nervous system can produce both oligoclonal bands that react with B. burgdorferi and ones that do not.
5. We find that some of the cystic structures of Lyme disease in the central nervous system of patients with MS. The cyst forms are  one of the means by which Borrelia burgdorferi can persist in the body for extended periods of time, under extremely adverse conditions, and reactivate into normal mobile spirochetes when the conditions are right. Perhaps certain environmental factors (e.g. low vitamin D) or co-infections with other organisms, such as Chlamydia, are responsible for Borrelia coming out of hiding and reactivating the cysts, driving demyelination and MS-type symptoms in certain patients.
***********
As we have seen, Borrelia burgdorferi is a helical-shaped organism, with a head and tails. These tails, or flagella, are how the organism propels itself through bodily fluids and tissues. It is represented by the the 41kDa band ..on the Western blot and is a common band seen in Lyme patients... this is considered diagnostic proof of exposure to Lyme disease.
*******
.. the immune systems of some patients who are genetically predisposed to autoimmune diseases try to kill off the Borrelia causing the Lyme disease by targeting the flagellar (tail) proteins that are biochemically similar to myelin sheaths. This causes their immune system to attack the myelin sheaths surrounding their nerves as well, leading to demyelination, the process that is hallmark to MS. The immune system of these patients is unable to differentiate between the flagellar protein of Borrelia and their myelin sheaths. Since demyelination is part of the disease process underlying MS, and since up to 70 percent of Lyme patients with unresolved symptoms can have demyelination with associated  peripheral neuropathy, it would appear  that this process is another common denominator in the two diseases.
**********
The primary difference between the two diseases seems to be that with MS there were more white matter lesions  on an MRI and higher amounts of myelin basic protein and oligobands present on the spinal tap. Moreover, Lyme disease did not usually cause demyelinating lesions in the cervical or thoracic spine.  So there were some differences, but the boundaries between the two diseases are easily blurred, and one disease could certainly be mistaken for the other.
********
Yet not all Lyme disease patients have demyelination and neuropathy. Could other bacterial organisms be present, causing these autoimmune  reactions and explaining why some patients get these symptoms and others do not? .. Chlamydia pneumonia has already been reported in the medical literature as having possible link to MS.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 27.02.2014 - 12:47:14

Todellakin myös USA:ssa on ongelmia eroittaa Lymen tauti ja MS-tauti, kuten seuraavasta esimerkistä huomataan.

Lyme Disease Mistaken for MS

02/17/08 17:58 Filed in: Lyme Disease Diagnosis|Lyme Disease Bacteria



Getting a correct diagnosis for Lyme disease is a significant step toward getting treatment, yet countless patients are misdiagnosed from the start. Here is a recent account of a North Carolina man who self-diagnosed, after having been put on medication for multiple sclerosis. The article below is from the Raleigh Newsobserver.com, February 19, 2008.

Patients push boundaries of Lyme disease debate.
Two factions hold opposing views on prevalence of tick-borne disease.

Jean P. Fisher, Staff Writer

Even as mounting evidence suggests the state may harbor more tick-borne illness than records indicate, patients with symptoms that match Lyme disease say doctors continue to turn deaf ears to their complaints. They say people are needlessly going untreated or misdiagnosed, leading to advanced illness and even disability. Read more about lyme disease diagnosis.

Dave Tierney of Cary thinks that's what happened to him. Plagued with unexplained fatigue, muscle aches, eye pain and other problems for years, Tierney was diagnosed with multiple sclerosis last year. In June, he left his job as a pilot with Delta Air Lines and began getting long-term disability benefits.

But after researching his symptoms on the Internet, Tierney became convinced he had chronic Lyme disease. An infectious disease doctor and a specialized laboratory test confirmed it. After three months of intravenous antibiotics, Tierney finds his Lyme symptoms much improved and he is back at the controls of an airplane.

"I could have been on MS medicine for the rest of my life," said Tierney, who returned to work this month.

http://www.lyme-disease-research-database.com/lyme_disease_blog_files/tag-multiple-sclerosis.html

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.02.2014 - 15:34:52

Ei liity suoraan MS:ään, mutta kokemuksesta voin sanoa, että tutkimuksen lopputulos tuntuu olevan faktaa.

Common Infections May Dull Mind

http://www.medpagetoday.com/MeetingCoverage/ISCNeuroEdition/44300

SAN DIEGO -- Mental sharpness appeared dulled with a history of exposure to five common pathogen, with a possible signal for faster cognitive decline as well, an observational study suggested.

Burden of exposure to Helicobacter pylori, cytomegalovirus, Chlamydia pneumoniae, and herpes simplex 1 and 2 was associated with poorer executive function and language skills among adults 55 and older (P=0.002 and P=0.04, respectively), Clinton Wright, MD, of the University of Miami Health System, and colleagues found.

Infectious burden index based on serum evidence of exposure to those pathogens showed the same direction of association with cognitive decline over 5 years, the group reported here at the International Stroke Conference.

But that association only approached significance for memory after adjustment for baseline performance, demographics, and vascular risk factors (P=0.07).

"We have a cross-sectional association and a hint of something longitudinal but it wasn't quite significant, and that might mean that we need longer follow-up or that there's no association with decline," Wright explained.

The period over which cognitive decline was measured may have been too short to determine an impact on granular measures of cognition other than memory, which is the most prominent form of decline with age, suggested Lee Schwamm, MD, vice-chair of neurology at Massachusetts General Hospital in Boston and a spokesperson for the American Stroke Association.

The analysis included 588 adults (mean age 71) with no prior stroke history in the diverse, community-based Northern Manhattan Study cohort. They underwent cognitive testing at baseline, and 287 had 5-year follow-up testing.

"This adds another piece of evidence to the story that chronic infectious burden is a bad thing," Schwamm told MedPage Today.

Infectious contributors have been sought, and found in some cases, for everything from cancers to Lyme disease to chronic fatigue and autoimmunity.

"There's a general interest in how exposure to infectious agents sets up biology processes we don't entirely understand and leads to organ damage," Wright agreed.

His group previously linked a higher burden of infectious exposures to elevated stroke risk and carotid artery plaque, which is suspected to be due to inflammation and vascular disease processes.

In the current study, "the fact that the association was strongest with executive function at baseline fits a nice biological hypothesis," Schwamm told MedPage Today.

"Because white matter disease and disseminated microvascular disease you think would, for sure, show up in executive function," he explained, noting that the latter is the most distributed across brain areas of all cognitive functions.

Adjustment for vascular risk factors in the current study did little to alter the associations between cognitive performance and infectious exposures.

While the observational findings couldn't determine causality or rule out confounding, there could eventually be applications for the clinic, Wright suggested.

"If we get to the point where enough studies have shown this connection, it may be time to consider a treatment trial" for pathogens determined to be of particular relevance, he suggested. "But that's a long way in future."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Rami Pvm 28.02.2014 - 17:46:10


HopeSprings 27.02.2014 - 15:34:52:
Ei liity suoraan MS:ään, mutta kokemuksesta voin sanoa, että tutkimuksen lopputulos tuntuu olevan faktaa.

Fantastista, tämä on ABSOLUUTTISTA faktaa, tämä on aivan fantastista... hei me tienataan tällä

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.03.2014 - 12:29:17

A team of University of Notre Dame researchers led by Mayland Chang and Shahriar Mobashery have discovered a new class of antibiotics to fight bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and other drug-resistant bacteria that threaten public health.


Discovery of a New Class of Non-β-lactam Inhibitors of Penicillin-Binding Proteins with Gram-Positive Antibacterial Activity

http://pubs.acs.org/doi/abs/10.1021/ja500053x

Infections caused by hard-to-treat methicillin-resistant Staphylococcus aureus (MRSA) are a serious global public-health concern, as MRSA has become broadly resistant to many classes of antibiotics. We disclose herein the discovery of a new class of non-β-lactam antibiotics, the oxadiazoles, which inhibit penicillin-binding protein 2a (PBP2a) of MRSA. The oxadiazoles show bactericidal activity against vancomycin- and linezolid-resistant MRSA and other Gram-positive bacterial strains, in vivo efficacy in a mouse model of infection, and have 100% oral bioavailability.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 05.04.2014 - 16:30:53

Human polymicrobial infections

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2805%2917745-9/fulltext

Context
Polymicrobial diseases, caused by combinations of viruses, bacteria, fungi, and parasites, are being recognised with increasing frequency. In these infections, the presence of one micro-organism generates a niche for other pathogenic micro-organisms to colonise, one micro-organism predisposes the host to colonisation by other micro-organisms, or two or more non-pathogenic micro-organisms together cause disease.
....
Where next
The medical community is recognising the significance of polymicrobial diseases and the major types of microbial community interactions associated with human health and disease. Many traditional therapies are just starting to take into account the polymicrobial cause of diseases and the repercussions of treatment and prevention.


Is Lyme disease always poly microbial? – The jigsaw hypothesis


http://www.lymepa.org/c05%20Lyme%20-%20Is%20It%20Always%20Polymicrobial.pdf

Summary
Lyme disease is considered to be caused by Borrelia species of bacteria but slowly evidence is
accumulating which suggests that Lyme disease is a far more complex condition than Borreliosis alone. This hypothesis suggests that it may be more appropriate to regard Lyme disease as a tick borne disease complex. Over recent years numerous different microbes have been found in ticks which are known to be zoonotic and can coinfect the human host. The hypothesis suggests that multiple coinfections are invariably present in the clinical syndromes associated with Lyme disease and it is suggested that these act synergistically in complex ways. It may be that patterns of coinfection and host factors are the main determinants of the variable clinical features of Lyme disease rather than Borrelia types. An analogy with a jigsaw puzzle is presented with pieces representing Borreliae, coinfections and host factors. It is suggested that many pieces of the puzzle are missing and our knowledge of how the pieces fit together is rudimentary. It is hoped that the hypothesis will help our understanding of this complex, enigmatic condition.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.05.2014 - 09:55:44

Wann ist eine Borreliose eine Neuroborreliose?

http://www.borreliose-berlin.de/wann_neuroborreliose.php

Käännös Suomen Lyme Borrelioosi yhdistyksen sivuilta http://borrelioosi.net/foorumi/viewtopic.php?t=2694:

Milloin borrelioosin katsotaan olevan neuroborrelioosia?

Borrelioosi ja siihen liittyvät neuropsykiatriset oireet.
Neurologian ja psykiatrian erikoislääkäri Martina Lorenz, Minden, Ala-Saksin osavaltio Saksassa.

On tarkoituksenmukaista selvittää, milloin borrelioosi-sairauden kroonistuessa sen neurologis- psykiatriset oireet merkitsevätkin neuroborrelioosia.
On muistettava että borrelioosin eri vaiheet menevät lomittain.

Oireet, jotka ilmaantuvat kun perifeerinen hermosto on sairastunut sekä likvortutkimuksen tulkinnan vaikeus

Saksan neurologisen tiedeyhteisön (Deutsche Gesellschaft für Neurologie= DGN) mukaan voidaan myös ilman positiivista likvortutkimuksessa ilmennyttä näyttöä osoittaa seuraavanlaisia borrelioosiin viittaavia oireita:
Punkin purtua reiden alueelle tai takalistoon iskiashermon alueelle, spirokeetta leviää iholta eteenpäin verisuonistoon ääreishermoston alueelle. Nyt ilmenee oire, joka on samankaltainen kuin hermojuurisyndrooma kuten välilevyluiskahduksessa. Kyseessä on kipu, joka säteilee ristiselästä ja takamuksesta jalkaan. Tarkalleen ottaen pitäisi puhua yhden perifeerisen hermojuuren tulehduksesta. Jos selkäydinpunktio, jossa tutkitaan proteiinien ja tulehdussolujen määrän kohoamista sekä borrelioosibakteerin vasta-aineita suoritettaisiin tässä tilanteessa, ei suurimmallakaan todennäköisyydellä voisi todeta neuroborrelioosia. Oireiden perusteella kyseeseen voisi kuitenkin tulla neuroborrelioosi. Tämä on vain yksi esimerkki siitä, kuinka on katsottava kriittisen tarkkaan tällä hetkellä voimassa olevia DGN:n säädöksiä.

Myös yhden yleisimmistä neuroborrelioosin oireista, kasvohermohalvauksen (perifeerinen fasialispareesi) ollessa kyseessä vain hyvin harvoin likvortutkimus antaa näytön borrelioosivasta-aineista. Aina on kuitenkin tiedossa olleen punkin pureman ja mahdollisen borrelioosiepäilyn ollessa otettava likvornäyte ja terapoitava antibiootein (Ceftriaxon)

Edelleen borrelioosibakteerin aiheuttamia perifeerisen hermoston sairauksia ovat: polyneuriitti (monihermotulehdus), polyradikuliitti (hermojuuren tulehdus) ja polyneuropatia (usean hermon toimintahäiriö-vaurio). Samoin käytännössä vastaantulevia ääreishermoston oireita ovat yläraajaan liityen: karpaalitunnelisyndrooma (medianushermon vaurio) sekä sulcus ulnaris syndrooma (ulnaarihermon viottuma/vaurio).
Punkin purema- anamneesin ollessa kyseessä on tutkimuksin poissuljettava neuroborrelioosin mahdollisuus; vaikkakaan likvortutkimukset suurella todennäköisyydellä eivät näytä positiivista tulosta = Borrelia vasta-aineita. Kaikesta huolimatta diagnoosina neuroborrelioosi on otettava huomioon.
Aina, kun tulee vastaan molemminpuolinen karpaalitunneli- ja/tai sulcus ulnaris syndrooma on ajateltava sairauksia kuten diabetes mellitus, erilaiset myrkytykset, kuten krooninen alkoholismi sekä myös borrelioosi.

Borrelioosi- infektiossa myös vegetatiivinen hermosto (riippumaton) vaurioituu: ilmenee uusiutuvia takykardioita (sydämen tiheälyöntisyyksiä), nopeutuneita pulsseja, hikoiluja, ihon lämpötilan muutoksia, lihasspasmeja, verenpaineen heittelyä samoin ääreisalueilla ilmenee vegetatiivisiä häiriöitä verenkierrossa kuten Raynaud-oireet (kylmäsormisuus).

Keskushermosto on vaurioitunut, kun kyseessä on aivotulehdus, aivokalvontulehdus tai selkäydintulehdus. Näissä tapauksissa ilmenee tasapainovaikeuksia, kehon toispuoleisia vaikeuksia, puhevikaa (afasiaa), virtsarakon toimivuus- ja tyhjentymisvaikeuksia samoin voi aiheutua epilepsian puhkeaminen sekä luonteen muuttumista. Dementian kaltaiset oireet, keskittymiskyvyn puute, univaikeudet, krooninen väsymysoireyhtymä, depression oireet, päänsäryt jopa hallusinaatiot voivat olla mahdollisia.


Miten neuroborrelioosi eroaa MS:sta?


Diagnoosia tehtäessä on huomioitava punkin purema ja erythema migransin olemassaolo. On myös borrelioosille tyypillisiä oireita, jotka on syytä ottaa huomioon. Magneettiresonanssikuvauksessa (MRT) MS-taudille tyypillistä plakkien kuviointia ei nähdä borrelioosissa. Borrelioosissa pesäkkeet voivat puuttua kokonaan. Likvordiagnostiikassa borrelioosissa solujen määrä on suurempi kuin MS:ssä (>50/mm3), samoin proteiinien määrä on koholla (>1g pro I). Borrelioosissa löydetään myös usein aktivoitunut B-solu määrä likvorissa. Parhaassa tapauksessa löytyy intratekaalisia vasta-aineita IgG, IgM sekä ryhmästä IgA. Lääketieteellisessä kirjallisuudessa pyydetään kiinnittämään huomiota siihen, että kliinisesti varmistetussa borrelioosi-aivotulehduksessa ja jopa pitkälle edenneessä aivojen tuhoutumisessa likvornäyte korkeintaan vain 30 %:ssa osoittautuu positiiviseksi.

Psykiatriset oireet:

Kyseessä olevat potilaat ovat borrelioosi -sairauden kroonistuneessa tilanteessa ja joiden tilaa myös kutsutaan ns. post-lyme-syndroomaksi. Ilmenee mielialan vaihtelua, depressiota, voimakasta väsymystä, univaikeuksia, saamattomuutta, uupuneisuutta, lisääntynyttä hermostuneisuutta, pelkoja, paniikkitiloja, keskittymiskyvyttömyyttä, unohtamista, samoin paikantamisvaikeuksia, sanojen löytämis- ja puhevaikeuksia. Monilla sairastuneilla ilmenee vaikeuksia ajattelussa, kirjoittamisessa; kuten kirjainten poisjättämistä tai väärään järjestykseen kirjoittamista.
Tyypillinen oire on myös häiriöt hienomotoriikassa., joka oikeastaan kuuluu neurologian alueelle. Potilaat kertovat myös kolhivansa itseään ovien karmeihin ja kaikenlaisiin kulmiin, sillä näitä ei vain huomaa.

Käytännön neurologis-psykiatrisia hankaluuksia

Potilailla, jotka kärsivät kroonisesta, jatkuvasta borrelioosista on edellä mainittujen oireiden kirjo laajuudessaan. Oireet voivat olla henkilöstä riippuen eriasteisia ja vuorotella. Oireet muuntautuvat selkeästi somatisaatiohäiriöön ja depression symptomatiikkaan. Kaikki tämä asettaa lääkärin vaikeaan tilanteeseen noudattaessaan tiedeyhteisön ohjeistusta: potilaalta otetaan mahdollisuus borrelioosiin ja edellä mainittujen oireiden yhteenkuuluvuuteen.
Jos näyttö vasta-aineista likvorissa, häiriö veri-aivoesteessä tai solujen kohonneita arvoja ei ilmene, kyseessä ei ole ohjeistuksen mukaan neuroborrelioosi. Jos potilaalta lisäksi on jäänyt huomaamatta puutiaisen purema, mahdollinen tapahtuma puuttuu anamneesista, ei asiaa voida todentaa. Vieläpä jos ei ole ilmennyt neurologisia puutoksia, on hylättävä ajatus mahdollisesta neuroborrelioosista.

Potilasta hoitavana lääkärinä minun siis on päätettävä, toiminko ohjeistuksen linjauksen mukaisesti vai otanko potilaan hätätilassaan vakavasti haluten hoitaa häntä.

Mahdollisuuksia on monia. Ensinnäkin voihan olla, että potilaalla ei olekaan borrelioosia ja sairauden oireet ovat jonkin muun sairauden aiheuttamia. Tehtäväni on tällöin lähettää potilas toisen asiantuntija-lääkärin luokse. Toisaalta on täysin mahdollista, että kyseessä on borrelioosi ja bakteeri on immuunisysteemiltä piilossa, eikä immuunisysteemi pysty reagoimaan (AK-Titer, Westwrn-Blot, LTT negatiiviset)
Mahdollista on myös, että jatkuvan tulehdustilan johdosta immuunipuolustus on voimaton (CD57- solujen väheneminen) eikä kykene muodostamaan vasta-aineita.
Tunnettua on myös, että immuunisysteemiä huiputetaan muuntamalla pinta-vasta-aineet immuunireaktion estämiseksi.
Mahdollista on myöskin, että potilaalla on lisäinfektio, jolloin jokin toinen taudinaiheuttaja on oireiston taustalla.

Erotusdiagnostiikka:

Somaatiomuotoisessa kivussa kyseessä on häiriö jossain elimessä, ja jonka taustalla on jokin psyykkinen tapahtuma. Kipusairaus puhkeaa yleensä äkkinäisesti, usein sitä on seurannut jokin onnettomuus, vaikea operaatio tai jokin vakava sairaus. Tyypillistä on, että ihminen keskittyy voimakkaasti kiputuntemukseen ja tuntee sen uhkaavana. Kipu on useimmiten tarkasti rajattavissa ja se on kestävää. Psykoterapiassa aiheuttajaksi paljastuu monia traumaattisia tapahtumia, kuten lapsena tai nuorena koettu hyväksikäyttö, koettu väkivalta tai heitteillejättö.

Tämänkaltaisesta kroonisesta kivusta borrelioosissa ei ole kyse ja tätä asianlaitaa puoltavat esim. seuraavat asiat:
- punkinpureman olemassaolo
- tuki- ja liikuntaelimistön oireisto
- nivelkivut
- iho-oireisto, esim. tuntomuutokset- ja puutokset
- sanojen hapuilu
- neurologinen oireisto
- ajoittaisesti puhkeavat kivut monilla kehon eri alueilla.

Mikä puoltaisi fibromyalgia- diagnoosia?

Fibromyalgian diagnoimisessa löydetään ns. tenderpoints:it, näissä pisteissä kipu on voimakas, kahdeksastatoista pisteestä yhdentoista on oltava positiiviset. Serotoniini sekä sen esiaste L-tryptophan ovat matalalla tasolla. Somatomedin-C, jota keho normaalisti tuottaa syvänunen vaiheessa on likvorissa matalalla tasolla. NON-REM unen häiriintyessä kehittyy Somatomedin C:n puute ja seuraa häiriöitä pienten verisuonten jäntevyydessä. Laboratorionäytteiden tason ja kivun tuntemus tenderpointseja painettaessa vallitsee tiivis yhteys. Selkäytimessä aine P:n taso on koholla, jolloin kivuntuntemus johdattuu keskushermostoon voimakkaammin. Syntyy häiriö melatoniinin ja serotoniinin välillä. Kilpirauhashormonien taso laskee. Yöllinen cortisolitaso nousee ja kasvuhormonitaso laskee. Cortico-Releasing-hormonin (CRH hypotalamuksesta) nousun johdosta on nähtävillä pelkotilojen ja depressioiden lisääntymistä. EMG:ssä nähdään ristiriitainen reaktio jännittyneessä lihaksessa. Lihasbiopsiassa näkyy epäspesivisiä muutoksia.
Sekundaarisen fibromyalgiasyndrooman voivat aiheuttaa borreliabakteeri, Ebstein-Barr-virus sekä coxackie-virukset. Tämän mielenkiintoisen syysuhteen näytön pitäisi lopultakin osoittaa, että fibromyalgia ei ole vain ?pelkkä psykogeeninen? reaktio. Oireet monimuotoisuudessaan osoittavat kuitenkin niiden olevan hyvin samankaltaisia kuin kroonistuneessa borrelioosissa.




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.05.2014 - 09:59:31

Jatkuu...

Borrelioosi-sairauden psykiatristen oireiden kehittymisen mahdollisia syntymekanismeja:

1. Vaskulaariset oireet: Pienten ja suurten verisuonten tulehdukset aiheuttavat verenkierron häiriöitä. SPECT-kuvauksessa näitä voidaan nähdä. Verisuonispasmien vuoksi voi ilmaantua lisääntyvästi migreenikohtauksia.
2. Neurotoksiinien aiheuttamat vauriot.
3. Tulehduspesäkkeiden aiheuttamat vauriot. SPECT-tutkimuksessa Fallon esittää tulehduspesäkkeiden ja verenkiertohäiriöiden aiheuttamaa heterogeenisista kuviointia vähentyneine virtauksineen.
4. Krooniset kivut voivat aiheuttaa reaktiivisen depression
5. Depression voi myös aiheuttaa syntyneet sosiaaliset ongelmat kuten partnerin ?tai työpaikan menettämiset sekä joutuminen eläkkeelle liian varhain.
6. Hormonaaliset häiriöt, kuten serotoniinin puute. (ks. esitelmä Dr. Petra Hopf-Seidel)

Serotoniinin tason lasku voi aiheuttaa kohtalokkaita seuraamuksia kuten depression ja psykiatrisia oireita, seuraamuksina voivat myös olla immuunipuolustuksen heikentyminen ja voimakas taipumus allergioiden puhkeamiseen, huonontunut haavojen paranemisprosessi, tonushäiriöt (liikkeen hallinnan häiriöt, suom. huom.) häiriöt ruokailutottumuksissa, kuten voimakas mieltymys makeaan. Voi ilmetä coronaarispasmeja sekä seksuaalisia häiriöitä.

On kylläkin mielenkiintoista mutta myös pelottavaa, kuinka borreliabakteeri saa koko organismin sekaisin ja kuinka moninainen ja kompleksinen tämä sairaus voi olla.

Juuri tästä johtuen on kroonisen borrelioosin hoidon oltava kokonaisvaltaista.
Antibioottisen terapian rinnalla ovat yhtä tärkeitä immuunisysteemin voimistaminen, stressin purkaminen, kuntoilu kuntohoitajan neuvomana, fysioterapeuttinen hoito, neurotoksiinien määrätietoinen häätäminen, ravinnon muuttaminen emäksiseksi ja kehon happamoitumisen estäminen. Apua tarjoavat avohoidossa tai sairaalahoidossa psykoterapia lähtökohtanaan kivunlievityksellinen terapia.

Tarvitsemme enemmän mielikuvitusta diagnosoidessamme borrelioosin ja vaihtaessamme tietoja kollegojen kesken, meidän on lisättävä yhteistyötä, lisättävä potilastietojen tilastointia sekä huolehdittava sairauden pakollisesta ilmoitusvelvollisuudesta.* Näillä toimenpiteillä ei potilas ehkä parane, kuitenkin pystymme näin purkamaan borrelioosi-potilaaseen kohdistunutta stigmaa, että kyseessä olisi puhtaasti psykosomaattinen sairaus

Yleisötilaisuus Berliinissä 6.9.08 Neurologian ja psykiatrian erikoislääkäri Dr. Martina Lorenz, www.borreliose-berlin.de

Prof. Dr. Brian Fallon, MD.,director; Lyme and Tick-Borne Diseases Research Center Columbia University.

Dr. Petra Hopf-Seidel: neurologian ja psykiatrin erikoislääkäri, Ansbach/Saksa; tutkimustyötä ja luentoja borrelioosista ja hoidoista.

* Vuoden 2011 alusta kaikki Saksan osavaltiot ovat sitoutuneet infektiotautien lainsäädäntöön liittyen ilmoitusvelvollisuuteen terveysviranomaiselle borrelioosisairauksissa, päätehtäväalueina ennaltaehkäisy ja hoitojen paraneminen. ( suom. huom.)

Käännös saksan kielestä: Marja Hoefs



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 04.05.2014 - 19:01:38

Mielenkiintoista tietoa borrelioosista ja sen hoidosta. Varmistin lääkäriltäni sen seikan, ettei Suomessa tehdä yhtä herkkiä borrelia-testejä kuin Saksassa. Toisena kiinnitin huomioni emäksiseen ruokavalioon ja toisaalta puolukan ja rukiin ristiriitaiseen käyttösuosituksiin, koska molempia pidetään "superterveellisinä" ja toisaalta happamina ruoka-aineina.
http://www.kotkansiipi.com/Page49.htm
http://www.whfoods.com/genpage.php?tname=foodspice&dbid=65
http://www.raikasweb.com/puolukka-todellinen-supermarja

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 05.05.2014 - 09:53:16

Hyvät linkit olet tähän ottanut.
Kiitos sinulle. - Marianna :)

http://www.kotkansiipi.com/Page49.htm
http://www.whfoods.com/genpage.php?tname=foodspice&dbid=65
http://www.raikasweb.com/puolukka-todellinen-supermarja

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.05.2014 - 13:38:59

John Hopkins University on tutkinut syitä miksi osa borrelioosia sairastavista kehittää heikosti vasta-aineita:

Serum Inflammatory Mediators as Markers of Human Lyme Disease Activity


http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0093243

Abstract

Chemokines and cytokines are key signaling molecules that orchestrate the trafficking of immune cells, direct them to sites of tissue injury and inflammation and modulate their states of activation and effector cell function. We have measured, using a multiplex-based approach, the levels of 58 immune mediators and 7 acute phase markers in sera derived from of a cohort of patients diagnosed with acute Lyme disease and matched controls. This analysis identified a cytokine signature associated with the early stages of infection and allowed us to identify two subsets (mediator-high and mediator-low) of acute Lyme patients with distinct cytokine signatures that also differed significantly (p<0.0005) in symptom presentation. In particular, the T cell chemokines CXCL9 (MIG), CXCL10 (IP-10) and CCL19 (MIP3B) were coordinately increased in the mediator-high group and levels of these chemokines could be associated with seroconversion status and elevated liver function tests (p = 0.027 and p = 0.021 respectively). There was also upregulation of acute phase proteins including CRP and serum amyloid A. Consistent with the role of CXCL9/CXCL10 in attracting immune cells to the site of infection, CXCR3+ CD4 T cells are reduced in the blood of early acute Lyme disease (p = 0.01) and the decrease correlates with chemokine levels (p = 0.0375). The levels of CXCL9/10 did not relate to the size or number of skin lesions but elevated levels of serum CXCL9/CXCL10 were associated with elevated liver enzymes levels. Collectively these results indicate that the levels of serum chemokines and the levels of expression of their respective chemokine receptors on T cell subsets may prove to be informative biomarkers for Lyme disease and related to specific disease manifestations.
.......

The detection of a subgroup of acute Lyme patients that display low levels of immune mediators in the blood (mediator-low) could represent a set of immunologically hyporesponsive individuals or patients that have immunologically cleared the infection for which inflammation has subsided. The finding that both mediator groups have similar duration of illness and identical erythema migrans presentation together with the observation that the mediator–low group is also enriched for seronegative patients argues against but does not fully exclude the latter possibility. Of note the mediator low group is heterogeneous in how Lyme patients cluster with controls suggesting that indeed there may be multiple mechanisms underlying the mediator low group. The failure to seroconvert is a well-known feature of antibiotic treated early Lyme disease but the underlying cause is not understood [11], [12]. It is also unlikely that the non-seroconverting Lyme disease patients were missed due to a delayed response because in the study design patients with a seronegative test result at diagnosis were re-tested following treatment and remained negative. This argues that the mediator low group represents a subgroup of Lyme patients that develop a diminished immune response that leads, in some cases, to poor antibody production.
.........

The analysis of chemokine and cytokine levels in the serum of Lyme disease patients has allowed us to define at least two subsets of Lyme patients which have distinct disease phenotypes differing in number of symptoms, extent of liver involvement, lymphocyte levels and seroconversion status. It is possible that the inflammatory mediator profiles identified may prove valuable as biomarkers of Lyme disease activity. Moreover, these chemokines likely identify immune pathways that are involved in the resolution of Lyme disease and as such may be potential therapeutic targets.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 23.05.2014 - 08:33:55

Tässä on "pähkinänkuoressa" mm. video borrelioosista.
http://www.youtube.com/watch?v=tGhwdGkeiOs&feature=player_embedded

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.05.2014 - 12:18:32

Promising discovery in fight against antibiotic-resistant bacteria

http://www.sciencedaily.com/releases/2014/05/140522175719.htm


Date:
May 22, 2014
Source:
University of British Columbia
Summary:
A small molecule that prevents bacteria from forming into biofilms, a frequent cause of infections, has been discovered by researchers. The anti-biofilm peptide works on a range of bacteria including many that cannot be treated by antibiotics. "Currently there is a severe problem with antibiotic-resistant organisms," says the lead author of the study. "Our entire arsenal of antibiotics is gradually losing effectiveness."

UBC’s Bob Hancock and his team of researchers have discovered a peptide that could help destroy biofilms, which are responsible for two-thirds of human infections.

Researchers at the University of British Columbia have identified a small molecule that prevents bacteria from forming into biofilms, a frequent cause of infections. The anti-biofilm peptide works on a range of bacteria including many that cannot be treated by antibiotics.

"Currently there is a severe problem with antibiotic-resistant organisms," says Bob Hancock, a professor in UBC's Dept. of Microbiology and Immunology and lead author of the study published today in PLOS Pathogens. "Our entire arsenal of antibiotics is gradually losing effectiveness."

Many bacteria that grow on skin, lung, heart and other human tissue surfaces form biofilms, highly structured communities of bacteria that are responsible for two-thirds of all human infections. There are currently no approved treatments for biofilm infections and bacteria in biofilms are considerably more resistant to standard antibiotics.

Hancock and his colleagues found that the peptide known as 1018-- consisting of just 12 amino acids, the building blocks of protein--destroyed biofilms and prevented them from forming.

Bacteria are generally separated into two classes, Gram-positives and Gram-negatives, and the differences in their cell wall structures make them susceptible to different antibiotics. 1018 worked on both classes of bacteria as well as several major antibiotic-resistant pathogens, including Pseudomonas aeruginosa, E. coli and MRSA.

"Antibiotics are the most successful medicine on the planet. The lack of effective antibiotics would lead to profound difficulties with major surgeries, some chemotherapy treatments, transplants, and even minor injuries," says Hancock. "Our strategy represents a significant advance in the search for new agents that specifically target bacterial biofilms."

Story Source:

The above story is based on materials provided by University of British Columbia. Note: Materials may be edited for content and length.

Journal Reference:

   César de la Fuente-Núñez, Fany Reffuveille, Evan F. Haney, Suzana K. Straus, Robert E. W. Hancock. Broad-Spectrum Anti-biofilm Peptide That Targets a Cellular Stress Response. PLoS Pathogens, 2014; 10 (5): e1004152 DOI: 10.1371/journal.ppat.1004152

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 02.06.2014 - 09:23:12

Ettei asia taas menisi liian yksinkertaiseksi, on takavuosina tehty myös tällainen päätelmä:

Wednesday, February 8, 2012 Memo: Borrelia Are NOT Gram-Negative Bacteria, And Might Become Resistant
Tags: abstracts, antibiotics, borrelia, chronic lyme, definition, diagram, lyme disease, macdonald, paper, resistance
For years, Borrelia have been thought to be Gram-negative because of their diderm and structural appearance upon staining. Borrelia - including Borrelia burgdorferi - are not Gram-negative bacteria, though - even though many people are still referring to them as such. They belong in their own category.

As I was telling Dr. MacDonald this week:

I found information confirming the fact that Borrelia is not Gram-negative or Gram-positive. It's its own special thing:

"Borrelia were thought to be Gram negative because of their double membrane structure, but genetic analysis places them - along with other spirochetes - into a separate eubacterial phylum. Ultrastructural molecular and biochemical studies have emphasized the wide taxonomic gap between spirochetes and Gram-negative bacteria."

- From "The Genus Borrelia" by Melissa Caimano. Prokaryotes (2006) 7:235-293.

"Although Borrelia spirochetes are often, but mistakenly described as Gram-negative bacteria due to their diderm, i.e. double-membrane envelopes, a closer examination reveals significant differences in composition and architecture. Probably most striking is the lack of LPS, the presence of major surface lipoproteins at the host-pathogen interface during transmission, persistence and ensuing pathogenic processes and the additional function of periplasmic flagella in defining cell shape. While surface lipoproteins such as the Osps interact with a variety of ligands in different organ tissues, they are also targets of the immune response and several have emerged as vaccine candidates."

- From Borrelia: Molecular Biology, Host Interaction and Pathogenesis. Edited by D. Scott Samuels and Justin D. Radolf. (2010)

So one could say they are Gram-negative-"like" - but strictly speaking, Borrelia is not Gram-negative bacteria."
He accepted this response, and is now stating that Borrelia burgdorferi is Gram-indeterminate.

There is additional information from the second source cited which indicates that Borrelia spirochetes are different from other bacteria, summarized here:

"Some of the identified periplasmic lipoproteins, i.e. the OppAs, are components of substrate transport complexes. Investigations into integral membrane proteins led to the identification of several Borrelia porins: P13, whose structure and function is unknown, DipA, which is specific for dicarboxylates and P66 (Oms66), which has a dual role as a pore-forming outer membrane protein with an extremely high single channel conductance and an adhesin for β3-integrin. The recently identified Tol homologs BesA, -B and -C appear to form a Type I 'channel' to export exogenous toxic agents such as antibiotics and to maintain infectivity by an unknown mechanism. Initial studies on envelope biogenesis pathways based on diderm proteobacterial model organisms already revealed significant deviations from the norm. This further bolsters the unique status of Borrelia among microbial pathogens."
darn Borrelia... Why do you have to be such a deviant? Why can't you just conform?

Anyway, the Type I 'channel' they're talking about above which exports or removes antibiotics and helps maintain infectivity is said here to do so using an unknown mechanism. Judging from research out there, this channel relates to transmembrane proteins which span the outer and inner membranes of the bacteria - and it appears to function like an efflux pump (in this case, a resistance-nodulation-division-like pump) which removes antibiotics and is involved in antibiotic resistance. Check out this paper (full text at link):

Source: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000009

An RND-Type Efflux System in Borrelia burgdorferi Is Involved in Virulence and Resistance to Antimicrobial Compounds

Ignas Bunikis1, Katrin Denker, Yngve Östberg1, Christian Andersen, Roland Benz, Sven Bergström. PLoS Pathog. 2008 Feb 29;4(2):e1000009.

Abstract

Borrelia burgdorferi is remarkable for its ability to thrive in widely different environments due to its ability to infect various organisms. In comparison to enteric Gram-negative bacteria, these spirochetes have only a few transmembrane proteins some of which are thought to play a role in solute and nutrient uptake and excretion of toxic substances. Here, we have identified an outer membrane protein, BesC, which is part of a putative export system comprising the components BesA, BesB and BesC. We show that BesC, a TolC homolog, forms channels in planar lipid bilayers and is involved in antibiotic resistance. A besC knockout was unable to establish infection in mice, signifying the importance of this outer membrane channel in the mammalian host. The biophysical properties of BesC could be explained by a model based on the channel-tunnel structure. We have also generated a structural model of the efflux apparatus showing the putative spatial orientation of BesC with respect to the AcrAB homologs BesAB. We believe that our findings will be helpful in unraveling the pathogenic mechanisms of borreliae as well as in developing novel therapeutic agents aiming to block the function of this secretion apparatus.



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.06.2014 - 10:45:31

Koska varsinaisten tutkimusten lukeminen ja varsinkin tulosten yhteenveto on varsin työlästä ja joissain tapauksissa oikeiden johtopäätösten tekeminen lähes mahdotonta, laitan tähän pari suomennettua esimerkkiä, joita sopii epäillä. Suomennoksissa on vikoja.


Kriittinen neurologisia oireita Borrelioosi sinun tarvitsee tietää


Kirjoittaja: Amélie Fontaine

Jotkin Borrelioosi, jotka sinun pitäisi näyttää varten neurologisia oireita ovat tunnottomuus, epänormaali tunteita, raajojen, Bell’s halvaus, Aivokalvontulehdus, Visio ongelmia, keskittämällä, muistin tappio, enkefalopatian, lepotila häiriöitä ja kognitiiviset alentuminen vaikeuksia.

Borrelioosi on tartunta tartunnan jakoviivojen vianselvitysmenettelyt vuoksi aiheutunut. Sairaus aiheuttaa Borrelia burgdorferi tunnetaan bakteeria. Tällaiset alueilla asuvien henkilöiden olisi varoa ja toteutettava jokaisen tarkoittaa tutkittavina, kun menee ulkona, koska jakoviivat ovat yleensä näkyvästi laiduntavat ja puustoisen sijainneissa. Borrelioosi oireet voivat sisältää singáw vianselvitysmenettelyt, joka laajentaa ajan ja useita flunssa kaltaiset oireita kuten sikaruton, elin kivut, väsyminen ja · kylmiä väristyksiä alalla. Borrelioosi oireita, jotka tulevat näkyviin aiemmassa vaiheessa, puutteellisuus joskus neurologisia oireita Käynnistä ilmeinen viikkoa tai jopa vuotta sen jälkeen, kun se on saanut tartunnan.

Tunnottomuus

Tunnottomuus on taudin tai vahingon luissa tyypillisiä oireita. Borrelioosi kärsivät usein ihmiset kokevat lomakkeen gammaknife sanoa, että kuten tapeilla ja neuloja pricking katsoo niiden ihon. Toisin kuin halvaus Jos potilailla ovat siirtäminen ei onnistu tunnottomuus aiheuttaa potilaille menettävän sensaatio.

Epänormaali tunteita raajojen

Potilaiden usein sanoa, että käsivarret ja jalat olosi heikko. Ne myös kohdata magâ, polttaminen, pintavikoja ja käsivarret ja jalat, pistelyä sensaatio.

Bellin halvaus

Bellin halvaus on toinen oire ottaa Lyme-tauteja. Bellin halvaus on ominaista äkillinen halvaus potilaan kasvohoito luissa komplikaatioita aiheuttamien kasvojen lihaksia. Potilaille voidaan ja yleensä tuntevat halvaantuneen vähintään puolet niiden kasvot tai enemmän.

Aivokalvontulehdus

Jopa 15 prosenttia Borrelioosi potilaiden tartunnan saaneiden kalvot, jotka sijaitsevat aivojen ja selkäytimen ympärille. Koe Aivokalvontulehdus potilaiden ominaista päätä ja päänsärkyä, että tyypillinen OTC lääkkeiden ole poistanut. Lisäksi ne kohdata kohonneen herkkyys valossa.

Vaikeuksia kuulon tai Visio

Potilaiden voi tuntea muutoksia niiden Visio. He tuntevat vääristymiä, sumea Visio, yö sokeus ja joskus ne jopa toimintansa näköpiirissä.

Ongelmia pitoisuus

Borrelioosi on kunnon, jonka tiedetään vaikuttavan potilaan pitoisuus. Kohdistus ja huomiota yhteen tehtävään puute on tällaiset potilaat ominaisuus.

Kognitiivinen mielialahäiriö

Muistiongelmat ovat Borrelioosi toinen ongelma. Kun yrittää muistaa, jotain saattaa olla vaikeaa palauttavat mieliin yksityiskohdat ja tuntuu vähän disoriented.

Enkefalopatian

Kun Borrelioosi on vasemmalle käsittelemätön hyvin varhaisessa vaiheessa, sitten se saattaa aiheuttaa Lyme enkefalopatian. Sinun tulee tietää tämän tautien, joka sisällyttää potilaan osaan dramaattinen mielialan keinut, Ärtyisyys, masennus ja osoitus yhteisestä ongelmista.

Vaarantamalla lepotila

Nukkuma tavat muuttuvat ihmisiä, jotka ovat sairastuneet Borrelioosi. Nämä ihmiset voivat kärsivät apnea, unettomuus ja muut unihäiriöistä ja häiriöitä.

Kognitiivinen arvon alentuminen

Borrelioosi voi myös aiheuttaa kognitiivinen arvon alentuminen. Potilaiden voi olla vaikea ajattelua ja tehdä järkeviä päätöksiä. Kognitiivinen alentuminen liittyy huono pitoisuus ja muistin tappio.

Muista, Borrelioosi käsitellään oikein alusta lähtien, on tärkeää ymmärtää täsmälleen mitä oireet ovat. Kaikki samat edelleen ennaltaehkäisy kuin hoito, niin noudattamalla jokaisen tarkoittaa tutkittavina välttämiseksi saaminen tartunta sairaus.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.06.2014 - 10:51:15

Tärkeät asiat tietää Bartonella


Kirjoittaja: Georges Jacquet



Asioista että tietoja bartonella tartunnan oltava se, että mahdollisesti useita harjoittajat; oireet täyden valikoiman ei aina voidaan tunnistaa samalla kertaa kuin bartonella on usein vaikea diagnosoida tarkasti; voi olla taudin ja akuutteja psyykkisiä häiriöitä; ja se on hyvin yleinen käsitellä bartonella antibioottien kanssa.

Bartonella ollessa lääketieteellisesti puhuminen viejän on vakavan tartunnan. Tämäntyyppinen bakteerien, se, joka aiheuttaa tartuntaa, voidaan inhabit ihmisiä ja eläimiä. Yhdeksän suvulla Bartonella bakteerien lajin tiedetään aiheuttavan tartunnan ihmisissä.

On olemassa useita harjoittajien tartunnan mahdollisuus

Bartonella on hyvin uudet toimijat lääketieteen alalla, tartunnan siirto reitti ei vielä täysin ymmärrettävä. Tartunnan asiantuntijan mukaan lentoliikenteen harjoittajat ovat todennäköisesti kirput ja jakoviivat ja lice. Tartunnan, kuten “Journal of lääketieteellisen mikrobiologia,” ensisijaiset lähteet ovat Euroopan rotilla löytyy kirput. Lisäksi on ehdotettu California Borrelioosi-kytkentä että Kissat ovat Borrelioosi kantajia. Katsovat, että sekä ihmisten että ihmisten vaikuttaa tätä tautia, on mahdollista, että bartonella-tartunta on useita harjoittajien.

Kaikki oireita ei ole havaittu vielä

Päänsärky, väsyminen, ruokahalu, sikaruton ja epätavallinen singáw kehittäminen ovat yleisin bartonella saastunnan oireita. Tyypillisiä oireita sisällyttää paisuttamalla pään, aseiden ja kaulan, jonka tiedämme ansiosta California Borrelioosi Association rauhaset. Lääkäreiden on noudatettu myös lisäedellytykset alemman vatsakipu, mahakatarri, tarjouksen ihon nodules, arka pohjat ja ärtymistä. Medscape tänään on tunnistettu muita epätyypillisiä oireita kuten vääristyneet tai blirred näky, vatsakipu, perna ja maksa, kudosten vakavia poikkeavuuksia kiehuu, niveltulehdus, neurologiset sairaudet ja olosuhteissa, kudosten ja venttiilien sydämen lukuun ottamatta yhteisen oireita.

On ollut mahdollinen yhteys havaittu tartuntojen ja akuutti pyschiatric sairaudet

Akuutteja psyykkisiä häiriöitä, kuten ahdistusta, masennusta ja paniikkikohtaukset ovat muutamia bartonella tartunnan joitakin lääketieteelliset selvitykset mukaan tulokset. James Schaller ja Glenn Burkland, sekä tutkijoiden uskovat, että tämän linkin psykiatrinen edellytykset ja bartonella tartunnan välillä on mahdollista ottaen huomioon neurologisia sairauksia, jotka on havaittu oireita ja todellinen potilaiden laatimat kertomukset.

Tietyt sairaudet ovat erittäin vaikea diagnosoida

Koska bartonella on eri oireet, joita ei ole täysin varmennettu, tosi taudinmääritys on jonkin verran vaikea todeta. Lisäksi kaksi yleisin bartonella kantojen testattaessa niiden tulokset eivät ole yhdenmukaisia. Muut tämän taudin liittyvät riskit ovat sen toimittamista sekä historiansa liittyvät epävarmuustekijät.

Antibioottien käytetään yleensä puhdistavaa Bartonella

Antibioottien, kuten Atsitromysiini, Doksisykliini, erytromysiini ja levofloxacin ovat yhteisten käsittelyjen bartonella. Ahdistuneisuus tai tartunnan alentavasta kärsivät potilaat kuin ne annostellaan anti-depressants ja anti-anxiety hoitoja. Perustuu sovittuihin valmistettu tapaustutkimuksia, Schaller ja Burkland ovat tehneet potilaille, jotka ovat voineet saada tartunnan Bartonella kanssa yleensä on suurempi annos psykiatrinen elämäntapaan. Psyykkisiä oireita, jotka johtuvat bartonella kadota, kun tartunta on onnistuneesti torjua antibioottien avulla.

Emme ole varma bartonella tartunnan syyt. Edelleen taudin oppiminen ja sen uusien suuntausten ymmärtäminen pitää voit ennen sen yhdessä vaiheessa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.06.2014 - 10:57:55

Babesioosi: asioita tiedettävä


- Kirjoittaja: Auguste Descamps  


Jotkut näyttävät yllättynyt vain jakoviivojen vianselvitysmenettelyt voi aiheuttaa monimutkainen tartunnan kuten babesioosi. Tietää ja ymmärtää tartunnan tietoja, sinun on tiedettävä babesioosin ja miten se on sopimus, sen oireet, miten tehdään se, miten se käsitellään, sen monimutkaisuuden ja estäminen se.

Basesiosis on harvinainen vielä monimutkainen ja vakava sairaus. Tietoa tämän tartunnan olisi turvattava voit siihen liittyvät vaarat. Antamaan sinulle tarpeeksi ymmärtämistä ja tietoisuutta babesioosi, tässä on joitakin olennaiset tiedot avulla voit havaita, diagonise ja käsitellä välittömästi vakavien tartunnan:

Mikä on Babesios ja siitä, miten voit ladata sen?

Babesia microti ja Babesia divergens alkueläimet veriteitse tarttuville tartunnan kutsutaan Babesia tai babesioosi. Tämä harvinainen tartunnan yleensä lähetetään jakoviivat, jotka harjoittavat Borrelioosi kautta. Tällöin on mahdollisuudet vaikuttaa Babesia ja Borrelioosi tartunnan samaan aikaan. Kukin näistä taudeista on yleine myöhäisessä vaiheessa keväällä varhaisessa vaiheessa syksyllä. Voi myös saada tartunnan Babesia saastuneiden verensiirto kautta.

Mitä oireita Babeosis on kokenut?

Jakoviivojen herkutella jälkeen Babesia on yleensä 7-28 päivän itämisaika ennen ongelmia ilmennyt. Voit todennäköisesti näyttää flunssa kaltaiset oireita kuten sikaruton, · kylmiä väristyksiä päänsärkyä ja lihaksen kipua. Ne voi kestää jopa useita kuukausia. Yleisimmin havaittavaa yöllä, voi tunnet joitakin anemia, masennus, pahoinvointi, Keltaisuus, oksentelu ja Hikoilevat. Usein oireet usein matkivat ne malarian

Mistä tietää, onko babesioosi?

Useissa tapauksissa aiemmin on epäonnistui, koska babesioosi on ollut virheellisesti kuin Malaria. Tärkein ero niiden välillä on, että malariaa aiheuttaa sikaruton oire kuin. Lisäksi opiskella oireet, teidän henkilökohtainen historia, mukaan lukien jakoviivojen vianselvitysmenettelyt ja verikokeen tarvitaan diagnosoida asianmukaisesti babesioosi. Erot näiden tautien on havaittavissa kanssa veren testaus. Potilaille, jotka kärsivät babesioosi yleensä on jotain kutsutaan Maltan risti, tai tetrads, punainen veren soluissa, samalla kun ne, jotka kärsivät malarian saattaa olla ring-kaltaiset muodostumista nämä samat soluissa. Lääkärit avulla useiden testien diagnosoimaan ongelmaa IFA testejä, PCC tekniikoita ja alustasta pysyy Giema.

Mikä on käsittelyn tilassa?

Babesioosi voidaan käsitellä anti-parasite lääkkeiden yhdistelmän avulla. Näkyviin tulee ei kanssa yhteisen antibioottien, koska tämä infektio ei johdu bakteerien, vaan pikemminkin loista. Klindamysiini ja muita antibiootteja kuten kiniini kuparisulfaatti voidaan käyttää yhdessä keskenään ja muiden tahojen kanssa. Voit halutessasi myös kokeilla toisen antibiootin nimeltä zithromycin, joka voidaan yhdistää malariaa vastaan huumeiden, jota kutsutaan atovaquone. Jotkin tilanne veren siirtoon voidaan käyttää babesioosi hoidossa.

Mitkä ovat sen monimutkaisuuden?

Kuten muiden sairauksien, joka ei ole asianmukaisesti viat babesioosin myös voi aiheuttaa merkittäviä ongelmia ihmisille ja erityisesti ikäihmiset, niitä, jotka kärsivät immuniteetti ongelmia ja niille, jotka ovat niiden perna kirurgisia poistaa osalta. Vakava anemia, alhainen verenpaine, maksan ongelmat ja jopa kuolemantapausten on raportoitu epäterveellisen hankituilla. Borrelioosi esiintyminen vaikeuttaa käsittelyä. Jos kuitenkin säilyttää hyvä terveys ja on kohtuudella vahva perustuslain, babesioosin todennäköisesti eivät edes rekisteröi omat tutka-järjestelmään.

Miten voidaan estää babesioosi?

Paras tapa estää babesioosi on Varmista, että olet ei saada pureman mukaan jakoviivat. Kun partaking fyysisen Ulkoilu kuten telttailu, Patikointi tai metsästys, on katettava paitsi elin. Kattavat itse hyvin ja eivät altista laitoksen osaa. Voidaan soveltaa myös hyönteisten karkotteet. Lopussa on usein tarkistat jakoviivat esiintyminen kehon tai sen jälkeen retkeilemään laiduntavat ja woody aloilla erityisesti aikaisin kuuluvat kevään lopusta, kesäksi ja. Jakoviivat löytyvät yleensä keväällä ja kesällä.

Älä huoli liian paljon tietoja saaneiksi babesioosi, se on erittäin harvinaisia tartunnan. Niin kauan kuin osaat estää se, tunnistaa sen oireet ja se käsitellään välittömästi lääkärin, asiakas voi suojautua tätä tautia.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 27.07.2014 - 10:25:17

Liitteenä mielestäni mielenkiintoinen linkki, jossa on asiaa borrelioosista ja puutiasaivokuumeesta. Yllätys minulle oli se, että USA:ssa oli aikanaan toimiva rokote myös borrelioosia vastaan (luulin että, se on mahdotonta).

http://areena.yle.fi/radio/2339863

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 30.07.2014 - 08:55:52

Lisää punkkiasiaa, jos esim. borrelioosista ja punkeista jaksatte vielä kuunnella lisää. Tässä linkki
http://areena.yle.fi/radio/2289483

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.08.2014 - 18:55:38

HIV and MS

http://www.economist.com/news/science-and-technology/21610864-curious-observation-may-lead-treatment-multiple-sclerosis-antithesis

IN SCIENCE, as in many other walks of life, what is unexpected is often what is most interesting and important. The idea, first mooted in 2011 by Julian Gold of the Prince of Wales Hospital in Sydney, Australia, that HIV infection—or maybe the drug treatment used to fight it—might protect against multiple sclerosis (MS), was certainly unexpected. Now, in a study just published in the Journal of Neurology, Neurosurgery and Psychiatry, Dr Gold has confirmed his suspicion. That is interesting. It may also be important.

Dr Gold’s original motive for investigating the connection was casual observation. He treats people with HIV and has acquaintances with MS. He realised one day that he had never come across a case of someone with both. A literature search confirmed the lack of connection. Of the 700,000 published papers on HIV and AIDS, and the 300,000 on MS, not one referred to a patient who had the pair of them. Eventually, he tracked down a single instance. Tellingly, that individual started to shrug off the symptoms of MS when he began taking drugs to combat his HIV.

This finding led a Danish team to compare 5,000 HIV-positive people with a control group of 50,000 of their uninfected peers. Unfortunately, these apparently large numbers did not yield enough instances of subsequent multiple sclerosis for a statistically significant result to emerge. Dr Gold and his colleagues therefore turned to the English Hospital Episode Statistics, which record all interactions between the people of England and hospitals belonging to their country’s National Health Service. They used this database to identify and track everyone in England with HIV who was discharged from hospital between 1999 and 2011. In total, they found 21,207 HIV-positive individuals and compared them with 5,298,496 controls of similar ages and ethnic backgrounds.

The rate of onset of MS in the controls suggested about 18 cases should have developed among the HIV-positive patients. In fact, the team found only seven. That result was statistically significant. It indicates that those infected and undergoing treatment are 60% less likely to develop MS than their uninfected peers. Moreover, further analysis showed this value leapt to 80% among those who had been infected and treated for more than five years.

Dr Gold’s results do not show whether it is the infection or its treatment that is suppressing MS. Either sounds plausible. The immediate cause of MS’s symptoms (which range from clumsiness, and even paralysis, to depression) is that the sufferer’s immune system is attacking his central nervous system—specifically, the fatty sheaths that insulate the nerve cells in it. HIV meddles with many sorts of immune-system cells and signalling pathways that are associated with multiple sclerosis, so this could be why the disease wanes in those infected with it. On the other hand, though the underlying cause of MS is unknown, many people suspect it is triggered by a yet-to-be-determined virus. If that is true, it may be that the antiviral drugs given to those with HIV are bringing relief by attacking this unknown culprit too.

If this second idea is the right one, it means a treatment for MS looks eminently plausible; it may simply be a question of repurposing some existing drugs. If HIV itself is the protective agent, devising a treatment will be harder. Dr Gold’s discovery would still be a useful pointer, though, to the molecular-biological crack into which a suitable pharmacological crowbar might be inserted. Either way, then, this does look like an important result, derived ultimately from an unexpected observation.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.08.2014 - 19:35:43

HIV and MS: Could a Link Lead to New MS Treatment?

http://www.medpagetoday.com/Neurology/MultipleSclerosis/44861

Two clinical trials are now underway that offer the first tests of an intriguing but still not widely accepted theory of multiple sclerosis -- that its trigger lies within a part of the human genome that medical research has largely ignored.

Some researchers in Great Britain and Europe now believe that MS results from activation of "human endogenous retroviruses," or HERVs -- remnants of retroviruses that infected humans eons ago and became incorporated into the germline, such as that it is now part of the human genome. This theory has prompted a group in the U.K. to begin a trial of the HIV drug raltegravir (Isentress) in about 25 MS patients, to see if the drug affects brain lesions seen in MRI scans. The trial is expected to conclude this August, with results potentially reported before the year ( is out.

Separately, a Swedish company called GeNeuro Innovation, founded by Swiss researcher Herve Perron, PhD, has developed a monoclonal antibody called GNbAC1 targeting a specific HERV element; safety results from a phase II trial are slated for presentation next month at the American Academy of Neurology's annual meeting.

Background
When the first full sequences of the human genome were released, one of the biggest surprises was how much of the genome appeared to encode retroviral elements such as integrase and helicase enzymes. By one estimate, 8% of the entire genome was made up of such sequences.

At first, these were assumed to be nonfunctional. But subsequent research established that, under some circumstances, they can become activated to express proteins. It has yet to be proven conclusively that these are pathogenic, as even the proponents of HERV theories of disease will admit. One of the leaders of the U.K. raltegravir trial, Julian Gold, MBBS, MD, of the Albion Street Centre in Sydney, Australia, told attendees at an MS conference last fall that current laboratory methods aren't currently able to provide such proof, at least not for MS.

But there is circumstantial evidence -- several laboratories have isolated HERV proteins from MS lesion samples, and Epstein-Barr virus (EBV), which has itself been a suspected environmental cause of MS, has been found to activate HERV expression in lab studies.

Gavin Giovannoni, MBBCh, of Barts and the London School of Medicine and Dentistry in London, who also helps lead the raltegravir trial with Gold, told MedPage Today that all herpes viruses, of which EBV is one, can trigger HERV expression. But, he said, "EBV is particularly effective in activating HERVs." Also, according to Gold, HERV expression has been linked to activation of both the innate and adaptive immune systems, providing a connection to the well-documented immunological and inflammatory features of MS.

Although the HERV theory doesn't explain everything about MS, such as the gender imbalance, Giovannoni said the conventional autoimmune paradigm has "lots of holes" too. "It doesn't explain everything about MS, and as part of a causation theory it should explain everything. It doesn't explain the epidemiology very well, it doesn't explain the sex ratio, it doesn't explain some of the responses to certain therapies," he said.

"That's a clue that we don't know the whole story."

The HIV Connection
Perhaps the most significant piece of evidence for the HERV theory of MS is even more indirect: People with HIV appear to be at vastly reduced risk for MS.  What does HIV status have to do with HERVs or MS? Because nowadays, essentially everyone with HIV in developed countries where broad-based epidemiological research can be conducted is treated with antiretroviral drugs.

Gold is an HIV specialist -- the Albion Street Centre, which he directs, is Australia's largest HIV outpatient clinic. His "aha" moment came when an HIV-positive patient who also had MS came under his care. This patient was first diagnosed with HIV infection in 1985 but managed to avoid developing AIDS before the advent of highly active antiretroviral therapy (HAART) in 1996. In a 2011 letter published in the European Journal of Neurology, Gold and colleagues described what happened after HAART was begun in 1996:

"Within months of commencing HAART, all MS symptoms gradually improved. Within 2 years, his urinary incontinence was controlled to the extent that he stopped wearing pads and fecal incontinence resolved. He has had no MS relapses."

The disease was not completely eliminated, the researchers indicated, because gadolinium-enhanced MRI scans made in 2002 continued to show lesions consistent with MS, even though clinical symptoms had largely disappeared.

Large-scale epidemiological studies have supported the notion that anti-HIV therapy may suppress MS pathology.
***

The Clinical Trials
There is no animal model for HERVs in MS, and the ability to study HERVs even in cell culture is limited, Gold said. He argued that "their exact role will only be obtained following appropriate clinical trials. If we wait for the laboratory to give us the answer, we will all have been retired."

Raltegravir was chosen for the U.K. trial for several reasons. One is that it is an HIV integrase inhibitor. "The integrases across HERVs and HIV are quite conserved," Giovannoni said, so that it is likely to be more effective in suppressing HERV elements than other types of antiretroviral drugs. He said it was also unique among antiretrovirals in also showing some potency against members of the herpesvirus family (though only in vitro -- this effect hasn't been studied clinically).

And, its manufacturer was willing to support the small, short-term trial. Gold pointed out that no company that markets MS medications is active in HIV drug development, or vice versa. He and Giovannoni were able to persuade raltegravir's maker, Merck's European subsidiary, to fund the 25-patient study which includes just 3 months of drug treatment after a 3-month baseline observation period. Gold said a longer and larger study would have been preferable but it could not be arranged.

The GNbAC1 monoclonal antibody's sponsor GeNeuro appears to have more resources, with France's Institut Merieux as a major investor. It has already completed a phase I safety study with the agent in healthy volunteers; the results to be presented at the AAN meeting next month are from 10 MS patients. According to the abstract, no safety problems were seen, and a larger efficacy study is warranted. However, GeNeuro has not said whether or when such a trial would be undertaken.

Caution Reigns
MS specialists in the U.S. contacted by MedPage Today were unanimous in urging caution about HERV theory, although some were warmer to it than others. Alessandro Serra, MD, of University Hospitals Case Medical Center in Cleveland, told MedPage Today that "many studies" had supported the association between HERV-expressed proteins and MS. However, these proteins also appear "in patients with other neurological conditions, and even in a proportion of healthy individuals," Serra said.

He said the debate in the community was over "whether HERVs are just bystanders within the normal immune response of MS patients, perhaps unable to handle these viruses, or whether they actually represent a key component of the pathogenic process of MS and even have a causative role."

Jerry Wolinsky, MD, of the University of Texas Health Science Center in Houston, pointed out that the search for MS triggers has been going on for decades and wound up in many blind alleys. Viruses have long been a popular suspect, but "thus far not fruitful."With regard to retroviruses lurking within the human genome, "to my knowledge there has been no consistently recovered retrovirus sequence associated with brain or other tissues from patients with multiple sclerosis," Wolinsky said.

"That does not mean that one might not be afoot, but the technology is well enough developed that it would be unusual to expect that one will be found in the future, given the failure to do so even with application of modern tools." Wolinsky added that the 2011 case report from Gold and colleagues, of the HIV/MS patient whose neurological symptoms resolved with HAART, did not persuade him. "The course of MS is very unpredictable," he said, and the disappearance of symptoms may simply have been "serendipitous."

Other experts were also supportive of research while agnostic or skeptical about the HERV theory. For example, Robert Bermel, MD, head of the Cleveland Clinic's Mellen Center for Multiple Sclerosis, told MedPage Today that "It becomes difficult ...  to separate the specific effect of antiretroviral therapy from the effect of altered immune status related to HIV, or from the natural tendency of MS disease activity to decline over time."

On the other hand, Anthony Reder, MD, of the University of Chicago, called the HERV theory "important" as well as plausible.

HERVs, he said, result from "hundreds of millions of years of battles with retroviruses. The residual DNA fragments do not produce complete viruses but DNA fragments and retrovirus proteins do leak out and are seen by the immune system."

Serra said he hoped that the two clinical trials wouldn't be taken as make-or-break for the HERV theory. "We need more rigorous models, especially animal models that have been lacking so far. I know there are groups that are looking into it."

In the meantime, everyone who spoke to MedPage Today emphasized that it would be premature for physicians or patients to try antiretroviral drugs on their own as MS therapies. Giovannoni said that some patients have told him that they had succeeded in obtaining raltegravir.

"That's a little premature and we wouldn't recommend it," he said.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.08.2014 - 22:35:07

HERV-W polymorphism in chromosome X is associated with multiple sclerosis risk and with differential expression of MSRV.

http://www.ncbi.nlm.nih.gov/pubmed/24405691

Abstract

BACKGROUND:
Multiple Sclerosis (MS) is an autoimmune demyelinating disease that occurs more frequently in women than in men. Multiple Sclerosis Associated Retrovirus (MSRV) is a member of HERV-W, a multicopy human endogenous retroviral family repeatedly implicated in MS pathogenesis. MSRV envelope protein is elevated in the serum of MS patients and induces inflammation and demyelination but, in spite of this pathogenic potential, its exact genomic origin and mechanism of generation are unknown. A possible link between the HERV-W copy on chromosome Xq22.3, that contains an almost complete open reading frame, and the gender differential prevalence in MS has been suggested.

RESULTS:
MSRV transcription levels were higher in MS patients than in controls (U-Mann-Whitney; p = 0.004). Also, they were associated with the clinical forms (Spearman; p = 0.0003) and with the Multiple Sclerosis Severity Score (MSSS) (Spearman; p = 0.016). By mapping a 3 kb region in Xq22.3, including the HERV-W locus, we identified three polymorphisms: rs6622139 (T/C), rs6622140 (G/A) and rs1290413 (G/A). After genotyping 3127 individuals (1669 patients and 1458 controls) from two different Spanish cohorts, we found that in women rs6622139 T/C was associated with MS susceptibility: χ2; p = 0.004; OR (95% CI) = 0.50 (0.31-0.81)] and severity, since CC women presented lower MSSS scores than CT (U-Mann-Whitney; p = 0.039) or TT patients (U-Mann-Whitney; p = 0.031). Concordantly with the susceptibility conferred in women, rs6622139*T was associated with higher MSRV expression (U-Mann-Whitney; p = 0.003).

CONCLUSIONS:
Our present work supports the hypothesis of a direct involvement of HERV-W/MSRV in MS pathogenesis, identifying a genetic marker on chromosome X that could be one of the causes underlying the gender differences in MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 02.09.2014 - 09:43:35

Monelta varmaankin jäi tämä ohjelma kroonistuneesta borrelioosista katsomatta.
http://areena.yle.fi/tv/2201783

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Rami Pvm 02.09.2014 - 16:04:24


Äijä 02.09.2014 - 09:43:35:
Monelta varmaankin jäi tämä ohjelma kroonistuneesta borrelioosista katsomatta.
http://areena.yle.fi/tv/2201783


Katsoin ja suhtauduin kuin kääkärikirjaan... noinko paljon minussa onkin sairauksia?  :o

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 03.09.2014 - 09:21:52

Niinpä, jos asia on kuten filmissä väitetään ja kuten monet ovat väittäneet ennenkin, siis kuten potilaiden puolustajat sanovat. Ja jos sinulla on kroonistunut borrelioosi syystä tai toisesta, ei pitkään sairastaneille anneta paljonkaan paranemisen mahdollisuuksia. Positiivista on kuitenkin se, että nuoremmille ja vähemmän aikaa sairastaneille annetaan toivoa, mikä on hyvä asia. Itse olen kokeillut pitkiä antibioottikuureja ja käytän yhä edelleen LDN:ää, ja oloni sekä toimintakykyni on parempi kuin muutama vuosi sitten. Mutta totuus on, että joka vuosi tulee "mittariin" yksi vuosi lisää, eikä tänne ole tietääkseni vielä kukaan jäänyt.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.09.2014 - 16:13:51

High-throughput screening of tick-borne pathogens in Europe

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4114295/

Due to increased travel, climatic, and environmental changes, the incidence of tick-borne disease in both humans and animals is increasing throughout Europe. Therefore, extended surveillance  tools are desirable.  To accurately screen tick-borne pathogens(TBPs), a large  epidemiological study was conducted on 7050 Ixodes ricinus nymphs collected from France, Denmark, and the Netherlands, using a powerful new high-throughput approach. This advanced methodology permitted the simultaneous detection of 25 bacterial, and 12 parasitic species (including; Borrelia, Anaplasma, Ehrlichia, Rickettsia, Bartonella,  Candidatus Neoehrlichia, Coxiella, Francisella, Babesia, and Theileriagenus) across 94  samples. We successfully determined the prevalence of  expected (Borrelia burgdorferi sensu lato, Anaplasma phagocytophilum, Rickettsia helvetica, Candidatus Neoehrlichia mikurensis, Babesia divergens, Babesia venatorum), unexpected (Borrelia miyamotoi), and rare (Bartonella henselae) pathogens in the three European countries. More over we detected Borrelia spielmanii, Borrelia miyamotoi, Babesia divergens, and Babesia venatorum for the first time in Danish ticks.This surveillance method represents a major improvement in epidemiological studies, able to facilitate comprehensive testing of TBPs, and which can also be customized to monitor emerging diseases.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 16.09.2014 - 12:53:10

Niinpä! Paljon on tehty bakteeri-infektioiden ja MS-taudin yhdistävää tutkimusta, mutta ne eivät ole johtaneet mihinkään konkreettiseen tulokseen. Missä syy? Ehkäpä, kun jotkut ovat joskus päättäneet, että MS-tauti on autoimmuunisairaus eikä sille voi mitään! Tässä linkissä on vanhan kertauksen makua, mutta se on silti asiaa.
http://owndoc.com/lyme/multiple-sclerosis-is-lyme-disease-anatomy-of-a-cover-up/

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 02.10.2014 - 09:10:46

Minosykliini on laajakirjoinen antibiootti, josta on tehty vähän ja ristiriitaista tutkimusta MS-taudin osalta. Nyt on kuitenkin meneillään suurempi tutkimus joka valmistunee vasta noin vuoden kuluttua. Kanadalaisessa pilotti-tutkimuksessa saatiin kuitenkin hyviä tuloksia RRMS-potilaiden osalta.
http://www.mymsaa.org/publications/msresearch-update-2013/tetracycline-antibiotics
http://msj.sagepub.com/content/13/4/517.abstract

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.10.2014 - 15:20:14

The role of infections in autoimmune disease

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665673/

Autoimmunity occurs when the immune system recognizes and attacks host tissue. In addition to genetic factors, environmental triggers (in particular viruses, bacteria and other infectious pathogens) are thought to play a major role in the development of autoimmune diseases. In this review, we (i) describe the ways in which an infectious agent can initiate or exacerbate autoimmunity; (ii) discuss the evidence linking certain infectious agents to autoimmune diseases in humans; and (iii) describe the animal models used to study the link between infection and autoimmunity
*******
Borrelia burgdorfeii
...
Neurological complications, including myelitis and peripheral neuropathy, can occur in 10–12% of untreated patients infected with Bb and can arise even after antibiotic treatment [110]. Patients with chronic neuroborreliosis have been reported to have antibodies reactive to nerve axons in their serum [111], as well as antibodies and T cells specific for myelin basic protein (MBP) in spinal fluid [112,113]. Patient serum that was reactive to axons and neuroblastoma cells was also cross-reactive with Bb flagellin [111,114]. Next, it was discovered that a mAb for flagellin was cross-reactive with human heat shock protein 60 and with neuroblastoma cell lines [115,116] and slowed neurite outgrowth in culture [117]. Antibody cross-reactivity has also been described between human central nervous system (CNS) proteins and Bb OspA [118]. Several host neural peptides were identified as cross-reactive with Bb-specific T cells from CSF of a patient with chronic neuroborreliosis using peptide libraries and biometric data analysis [119]. However, studies such as those in non-human primates suggest that bystander inflammatory responses to the persistently infective pathogen may explain more clearly the CNS complications of this disease [120–122].

Multiple sclerosis

Multiple sclerosis (MS) is characterized by a loss of the myelin sheath surrounding axons in the CNS [201]. Demyelination is associated with elevated levels of CD4+ T cells specific for major myelin proteins, and the disease is generally thought to be autoimmune [202–204]. Although it is not known precisely what triggers the development of MS, it is well established that relapses or disease flares in patients diagnosed with the relapsing–remitting form of MS are often associated with exogenous infections, particular upper respiratory infections. In total, more than 24 viral agents have been linked to MS [205,206]. Most of the associations have been circumstantial, but some studies have found evidence of specific pathogens in human tissue. Antigens from herpesvirus type 6 were found in MS plaques but not from tissues from other neurological disorders [207]. Similarly, compared with CSF from patients with other neurological diseases, CSF from MS patients was shown to have higher levels of the bacteria Chlamydia pneumoniae[208]. In vitro studies have also provided evidence linking MS and infectious agents. MS patients have activated T cells specific for MBP [209–211]. Eight pathogen-derived peptides, including epitopes from HSV, adenovirus and human papillomavirus, were identified that are able to activate MBP-specific T cell clones derived from MS patients [212]. Significantly, these peptides were found to be presented most efficiently by subtypes of HLA-DR2 that are associated with susceptibility to MS. Despite the difficulty in linking MS to any one pathogen, the amount of epidemiological evidence reported over the years shows that environmental factors play a strong role in disease development, and suggests that a cumulative lifetime exposure to certain microorganisms can influence disease development [213–216]. In addition, a recent study showed that the degree of concordance for monozygotic twins (generally reported at 40% or less) was influenced by environmental factors [217].
*******
CD4-deficient mice showed less severe disease than CD8-deficient mice [236,237]. Collectively, these studies suggest that macrophages are responsible primarily for myelin destruction in the MHV model, but that T cells are required to recruit macrophages into the CNS. Like MHV, SFV leads to a transient clinical disease [238,239]. The virus is, for the most part, cleared from the CNS by day 6 post-infection, while demyelination peaks at day 14 and then wanes [240,241]. Demyelination is not seen in nude or SCID mice, demonstrating that it is T cell-mediated [240,242]. In BALB/c mice it is thought that demyelination is due to cytolytic damage of virus-infected oligodendrocytes, although this has not been proved definitively. Depletion of CD8+ T cells virtually abolished lesions of demyelination, whereas depletion of CD4+ T cells did not have that effect [243]. Other studies in BALB/c mice have shown that Th1-type cytokines are involved in viral clearance but not demyelination [244,245]. In C57/Bl6 mice, molecular mimicry may also play a role in demyelination. Infected mice have MBP-reactive T cells [246], and antibodies reactive to MBP and myelin oligodendrocyte protein (MOG) [247]. Computer algorithms uncovered homology between an epitope in the SFV surface protein E2 and MOG18–32[248]. Mice primed with either peptide develop paralytic symptoms with histopathology resembling that of mice infected with SFV. The authors of that study concluded that the cross-reactive antibody response was mainly responsible for the demyelinating lesions.
*****
The argument for infection-induced pathology is much stronger for diseases associated with one or two specific pathogens than for diseases with multiple causal associations. For example, the fact that infection with C. jejuni is a common antecedent to GBS makes a strong argument that this disease is infection-triggered. In contrast, for diseases such as TID and MS that have been associated with dozens of pathogens, but none in particular, much more needs to be done to make a convincing case. The most compelling proof would be the disappearance of symptoms with the clearance of the infection. This is the case in Lyme disease, where treatment with antibiotics alleviates acute arthritis. However, as outlined previously in this paper, there are many ways a pathogen can cause disease even after the infection has been cleared. In these cases, epidemiological studies showing that people infected with a particular agent have an increased incidence of these diseases compared with people never infected, while not wholly definitive, would certainly strengthen the infection-induced autoimmunity argument.
*****
The heterogeneity of the human population, rather than the weakness of the data, may be in play in instances where the evidence linking infection and autoimmunity is tenuous or even conflicting. It is not difficult to imagine that some people may be more susceptible to developing autoimmune disease following a particular infection than others, or that mimic peptides derived from different infectious agents may be able to trigger a particular autoimmune disease depending on the ability of the infected individual to present various epitopes in the context of their various HLA molecules. Defining the genetic markers that predispose patients to different autoimmune diseases with a suspected infectious trigger would be an important contribution to defining the underlying disease pathogenesis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 05.10.2014 - 09:59:37

Mielenkiintoista luettavaa! LDN parantaa ihmisen immuunipuolustusta oikein otettuna. Suomenkielisiltä "pääsivuilta" voi lukea lisää asiasta. Viimekesänä tilatessani LDN:ää Helsingin yliopiston apteekista, ei tarvinnut enää selvittää valmistusaineosia ja määriä, koska LDN on nykyisin "tuotteistettu" reseptilääke ja sen valmistus on vakioitu.
http://ldn.gehennom.org/

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Gwbh Pvm 09.10.2014 - 21:38:00

Mite helposti lääkärit tätä LDN kirjoittavat, onko yleisessä käytössä jos ei ole halukas ottamaan vakilääkkeitä? Onko tietoa kuinka paljon MS tautia sairastavavia tätä käyttää? Kyselen vaikka diagnoosini ei vielä satavarma olekaan mutta ainakin nää uudet immunosupressiolääkkeet pelottavat.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 10.10.2014 - 08:58:25

LDN on vastikään tuotteistettu, eikä se ole varsinainen MS-tautilääke. Kuinka paljon MS-potilaista sitä käyttää, ei kai kukaan tiedä. MS-tauti on tämänhetkisen näkemyksen mukaan ns. autoimmuunisairaus, mutta sekin on pelkkää teoriaa. Nykyisin ei ole mitään reaaliaikaista tutkimus tai seurantamenetelmää, jolla voisi myelinitupen tuhoa seurata. Jättiannos kortisonia on virallinen ja tulehdusta elimistössä heti rauhoittava ensihoito MS-taudin pahenemisvaiheessa. LDN on taas elimistön immuunipuolustusjärjestelmää tuleva lisälääkitys, joka perustuu aivan toisenlaiseen teoriaan. Siinä vaiheessa, kun ihmiselle ei ole apua tarjolla mistään, ei LDN ole ainakaan minun oloani huonontanut, vaikka olenkin käyttänyt sitä jo useamman vuoden.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Gwbh Pvm 11.10.2014 - 15:46:53

Tiedän ton kortisonipulssin kun itse olen nyt saanut 2 kertaa vaikkei mulla diagnoosia vielä olekaan. Nyt oltaisiin kuitenkin aloittamassa jokin lääke ettei oireet enää tästä pahenisi ja LDN ei kuulunut näihin neurologin ehdottamiin lääkkeisiin. Siis kai kuitenkin useimmilla ms ihmisillä on jokin ylläpitolääke ja sit pahiksiin kortisonipulssi?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja VPS358 Pvm 11.10.2014 - 19:16:12

Sori, että masennan, mutta mäsään Ei ole olemassa mitään "ylläpitolääkettä", oikeastaan ei mitään joka parantaisi. On vaan oireenmukaista ja oireita vähentävää...
Toisia ABCR:t auttaa, osalle taas ei ja jossain vaiheessa ns. nostetaan kädet pystyyn...

T: Vesku, lääkeetön jo vuosia...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Äijä Pvm 12.10.2014 - 10:51:12


Gwbh 11.10.2014 - 15:46:53:
Tiedän ton kortisonipulssin kun itse olen nyt saanut 2 kertaa vaikkei mulla diagnoosia vielä olekaan. Nyt oltaisiin kuitenkin aloittamassa jokin lääke ettei oireet enää tästä pahenisi ja LDN ei kuulunut näihin neurologin ehdottamiin lääkkeisiin. Siis kai kuitenkin useimmilla ms ihmisillä on jokin ylläpitolääke ja sit pahiksiin kortisonipulssi?

Olet käsittääkseni nuori, joten sinulla on hyvät mahdollisuudet saada oikeaa hoitoa vaivoihisi. Älä missään tapauksessa nosta käsiäsi ns. pystyyn ja anna periksi. Diagnoosistasi riippumatta etsi "hengenheimolainen" lääkärien ja alan tutkijoiden joukosta, mikä voi olla työlästä. Sillä tämän päivän "virallinen" totuus tai käypä hoito suositus, on huomenna todennäköisesti historiaa.
       Tämä ei ole varsinaisesti mikään keskustelupalsta, mutta huomaan kyllä, että tämän sivuston useimmat palstat on valloittanut asiaankuulumaton lähettäjä. Mitä vertaistukeen yleisesti tulee, antivertaistukea tulet saamaan täällä, kuten muuallakin kirjoitellessasi ns. sosiaaliseen mediaan. Luota kuitenkin itseesi, ensi järkytyksestäsi toivuttuasi, ja liiku paljon sekä syö terveellisesti. Mahdollisuutesi ovat paremmat, kuin meillä jo kauemmin sairastaneilla. Äläkä stressaa turhista asioista, vaan keskity itseesi, nyt on sen aika.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Gwbh Pvm 12.10.2014 - 20:02:04

Moi, en suinkaan ole nuori, ikä 46 ja eka neurologi oli jo sitämieltä ettei minulla ikäni puolesta voisi olla ms. Uusia lääkkeitä,vaikka ei parantavia,on koko ajan tulossa mutta aina on se sivuvaikutusten takia pelottavaa. Ja en kuitenkaan haluaisi olla mikään koekaniini. No huomenna on lääkäri jolta kuulen uuden mangneettin ja verikokeiden tulokset. Kortisonipulssin vaikutus jäi melko pieneksi mutta onneksi varpaat liikkuu :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.11.2014 - 23:43:42

Is Multiple Sclerosis an Autoimmune Disease?

http://www.hindawi.com/journals/ad/2012/969657/

Abstract

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) with varied clinical presentations and heterogeneous histopathological features. The underlying immunological abnormalities in MS lead to various neurological and autoimmune manifestations. There is strong evidence that MS is, at least in part, an immune-mediated disease. There is less evidence that MS is a classical autoimmune disease, even though many authors state this in the description of the disease. We show the evidence that both supports and refutes the autoimmune hypothesis. In addition, we present an alternate hypothesis based on virus infection to explain the pathogenesis of MS.
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. Is MS an Autoimmune Disease?

From most references gleaned in the literature, MS is boldly stated as an autoimmune disorder. However, the evidence for such a statement is weak and circumstantial. We have updated and revised criteria for determining whether a disease is autoimmune in nature [14]. The main criterion of a given autoimmune disease is that a precise autoantigen be present in all patients with the disease. Despite multiple attempts to identify various proteins, lipids, and gangliosides in myelin as potential MS antigens, none have been proven or confirmed. Secondly, administration of autoantibody or T cells induces autoimmune disease in normal animals. These approaches have been attempted in animal models of MS with contrasting results [15, 16]. A third criterion is the ability to induce lesions by immunizing animals with relevant autoantigen. This had been partially achieved but with problems. The fact that multiple different antigens can induce the disease process in animal models without one specific antigen being superior to the other makes the results ambiguous from the standpoint of identifying the relevant antigen. The fourth criterion is the ability to isolate autoantibody or autoreactive T cells from the lesion or from serum. Many investigators have suggested a higher precursor frequency of T cells, specifically of the CD4 subgroup, in patients with MS when compared to healthy controls, which recognize MBP, proteolipid protein (PLP), MOG, or other such antigens from myelin. Unfortunately, because similar positive results are obtained from normal individuals, this criterion is not satisfied. The fifth criterion is the correlation between the autoantigen or the autoreactive T cells with disease activity. Autoreactive T cells occur with greater frequency in patients experiencing an exacerbation than in patients with progressive disease, which suggests a possible correlation between auto-reactive T cells and disease activity. Even though the precursor frequency of autoreactive T cells may be higher in MS than in normal controls, the presence of autoreactive T cells demonstrated in normal controls makes a definitive conclusion about MS as autoimmune more difficult to accept. The sixth criterion is the presence of other autoimmune disorders or autoantigens associated with the disease. This issue has been addressed by a number of investigators, and there have been occasional case reports demonstrating the presence of MS with other autoimmune diseases, for example, myasthenia gravis [17] and diabetes mellitus [18]. However, population-based cohort studies performed in the Olmsted county, Minnesota, failed to show any association between autoimmune diseases and MS [19]. The only possible increased odds ratio was found with thyroid disease, when both hyperthyroidism and hypothyroidism were combined. In addition, rare cases have been described in patients with both MS and inflammatory bowel disease [17, 18]. There have also been multiple studies looking at the presence of autoantibodies, a characteristic of patients with autoimmune diseases, such as the antibodies seen in Sjögren’s syndrome, systemic lupus erythematosus (SLE), or myasthenia gravis, but to date, no evidence indicates that the presence of these antibodies is greater in MS patients than in normal controls. Of interest, this differs greatly from neuromyelitis optica (NMO) [20, 21], where there is clearly an association between the presence of autoantibodies and NMO (discussed later in this paper).

3. Immune Manifestations of MS: Role of Antibodies

There is evidence to suggest that part of the immunopathogenesis of MS is mediated by antibodies. Studies have indicated intrathecal production of antibodies, which occur after clonal expansion manifested by the identification of oligoclonal bands after CSF electrophoresis [22]. Studies at the Mayo Clinic, Austria, and Germany reported on the heterogeneity of MS lesions in CNS tissue and their implications for the pathogenesis of demyelination. A detailed immunohistochemical study was performed in active MS lesions from 83 biopsies and autopsies of MS patients, following, which were identified four different pathologic subtypes of active MS lesions. One of the subtypes, Pattern II, demonstrated the presence of macrophages and T cells but, in addition, a prominent display of antibodies and complement [9]. This data provided evidence that lesion patterns were heterogeneous among patient subgroups but homogeneous in the same patient. Barnett and Prineas studied acute MS lesions and found complement activation, oligodendrocyte apoptosis, and remyelination, findings that overlapped the Mayo/Germany/Austria studies [23]. A recent study identified activated complement (C3d and C9neo) on fragmenting myelin sheaths in the outer actively demyelinating lesions in 20 patients with relapsing MS (58/58 active lesions) [24]. The authors reported the presence of activated complement on disintegrating sheaths in diverse diseases affecting white matter, including viral and autoimmune encephalitis, NMO, and even ischemic infarcts, suggesting that this phenomenon is not limited to MS. In a more recent study, Breij et al. [25] investigated to what extent the four pathological pattern criteria translated to active lesions from patients with established MS. These authors concluded that MS lesions displayed a homogenous profile. The authors were unable to confirm the lesion heterogeneity or interindividual heterogeneity with respect to Ig and complement immuno-reactivity. However, it is possible that all the lesions studied were not active. It is possible that the heterogeneous features reported in active MS lesions that were sampled at varied time-points are the evolution of a single pathophysiological process, rather than discrete immunopathogenic patterns. This may be the case, or the majority of active lesions will present with Pattern II phenotype, as supported by findings of a study by Barnett and Sutton, where the authors described that in 22 patients drawn from a large unselected pool of MS material, 33 actively demyelinating lesions presented Pattern II pathology [26]. The four-pattern system has not been completely independently verified to date because of the lack of available highly comparable pathologic material.

The response to plasma exchange (PLEX) in acute fulminant MS provides further evidence for the role of immunoglobulin or serum components in the disease. Rodriguez et al. demonstrated conclusively for the first time the detrimental effect of plasma components in inflammatory demyelinating diseases of the CNS; PLEX in acute episodes of fulminant CNS inflammatory demyelination, which did not respond to high-dose methylprednisolone, led to a marked neurologic improvement in 6 patients [27]. These results were confirmed in a randomized, sham-controlled, double-masked study of PLEX without concomitant immunosuppressive treatment in patients with recently acquired, severe neurological deficits resulting from attacks of inflammatory demyelinating disease, who failed to recover after treatment with intravenous corticosteroids [28]. A retrospective study investigated 19 patients treated with PLEX for an attack of fulminant CNS inflammatory demyelinating disease. All patients with pattern II , but none with pattern I or pattern III , achieved moderate to substantial functional neurological improvement after PLEX [29]. The fact that all cases, which responded to PLEX, had a biopsy demonstrating Igs and complement, whereas none that responded showed this immunologic pattern, provided the strongest proof that the pathologic patterns are unique and have therapeutic significance. Numerous publications during the last few decades have supported the idea that CSF oligoclonal bands correlate to the level of B-cell involvement in MS [30]. In addition, evidence indicates that oligoclonal bands may have a prognostic value. One prospective study of patients with acute isolated demyelinating episode demonstrated intrathecal immunoglobulin synthesis to be a better predictor of MS progression than MRI [31]. Another prospective study showed that presence of CSF oligoclonal bands in early MS generally correlated with a worse outcome [32]. A recent study showed strong correlation between levels of oligoclonal bands (OCBs) and prognosis for MS disability [33].

4. Antigen: Specificity of Antibodies Found in MS
After several years of research, confirmation of the antigen-specificity of antibodies in MS is still lacking. Due to their broad reactivity, IgG in CSF of patients with MS may represent synthesis of “nonsense” antibodies irrelevant to pathogenesis [34–36]. However, other experiments found molecular uniformity and temporal persistence of the Ig response in MS, thus conflicting with the nonsense antibody proposal [37]. It is possible that relevant antigens are limited to the myelin sheath. Studies demonstrated the serological and/or CSF presence of antibodies directed against MBP and/or myelin/oligodendrocyte glycoprotein (MOG) in patients with MS [38]. However, myelin-specific antibodies are not limited to MS. ..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.11.2014 - 23:49:59

Using an enzyme-linked immunosorbent assay, Karni et al. compared levels and frequencies of anti-MOG antibody between patients with MS, patients with other neurological disorders, and healthy control subjects [39] and found minor differences. In a parallel line of research, some reports suggested lipids or carbohydrates as possible candidate antigens for the humoral immune response [40, 41]. Anti-alpha-glucose-based glycan IgM antibodies have been suggested to be predictors of relapse activity in MS after the first neurological event [42]. Others suggested that serum anti-Glc(alpha1, 4)Glc(alpha) antibodies serve as biomarkers for relapsing-remitting MS [43]. Antibodies to myelin proteins, lipids, and carbohydrates can be extracted from the tissue and sera of some MS patients.

5. Immune Manifestations of MS: Role of T Cells
5.1. CD4+ T Cells as Initiators of Disease versus Effectors in Destruction of Myelin

The area of greatest confusion in the MS literature concerns the role of CD4+ T cells in disease pathogenesis. CD4+ cells predominate in experimental autoimmune/allergic encephalomyelitis (EAE) as the effectors that induce disease and destroy myelin. Therefore, due to the influence of the experimental model, many investigators have attempted to show that CD4+ T cells also play a pathogenic role during the evolution of MS. Unfortunately, many findings regarding the role of CD4+ T cells reported have not been reproduced elsewhere [44]. However, there is strong experimental evidence that any immune response must begin through the engagement of the antigen recognized by receptors on CD4+ T cells. In concept, dendritic cells, both outside and/or inside the CNS, take up the exogenous or endogenous antigen and present it to CD4+ T cells. As a result, these CD4+ T cells differentiate into four distinct subtypes depending on the inflammatory milieu (Figure 1). The first is the Th1-type CD4+ T cell, which primarily secretes IFN-γ and TNF-α. The second is a CD4+ T cell frequently called Th2, which secretes primarily TGF-β and IL-10. The third is a CD4+ TREG cell that performs a regulatory function [45]. These T cells express a number of transcription factors including FoxP3 and other molecules [46, 47]. These cells play a major role in downregulating the immune response [48–50]. Finally, there are CD4+ T cells that primarily secrete IL17 called Th17 cells. These Th17 cells induce most of the pathology in EAE. There is evidence of their presence in the MS plaque, where they may preferentially recruit IFN-γ [51]. Data suggest that CD4+ T cells from MS patients use unique human T-cell beta-receptors [52]. In these studies, the investigators used T-cell lines from MS patients as well as healthy controls and showed that these CD4+ T-cell lines reacted against specific human myelin basic proteins, the first being residues 84–102 and the second being residues 143–168. They showed that the CD4+ T-cell receptors being used were primarily of the Vβ17 and Vβ12 family. Vβ12 receptors were used frequently in recognition with the MBP (84–102) peptide, while Vβ17 mostly reacted against MBP (143–168).
969657.fig.001
Figure 1: CD4+ T Cells differentiated into subsets. CD4+ T cells can differentiate into different subtypes based on the factors within the inflammatory milieu with which T cells come into contact. TH1+ cells secrete IFN-γ and tumor necrosis factor (TNF) and mediate the pathology in experimental autoimmune encephalomyelitis (EAE). Many of the results previously attributed to TH1 cells are actually mediated by Th17+ cells. Th17+ cells secrete IL17, IL21, and IL22. These cells have been identified in MS lesions, where they may serve as important effectors. As a result of  TGF-β stimulation, CD4+ T cells develop into T-regulatory cells. These cells downregulate the immune response and express FOXP3, CD25, and IL10. The mechanism of suppression is by the secretion of factors such as IL10. TH-helper cells provide help to other T cells, such as CD8+ T cells or B cells. Th-helper cells secrete IL2, IL10, and IL21. Th2+ cells downregulate the immune response and are associated with recovery from acute attacks in EAE and, possibly, MS. The cytokines that mediate the downregulation of the immune response are IL4 and IL10, in addition to IL13 and IL5.

The presence of unique T-cell receptor V-β gene usage has generated a series of experimental animal trials as well as early human trials with the goal of deleting specific V-β T cells in MS patients [53]. These experiments have been relatively successful in EAE; however, the approach has been less effective in human patients. Of interest, investigators have also isolated MBP-reactive CD4+ T-cell lines from normal human blood [54]. The fact that these T-cell lines respond to MBP [55], similarly to what is observed in MS patients, has raised major questions as to the specificity of the response of CD4+ T-cell lines to myelin antigen in MS patients [56]. These CD4+ T-cell lines obtained from non-MS patients secreted IL2 similar to that seen with MS patients. All of the T-cell lines isolated from the peripheral blood were of the CD4 phenotype [57]. Investigators have examined peripheral blood lymphocytes from MS patients and other neurological controls in effort to study specific T-cell populations against purified human MBP and other brain antigens [58]. Investigators showed that lymphocytes from MS patients were more likely to react against MBP. Unfortunately, they discerned only minor differences between MS patients and normal controls as to the specificity of the response to any brain tissue antigens. The majority of responses were found in patients with chronic progressive MS, a phase when T cells are least active in the disease. These results also have raised concerns about the specificity of the T-cell immune response to myelin antigens in MS patients given the not easily discernible differences between MS patients and normal individuals. Even those investigators claiming to show a positive, “statistically significant” response show such an overlap in the results between patients and controls that these assays have never been developed as a diagnostic test for MS [59].

Recent work has focused on Th17+ cells in MS [60, 61]. Investigators looked at evidence implicating IFN-γ producing hybrid T cells (so-called Th1 cells as well as IL17+ lymphocytes (Th17+ cells)) in MS. They compared this to animals with EAE and demonstrated expansion of Th17 lymphocytes from the blood of healthy controls as well as from patients with relapsing MS. In response to IL23, which is known to expand the Th17 phenotype, they showed simultaneous expressions of IFN-γ and IL17. They noted that patients with relapsing-remitting MS had increased production of IFN-γ by Th17 cells. The same findings were also present in the experimental model. Both these data sets support the hypothesis that Th17 cells play a role in the pathology of MS and EAE. However, the presence of Th17 cells does not automatically prove that they play a role in pathogenesis [62]. No data is available that deletion of Th17 cells improves MS or that elevated Th17 cells in lesions correlate with disability. This is in contrast to the work done on CD8+ T cells (discussed hereinafter), which reveals a strong correlation between CD8+ T cells, perforin, and other molecules as secreted by CD8+ T cells with disease disability.
5.2. CD8+ T Cells: Primary Mediator of Effector Function in the MS Plaque

Pathological studies demonstrate that the CD8+ T cell is the most common T cell observed in the MS plaque. Conventional perception is that CD8+ T cells have two major functions: cytotoxicity and suppression. In MS, because of the strong bias of the experimental autoimmune encephalomyelitis (EAE) models, the CD8+ T cell has been primarily thought to play a suppressive role. In EAE, the CD4+ T cell, through its Th1 and Th17 function, mediates the disease and induces the inflammatory response, neurological deficits, paralysis, and histological findings. In EAE, CD8+ T cells are associated with recovery of neurologic function and have been shown to have suppressive properties. In contrast, in the MS plaque, the CD8+ T cells appear to play a much more aggressive role rather than just suppressing the inflammatory response. CD8+ T cells interact with major histocompatibility (MHC) class I antigens to induce their response. In normal CNS, class I MHC is observed only in vascular cells and rare meningeal cells. However, in the midst of an inflammatory process such as MS, class I MHC is observed in astrocytes, oligodendrocytes, and neurons and even rarely on axons [63]. In addition, the CD8+ T cells correlate with axonal injury, and there is strong evidence in vitro that CD8+ T cells play a major role in transecting axons [64, 65]. Relapses of MS are associated with increased CD8+ T cell cytotoxicity in the CSF [66]. A number of clinical trials with monoclonal antibodies, specifically against CD4+ T cells [67], failed to show any therapeutic benefit in MS as opposed to broader spectrum antibodies (alemtuzumab CD52), which are able to deplete all T cells [68], including CD8+ T cells. It is also important to emphasize that CD8+ T cells may play a major role in a number of proven autoimmune disease including SLE, diabetes mellitus, Crohn’s disease, Graves’ disease, and autoimmune Addison’s disease [63]. Finally, CD8+ T cells show oligoclonal expansion in MS brains, blood, and CSF that have not been reported with CD4+ T cells [69–71]. Some of the cytotoxic T cells react against autoantigens such as myelin-basic protein [72]. If these cells traveled randomly in the CNS, then presumably their CD3 junction region length would show a normal Gaussian distribution. In contrast, there is skewing of the CDR3 junction regions in MS, suggesting a selective infiltration or expansion of CD8+ T cell clones into the CNS [71]. ....

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 29.11.2014 - 00:00:49

..Moreover, the T-cell receptors of the CD8+ T cells demonstrate distinct CD8+ T-cell clones with conserved specificity implying recognition of a similar antigen that results in their proliferation in the CNS. Much effort has focused on the potential role of IL17 in the MS plaque, and because of the bias of experiments in EAE, it has been proposed that this comes from the CD4+ T cells. However, there is evidence that IL17 is also made by CD8+ T cells [73]. Defining IL17+ CD8+ T cells opens up new avenues for future research and new targets from the standpoint of immunotherapy. CD8+ T cells secrete a number of molecules including granzymes and perforin. Strong evidence suggests that perforin contributes to axonal injury in the MS plaque (Figure 2). The presence of perforin correlates with neurologic disability and with the presence of “black holes” on MRI. Therefore, CD8+ T cells play a critical role during the acute inflammatory phase of the disease as well as during the neurodegenerative phase. CD8+ T cells account for axonal damage in MS as well as long-term neurological deficits. There is evidence that CD8+ T cells play a major role in the secondary progressive phase of the disease by the secretion of lymphotoxin [74]. In studies of cytokine secretion in patients with secondary progressive MS and normal controls, investigators found clear evidence of anti-CD3-stimulated CD8+ T cells in the patients with secondary progressive MS. These cells secreted lymphotoxin and other cytokines, which play a critical role in the evolution of the progressive phase of the disease. This provides strong evidence that the CD8+ T cell plays a role in the neurodegenerative aspect of the progressive phase of the disease as well as in the early acute phase.
It is also important to emphasize a possible regulatory role for CD8+ T cells in MS. Investigators have identified CD8+/CD25+ Foxp3+ as regulatory T cells in MS patients [75]. In these studies, they examined the peripheral blood, CSF, and CD8+ T cell clones from patients with MS exacerbations, patients with remissions, healthy individuals, and patients with other inflammatory neurological diseases. The inhibition of CD4+ self-reactive T-cell proliferation by CD8+ regulatory cells was mediated by IL10 and transforming growth factor beta (TGF-β). Any attempt to delete CD8+ T cells from the MS lesion could potentially worsen the disease by eliminating regulatory cells. Therefore, caution must be taken in any effort to manipulate the CD8+ population.
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10. Conclusions

In MS, for an oligodendrocyte to be injured by inflammatory cells, it must express MHC class I or class II genes. CD8+ T cells can then engage a novel protein that is expressed in the context of class I MHC. CD8+ T cells would then secrete perforin, granzyme, or other factors that may directly injure or kill the oligodendrocyte resulting in demyelination. Antibodies, through molecular mimicry, may recognize autoantigens of the CNS and can also injure the oligodendrocyte by binding to the surface of the cell and, in association with complement, may induce direct injury to myelin or the oligodendrocytes. This partially leads us to the autoimmune hypothesis. In addition, the B cells may also present virus antigens in the context of class II MHC molecules. The oligodendrocyte or microglia itself may also express class II MHC. This presentation of the viral antigen must be processed, which allows the CD4+ T cells to be engaged with class II MHC to induce injury, the common mechanism of injury presumed to be present in experimental autoimmune encephalomyelitis. The oligodendrocyte may die as a consequence of direct and persistent virus infection. These mechanisms of injury may be independent or occur concurrently in each brain. All of these mechanisms lead to demyelination that the host may correct by transient remyelination. Ultimately, the demyelination process overtakes remyelination resulting in axonal damage, thus leading to permanent neurologic deficits. At the present time, there is no clear evidence that these patterns of injury relate to various stages of the disease course and do not correlate with the clinical subtypes of relapsing-remitting multiple sclerosis, secondary progressive multiple sclerosis, or primary progressive multiple sclerosis, although this is yet to be determined.

Many of the observed findings have subsequently led investigators to false conclusions regarding MS pathogenesis. Immune cells are present in the MS plaque, and the immune system is important in the pathogenesis of the disease because a number of immunomodulatory and immunosuppressive therapies do decrease relapses and the number of gadolinium-enhancing lesions in MS brain. However, the long-term consequences of immunosuppression on disease course are unknown because most published clinical trials end after two years of observation, an insufficient period of time to address the long-term consequences of these treatments. It is increasingly evident that CD8+ T cells and their effector molecules may directly affect the disease process. Unfortunately, despite years of documentation of involvement of CD8+ T cells in MS lesions, scant experimentation has been performed on this aspect of the immune response. This is probably due to the bias of the experimental model, EAE, in which CD8+ T cells play only a regulatory role whereas CD4+ T cells play a major effector role in disease pathogenesis. Once we move away from the experimental model and begin to investigate MS in humans, it becomes apparent that the MHC class II CD4+ T-cell immune response yields less important critical data of the MHC class I CD8+ T-cell immune response. The most important diagnostic test for MS continues to be the presence of increased CSF IgG and the presence of specific oligoclonal bands in the CSF but not in the serum. Therefore, it is critical to identify the specificity of these bands. Ultimately, it may be proven that CSF oligoclonal IgG bands play a neuroprotective rather than a pathologic role [137–140].

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.12.2014 - 22:21:45

Lyme and associated tick-borne diseases: global challenges in the context of a public health threat

http://journal.frontiersin.org/Journal/10.3389/fcimb.2014.00074/full

Lyme disease, caused by Borrelia burgdorferi and transmitted by ticks, was initially considered a recent, rare and regional occurrence. We now have evidence that very similar bacteria infected humans in Europe during the ice age (Keller et al., 2012). Evidence-based data are scarce therefore many aspects of the disease remain controversial (Auwaerter et al., 2011; Lee and Vielmeyer, 2011; Perronne, 2012), but in 2013 the Centers for Disease Control and Prevention (CDC) revised their annual estimates from 30,000 cases to 300,000 cases in the USA alone. Having dramatically increased their numbers, the CDC are now calling Lyme disease “a tremendous public health problem in the United States” (CDC, 2011).
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These recent historical, geographical and microbial data should prompt the medical community to realize that cases of persisting post tick-bite syndromes are probably due to multiple pathogens and that these occult infections will require a new approach if not an actual paradigm shift.
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Classical forms of Lyme disease are usually easy to manage, but these medical conditions with pleomorphic non specific symptoms may prove confusing to physicians (Strle and Stanek, 2009). Lyme disease may mimic chronic inflammatory or degenerative diseases, including a wide range of auto-immune diseases. Although practitioners from every medical specialty are likely to have encountered cases of Lyme disease, they may have failed to recognize it, no matter how skilled they are.
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Modern medical practice expects to rely on evidence. Most physicians would not consider diagnosing Lyme disease without serological proof. Yet the failure to diagnose seronegative neuroborreliosis, especially the acute or severe forms, can have dire consequences including chronic neurologic sequelae or even death. A review of the literature shows that a diagnosis of Lyme neuroborreliosis is often difficult to prove (Blanc et al., 2007; Bennet et al., 2008; Tveitnes et al., 2009; Makhani et al., 2011). The sensitivity of intrathecal antibody index (measuring specific antibodies within the cerebro-spinal fluid) ranges from 55 to 80%. In a Swedish study, antibodies were present in serum of only 23% of children with neuroborreliosis (Bennet et al., 2008). Cognitive tests or SPECT brain imaging may help to provide objective evidence (Tager et al., 2001; Roche-Lanquetot et al., 2008; Fallon et al., 2009; Donta et al., 2012). Pragmatic diagnostic criteria including response to empiric antibiotic treatment are used to diagnose neuroborreliosis (Blanc et al., 2007). Should this strategy be recommended in other clinical presentations as well? In fact some clinicians will not hesitate to classify as Lyme disease cases, seronegative patients with a highly compatible clinical picture, provided other diagnoses have been ruled out. In a major clinical trial on Lyme disease, 40% of the enrolled patients were seronegative. These patients had a history of erythema migrans, neurologic or cardiac symptoms, radiculoneuropathy or arthritis (Klempner et al., 2001). Clinicians, often unaware of the difficulties involved in diagnosing Lyme disease, will fall back on “weak” alternative diagnoses (“viral,” “idiopathic,” “auto-immune,” “degenerative,” “inflammatory,” or “psychosomatic”) (Kennedy, 2013). New techniques are needed to accurately assess these patients. This current over-reliance on inaccurate testing procedures not only flaws the diagnosis of individual patients but it also has epidemiological consequences especially as new species and variants continue to be identified on all continents (Hao et al., 2011; Rudenko et al., 2011).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.12.2014 - 22:25:23

Lyme disease -induced polyradiculopathy mimicking amyotrophic lateral sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/24397499

Abstract

IMPORTANCE:
To describe a case of predominantly motor polyradiculopathy secondary to Lyme disease that can mimic motor neuron disease and has been rarely reported.

OBSERVATIONS:
A 64-year-old man presented with a 1-month history of rapidly progressive weakness involving bulbar, upper limb and lower limb muscles. The physical examination showed widespread weakness, atrophy, fasciculation, and brisk reflexes. The initial electrodiagnostic test showed widespread active and chronic denervation findings. The initial physical and electrodiagnostic findings were suggestive of Amyotrophic Lateral Sclerosis (ALS). However, blood serology indicated possible Lyme disease. Thus, the patient was treated with doxycycline. The clinical and electrodiagnostic findings were resolved with the treatment.

CONCLUSION AND RELEVANCE:
The diagnosis of Lyme disease can be very challenging and it can mimic other neurological disorders such as ALS or Guillain-Barre syndrome (GBS). Careful and detailed examination and investigation are required to confirm the diagnosis and to prevent misleading inaccurate diagnoses.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.12.2014 - 22:34:39

Analysis of overall level of evidence behind Infectious Diseases Society of America practice guidelines

http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&Cmd=ShowDetailView&TermToSearch=21220656

Abstract

BACKGROUND:
Clinical practice guidelines are developed to assist in patient care. Physicians may assume that following such guidelines means practicing evidence-based medicine. However, the quality of supporting literature can vary greatly.

METHODS:
We analyzed the strength of recommendation and overall quality of evidence behind 41 Infectious Diseases Society of America (IDSA) guidelines released between January 1994 and May 2010. Individual recommendations were classified based on their strength of recommendation (levels A through C) and quality of evidence (levels I through III). Guidelines not following this format were excluded from further analysis. Evolution of IDSA guidelines was assessed by comparing 5 recently updated guidelines with their earlier versions.

RESULTS:
In the 41 analyzed guidelines, 4218 individual recommendations were found and tabulated. Fourteen percent of the recommendations were classified as level I, 31% as level II, and 55% as level III evidence. Among class A recommendations (good evidence for support), 23% were level I (≥1 randomized controlled trial) and 37% were based on expert opinion only (level III). Updated guidelines expanded the absolute number of individual recommendations substantially. However, few were due to a sizable increase in level I evidence; most additional recommendations had level II and III evidence.

CONCLUSIONS:
More than half of the current recommendations of the IDSA are based on level III evidence only. Until more data from well-designed controlled clinical trials become available, physicians should remain cautious when using current guidelines as the sole source guiding patient care decisions.

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(Suomessahan borrelioosin hoidossa mennään IDSA:n ohjeistuksen mukaisesti...)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.01.2015 - 13:40:45

Lyme is often Misdiagnosed as other Disease and Disorders

http://www.lyme-symptoms.com/LymeMimics.html

Many  found  their  "misdiagnosed" disease or syndrome disappeared after receiving treatment for Lyme Disease .
This does not say that a Lyme disease infected person may not also have another disease, disorder, or syndrome.

Samoilta sivuilta olen laittanut aikaisemmin "comparison chart" osan, mutta tässä loput. Oireita on melkoisesti ja kaikilla yksilölliset, kuten MS-taudin oireet. Tottakai erojakin on (esim. kivut liikkuvat paikasta toiseen), ja ongelmana on se, että borren diagnomiseen tarvitsee asiantuntevan infektiolääkärin ja liudan verikokeita. Aikonaan omalla kohdalla borrelioosi suljettiin pois ilman verikokeita tai infektiolääkärin diagnoosia, vaikka olin jo silloin sairastunut borrelioosiin ja lisäinfektioihin.  Mutta eiväthän neurologit niitä etsi vaan MS-tautia. Etsivä löytää..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.02.2015 - 19:39:12

Ja juuri kun luulin, että infektiot oli suurimmalta osin kukistettu, sain viimeisten verikokeiden tulokset Saksasta: aktiivisesti jylläävät borrelioosi, keuhkoklamydia ja EBV-virus. Itse asiassa nämä olivat ainoat jotka tutkitutin viidestä infektiosta, mutta tämä osoittaa sen, miten vaikea näistä on päästä eroon. Myös sen, miten yhden kerran negatiivinen tulos voi kuuukausien jälkeen muuuttua positiiviseksi, koska bakteerit piiloutuvat hyvin. Tai ehkä syynä on se, että yhdestä punkin puremasta sain kolme borrelia kantaa. Vaikka kuinka isken päätä seinään, se ei kuitenkaan tapa noita bakteereita, joten joudun turvautumaan uudelleen joko konservatiiviseen aseistukseen eli antibiootteihin ja malarialääkitykseen, tai sitten monien suosimaan homeopaattiseen hoitoon. Toisaalta minulle ei ole vieläkään selvää mitkä ovat MS-tautini oireet, koska infektiot sekoittavat kuvioita. Ja tarina jatkuu..



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 14.02.2015 - 13:11:54

Common Allergy Medication May Be Effective at Killing the Bacteria That Causes Lyme Disease

http://www.infectioncontroltoday.com/news/2015/02/common-allergy-medication-may-be-effective-at-killing-the-bacteria-that-causes-lyme-disease.aspx

A new study funded by the Bay Area Lyme Foundation and conducted by Stanford School of Medicine researchers shows that loratadine, which is a common antihistamine frequently taken to treat allergy symptoms, may be able to help kill Borrelia burgdorferi, the bacteria associated with Lyme disease. Lyme disease is a potentially debilitating condition with 300,000 new cases in the US each year. The study was published in the open access publication Drug Design, Development and Therapy.

"Our results bring us closer to the possibility of discovering the first targeted therapy to treat Lyme disease," says Jayakumar Rajadas, PhD, director of the Biomaterials and Advanced Drug Delivery Lab (BioADD) at Stanford School of Medicine, and lead author of the study. "It's exciting to see first-hand that our insights into the metabolic activity of this elusive bacteria may give us the ability to actually kill it."

The results of this new laboratory study show that loratadine (trade name Claritin®) and specifically its metabolite, desloratadine, are able to prevent manganese (Mn) from entering the cell wall of the bacteria that causes Lyme disease, starving the bacteria and causing it to die in test tubes.  The antihistamine accomplishes this by inhibiting the bacteria's transport system, BmtA (Borrelia metal transporter A).

[Suomessa vastaava lääke on nimeltään Aerius, sisältäen desloratadiinia]

Manganese is required for certain metabolic processes of Borrelia burgdorferi and also plays an important role in numerous biological processes in the human body.  Previous research shows that in general, bacteria scavenge the body for trace metals that circulate in the blood and have developed special adaptations on their cell walls to internalize these metals.  These adaptations are called transport proteins, and BmtA is the specialized transport protein for Borrelia burgdorferi.  BmtA binds with manganese to bring it into the bacteria, and studies have shown that BmtA and manganese are required to make the bacteria harmful to the human body.(1)

"Because current treatments do not work for everyone and the bacteria that causes Lyme disease offers many treatment challenges, this study offers encouraging insights for researchers, and hope for the 80 million Americans at risk of getting Lyme disease," says Bonnie Crater, founder and science committee chairperson of the Bay Area Lyme Foundation, the leading private funder of innovative Lyme disease research in the US.  "We are grateful to the BioADD team for their commitment to finding solutions to this difficult disease."

Currently, patients with Lyme disease are typically prescribed a two- to four-week week course of antibiotics, but approximately 10 percent to 20 percent of patients treated with this regimen will have lingering symptoms of fatigue, pain, or joint and muscle aches.(2)

Increasing in threat due to rising prevalence across the US, Lyme disease is a potentially debilitating infection caused by bacteria transmitted through the bite of an infected tick to people and pets. If caught early, most cases of Lyme disease can be effectively treated, but it is commonly misdiagnosed due to lack of awareness and unreliable diagnostic tests. There are about 300,000 new cases of Lyme disease each year, 10 times more than previously reported, according to statistics released in 2013 by the CDC. As a result of the difficulty in diagnosing and treating Lyme disease, as many as one million Americans may be suffering from the impact of its debilitating long-term symptoms and complications, according to Bay Area Lyme Foundation estimates.

Source: Bay Area Lyme Foundation

References

1. Ouyang Z et al: A manganese transporter, BB0219 (BmtA), is required for virulence by the Lyme disease spirochete, Borrelia burgdorferi. Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3449-54.. http://www.ncbi.nlm.nih.gov/pubmed/19218460

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 14.02.2015 - 13:27:13

Cordycepin is a novel chemical suppressor of Epstein-Barr virus replication

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4303894/

Cordyceps species are known to produce numerous active components and are used for diverse medicinal purposes because of their varied physiological activities, including their ability to protect the liver from damage as well as their anticancer, antidepressant, anti-inflammatory, hypoglycemic, antimicrobial effects. Cordycepin, an adenosine derivative, differs from adenosine in that its ribose lacks an oxygen atom at the 3′ position. Several research groups have reported that cordycepin has antiviral activity against several viruses including influenza virus, plant viruses, human immunodeficiency virus(HIV), murine leukemia virus, and Epstein-Barr virus (EBV). In this study, we identify the epigenetic mechanisms by which cordycepin exerts its anti-gammaherpesvirus effects. We show that cordycepin possesses antitumor and antiviral activity against gastric carcinoma and EBV, respectively.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 17.04.2015 - 17:09:56

Progressive multiple sclerosis cerebrospinal fluid induces inflammatory demyelination, axonal loss, and astrogliosis in mice

http://www.ncbi.nlm.nih.gov/pubmed/25111532

Abstract

Multiple sclerosis (MS) is an autoimmune disease characterized by inflammatory demyelination and neurodegeneration throughout the CNS, which lead over time to a condition of irreversible functional decline known as progressive MS. Currently, there are no satisfactory treatments for this condition because the mechanisms that underlie disease progression are not well understood. This is partly due to the lack of a specific animal model that represents progressive MS. We investigated the effects of intracerebroventricular injections of cerebrospinal fluid (CSF) derived from untreated primary progressive (PPMS), secondary progressive (SPMS), and relapsing/remitting (RRMS) MS patients into mice. We found discrete inflammatory demyelinating lesions containing macrophages, B cell and T cell infiltrates in the brains of animals injected with CSF from patients with progressive MS. These lesions were rarely found in animals injected with RRMS-CSF and never in those treated with control-CSF. Animals that developed brain lesions also presented extensive inflammation in their spinal cord. However, discrete spinal cord lesions were rare and only seen in animals injected with PPMS-CSF. Axonal loss and astrogliosis were seen within the lesions following the initial demyelination. In addition, Th17 cell activity was enhanced in the CNS and in lymph nodes of progressive MS-CSF injected animals compared to controls. Furthermore, CSF derived from MS patients who were clinically stable following therapy had greatly diminished capacity to induce CNS lesions in mice. Finally, we provided evidence suggesting that differential expression of pro-inflammatory cytokines present in the progressive MS CSF might be involved in the observed mouse pathology. Our data suggests that the agent(s) responsible for the demyelination and neurodegeneration characteristic of progressive MS is present in patient CSF and is amenable to further characterization in experimental models of the disease.



Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 17.04.2015 - 17:19:08

Indications of Th1 and Th17 responses in cerebrospinal fluid from patients with Lyme neuroborreliosis: a large retrospective study

http://www.jneuroinflammation.com/content/8/1/36


Edellisessä artikkelissa selkäydinnesteen Th17 oli korostunut. Tämä tutkimus taas selvittää Th17:sta  neuroborrelioosissa:


Abstract
Background
Previous studies indicate that successful resolution of Lyme neuroborreliosis (NB) is associated with a strong T helper (Th) 1-type cytokine response in the cerebrospinal fluid (CSF) followed by a down-regulating Th2 response, whereas the role of the recently discovered Th17 cytokine response is unknown.

Methods
To investigate the relative contribution of different Th associated cytokine/chemokine responses, we used a multiple bead array to measure the levels of CXCL10 (Th1 marker), CCL22 (Th2 marker), IL-17 (Th17 marker) and CXCL8 (general inflammation marker), in serum and in CSF from untreated patients with confirmed NB (n = 133), and non-NB patients (n = 96), and related the findings to clinical data. Samples from patients with possible early NB (n = 15) and possible late NB (n = 19) were also analysed, as well as samples from an additional control group with orthopaedic patients (n = 17), where CSF was obtained at spinal anaesthesia.

Results
The most prominent differences across groups were found in the CSF. IL-17 was elevated in CSF in 49% of the patients with confirmed NB, but was not detectable in the other groups. Patients with confirmed NB and possible early NB had significantly higher CSF levels of CXCL10, CCL22 and CXCL8 compared to both the non-NB group and the control group (p < 0.0001 for all comparisons). Patients in the early NB group, showing a short duration of symptoms, had lower CCL22 levels in CSF than did the confirmed NB group (p < 0.0001). Furthermore, patients within the confirmed NB group showing a duration of symptoms <2 weeks, tended to have lower CCL22 levels in CSF than did those with longer symptom duration (p = 0.023). Cytokine/chemokine levels were not correlated with clinical parameters or to levels of anti-Borrelia-antibodies.

Conclusion
Our results support the notion that early NB is dominated by a Th1-type response, eventually accompanied by a Th2 response. Interestingly, IL-17 was increased exclusively in CSF from patients with confirmed NB, suggesting a hitherto unknown role for Th17 in NB. However, for conclusive evidence, future prospective studies are needed.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.05.2015 - 14:14:27

Drug Combinations against Borrelia burgdorferi Persisters In Vitro: Eradication Achieved by Using Daptomycin, Cefoperazone and Doxycycline

http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.01172071


Abstract

Although most Lyme disease patients can be cured with antibiotics doxycycline or amoxicillin using 2-4 week treatment durations, some patients suffer from persistent arthritis or post-treatment Lyme disease syndrome. Why these phenomena occur is unclear, but possibilities include host responses, antigenic debris, or B. burgdorferi organisms remaining despite antibiotic therapy. In vitro, B. burgdorferi developed increasing antibiotic tolerance as morphology changed from typical spirochetal form in log phase growth to variant round body and microcolony forms in stationary phase. B. burgdorferi appeared to have higher persister frequencies than E. coli as a control as measured by SYBR Green I/propidium iodide (PI) viability stain and microscope counting. To more effectively eradicate the different persister forms tolerant to doxycycline or amoxicillin, drug combinations were studied using previously identified drugs from an FDA-approved drug library with high activity against such persisters. Using a SYBR Green/PI viability assay, daptomycin-containing drug combinations were the most effective. Of studied drugs, daptomycin was the common element in the most active regimens when combined with doxycycline plus either beta-lactams (cefoperazone or carbenicillin) or an energy inhibitor (clofazimine). Daptomycin plus doxycycline and cefoperazone eradicated the most resistant microcolony form of B. burgdorferi persisters and did not yield viable spirochetes upon subculturing, suggesting durable killing that was not achieved by any other two or three drug combinations. These findings may have implications for improved treatment of Lyme disease, if persistent organisms or detritus are responsible for symptoms that do not resolve with conventional therapy. Further studies are needed to validate whether such combination antimicrobial approaches are useful in animal models and human infection.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.05.2015 - 12:50:26

Is it Lyme or MS? (revisited)

http://lymemd.blogspot.fi/2015/03/is-it-lyme-or-ms-revisited.html

A 45 year old male recently presented to my practice. He suffered with a progressive, debilitating, multisystem disease over a period of 5 years. An MRI of the brain was performed and the results were unnerving. The scan showed numerous white matter lesions, greater than 20. The diagnosis of MS was suggested by the radiologist.

Mainstream authorities all agree: There is no diagnostic test for MS. The diagnosis can only be made when other causes of the symptoms and findings have been ruled out. It is a diagnosis of exclusion. MRI protocols, proteins in the spinal fluid, abnormal evoked potentials, alone or in combination cannot conclusively make the diagnosis the MS.

This patient lives in a Lyme endemic area and has had numerous tick bites over a period of many years. He suffers with fatigue, weakness, trouble walking, poor endurance, headaches, cognitive symptoms and memory loss, depression, tinnitus, night sweats, flulike symptoms, migratory joint pain, mood swings and episodes of rage.

The left lower extremity was particularly weak showing a “foot drop,” apparent with gait testing. The patient was instructed to walk on his heels but the left foot is unable to elevate and the foot flops to the floor. An EMG showed the cause to be inflammation of the peroneal nerve, a peripheral nerve. This is not a feature of MS which involves only the central nervous system. Lyme, however, effects all aspects of the nervous system.

White matter lesions in the brain reflect damage of heavily myelinated nerve fibers in the deep portions of the brain. Myelin is a white, fatty, insulating substance which covers these neurons. Some nerve cells are not covered by myelin, for example, those covering the top of the brain. These nerve cells have a gray appearance hence the cortex (outer surface) of the brain, is composed of gray matter.
White matter lesions can have many causes. They can be normal; you are allowed one per decade of life. The lesions may be seen with atherosclerosis, diabetes causing small blood vessel disease, hypertension, migraines, infections, vasculitis and Lyme disease and there are many other potential causes listed in texts and various sources.

Multiple sclerosis is characterized as a demyelinating disease. It results from an autoimmune process which attacks this coating of the deep nerve cells. MS is divided into 4 types. In 85% of cases it is relapsing and remitting. Patients have discrete neurological events (central nervous system only) which generally get better over time. MS is not diagnosed based on a single event. Subsequent events occur over time involving different parts of the central nervous system.

Typical “events” may include: optic neuritis with loss of vision; weakness, generally localized; numbness and shooting pains originating from the central nervous system, vertigo and loss of bowel and/or bladder function.  In most cases patients get better. Interim periods of time, devoid of symptoms, are followed recurring events causing different symptoms. Over time, the symptoms may not remit and become permanent.

These events are dramatic and distinct. MS is a disease of fits and starts.

The Multiple Sclerosis Society states common symptoms of MS include: fatigue, trouble walking, numbness and tingling, weakness, changes in vision, changes in bowel and bladder function, changes in cognition, depression and pain. The National Multiple Sclerosis Society states that one half of MS patients end up with a chronic pain syndrome. By my way of thinking, the recognition of such symptoms after the fact speaks to a more insidious, gradual inflammatory brain disorder and a multisystem disorder more characteristic of late Lyme disease. Why has the disease morphed?

MS is not defined by MRI findings. In the case of the above mentioned patient, there is a history of tick bite, positive Lyme test and evidence of a progressive, multisystem disease. These white matter lesions, numerous as they are, are most likely the results of Lyme, neuroborreliosis.

The cause(s) of MS are thought to be both genetic and environmental (including infection).

MS has an interesting epidemiology. Cases are rare around the equator. The incidence increases proportionally to the distance one is away from the equator. For example, it is more prevalent in the Northern U.S. and Candida and Northern Europe and Scandinavia. The rule does not hold true for the Asian continent where the incidence remains relatively low throughout the continent. Sporadic epidemics of MS have been described, suggesting an unknown, probably viral, infectious cause. Chamydia pneumonia has been shown to be the culprit in some cases. Coincidently, there is a lot of overlap between the geographic distribution of MS and Lyme.

The MS Society has a clear opinion about Lyme: it is not associated with MS. It is easy for the Society to make this claim: they follow the IDSA approach. Lyme responds to 3 weeks of antibiotics. White matter lesions in a previously treated Lyme patient are therefore the result of MS, not Lyme.

How Lyme causes these lesions is not entirely clear. It has been proposed that the highly immuno-inflammatory proteins expressed on the surface of Lyme spirochetes may evoke an autoimmune reaction, one that has not yet been categorized. This raises the question: are some forms of neuro-Lyme a type of MS or a close relative? Can Lyme cause MS?

This is a murky arena. A subset of patients may respond best to MS therapy combined with Lyme therapy. Perhaps some patients do have both Lyme and MS.

There exist 10 FDA approved drugs for the long term management of MS. Some suppress the immune system, like drugs used by rheumatologist for rheumatoid arthritis. Others modulate immune responses and others have anti-viral properties. Neurologist typically treat acute flares of disease with high doses of intravenous steroids. Many of my patients got worse when given steroids. When patients have Lyme (and are also treated by neurologists for MS) I like to steer them to immune modulating and antiviral therapy (interferon).

Clearly, MS is a real disease, apart from Lyme. Not all MS is caused by Lyme. However, there seems to be a large universe of patients suffering with Lyme disease who have been incorrectly diagnosed with MS.

P.S. After only a month of oral doxycycline the patient has experienced dramatic improvements in many symptoms.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 26.06.2015 - 16:54:53

Your Viral Infection History from a Single Drop of Blood

http://www.hhmi.org/news/your-viral-infection-history-single-drop-blood


Summary
New technology developed by HHMI researchers makes it possible to test for current and past infections with any known human virus by analyzing a single drop of blood.

Highlights
- With VirScan, scientists can run a single test to determine which viruses have infected an individual.
- VirScan works by screening the blood for antibodies against any of more than 200 species of viruses known to infect humans.
- The comprehensive analysis can be performed for about $25 per blood sample.
- The test is currently used as a research tool and is not commercially available.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 26.06.2015 - 16:58:22

Resveratrol Prevents EBV Transformation and Inhibits the Outgrowth of EBV-Immortalized Human B Cells

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0051306

Background

Epstein Barr virus-associated lymphoproliferative disease is an increasing complication in patients with immunosuppressive conditions. Although the current therapies for this disorder are effective, they are also associated with significant toxicity. In an attempt to identify newer therapeutic agents, this study investigated the effects of Resveratrol, a naturally occurring polyphenolic compound, on the EBV transformation of human B cells.

Methodology/Principal Findings

This study demonstrates that resveratrol prevents EBV transformation in human B cells. These effects are mediated by specific cytotoxic activities of resveratrol against EBV-infected B cells that are associated with the downregulation of the anti-apoptotic proteins Mcl-1 and survivin. This occurs as a consequence of the inhibition of EBV-induced NFκB and STAT-3 signaling pathways and a resveratrol-induced decrease in the expression of the oncogenic viral product LMP1 in EBV-infected B cells. In addition, resveratrol decreased the expression of miR-155 and miR-34a in EBV-infected B cells, blocked the expression of the anti-apoptotic viral gene BHRF1, and thus interrupted events that are critical for EBV transformation and the survival of EBV-transformed cells.

Conclusions/Significance

These results suggest that resveratrol may therefore be a potentially effective therapeutic alternative for preventing EBV-associated lymphoproliferative diseases in immune compromised patients.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.07.2015 - 21:00:09

Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection

http://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1004976

Abstract

Lyme Disease caused by infection with Borrelia burgdorferi is an emerging infectious disease and already by far the most common vector-borne disease in the U.S. Similar to many other infections, infection with B. burgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure. However, clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies. This is further supported by reports of frequent repeat infections with B. burgdorferi in endemic areas. The mechanisms underlying such a lack of long-term humoral immunity, however, remain unknown. We show here that B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment. This failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates. These showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain of B. burgdorferi. The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of B. burgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction. Furthermore, influenza immunization administered at the time of Borrelia infection also failed to induce robust antibody responses, dramatically reducing the protective antiviral capacity of the humoral response. Collectively, these studies show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat.

http://news.ucdavis.edu/search/news_detail.lasso?id=11254
....
The bacteria initially trigger a strong immune response in an infected animal, but findings from this study indicate that the bacteria soon cause structural abnormalities in “germinal centers” — sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.

For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria and launching a protective immune response against future infections.

The researchers found that following Borrelia burgdorferi infection, this process even prevented induction of strong immune responses to an influenza infection.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.08.2015 - 16:10:19

DESY X-ray source reveals decoy protein of a herpes virus at work

http://phys.org/news/2012-08-desy-x-ray-source-reveals-decoy.html


EBV näyttää heikentävän immuunipuolustustusta:

With the help of DESY's X-ray source DORIS III, an international team of scientists decoded an important weapon used by a widespread human herpes virus. The study reveals at the molecular level how the Epstein-Barr virus (EBV) deactivates the alert system of the body's immune defence by using a molecular decoy. The analysis has implications on the development of new therapies and drug compounds, as the team led by Savvas Savvides from Ghent University (Belgium) and colleagues from the European Molecular Biology Laboratory (EMBL), Grenoble (France) and Hamburg (Germany), report in Nature Structural & Molecular Biology.

The Epstein-Barr virus is a member of the herpes virus family and can causes a range of diseases including the glandular fever (mononucleosis), also known as "kissing disease". Moreover, it plays a role in at least one type of cancer. The pathogen also labeled "human herpes virus 4" is extremely widespread, with 90 to 95 per cent of the adult population infected worldwide. Often, the infection is asymptomatic and the virus usually remains latent in the human body.

It was already known that the Epstein-Barr virus secretes a protein named BARF1 that blocks the protein hCSF-1 in the human body. hCSF-1 (human CSF-1) is a so-called growth factor which plays an essential role in the immune defence by stimulating the growth of white blood cells (leucocytes).

For the first time the scientists now shed light upon how the hCSF-1 blocking works at the molecular level. Using different methods at the European Synchrotron Radiation Facility ESRF, at the Swiss Light Source SLS and at Deutsches Elektronen-Synchrotron DESY the authors investigated the molecular structures of BARF1, hCSF-1 and the combination of the two. At the EMBL beamline X33 at DESY's particle accelerator DORIS III, it was also possible to elucidate the protein structure in solution to investigate the proteins under conditions closer to their natural environment.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.08.2015 - 16:15:56

Antivirus immune activity in multiple sclerosis correlates with MRI activity

http://www.ncbi.nlm.nih.gov/pubmed/25939660

OBJECTIVE:

The objective of this study was to determine whether reactivation of Epstein-Barr (EBV) or activation of the anti-EBV immune response correlates with MS disease activity on MR imaging.

METHODS:

Subjects with early, active relapsing-remitting MS were studied for 16 weeks with blood and saliva samples collected every 2 weeks and brain MRI performed every 4 weeks. We isolated peripheral blood mononuclear cells from each blood sample and tested the immune response to EBV, autologous EBV-infected lymphoblastoid cell lines (LCL), human herpesvirus 6 (HHV6), varicella zoster virus (VZV), tetanus, and mitogens. We measured the proliferative response and the number of interferon-γ secreting cells with ELISPOT. We measured the amounts of EBV, HHV6, and VZV DNA in blood and saliva with quantitative PCR. On MRI, we measured number and volume of contrast enhancing and T2 lesions. We tested for correlation between the immunologic assays and the MRI results, assessing different time intervals between the MRI and immunologic assays.

RESULTS:

We studied 20 subjects. Ten had enhancing lesions on one or more MRI scans and one had new T2 lesions without enhancement. The most significant correlation was between proliferation to autologous LCL and the number of combined unique active lesions on MRI 4 weeks later. Both proliferation and number of cells secreting interferon-γ in response to LCL correlated with the number of enhancing lesions 8 weeks later.

CONCLUSIONS:

We find evidence for correlation of antiviral immune responses in the blood with subsequent disease activity on MRI scans.

Avainsana on korrelaatio, ei kausaatio, mutta silti mielenkiintoista.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 27.09.2015 - 13:26:20

Lyme Borreliosis and Deficient Mannose-Binding Lectin Pathway of Complement.

http://www.ncbi.nlm.nih.gov/pubmed/25416809

Abstract

Risk factors for the widely endemic and much-debated tick-borne infection, Lyme borreliosis (LB), are unknown. The mannose-binding lectin (MBL) pathway of the complement cascade has an essential role in the eradication of Borrelia burgdorferi. A sufficient concentration of biologically active MBL in body fluids is an indicator of proper function of the MBL pathway. In this study, we investigated whether impaired MBL pathway function, represented by reduced serum MBL concentration, predisposes individuals to LB. First, we determined a serum MBL concentration cut-off level associated with diminished MBL pathway function in a group of 201 individuals. Then, we identified 350 borrelia Ab+ LB patient serum samples and 350 Ab- control samples from the archives of our laboratory and measured serum MBL concentrations in both sample groups. The concentration data were analyzed statistically using logistic regression, controlling for MBL cut-off, age, gender, and age and gender interaction. Serum MBL concentrations < 787 and < 445 ng/ml were associated with diminished and deficient MBL pathway function, respectively. Using these cut-offs, diminished (41.4 versus 27.4%, p = 0.0027) and deficient (26.3 versus 17.1%, p = 0.0361) MBL pathway functions were observed statistically more frequently in the LB patient samples than in the control samples. Also, the age-adjusted median serum MBL concentrations were significantly lower in the LB patient samples than in the non-LB controls. Our findings indicate that a deficiency in the MBL pathway of the complement cascade is a risk factor for developing disseminated Ab+ LB.

Komplementtijärjestelmän lektiinitien heikentynyt toiminta on disseminoituneen borrelioosin kehittymisen riskitekijä. Ts. neljänneksellä väestöstä tämä aktivaatiotie toimii puutteellisesti. Siihen liittyy muun muassa lisääntynyt tiettyjen hengitystieinfektioiden ja toisaalta autoimmuunisairauksien riski. Tässä suomalaisessa tutkimuksessa havaittiin lektiinitien toiminnan puutos useammin borrelioosipotilailla kuin verrokeilla. Eli jos kuulut tähän 25%, riski sairastua infektioihin ja autoimmuunisairauksiin on suurempi kuin muilla.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.10.2015 - 18:59:28

New finding will help target multiple sclerosis immune response

http://www.sciencedaily.com/releases/2015/10/151029102906.htm

Researchers have made another important step in the progress towards being able to block the development of multiple sclerosis (MS) and other autoimmune diseases.

Published today in the journal Nature Communications, the researchers at the University of Adelaide have identified a key protein involved in a 'super-inflammatory' immune response that drives the progression of MS and other autoimmune diseases.

The protein is a specific 'chemokine receptor' involved in moving the body's immune response cells, the T-cells, around the body when they are in the super-inflammatory mode needed to fight persistent infections or conversely, as in the case of autoimmune diseases like MS, attacking the body's own tissues. This chemokine receptor, called CCR2, is a different receptor than was widely assumed to be involved.

"Everybody has been focussing on the CCR6 receptor as the one to target to control this inflammatory response," says project leader Professor Shaun McColl, Director of the Centre for Molecular Pathology at the University of Adelaide.

"We've now shown that the receptor to target is actually CCR2. Blocking CCR6 makes the disease worse. If we can find an antagonist to block the CCR2 receptor specifically on these T-cells, we should be able to control the progression of MS."

MS is an incurable neurodegenerative disease, currently affecting 23,000 people in Australia and the most common disease of the central nervous system in young adults.

"We still can't control MS well, there's a great need for new therapies," says Professor McColl.

The University of Adelaide research was conducted by PhD student Ervin Kara under the supervision of Professor McColl and research fellow Dr Iain Comerford, also in the University's School of Biological Sciences.

Another potential benefit of the research is in making improved vaccines to fight infection.

"Unlike in autoimmune diseases, where the body's immune response is destroying its own cells and the aim is to block T-cell migration, with persistent infection we want to turn on the super-inflammatory response and enhance the migration of the immune cells to sites where they are needed," says Professor McColl. "This research may help guide development of vaccines that can better force that immune response."


Sekä krooniset infektiot että autoimmuunitaudit voivat hyötyä tästä tutkimuksesta.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 30.10.2015 - 19:08:54

Tried-and-True Antibiotic May Block Conversion to MS

http://www.medpagetoday.com/clinical-context/MultipleSclerosis/54038

BARCELONA -- After a first demyelinating event, a broad-spectrum tetracycline antibiotic may prevent conversion to multiple sclerosis (MS), researchers reported here.

In a phase III multicenter Canadian study, patients randomized to minocycline had a significant 44.6% relative risk reduction in progressing to MS over 6 months, reported Luanne Metz, MD, of the University of Calgary, at the European Committee for the Treatment and Research in Multiple Sclerosis meeting.

"We feel that this should be considered a treatment for MS," Metz said. "If you treat people with a simple prescription, you don't need to do complex paperwork or get insurance going. It's a well tolerated drug that requires no safety monitoring whatsoever."

She said she believes a typical regimen of the drug would cost $500 to $600 annually in Canada (about $387 to $460 U.S.).

Current therapies work better if they're given to patients soon after their first clinical demyelinating event. However, insurance coverage for therapies varies by country and region, which may result in treatment delays until patients have a second clinical attack.

In addition, currently available oral therapies may not be ideal because of safety concerns.

Minocycline is an oral antibiotic with a recognized safety profile, widely available, and can be obtained in a lower-cost generic formulation, Metz said. It has many immune-modulating properties, including blocking the transmigration of leukocytes and reducing the activity of activated microglia, she noted.

Preclinical and preliminary clinical studies suggest that minocycline may be a therapeutic option in MS, both as a monotherapy and as an add-on to treatment, she added.

Her group enrolled 142 patients, with a mean age of 35.8, who had their first demyelinating event no more than 180 days before enrollment, and had at least two T2 hyperintense lesions on brain MRI.

The majority of patients (68.3%) were women, the onset was monofocal in 76.8%, and the median expanded disability status scale (EDSS) score was 1.5.

Patients were randomized to placebo or to 100 mg of oral minocycline twice a day, and were treated for 24 months or until they developed MS.

The primary outcome was the proportion of participants who developed MS by 6 months.

Overall, Metz and colleagues found that the risk of conversion to MS within 6 months was 61.4% in the placebo group compared with 34% in the minocycline group -- making for a relative risk reduction of 44.6% and an absolute risk reduction of 27.4% (P=0.001).

The number needed to treat (NNT) was four patients, they added.

By 1 year, the absolute risk reduction was 25.1% and the relative risk reduction was 37.6%. The NNT remained four, they reported (P=0.002).

Findings at 2 years weren't significant, but Metz said the study was underpowered to detect a difference at this point in time.

She added that there were no unexpected safety issues.

Metz concluded that minocycline can reduce conversion to MS, and should be considered for initial treatment as well as for combination therapy trials, given both its safety and low cost.

"This is exciting because it's oral, it's low cost, and we have lots of safety data," Dennis Bourdette, MD, of Oregon Health & Science University in Portland, told MedPage Today. "It would be a good alternative for CIS [clinically isolated syndrome]." Bourdette was not involved in the study.

"We have a lot of CIS patients who don't want to go on anything yet, particularly the expensive drugs which are either injectable or oral but have side effects," he added. "Some of those patients prefer to just be followed. But if you could put them on minocycline, you'd still follow them and then if they break through, you can give them something else."

John Corboy, MD, of the University of Colorado Denver, who also wasn't involved in the study, agreed that minocycline could be a useful tool for early disease.

"Minocycline has a long safety track record which is generally quite favorable, including with long-term use, for example in treating acne," Corboy told MedPage Today. "Thus while we may not wish to put it in the drinking system, we would expect large numbers of patients to tolerate it well."

Toisin sanoen: jos lääkäri epäilee MS-tautia, hänen pitäisi heti määrätä minosykliinikuuri. Saman tien voisi tutkia kaikki mahdolliset krooniset infektiot. Eikä maksa paljoa...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Hartti Pvm 30.10.2015 - 20:31:55

Jep, Minosykliini voi toimia monille ihan tosi hyvikin tässä sairaudessa. Sitä pitäisi ehdottomasti määrätä ja käyttää täälläkin, mutta totta puhuen en usko että joku perusneuro edes miettii tätä vaihtoehtoa sikäli mikäli edes tajuaa olevansa diagnosoimassa MS-tautia ennen kuin on liian myöhäistä.

Se on aika tärkeää tämän sairauden kanssa että kyetään tunnistamaan se ajoissa. Liikaa on lukenut tarinoita siitä että sitä ei kyetä diagnosoimaan ajoissa tai mennään tutkimuksissa niin metsään kuin mahdollista. Pidän itseäni esimerkkinä.

Kannattaa ehkä jutella tästä em. lääkkeestä lääkärin kanssa jos mahdollista.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 14.11.2015 - 00:00:34

Classic microscopy reveals borrelia bacteria

http://phys.org/news/2013-06-classic-microscopy-reveals-borrelia-bacteria.html

A simple method has been found that tells people who have become seriously ill after a tick bite once and for all whether they have bacteria in their blood.

Over the past year, two experienced biologists at Oslo University have seen something that very few scientists experience. They have been sought out by a persistent stream of people from all over Norway who are asking for help.

"People so sick that they can barely stand up have come here to Kristine Bonnevie Building at the University's Blindern campus. They are desperate, because they have not been diagnosal, and therefore have not received appropriate treatment.

Many of them suspect that they have developed chronic borreliosis following a tick bite, and that they have had the disease for a long time. But the tests used by the public health service do not detect it. They come to us with blood samples that they want us to test. They have heard rumours that we have developed a method that can give them answers", explain Ivar Mysterud and Morten Laane. The remarkable new method has just been published in the journal Biological and Biomedical Reports.

When the body is attacked by a bacterium, antibodies develop that can be detected in blood samples and in spinal fluid.

"If the tests do not show that the body has developed antibodies against Borrelia bacteria, this is taken as evidence that tick bite is not the cause of the patients' symptoms".

Suppresses the body's defences

"We believe, contrary to the official stance, that the antibody reaction wanes in people who have been sick for a long time, and that only a small minority of those with chronic borreliosis test positive. The Borrelia infection suppresses the immune system so that it does not function properly. This is one of several reasons that it is difficult to give a definite diagnosis.

The tests used today succeed only partly in detecting the disease due to tick bite. Through intensive studies over many years, the two biologists have formed a picture of the life cycle of the Borrelia bacterium and all the different forms that it takes. Borrelia is a thread-like, spiral bacterium, or spirochaete. It can bore into our blood cells and moves around the body with our blood circulation.

"As a result, the bacteria spread rapidly and in principle can infect all tissues and organs, including the brain. This is why the symptoms are so many and varied. In the early phase, the symptoms tend to be mild, such as headache, muscular pain and fever. In some cases, however, the disease may last a long time, or become chronic, and the symptoms may vary enormously: stabbing pains, impairments in short-term memory, persistent fatigue, unusually long recovery time after exertion, permanent skin changes, joint pain, paralysis, nervous disorders and depression. One important reason that chronic borreliosis often remains undiagnosed is that the symptoms are not well understood. The diagnosis chronic borreliosis is controversial. The Norwegian health service believes that a four-week course of antibiotics should be enough to kill all Borrelia bacteria in the body, but it is not that simple, according to the two biologists.

"There are strong indications that once the bacterium gets into your bloodstream, it's there for the rest of your life", they say.
***************
By developing some smart microscopy techniques, researchers have now succeeded in making the Borrelia bacteria stand out clearly - including in the blood of individuals who have no symptoms of disease.

Revealing the bacteria


"Using our method, the Borrelia bacteria in the red blood cells stand out clearly after one to two days at room temperature. We manage to make the bacteria visible without using staining (which can only be used on dead preparations). Keeping the bacteria alive allows us to monitor the bacteria through the microscope.

The researchers add a dilute saline solution to the blood preparation. The blood cell then swells up and most of the blood plasma breaks up and disappears.

"The swollen red blood cells become clearly visible. The images are sharper and clearer than those produced by other methods we know of, and they often show incredible details. We can observe how the bacteria emerge from the blood cells. Not all of the structures seen when the blood cells expel material are classically shaped Borrelia bacteria. Visualization of various Borrelia life stages can be enhanced by adjusting the concentration of the salt solution to give more detail.

A common conception is that Borrelia bacteria in human blood have a spiral or zig-zag shape. However, the absence of such shapes in the blood does not exclude the presence of the bacteria. The researchers see examples of the bacteria straightening out after 24 hours, or they may exist as tiny structures with simple geometrical shapes, or form round structures (the aforementioned cyst stage).

"Our experiments show that virtually all the bacteria change into the cystic form in the course of just one hour. We can then expose them to almost any antibiotic medication, but nothing destroy these.

It is well known that these bacteria migrate and thrive in parts of the body with little oxygen, such as joint tissue. They lie there and wait for the host's health to deteriorate. Bacteria constantly leak out into the bloodstream. he patient is given antibiotics, which destroy the bacteria that leak out, the immune system recovers and the treatment stops. But the source is still in the body.

Extremely complex

Research on Borrelia and tick-borne diseases has exploded internationally in recent years. For all that, Mysterud and Laane maintain that knowledge about the bacteria remains very limited.

"We may find Borrelia in the blood, while the symptoms have nothing to do with borreliosis. Conversely, the symptoms may be absolutely typical of borreliosis. There are many shades in between, but this is never discussed. The exchange of views now in progress barely scratches the surface, because this is actually staggeringly complex. I have pointed out a problem that nobody has taken very seriously, in my view - at least not many doctors", says Laane.

Pitäisiköhän hankkia mikroskooppi, tutkia ja todistaa borre itse kun muuten ei kukaan usko. Ole oman itsesi lääkäri ja labra. Ja hoitohenkilökunta..


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.12.2015 - 15:00:10

Germ that causes cat scratch disease not necessarily mild

http://news.vin.com/VINNews.aspx?articleId=16570

The pathogen best known for causing cat scratch disease is responsible for a host of serious illnesses in humans that may be misdiagnosed due to lack of awareness in the medical community.

Researchers studying the Bartonella genus of bacteria say veterinarians and veterinary staff, along with others who work with animals — including groomers, trainers and shelter and rescue organization personnel — are at particular risk of infection owing to their frequent exposure to animals and animal parasites such as fleas.

“I think it’s more common than we think in the veterinary community,” said Dr. Bruno Chomel, a DVM and professor in the Center for Vectorborne Diseases at the University of California, Davis.
*******
Twenty years ago, only two Bartonella species were known. One, B. henselae, was identified as the agent behind cat scratch disease, a condition believed to be transmitted by a cat scratch or bite that causes swelling of the lymph nodes along with fever, headache, fatigue and/or poor appetite. Conventional wisdom said — and says still — that “cat scratch fever” is nothing to worry about for most people: Except in those with immune system deficiencies such as AIDS, the infection goes away on its own or with a short course of antibiotics. Bartonella became synonymous with mild illness.

But researchers say the picture is more complicated than that. Today, the number of Bartonella species identified is 26 and counting. Species exist that co-evolved with dogs, cattle, squirrels and ground hogs. Arthropods including fleas, lice and possibly ticks transmit the germ to mammals.

Those who study Bartonella characterize it as a “stealth pathogen” because of its ability to evade detection even at levels that cause illness. The bacterium has been found to invade and colonize a variety of cell types — not only blood cells such as erythrocytes and macrophages but vascular endothelial cells and dendritic cells of the nervous system, as well.
*********
Barnes, 54, was diagnosed with multiple sclerosis (MS) in 2005. Up to that point, he was a healthy man who jogged regularly and ran up and down bleachers at the local high school for exercise.

One day, shortly after a bout of 103-degree fever and vomiting that he attributed to food poisoning, Barnes was jogging around a track. On the third lap, his left leg stopped cooperating, causing him to stumble. A week or so later, Barnes began tripping again while jogging, this time on the second lap.

Thus began his journey through the medical system. One physician suspected a herpes virus. Another thought it might be Guillain-Barre, a rare neurological syndrome in which the body’s immune system attacks part of the peripheral nervous system. Following an MRI and spinal tap, Barnes was told he had MS and that he would likely end up in a wheelchair.

Barnes was not so sure. “I wasn’t trying to balk at the diagnosis but because I had this huge fever (five months earlier) in December when all of this started, I thought maybe I had something else,” he said. “It sounded more inflammatory and (like an) infection.”
*******
It turned out that Barnes had an infection of B. henselae, the same species of Bartonella that causes cat scratch disease. His case and that of five other similarly infected patients was published in a study that appeared in the Journal of Clinical Microbiology in September 2008.

Whether the Bartonella infection had anything to do with his neurological symptoms or was mere coincidence was a point of debate and discussion among various doctors. “I have so many ologists, I don’t know what I’m doing,” Barnes commented wryly.

His condition worsened in the meanwhile. He fell frequently, once breaking a rib.

Finally in August 2007, he was prescribed two antibiotics to combat the Bartonella: doxycycline and rifampin. Within a month, he said his toes, which had had a cadaverous gray tone, “started pinking up.”

A couple months later, he noticed his fatigue lifting. By the following summer, he could stand on one leg, cross the other over his standing knee and look at the bottom of his foot — a position he had not been able to assume in three years.

His odyssey didn’t end there, unfortunately. Barnes stopped taking the antibiotics after a year. Breitschwerdt continued to monitor his blood. At first, Barnes was negative for Bartonella. But six months later, the bacteria reappeared.

Barnes went back on antibiotics. In February this year, he sent another blood sample to Breitschwerdt. The B. hensalae showed up still, and this time, not one strain, but two.

Was it the result of a new exposure or something that had been in hiding? The answer may never be clear.

Barnes said that as far as he knows, in 26 years as a clinician, he has never had a patient with a Bartonella infection. But he has spent plenty of time among animals and in the outdoors. “My dad was a vet,” he said. “I was always catching frogs and toads (as a boy). So I think I’m exposed to all this junk.”

Despite the ongoing infection, Barnes said he is doing much better — on the order of 60 to 70 percent improved, in his estimation. That tells him that while he truly may have MS, there’s a relationship between his MS and Bartonella.

“I’m not saying I have just Bartonella or just MS,” he said. “But what if, of all the 400,000 people with MS right now, what if 2 percent of them are Bartonella-induced? People get their panties in a wad if I say that Bartonella causes MS. But (the diagnosis of Bartonella infection) helped me. I should be in a wheelchair right now.”


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.12.2015 - 14:36:06

Certain herpes viruses can infect human neurons

http://www.sciencedaily.com/releases/2015/12/151204121405.htm

For years, researchers have noted a tantalizing link between some neurologic conditions and certain species of the herpes virus. In patients with Alzheimer's disease, multiple sclerosis, and cerebellar ataxia, among other neuropathies, the cerebrospinal fluid teems with Epstein-Barr virus (EBV). Yet, the nature of that link has remained unclear, as it has been assumed that EBV, as well as other viruses in the same sub-family, called gammaherpesviruses, cannot infect neurons.

Now, thanks to investigators from the Perelman School of Medicine at the University of Pennsylvania, researchers in this field know better. Erle S. Robertson, PhD, a professor of Microbiology and Otorhinolaryngology and Director of the Tumor Virology Training Program at the Abramson Cancer Center, and colleagues published in mBio this week that EBV and a related virus, Kaposi's sarcoma-associated herpesvirus (KSHV), can infect and replicate in both cultured and primary neurons.

Though by no means proving causality, those data do suggest viral infection could underlie at least some of the symptoms of those brain disorders, as well as the potential utility of antiviral drugs as a novel therapeutic strategy.

According to Robertson, several lines of evidence suggested the possibility that gammaherpesviruses could infect brain tissue. First, the viruses are enriched in the cerebrospinal fluid and brain tissue of individuals with such conditions as multiple sclerosis (MS) and Alzheimer's disease. In addition, individuals with a history of infectious mononucleosis caused by EBV are more likely to develop MS, while those who have never been infected with EBV are less likely to do so. Particularly tellingly, the drug acyclovir, which can inhibit EBV and related viruses, has been examined as a potential treatment for MS, with some positive, albeit inconclusive, results.

Still, says Robertson, the ability of gammaherpesviruses to infect neurons has been "controversial." Devan Mehta, a student in Robertson's lab, working with postdoctoral fellow Hem C. Jha, PhD, and Dennis Kolson, MD, PhD, a professor of Neurology, tested the link directly. Using genetically modified viruses that express green fluorescent protein (GFP), Mehta infected human neuroblastoma cells (neurons differentiated from cancer cells) and primary human fetal neurons, monitoring the infection over time by microscopy and protein expression.

In both cell types, infection with either EBV or KSHV resulted in the appearance of a fluorescent signal in the infected cells, as well as the appearance of key viral proteins. The media in which infected cells were grown also contained functional virus particles capable of infecting other cells, indicating a mode of infection that tears open host cells. On the other hand, treatment of infected cells with acyclovir reduced the production of virus particles.

"I couldn't believe it," Robertson said. "After 50 years of studying EBV, nobody had ever seen the virus in nerve cells. But maybe they just never looked."

According to Robertson, these data suggest that viral infection of neurons could be associated with neuropathology, though he emphasizes that it is not the same as establishing causality. Such proof, if it ever comes, could be years away.

"There's likely to be association of this virus with neurons," he stated. "But more studies will be necessary to know whether it is actually associated with disease pathology.

Why EBV and KSHV infection of neurons results in a specific destructive form of infection will also be explored in future research. In contrast, when these viruses infect other cell types, such as B cells, they enter a latent mode, in which virus particles are relatively dormant. But, when they infect neurons, the particles apparently direct the cells to produce large amounts of virus, burst, and die, which explains why the growth media bathing infected cells could be used to infect other cells. "That's an interesting twist," Robertson said.

If nothing else, the ability of gammaherpesviruses to infect neurons provides a new model system for studying viral life cycles. But these viruses ultimately may also prove useful in studying disease etiology. "If you can infect nerve cells, that's likely to have some sort of pathology," he said.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.12.2015 - 14:39:59

How cells are foiled by a herpesvirus family member in the virus-host arms race

http://www.sciencedaily.com/releases/2015/12/151204183624.htm

Not every virus wants to go viral -- at least, not immediately. Some want to slip in quietly. Hide. Wait for the perfect opportunity to attack.

In order to do so, the virus has to find a way to enter the cells of the human body without tripping the alarm, and stay there without notice. It's how HIV works, and also how viruses in the herpesvirus family, like human cytomegalovirus (HCMV), do their business.

In a new study published in Science Advances, a group of University of Wisconsin-Madison researchers show that individual cells in the human body have an armament designed to prevent HCMV from achieving and maintaining this latency, to shine a spotlight on the virus so the immune system knows to fight. But the virus, in turn, has developed ways to thwart these defenses.

"We call it an arms race," says study leader Rob Kalejta, professor of molecular virology and oncology at UW-Madison. "Virus evolves a mechanism to persist, human cells evolve a way to defeat that mechanism, virus evolves a way to defeat what the cell just evolved."

The study shows there are potential ways to intervene in that process, says Albright. Its co-lead authors are UW-Madison graduate student Emily Albright and former postdoctoral researcher Song Hee Lee.

HCMV infects people at high rates all around the world. People with compromised or weakened immune systems are especially vulnerable. In newborn babies, the virus can cause deafness, intellectual disability and learning disorders. Other viruses in the herpesvirus family can cause cancer, shingles and mononucleosis. Once people are infected, they will have the virus their entire lives, due to its ability to cycle between latent and active states in the body.

"Our immune system does a pretty good job at fighting lytic (active) herpesviruses, but it has no chance against the latent reservoir," says Kalejta.

The human immune system is made of two main branches: innate and adaptive. One is more general -- the immediate response to a cut in your skin -- and the other more specialized, responding specifically to a variety of pathogens that invade the body. But there is a third, more recently described, arm called intrinsic immunity, where individual cells in the body protect themselves from infection without calling on the body's immune defenses.

Active HCMV is obvious to the body's innate and adaptive immune systems, producing proteins and other viral material that serve as red flags to the body's security system.

But latent HCMV shuts down the processes that allow it to be found.

Previous studies in the lab showed that once HCMV is inside the cell, it quickly becomes latent by entering the cell's nucleus and co-opting a cellular protein called Daxx -- part of the intrinsic immune system -- to shut down its own replication, the process of reproducing its genetic material to make more copies of itself. This process would otherwise trigger a healthy immune system to respond. Instead, it can hide and wait for a time when a person's immune system is weakened.

In the new study, expanding upon what scientists previously understood about intrinsic immunity, the researchers found that cells can subsequently respond to latent HCMV by employing other cellular proteins called lysine demethylases to reactivate the virus.

"When you think about defending yourself against a virus, you usually think about turning it off, but this is what the virus wants to do when it goes latent," Kalejta says. "So this intrinsic immune system is trying to convert it from a latent to a lytic infection so that we at least have a fighting chance against it."

But the wily virus fights back.

The research team learned the virus brings with it to the cell a protein called UL138 that blocks the cellular lysine demethylases from turning the virus back on.

"We showed that UL138 prevents the cellular proteins from getting to the viral genome, and if they can't get there, they can't turn it on," says Albright.

The researchers are not yet sure how UL138 accomplishes this. The cellular proteins are located in the nucleus of the cell, where the virus maintains its genetic material. But UL138, the viral protein, is actually located outside the nucleus, at a cellular component called the Golgi. The viral protein outside the nucleus is somehow preventing the cellular proteins in the nucleus from accessing the viral genome, which is also in the nucleus.

"We'd like to know how that works," Albright adds.

The study of HCMV is revealing new ways in which human cells function, highlighting the role of proteins and other factors that have never been described in these ways before. It is opening new avenues of scientific inquiry.

"We've shown that cells can defend themselves against latent viruses," says Kalejta.

"So if cells can do that, maybe scientists can, too. We are years away from that, but it gives us hope that cures are possible."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.01.2016 - 14:47:06

Bacterial toxins and Multiple Sclerosis.

http://www.unboundmedicine.com/medline/citation/17707408/Bacterial_toxins_and_Multiple_Sclerosis_

Abstract

The primary pathogenetic mechanism responsible for the distinctive demyelinating lesions in the Central Nervous System (CNS) in Multiple Sclerosis (MS), first described in remarkable detail by Charcot more than 170 years ago, remains one of the most baffling conundrums in medicine. A possible role for bacterial cell molecules and transportable proteins in the pathogenesis of MS is reviewed. The ability of bacterial toxins to distort immunity and to cause distinctive toxic damage in the nervous system is discussed in the light of largely forgotten data linking bacterial nasopharyngeal infections with optic neuritis, optochiasmatic arachnoiditis and MS. While the blood-brain barrier substantially protects the CNS from hematogenous toxins, there is a route by which the barrier may be by-passed. Data is reviewed which shows that the CSF and extra-cellular fluid circulation is bi-directionally linked to the lymphatic drainage channels of the nasopharyngeal mucosa. While this provides a facility by which the CNS may mount immunological responses to antigenic challenges from within, it is also a route by which products of nasopharyngeal infection may drain into the CNS and be processed by the immune cells of the meninges and Virchow-Robin perivascular spaces. If potentially toxic bacterial products are identified in early MS tissues at these sites, this would provide an entirely new insight into the pathogenetic mechanisms of this frustratingly enigmatic disease.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 17.01.2016 - 14:42:11

Common virus plus low sunlight exposure may increase risk of multiple sclerosis

http://www.sciencedaily.com/releases/2011/04/110418161658.htm

New research suggests that people who are exposed to low levels of sunlight coupled with a history of having a common virus known as mononucleosis may be at greater odds of developing multiple sclerosis (MS) than those without the virus. ****

"It's possible that vitamin D deficiency may lead to an abnormal response to the Epstein-Barr virus," Ebers said.

He noted that low sunlight exposure in the spring was most strongly associated with MS risk. "Lower levels of UVB in the spring season correspond with peak risk of MS by birth month. More research should be done on whether increasing UVB exposure or using vitamin D supplements and possible treatments or vaccines for the Epstein-Barr virus could lead to fewer cases of MS."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.02.2016 - 18:58:50

Varicella Zoster Virus and Relapsing Remitting Multiple Sclerosis

http://www.hindawi.com/journals/msi/2011/214763/

Multiple sclerosis (MS) is an immune-mediated disorder; however, little is known about the triggering factors of the abnormal immune response. Different viruses from the herpes family have been mentioned as potential participants. Here, we review the evidences that support the association of varicella zoster virus (VZV) with MS. Epidemiological studies from geographical areas, where incidence of MS has increased in recent decades, pointed out a high frequency of varicella and zoster in the clinical antecedents of MS patients, and also laboratory investigations have found large quantities of DNA from VZV in leucocytes and cerebrospinal fluid of MS patients restricted to the ephemeral period of MS relapse, followed by disappearance of the virus during remission. The above observations and the peculiar features of VZV, mainly characterized by its neurotropism and long periods of latency followed by viral reactivation, support the idea on the participation of VZV in the etiology of MS. However, as with reports from studies with other viruses, particularly Epstein Barr virus, conflicting results on confirmatory studies about the presence of viral gene products in brain tissue indicate the need for further research on the potential participation of VZV in the etiology of MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.02.2016 - 19:04:14

Herpes Zoster and Multiple Sclerosis

http://jid.oxfordjournals.org/content/204/2/177.full

Multiple sclerosis (MS), a demyelinating disease of the central nervous system, has been considered multifactorial, and viruses may have a role in disease pathogenesis. Evidence suggests that certain viruses may trigger autoimmune neurological processes that lead to MS in genetically susceptible individuals [1, 2].

In this issue of the Journal, Kang et al analyze a database of 349,477 patients who had herpes zoster (experimental group) as a risk factor for MS (study outcome variable) in a region of the world historically considered low risk for MS. The authors compare their data with a randomly selected control group, more than 3 times as large as the initial sample (n = 1,262,200), of participants who did not have herpes zoster. Their results show that the herpes zoster group had a 3.96 times greater risk of developing MS than did the control group (95% confidence interval [CI], 2.22–7.07, P ≤ .001).

This Kang et al study provides clear epidemiological observations suggesting a role for herpes zoster in the development of MS [3]. Previous studies noted that certain herpes viruses may trigger proinflammatory and autoimmune cascades through particles such as the Toll-like receptor 4 (TLR-4) [3, 4], and that infectious environmental factors associated with MS may also belong to the herpesviridae family [4, 5].

This study highlights the time elapsed from the event of shingles until the occurrence of MS (approximately 100 days). In addition, evidence suggests that up to 30% of relapses among MS patients are associated with an infectious process [6, 7]. A possible explanation is the reactivation of latent herpes viruses by other infectious agents, and cross-recognition of common viral antigens with antigens found in the myelin sheath, which thereby induces molecular mimicry or superantigens [8–10]. The time lag for the occurrence of MS could be explained by a series of processes required by the immune systems of genetically susceptible individuals to reach a “threshold” and start the disease process. The threshold may also explain, in part, the observation that some patients have higher recurrence rates of MS around certain months of the year [11]. Some viruses of the herpesviridae family cause B cells to express alpha and beta crystal, a small stress protein that is normally absent from lymphoid tissues and has been considered an immunodominant antigen in the central nervous systems of MS patients [12].

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2016 - 15:47:31

Association between multiple sclerosis and cystic structures in cerebrospinal fluid.

http://www.ncbi.nlm.nih.gov/pubmed/11787831

Tutkimus vuodelta 2001 borrelioosi kystista aivoselkäydinnesteessä:

BACKGROUND:
The aim of the study was to search for infectious agents in the cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS).

PATIENTS AND METHODS:
CSF from ten patients with the diagnosis relapsing remitting MS and from five controls without MS were examined by transmission electron microscopy (TEM), dark field microscopy (DF), interference contrast microscopy (ICM) and UV-microscopic examination of acridine orange staining (AO). All CSF samples from patients and controls were cultured.

RESULTS:
Cystic structures were observed in CSF of all ten patients by AO and TEM. DF revealed eight cyst-positive patients out of nine. One of five control persons had such structures in the CSF; this person had suffered from erythema migrans. Spirochete or rod-like structures emerged after culturing two of the MS patient CSF samples and these structures could be propagated.

CONCLUSION:
A significant association of CSF cysts and MS was identified in this small study among residents in a coastal area of southern Norway. The cysts could be of spirochetal origin. Our study may encourage other researchers to study larger patient groups.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2016 - 15:52:44

Multiple Sclerosis After Infectious Mononucleosis

http://archneur.jamanetwork.com/article.aspx?articleid=793221

Results  
A total of 104 cases of multiple sclerosis were observed during 556 703 person-years of follow-up, corresponding to a standardized incidence ratio of 2.27 (95% confidence interval, 1.87-2.75). The risk of multiple sclerosis was persistently increased for more than 30 years after infectious mononucleosis and uniformly distributed across all investigated strata of sex and age. The relative risk of multiple sclerosis did not vary by presumed severity of infectious mononucleosis.

Conclusions
The risk of multiple sclerosis is increased in persons with prior infectious mononucleosis, regardless of sex, age, and time since infectious mononucleosis or severity of infection. The risk of multiple sclerosis may be increased soon after infectious mononucleosis and persists for at least 30 years after the infection.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2016 - 15:59:04

Rare infections mimicking MS

http://www.clineu-journal.com/article/S0303-8467%2810%2900113-7/abstract

The diagnosis of multiple sclerosis (MS), despite well defined clinical criteria is not always simple. On many occasions it is difficult to differentiate MS from various non-MS idiopathic demyelinating disorders, specific and infectious inflammatory diseases or non-inflammatory demyelinating diseases. Clinicians should be aware of various clinical and MRI “red flags” that may point to the other diagnosis and demand further diagnostic evaluation. It is generally accepted that atypical clinical symptoms or atypical neuroimaging signs determine necessity for broad differential diagnostic work up. Of the infectious diseases that are most commonly mistaken for MS the clinician should take into account Whipple's disease, Lyme disease, Syphilis, HIV/AIDS, Brucellosis, HHV-6 infection, Hepatitis C, Mycoplasma and Creutzfeld-Jacob disease, among others. Cat scratch disease caused by Bartonella hensellae, Mediterranean spotted fever caused by Riketssia connore and Leptospirosis caused by different Leptospira serovars rarely cause focal neurological deficit and demyelinating MRI changes similar to MS. When atypical clinical and neuroimaging presentations are present, serology on rare infectious diseases that may mimic MS may be warranted. This review will focus on the infectious diseases mimicking MS with presentation of rare illustrative cases.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2016 - 16:11:11

Decreased CD8+ T cell response to Epstein-Barr virus infected B cells in multiple sclerosis is not due to decreased HLA class I expression on B cells or monocytes

http://bmcneurol.biomedcentral.com/articles/10.1186/1471-2377-11-95

Patients with multiple sclerosis (MS) have a decreased frequency of CD8+ T cells reactive to their own Epstein-Barr virus (EBV) infected B cells. We have proposed that this might predispose to the development of MS by allowing EBV-infected autoreactive B cells to accumulate in the central nervous system. The decreased CD8+ T cell response to EBV results from a general CD8+ T cell deficiency and also a decreased proportion of EBV-specific T cells within the total CD8+ T cell population. Because decreased HLA class I expression on monocytes and B cells has been reported in MS and could influence the generation and effector function of EBV-specific CD8+ T cells, the present study was undertaken to measure the expression of HLA molecules on B cells and monocytes in patients with MS.
******
We have hypothesized that a genetically determined defect in the elimination of EBV-infected B cells by cytotoxic CD8+ T cells might predispose to the development of MS by allowing EBV-infected autoreactive B cells to accumulate in the central nervous system.
*****
The decreased CD8+ T cell response to EBV-infected B cells in MS patients is not due to decreased HLA class I expression on monocytes or B cells. In a small proportion of patients decreased HLA class II expression on B cells might impair the CD8+ T cell response to EBV by reducing CD4+ T cell help.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.02.2016 - 21:24:53

Study details source of mental problems associated with MS

https://www.sciencedaily.com/releases/2016/01/160126175036.htm#

A study out today sheds new light on multiple sclerosis (MS), specifically damage in the brain caused by the disease that may explain the slow and continuous cognitive decline that many patients experience. The findings, which appear in the Journal of Neuroscience, show that the brain's immune system is responsible for disrupting communication between nerve cells, even in parts of the brain that are not normally considered to be primary targets of the disease.

"This study identifies for the first time a new disease mechanism in MS which causes damage to neurons independent of the loss of white matter and demyelination that is the hallmark of the disease," said the lead author, neurologist Matthew Bellizzi, M.D., Ph.D., with the Center for Neural Development and Disease at the University of Rochester Medical Center (URMC). "This damage represents another component of the disease and one that is not prevented by the current immunosuppressive drugs employed to treat MS."
*****
One of the culprits appears to be a cell in the central nervous system's defenses called microglia. Microglia serve as the brain's "first responders" and are activated to help fight infection or other assaults on the nervous system and clean up the debris from damaged cells.

One of the functions of microglia is to maintain the health of the synapse so that it can function normally to help the hippocampus with learning and memory.However, when the immune system is over-activated during MS, distress signals are sent throughout the brain causing the microglia to switch from their normal nurturing role and take up an aggressive pro-inflammatory response.

The microglia release a molecule called platelet-activating factor (PAF) that affects the excitatory signaling that neurons use to activate one another and encode new memories. High levels of PAF can lead to an over-activation of these signals that, like a power surge, destroys the receiving end of the synapse. This, in turn, causes more microglia and other immune cells to rush to the site of injury, triggering a chronic and self-perpetuating cycle of destruction.

"The cumulative effect is like trying to put out a fire with gasoline," said Gelbard.

The researchers believe that this phenomenon is ultimately responsible for much of the cognitive impairment and progressive decline that many individuals with the disease experience.

While the activation of microglia and resulting damage to the synapse is not impacted by the drugs currently used to treat MS, the researchers are now focused on potential drug candidates known to suppress the signaling pathways that cause the nerve cells and microglia to become overactive, including a drug that is being investigated to treat HIV-associated neurological disorders.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.02.2016 - 16:19:56

Immunopathology of Japanese macaque encephalomyelitis is similar to multiple sclerosis.

http://www.ncbi.nlm.nih.gov/pubmed/26857488

Abstract

Japanese macaque encephalomyelitis (JME) is an inflammatory demyelinating disease that occurs spontaneously in a colony of Japanese macaques (JM) at the Oregon National Primate Research Center. Animals with JME display clinical signs resembling multiple sclerosis (MS), and magnetic resonance imaging reveals multiple T2-weighted hyperintensities and gadolinium-enhancing lesions in the central nervous system (CNS). Here we undertook studies to determine if JME possesses features of an immune-mediated disease in the CNS. Comparable to MS, the CNS of animals with JME contain active lesions positive for IL-17, CD4+ T cells with Th1 and Th17 phenotypes, CD8+ T cells, and positive CSF findings.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Oireeron_fibro Pvm 28.02.2016 - 19:15:37

Mielenkiintoinen ketju. Itse olen tutkinut mm. fibron parantamismahdollisuuksia pallolaajennuksen avulla. Ilmeisesti keuhkoklmydialla on osuutta ahtaumiin, olipa diagnoosi sitten MS-tauti tai fibromyalgia. Sma ongelma, fibrossa operaatiosta käytetään nimeä TVAM ja MS taudin kohdalla CCSVI.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Oireeron_fibro Pvm 28.02.2016 - 19:17:32

Laitetaan vielä lisäinfoa MS-taudin kanssa painiville.

Tässä esityksiä MS-taudista ja borresta sivujuonteineen. Ovat juuri pidetystä LDN2016 konferenssista huippulääkäreiden esityksiä jossa on paljon tietoa aiheesta.

Armin Schwarzbach (borrelioosi sivujuonteineen)
https://vimeo.com/156196839
http://www.ldn2016.com/sites/default/files/Armin_Schwarzbach.pdf

Jarred Younger (MS-taudin hoitaminen, jossa mukana LDN)
http://www.ldn2016.com/sites/default/files/Jarred-Younger.pdf
Videoitu esityskin on olemassa, mutta en löydä linkkiä..

Kommentoikaapa näitä, itse en ole ehtinyt katsoa MS aiheisia vielä läpi.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 29.02.2016 - 18:57:23

”Krooninen bakteeri-infektio saattaa olla melkein missä tahansa. Minulla ei ole ollut, ehkä tikku sormessa lapsena, tai ei sekään. Tutkijat selvittävät kroonisten infektioiden roolia syövän kehittymisessä .... Yhdeksän tunnistettua syöpää aiheuttavaa virusta tai bakteeria aiheuttaa arviolta 17 prosenttia syöpäsairauksista koko maailmassa - toisin sanoen, vuosittain diagnosoidaan noin 1,6 miljoonaa syöpätapausta, joissa taustalla on virus- tai bakteeri-infektio.”
http://www.biomedicum.fi/index.php?page=356&lang=1

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.03.2016 - 00:05:08

Kiitti LDN2016 linkeistä. Armin Schwartzbach oli aikaisemmin  BCA:n Infectolabissa kunnes perusti oman labran tutkimaan borrea ja lisäinfektioita. Hän mainitsee CD3/CD57 testin, joka antaa suuntaa mahdollisesta immuunisuppressiivisesta tilasta. Normaali arvo on 130-360. Minulla on ollut alimmillaan 39, mutta monilla pitkään sairastaneilla saattaa olla vielä alhaisempi arvo. Samaan aikaan valkosolut ovat olleet joko normaalin alarajan alla tai siinä alarajan pinnassa. Antibiootti ja malarialääkityksen jälkeen aloitin LDN:n puolitoista vuotta sitten. Reseptin sain infektiolääkäriltä. Muita muuttujia ei ollut, ja kolmessa kuukaudessa CD57 nousi 47:stä 85:een, seuraavan 5kk aikana 134:ään eli hieman normaalin rajan yläpuolelle. Jos ottaa huomioon, että CD57 testin varianssi saattaa olla +/- 50 (aika paljon), arvot ovat silti parantuneet. Syynä voi olla (i) normaali immuunipuolustuksen parantuminen, tai (ii) LDN:n auttama  immuunijärjestelmän parantuminen. Vuosi sitten testeistä paljastui, että minulla oli vielä borre, keuhkoklamydia ja EBV, vaikka oloni oli edellistä vuotta parempi, ja CD57 oli siis 134. Sain antibiootteja pulssihoitona vähän aikaa viime vuonna ja tämän vuoden testeissä ainoastaan EBV jylläsi, ja CD57 noussut hieman 138:aan ja valkosolut normaalille tasolle.
Auttaako LDN sitten immuunisuppressiiviseen tilaan?  Mielestäni auttaa, vaikka CD57 ei olisikaan kaikkein luotettavin testi sen tilan mittaamiseen. Auttaako se infektioihin? Kiertoteitse auttamalla omaa immuunipuolustusta. Lisää tieteellistä tutkimusta tarvitaan, niin kuin monessa muussakin mielenkiintoisessa näkökulmassa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 01.03.2016 - 13:15:08

Mikrogliat muuttuvat, mutta miksi?
http://www.utu.fi/fi/Ajankohtaista/Artikkelit/Sivut/turussa-etsitaan-laaketta-etenevaan-ms-tautiin.aspx

https://www.utu.fi/fi/Ajankohtaista/mediatiedotteet/vaitostiedotteet/Sivut/uusia-kuvantamismenetelmia-etenevan-ms-taudin-.aspx

"Yksi PET-kuvan paljastama muutos tapahtuu aivojen mikroglia-soluissa. Niiden tehtävänä on normaalioloissa putsata aivoista haitallisia aineita ja roskaa. Terveissä aivoissa kaikista aivosoluista noin 10 prosenttia on mikroglia-soluja, MS-taudissa ne vielä tuntemattomasta syystä muuttavat muotoaan ja toimintaansa ja aktivoituvat.

– Tiedämme neuropatologian tutkimuksista, että mitä pidemmälle tauti on edennyt, sitä enemmän mikroglian aktiivisuutta ilmenee. Haluamme selvittää, miten hyödyllinen, roskaa putsaava solu muuttuu tulehduksen yhteydessä haitalliseksi ja mikä vaikutus tällä on tautiprosessiin, muun muassa neurodegeneraation kehittymiseen, Airas sanoo.

Turkulaisten työtä vie eteenpäin myös kolme vuotta sitten alkaneet eläinmallitutkimukset.

– Turku on maailman ensimmäinen paikka, jossa etenevän MS-taudin eläinmallia käyttäen on pystytty in vivo PET-tutkimuksen avulla osoittamaan MS-lääkityksen vähentävän mikroglia-aktiivisuutta, Airas sanoo.
MS-PET-tutkimusryhmä etsii parhaillaan monipuoliset metodologiset taidot omaavaa post-doc tason tutkijaa prekliinisen ryhmän vahvistukseksi. Aiheesta kiinnostuneet voivat ottaa yhteyttä Laura Airakseen sähköpostiosoitteeseen laura.airas@utu.fi."

Teksti: Erja Hyytiäinen
Kuvat: Tutkimusryhmä, Erja Hyytiäinen

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.03.2016 - 15:55:42

Body's immune system may play larger role in Alzheimer's disease than thought

https://www.sciencedaily.com/releases/2016/02/160223074923.htm

February 2016
Immune cells that normally help us fight off bacterial and viral infections may play a far greater role in Alzheimer's disease than originally thought, according to University of California, Irvine neurobiologists with the Sue & Bill Gross Stem Cell Research Center and the Institute for Memory Impairments and Neurological Disorders.

The researchers discovered this when Alzheimer's disease mice genetically modified to lack these key immune cells in their blood developed the distinctive brain plaques associated with the neurodegenerative disorder much more quickly.

According to Mathew Blurton-Jones, assistant professor of neurobiology & behavior, and doctoral student Samuel Marsh, their findings could lead to the creation of new techniques to help identify, or perhaps even treat, individuals at risk of developing the disease.

Alzheimer's is the leading cause of age-related dementia and is thought to be driven by the accumulation of a protein called beta-amyloid that aggregates to form amyloid plaques in the brain. Microglia, immune cells that reside in the brain, attempt to clear this buildup, but in Alzheimer's, they appear to be fighting a losing battle. While many studies have explored the role of microglia in Alzheimer's, very few researchers have asked whether a different set of immune cells called T-cells and B-cells that reside outside the brain and play a large part in autoimmune diseases might also impact Alzheimer's.

To test this idea, Blurton-Jones and Marsh bred genetically modified Alzheimer's disease mice to lack three key immune cell types: T-cells, B-cells and NK-cells. Six months later, when the brains of these mice were compared to those of Alzheimer's mice with intact immune systems, the scientists found a more than twofold increase in beta-amyloid accumulation.

"We were very surprised by the magnitude of this effect," Blurton-Jones said. "We expected the influence of the deficient immune system on Alzheimer's pathology to be much more subtle."

To understand how the loss of these immune cells was increasing beta-amyloid, he and Marsh examined the interactions between these peripheral cells and microglia within the brain.

"We found that in Alzheimer's mice with intact immune systems, antibodies -- which are made by B-cells -- accumulated in the brain and associated with microglia. This, in turn, helped increase the clearance of beta-amyloid," Marsh said.

To further confirm the importance of this interplay between immune cells in the blood and those in the brain, the researchers transplanted healthy bone marrow stem cells into the immune-deficient Alzheimer's mice. Since T-, B- and NK-cells develop from bone marrow stem cells, this transplantation led to a reconstitution of the missing immune cells. This allowed the B-cells to produce antibodies that once again reached the brain and aided microglia in eradicating the beta-amyloid.

"We know that the immune system changes with age and becomes less capable of making T- and B-cells," Blurton-Jones said. "So whether aging of the immune system in humans might contribute to the development of Alzheimer's is the next big question we want to ask."
******
Eli valkosolut puhdistavat aivoista ylimääräisiä beta-amyloideja, ilman valkosoluja haitallisten beta-amyloidien määrät kasvavat.  Edellä  mainitun suomalaisen tutkimuksen mukaan MS-lääkitys vähentää mikroglia-aktiivisuutta - MS-lääkityshän vähentää valkosoluja, joten eikö lopputulos ole arvattavissa. Suomalaisten mukaan mikroglia muuttuu haitalliseksi. Vai onko se tulehdus haitallinen ja mikroglia ylikuormitettu..
Myöskin aikaisemmin mainittu CD57-testi laskee juuri Natural Killer, NK-solujen, määrää veressä. Immunisuppresiivisesta tilasta kärsivillä luku yleensä alhainen.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.03.2016 - 01:37:51

New Lyme-disease-causing bacteria species discovered

http://www.cdc.gov/media/releases/2016/p0208-lyme-disease.html

The Centers for Disease Control and Prevention, in collaboration with Mayo Clinic and health officials from Minnesota, Wisconsin, and North Dakota, report the discovery of a new species of bacteria (Borrelia mayonii) that causes Lyme disease in people. Until now, Borrelia burgdorferi was the only species believed to cause Lyme disease in North America.

Scientists at the Mayo Clinic in Rochester, Minnesota, first suspected the possibility of new bacteria after lab tests from six people with suspected Lyme disease produced unusual results, according to the findings published today in Lancet Infectious Diseases. Additional genetic testing at the Mayo Clinic and CDC found that the bacteria, provisionally named Borrelia mayonii, is closely related to B. burgdorferi.

“This discovery adds another important piece of information to the complex picture of tickborne diseases in the United States,” said Dr. Jeannine Petersen, microbiologist at the Centers for Disease Control and Prevention.

So far, new Lyme species found only in upper Midwest

Limited information from the first six patients suggests that illness caused by B. mayonii is similar to that caused by B. burgdorferi, but with a few possible differences. Like B. burgdorferi, B. mayonii causes fever, headache, rash, and neck pain in the early stages of infection (days after exposure) and arthritis in later stages of infection (weeks after exposure). Unlike B. burgdorferi, however, B. mayonii is associated with nausea and vomiting, diffuse rashes (rather than a single so-called “bull’s-eye” rash), and a higher concentration of bacteria in the blood.

The researchers believe that, like B. burgdorferi, B. mayonii is transmitted to humans by the bite of an infected blacklegged (or “deer”) tick. B. mayonii has been identified in blacklegged ticks collected in at least two counties in northwestern Wisconsin. The likely exposure sites for the patients described in Lancet Infectious Diseases are in north central Minnesota and western Wisconsin. It is highly likely, however, that infected ticks are found throughout both states.

The newly recognized species was discovered when six of approximately 9,000 samples drawn from residents of Minnesota, Wisconsin, and North Dakota with suspected Lyme disease between 2012 and 2014 were found to contain bacteria that were genetically distinct from B. burgdorferi. Scientists analyzed the DNA sequences of these bacteria and found that they belonged to a previously unrecognized Borrelia species. Blood from two of the patients was also tested by culture at CDC, whereby the organism is grown in the laboratory.

To date, the evidence suggests that the distribution of B. mayonii is limited to the upper midwestern United States. The new species was not identified in any of the approximately 25,000 blood samples from residents of 43 other states with suspected tickborne disease taken during the same period, including states in the Northeast and Mid-Atlantic region where Lyme disease is common.

Current tests, treatments should work for new Lyme strain

Results from the cases described in this report suggest that patients infected with B. mayonii will test positive for Lyme disease with currently available Food and Drug Administration-cleared Lyme disease tests. Specific identification of the organism can be made by using polymerase chain reaction assays (PCR.), which detects the DNA of the Lyme disease bacteria. In some instances, B. mayonii bacteria may also be seen on a blood smear.

The patients described in this report were treated successfully with antibiotics commonly used to treat Lyme disease caused by B. burgdorferi. CDC recommends that health care providers who treat people infected with B. mayonii follow the antibiotic regimen described by the Infectious Diseases Society of America.
*******
CDC kannattaa IDSA:n hoito-ohjeita, jotka pätevät uuteen infektioon, muttei krooniseen (ai niin, eihän sellaista ole olemassakaan). Ja borrelia kantoja on kymmeniä, ellei satoja, niitä kaikkia ei vaan vielä ole löydetty. Suomessahan on ainakin 8 kantaa (kts aikaisemmin esitetty ruotsalaisten tutkimus).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 04.03.2016 - 16:28:45

Sivulla 12 on linkki artikkeliin EBV immuuniterapiatutkimuksesta. Tässä itse tutkimus vuodelta 2014:

Epstein-Barr virus-specific adoptive immunotherapy for progressive multiple sclerosis

http://www.ncbi.nlm.nih.gov/pubmed/24493474

Defective control of Epstein-Barr virus (EBV) infection by cytotoxic CD8(+) T cells might predispose to multiple sclerosis (MS) by allowing EBV-infected autoreactive B cells to accumulate in the central nervous system. We have treated a patient with secondary progressive MS with in vitro-expanded autologous EBV-specific CD8(+) T cells directed against viral latent proteins. This adoptive immunotherapy had no adverse effects and the patient showed clinical improvement with reduced disease activity on magnetic resonance imaging and decreased intrathecal immunoglobulin production. This is the first report of the use of EBV-specific adoptive immunotherapy to treat MS or any other autoimmune disease.
****
Potilaan aivoissa olevien plakkien määrä ja koko vähenivät, ja IgG index pieneni 0.79:stä 0.63:een (normaali <0.70). Jos tarvitaan molemmat, plakkien määrä ja IgG index, määrittelemään sairaus, niin tämä potilas parani..
*****

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.03.2016 - 14:42:26

Immune factor allows viral infections to become chronic

https://www.sciencedaily.com/releases/2016/03/160307113551.htm

March 7, 2016
Many viral diseases tend to become chronic -- including infections with the HI virus. In persons affected, the immune response is not sufficient to eliminate the virus permanently. Scientists at the University of Bonn have now identified an immune factor which is partially responsible for this. Their results give rise to hopes for new therapeutic approaches. The work, which included researchers from the University of Cologne and the Technical University of Munich, is being published in the journal Nature Immunology.

The HI virus triggers the immunodeficiency disease AIDS. The infection has a chronic course -- the immune system is not able to get rid of the pathogen. This is due among other things to the fact that the virus directly attacks and destroys certain immune cells known as helper T cells.

However, many helper T cells are not affected by the virus at all. Nonetheless their function is impaired in the case of AIDS. Normally, helper T cells secrete inflammatory messengers during an infection. As a result of this chemical distress call, killer T cells (the body's own defense troops) become ready to fight and are guided to the site. By contrast, in AIDS and other chronic infections, the helper T cells remain silent. But why is that?

To answer this question, the researchers initially analyzed which genes in the silent helper cells of HIV patients are active. Result: In chronic inflammation, the immune function of the helper T cells is inhibited by various signaling pathways. These signaling pathways in turn are apparently controlled by a single molecule known as tumor necrosis factor (TNF).

This factor appears to be responsible for the weak immune response. "We investigated mice suffering from a chronic viral infection similar to an HIV infection and inactivated the TNF molecule in them," explains Dr. Marc Beyer from Life and Medical Sciences Institute (LIMES) of the University of Bonn. "As a result, the helper T cells worked normally once again. After ten days, the animals had completely eliminated the virus; they were healthy."

Misdirected protective function

Paradoxically, the tumor necrosis factor has exactly the opposite effect in acute viral attacks: It brings the immune system up to full speed and additionally ensures that cells infected with the virus commit suicide. "Therefore, in an acute infection, large quantities of TNF are formed very rapidly," says Dr. Zeinab Abdullah from the Institute of Experimental Immunology at the University Hospital Bonn. "In chronic infections, on the other hand, the body secretes small amounts of TNF over a long period of time. This appears to cause the helper T cells to shut down to some extent."

The researchers suspect that this is a protective mechanism. A prolonged strong immune reaction can in particular destroy healthy tissues as well -- with life-threatening consequences. TNF could act as a type of emergency brake which prevents this. Exactly what the tumor necrosis factor does on a molecular level is still largely unknown. The scientists involved now want to examine this question in detail.

The results may establish new therapeutic options in the medium term. Thus there are drugs which inhibit the effect of TNF. These TNF blockers are used in the treatment of autoimmune diseases such as rheumatism, for example. They are to prevent defense cells from attacking the body itself. "Among other things, we want to investigate what effects these drugs have in rheumatism patients who are additionally suffering from a chronic viral infection," says Marc Beyer.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.03.2016 - 21:14:25

The participation of varicella zoster virus in relapses of multiple sclerosis

http://www.ncbi.nlm.nih.gov/pubmed/24635924

OBJECTIVE:
Recent studies have documented the apparent participation of varicella zoster virus (VZV) in the etiopathogenesis of multiple sclerosis (MS). The present study aimed to corroborate the possible presence of VZV during exacerbations of MS.

DESIGN:
Fifty-three patients with definite MS were included; of them, 31 were studied during the first week of a clinical relapse, whereas 16 were studied during remission; 6 patients with progressive MS were also studied. Genes from 5 herpes viruses: varicella zoster, herpes simplex 1 and 2, Epstein-Barr and herpes 6 were studied by polymerase chain reaction in cerebrospinal fluid and in peripheral blood mononuclear cells (PBMC). As controls 21 patients with inflammatory or functional neurological disorders were included.

RESULTS:
DNA from varicella zoster virus was found in the CSF from all MS patients studied during relapse (100%) and in the PBMC from 28 of them (90%). However, VZV DNA was found in the CSF only in 5 MS patients studied during remission (31%) and in the PBMC from 3 of them (19%). VZV DNA was also found, but in lower amounts, in the CSF (83%) and PBMC (33%) from patients with progressive MS. In contrast, VZV was not found either in CSF or in PBMC from controls. Results from the other herpes viruses tested were similar in MS patients and in controls.

CONCLUSIONS:
Our results corroborate the conspicuous, but ephemeral presence of VZV during relapses of MS and support the idea of VZV involvement in the etiopathogenesis of MS. Recent epidemiological and molecular studies as well as reports of severe VZV infections triggered by specifically induced immunosuppression during therapy of MS give additional support to this potential association.
*******
Vesirokkoviruksesta tuli mieleen antibioottikuurin alussa saadut herxit (Herxheimer reaktio), jolloin sain vesirokkorakkuloita kasvoihin aivan kuin silloin kun sairastin vesirokon. Ne hävisivät päivässä, mutta muistuttivat siitä, että virus säilyy elimistössä ja saattaa "herätä" ärsytettynä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 25.03.2016 - 23:29:01

Paradigm shift: 'We need to study lumps of bacteria'

https://www.sciencedaily.com/releases/2016/03/160323115917.htm

March 23, 2016
New research from the University of Copenhagen reveals that bacteria which agglutinate [combine into a mass] before entering the body are far more resistant than single-celled bacteria. This may be the cause of chronic infections.

Since the discovery of bacteria researchers have primarily studied bacteria as organisms that enter the body individually and only then accumulate or agglutinate, creating what is known as biofilm. However, a new study conducted by researchers at the Faculty of Health and Medical Sciences at the University of Copenhagen, among others, indicates that this view of bacteria needs to be revised.

"Bacteria that enter the bloodstream as biofilm are stronger than bacteria that enter the body separately. This is something we have to pay far greater attention to in trying to prevent infections, for example in connection with operations," says Professor Thomas Bjarnsholt from the Costerton Biofilm Center at the University of Copenhagen. He is the senior researcher behind the study, which is about to be published in the acclaimed online journal mBio.

Biofilm may be the cause of chronic infections. The research team behind the study has examined bacterial environments containing both biofilm and single-celled bacteria.

Here the researchers have found a significantly different type of growth than previously seen. The biofilm takes the main part of the nourishment available and thus outmatches the single-celled bacteria. This makes biofilm the most important player. According to Thomas Bjarnsholt, this is something we need to pay attention, for example when performing operations.

"We have a lot of bacteria on and in our skin which are clustered as biofilm and potentially pathogenic if they enter the skin. In this way biofilm can penetrate or be pushed into the body when the surgeon cuts a hole in the skin containing the biofilm," says Thomas Bjarnsholt.

"Antibiotics are not designed to fight biofilm," says Postdoc Kasper Kragh, who is the main author of the research article. "Often antibiotics are not sufficient to fight chronic infections. This may partly be because antibiotics are to a large extent designed to fight single-celled bacteria, not biofilm."

"We have to take a few steps backwards and, with an open mind, examine how bacteria cause infections and how we can fight them," he adds.

"Hopefully by learning how and when bacteria form biofilm we will be able to find a better way to prevent and treat chronic bacterial infections," concludes Kragh.
*******
Mielenkiintoista, että bakteerit tunkeutuvat elimistöön biofilmin suojaamana. Aikaisemmin oletettiin, että biofilmit kehittyvät suojelemaan bakteereita vasta elimistössä.  Infektiolääkärit ovat puhuneet kauan aikaa biofilmeistä ja yrittäneet löytää niihin tepsiviä lääkkeitä ja luonnonlääkkeitä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Juliane85 Pvm 26.03.2016 - 16:53:34

Erittäin kiinnostava alue. Kun opiskelisin nyt, ”valitsisin” biokemia tai kemian.

”Bakteerien muodostamaa biofilmiä on vaikea tuhota”:
http://www.aka.fi/fi/tietysti/terveys/nyt-pinnalla1/bakteerien-muodostamaa-biofilmia-on-vaikea-tuhota/
”Useimmilla meistä on syöpävirus, mutta vain harvalla se aktivoituu.”
http://www.eskojalkanen.net/media/artikkelit/sy%C3%B6p%C3%A4-aikamme-vitsaus
- Marianna D. :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 01.04.2016 - 20:45:53

Hidden in plain sight: Well-known drug could yield new treatment for herpes viruses

https://www.sciencedaily.com/releases/2016/03/160314161234.htm

Today, there is only one class of antiviral medicines against herpesviruses -- a family of viruses that cause mononucleosis, herpes, and shingles, among other illnesses -- meaning options for treating these infections are limited. If viruses become resistant to these frontline treatments, a growing problem particularly in clinical settings, there are no alternative drugs to serve as backup.

In a search for new drugs to treat viral infections, scientists from the University of Utah School of Medicine found that a medicine routinely used to treat heart failure, spironolactone, has an unexpected ability to block infection by Epstein Barr virus (EBV), a herpesvirus that causes mono and is associated with several human cancers. They find that the drug's antiviral properties stem from its ability to block a key step in viral infection that is common to all herpesviruses. Spironolactone's target is distinct from that of existing drugs, revealing that it could be developed into a new class of anti-herpesvirus drug.

"It's remarkable that a drug we have used safely in the clinic for over 50 years is also an effective EBV inhibitor," says senior author Sankar Swaminathan, M.D., chief of infections disease at University of Utah Health Care and professor of internal medicine. "It goes to show how basic research can reveal things we would never have found otherwise." In collaboration with research assistant professor of internal medicine Dinesh Virma, Ph.D., and Jacob Thompson, he published the study in the Proceedings of the National Academy of Sciences.

Swaminathan's team uncovered spironolactone's antiviral properties in a screen to identify drugs that work through a mechanism that is different from that of existing anti-herpesvirus drugs. Currently available drugs block a middle step of the viral infection cycle by inhibiting virus' ability to replicate DNA. They found that like these drugs, spironolactone can block EBV replication in cells, but it does so by targeting the so-called SM protein, required for a late step in the infection cycle.

Importantly, spironolactone's ability to block viral infection appears to be independent from its ability to treat heart failure. Previous studies showed that the drug treats heart failure through a different, metabolic mechanism. This study demonstrates that a drug similar to spironolactone shares its ability to treat heart failure but not its antiviral properties. Together the results suggest the two mechanisms are separable.

"We think there is great potential to modify this molecule so that it can work as an antiviral without having undesired side effects," explains Swaminathan. Spironolactone could be developed as a new medicine against EBV, a common and dangerous infection among transplant and other immunocompromised patients.

But because all herpesviruses depend on SM-like proteins to spread infection, the work also has broader implications. Spironolactone could be a template for a new class of drug directed against all herpesviruses.

"We have found a new therapeutic target for herpesviruses," says Swaminathan. "We think it can be developed it into a new class of antiviral drugs to help overcome the problem of drug resistant infections."
********
Vaikka EBV-virusta on epäillty MS:n aiheuttajaksi, ei ainakaan minulta virusta tutkittu diagnoosia tehtäessä. Myöhemmin Saksassa arvot olivat 650-700, kun normaali olisi ollut <2.  Siten jo henkilökohtaisista syistä EBV:hen tepsivä lääkitys kiinnostaa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.04.2016 - 20:17:09

Viral triggers of multiple sclerosis

http://www.sciencedirect.com/science/article/pii/S0925443910001225

In 1894, Pierre Marie, a former student of Charcot, argued strongly that infection was the cause of multiple sclerosis. He felt that infectious pathogens, or more likely combined infections, initiate MS [3]: “These gentlemen, are suppositions, and I put them before you without unreasonably insisting upon them. The one point in this discussion which I would fix in your minds is the following fact, a fact, thank God, has been well established, viz., that the cause of insular sclerosis in intimately connected with infectious diseases.” More than a century later, intriguing epidemiological but weak immunological and virological evidence has resulted in a bewildering list of usual suspects including measles, rabies, scrapie-like agent, Carp agent, paramyxovirus, coronavirus, Epstein–Barr virus, herpes zoster, herpes simplex virus, human herpesvirus 6, rubella, mumps, canine distemper, Marek's Semliki forest virus, animal and human retroviruses, and human T-cell lymphoma virus type I. Almost universally, these associations have later not withstood scrutiny. Such unclarity and vagueness spurred the notion that a pathogenic role of infectious agents in MS cannot be established unless experiments provide unequivocal evidence that the postulates of Koch have been met.
Traditionally, microbiologists have used postulates formulated by Robert Koch and Friedrich Loeffler to demonstrate whether a particular microbe causes a specific disease: a microorganism must be (1) found in abundance in all organisms suffering from the disease, but should not be found in healthy animals; a microorganism must be (2) isolated from the host with the disease and grown in pure culture; (3) the specific disease must be reproduced when a pure culture of the microbe is inoculated into a healthy susceptible host; and (4) the pathogen must be recoverable from the experimentally infected host [4]. These postulates retain historical importance, but fulfillment of all four postulates is not required to demonstrate causality, even in infectious diseases.
******
10. Conclusions and future perspectives

The relationship between infections and autoimmune diseases is complex and the mechanisms by which infectious pathogens could trigger MS are likely dynamic, i.e., they might change over time and not be mutually exclusive. Epidemiological observations indicate that viral infections could contribute to MS development not only as triggers of disease exacerbations but also as etiological agents, i.e., long before the disease becomes clinically apparent. The two- to three-folds increased risk of developing MS among individuals with history of IM compared with subjects who acquired EBV without symptoms, the almost universal seropositivity for EBV in adults and children with MS, and the steep and monotonic increase in MS risk with increasing titers of antibodies to EBV in apparently healthy adults could suggest that EBV infection is causally linked to MS development. The mechanisms responsible for this association are far from understood. Moreover, the incidence of IM in Western countries (≥ 5%) [64] exceeds the prevalence of MS in comparable populations (0.1%) by far (more than 50-fold) suggesting that yet unidentified genetic and/or additional environmental factors determine whether symptomatic EBV infection indeed predisposes to MS.

Although one particular MS-causing agent might still be discovered, current data suggest that multiple infections along with noninfectious environmental factors trigger the development of MS. These factors are likely ubiquitous, i.e., highly prevalent in the general population, and they require a permissive genetic background that predisposes for MS development. Future studies investigating infectious pathogens in a complex and heterogenous disease such as MS will benefit from careful and detailed clinical, pathological, and neuroimaging-based patient characterizations and from reproducibility in different study populations. In addition, novel humanized animal models of autoimmune diseases that are simultaneously permissive for viral pathogens which usually infect only humans [104] and [105] should allow investigation of specific aspects of host–pathogen interactions during autoimmune CNS inflammation in vivo. The integration of these data might eventually allow us to better define the role of viruses in the etiology and pathogenesis of MS and how virus–host interactions could be targeted for MS therapy.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.04.2016 - 15:07:23

Zika virus may now be tied to another brain disease

https://www.sciencedaily.com/releases/2016/04/160411082335.htm

April 11, 2016

The Zika virus may be associated with an autoimmune disorder that attacks the brain's myelin similar to multiple sclerosis, according to a small study that is being released today and will be presented at the American Academy of Neurology's 68th Annual Meeting in Vancouver, Canada, April 15 to 21, 2016.

"Though our study is small, it may provide evidence that in this case the virus has different effects on the brain than those identified in current studies," said study author Maria Lucia Brito Ferreira, MD, with Restoration Hospital in Recife, Brazil. "Much more research will need to be done to explore whether there is a causal link between Zika and these brain problems."

For the study, researchers followed people who came to the hospital in Recife from December 2014 to June 2015 with symptoms compatible with arboviruses, the family of viruses that includes Zika, dengue and chikungunya. Six people then developed neurologic symptoms that were consistent with autoimmune disorders and underwent exams and blood tests. The authors saw 151 cases with neurological manifestations during a period of December 2014 to December 2015.

All of the people came to the hospital with fever followed by a rash. Some also had severe itching, muscle and joint pain and red eyes. The neurologic symptoms started right away for some people and up to 15 days later for others.

Of the six people who had neurologic problems, two of the people developed acute disseminated encephalomyelitis (ADEM), an attack of swelling of the brain and spinal cord that attacks the myelin, which is the coating around nerve fibers. In both cases, brain scans showed signs of damage to the brain's white matter. Unlike MS, acute disseminated encephalomyelitis usually consists of a single attack that most people recover from within six months. In some cases, the disease can reoccur. Four of the people developed Guillain-Barré syndrome (GBS), a syndrome that involves myelin of the peripheral nervous system and has a previously reported association with the Zika virus.

When they were discharged from the hospital, five of the six people still had problems with motor functioning. One person had vision problems and one had problems with memory and thinking skills.

Tests showed that the participants all had Zika virus. Tests for dengue and chikungunya were negative.

"This doesn't mean that all people infected with Zika will experience these brain problems. Of those who have nervous system problems, most do not have brain symptoms," said Ferreira. "However, our study may shed light on possible lingering effects the virus may be associated with in the brain."

"At present, it does not seem that ADEM cases are occurring at a similarly high incidence as the GBS cases, but these findings from Brazil suggest that clinicians should be vigilant for the possible occurrence of ADEM and other immune-mediated illnesses of the central nervous system," said James Sejvar, MD, with the Centers for Disease Control and Prevention in Atlanta and a member of the American Academy of Neurology. "Of course, the remaining question is 'why'-why does Zika virus appear to have this strong association with GBS and potentially other immune/inflammatory diseases of the nervous system? Hopefully, ongoing investigations of Zika virus and immune-mediated neurologic disease will shed additional light on this important question."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.04.2016 - 15:20:47

Kirjoitin aikaisemmin: "Vaikka EBV-virusta on epäillty MS:n aiheuttajaksi, ei ainakaan minulta virusta tutkittu diagnoosia tehtäessä. Myöhemmin Saksassa arvot olivat 650-700, kun normaali olisi ollut <2.  Siten jo henkilökohtaisista syistä EBV:hen tepsivä lääkitys kiinnostaa."

Tuli pieni kirjoitusvirhe. Oikeasti normaali arvo olisi ollut <20.

Mielenkiintoista kohdallani on myös se, että tänä vuonna ulkomailla otetussa likvorissa IgG index pieneni siitä mikä se oli diagnoosia tehtäessä 2008. Se puolittui, mutta on vielä korkeampii kuin normaali <0.60. Olen kuulut neurologeilta, ettei MS-taudissa IgG index muutu. Mutta koska se on vielä normaalin yläpuolella, on minulla siis MS.  Infektiolääkäreiden mielipide olisi varmaan erilainen, onhan minulla vielä aktiivisia infektioita, ennen kaikkea produktiivinen EBV. Faktat eivät muutu, mutta tulkinnat näyttävät muutuvan riippuen siitä keltä kysyy..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja Caroline80 Pvm 16.04.2016 - 12:21:25


HopeSprings 15.04.2016 - 15:20:47:
Faktat eivät muutu, mutta tulkinnat näyttävät muutuvan riippuen siitä keltä kysyy..
Mulla taas on joko MS tai Transverse myelitis http://www.mayoclinic.org/diseases-conditions/transverse-myelitis/basics/definition/con-20028884
Oireeni eivät puhtaasti sovi kumpaankaan, totesi jopa eräs neurologikin. En siitä eroon pääse.  :)

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.05.2016 - 23:35:01

Research Breathes New Life into Theory Supporting Possible Viral Etiology of Multiple Sclerosis

http://www.hcplive.com/journals/targeted-therapies-multiple-sclerosis/2014/october-2014/research-breathes-new-life-into-theory-supporting-possible-viral-etiology-of-multiple-sclerosis-

Several clusters of multiple sclerosis (MS) have been identified around the world, some of which have occurred in association with exposure to infectious agents, while others have suggested an influence of environmental toxins, such as heavy metals.1,2

Although MS is likely a result of multifactorial influences, there is some evidence that viruses play a role in the disease. For example, in the Faroe Islands, which lie northwest of Scotland and halfway between Iceland and Norway, native residents began to develop MS starting in 1943 after British occupation of the island during World War II. Although no virus was ever identified, John F. Kurtzke, MD, creator of the Kurtzke Expanded Disability Status Scale, said he believes the Faroe Island cluster suggests a viral etiology of MS.3-5

In a scientific paper published in 2013 in the journal Brain, Kurzke wrote, “As of 1999, we had found 189 suspected cases, and we had agreed that 83 of them were examples of MS… There is no evidence that MS occurred among native-born resident Faroese before July 1943, when symptoms began in one patient… The abrupt onset indicates that the disorder had to have been introduced into the islands at a single time.”
*****
In 1996, Gold noticed that one of his patients who had both MS and HIV experienced a reduction in symptoms after starting antiretroviral therapy. Over 12 years of therapy, the patient continued to experience few symptoms of MS. Based on this case, Gold hypothesized that the antiretroviral medication, the immunosuppression associated with HIV, or both, might slow the progression of MS.
*****
In a secondary analysis, investigators analyzed MS cases that were identified in patients 1 year or more after they acquired HIV. A total of 3 such cases were identified. Although this number was smaller than the expected number of 13 cases of HIV that would be expected to occur in a similar population without HIV, the result was no longer statistically significant (hazard ratio: 0.25; 95% CI: 0.07-0.65). The lack of statistical significance may be a result of the small number of MS cases observed in patients with HIV.

According to Gold, who presented his research in MS at the Barts and London School of Medicine and Dentistry on MS Research Day in 2013, “As a result of these observations, we are now launching a unique clinical trial … the INSPIRE trial.” This trial will begin with a pilot phase in which patients with RRMS will receive raltegravir over a 3-month baseline period and a 3-month treatment period. Patients will be evaluated for the primary outcome of new gadolinium-enhancing lesions.7,8

Gold compares the pathophysiology of MS with a car lying in pieces: “It’s very complicated…all over the world there are researchers working on little bits to do with MS. Some are working on vitamin deficiencies, and others are working on Epstein-Barr virus (EBV), and others are working on hypoxia, but nobody has been able to put all these pieces together and drive it away.”

The pathophysiology of MS is very complex and the involvement of viruses is far from certain. For now, the use of antiviral agents in patients with MS should be limited to the clinical trials setting.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.05.2016 - 23:43:47

Scientists discover way to improve effectiveness of antibiotics

https://www.sciencedaily.com/releases/2016/03/160331082641.htm

Scientists at Nanyang Technological University, Singapore (NTU Singapore) have discovered that antibiotics can continue to be effective if bacteria's cell-to-cell communication and ability to latch on to each other are disrupted.

This research breakthrough is a major step forward in tackling the growing concern of antibiotic resistance, opening up new treatment options for doctors to help patients fight against chronic and persistent bacterial infections.

The study, led by Assistant Professor Yang Liang from the Singapore Centre for Environmental Life Sciences (SCELSE) at NTU, found that a community of bacteria, known as biofilm, can put up a strong line of defence to resist antibiotics. The NTU team has successfully demonstrated how biofilms can be disrupted to let antibiotics continue their good work.

The research was published recently in Nature Communications, am academic journal by the Nature Publishing Group.

"Many types of bacteria that used to be easily killed by antibiotics have started to develop antibiotic resistance or tolerance, either through acquiring the antibiotic resistant genes or by forming biofilms," said Asst Prof Yang, who also teaches at NTU's School of Biological Sciences.

"The US Center for Disease Control estimates that over 60 per cent of all bacterial infections are related to biofilms. Our study has shown that by disrupting the cell-to-cell communication between bacteria and their ability to latch on to each other, we can compromise the biofilms, leaving the bacteria vulnerable and easily killed by antibiotics."

Bacterial resistance to antibiotics is rapidly growing world-wide and this puts at risk the ability to treat common infections in the community and hospitals.

The World Health Organisation states on its factsheet on Antimicrobial resistance that "without urgent, coordinated action, the world is heading towards a post-antibiotic era, in which common infections and minor injuries, which have been treatable for decades, can once again kill."

Associate Professor Kevin Pethe, an expert in antibiotic development and infectious diseases from NTU's Lee Kong Chian School of Medicine, said that this discovery may yield new treatment options that doctors can employ against chronic and persistent bacterial infections.

"Being able to disable biofilms and its protective benefits for the bacteria is a big step towards tackling the growing concern of antibiotic resistance," said Assoc Prof Pethe.

"While the scientific community is developing new types of antibiotics and antimicrobial treatments, this discovery may help to buy time by improving the effectiveness of older drugs."

How the discovery was made

Asst Prof Yang's team discovered the mechanisms of how bacteria are able to tolerate antibiotics by using a common bacterium Pseudomonas aeruginosa.

The bacteria were allowed to form a wall of biofilm in a microfluidic system. An antibiotic was then introduced. A large portion of the bacterial cells were killed by the antibiotic, leaving only a small fraction of antibiotic-tolerant cells. However, these cells were able to reproduce rapidly and dominate the community.

The scientists then used an FDA-approved drug that disrupts cell-to-cell communication (known as quorum sensing) and 'velcro'-like cells that can move and "stick" to each other. This drug was added to the antibiotic and together they managed to kill all the bacterial cells.

The same tests were then performed on mice with infected implants. It was found that only mice treated with a combination of anti-biofilm compound and antibiotics had their infections completely eradicated.

Interdisciplinary research

This discovery breakthrough was made possible through an interdisciplinary approach, where experts from three different fields -- microbiology ecology, systems biology and chemical biology -- came together to tackle the problem.

The NTU research team included proteomics expert Assoc Prof Newman Sze Siu Kwan from NTU's School of Biological Sciences. Proteomics was the key method used to discover chemical signals that bacterial cells in the biofilm use to communicate with each other.

Another researcher in the team is Professor Michael Givskov, a world-leading scientist in the area of biofilm research and bacterial cell-to-cell communication at SCELSE. Together, the team found that traditional methods of isolating the bacteria from the biofilm for observation did not work, as the bacteria behave differently after being isolated from the biofilm.

This study, supported by the Ministry of Education Academic Research Fund, took Asst Prof Yang and his team four years to complete. Moving forward, they will seek more ways to improve efficiency of antibiotics for persistent infections.

"What we hope to do is to develop new compounds that are able to better target biofilms. This will help existing drugs perform better at overcoming biofilm infections, which is commonly seen in cases of patients with artificial implants and chronic wounds, as they have very limited effective treatment options that are effective," said Asst Prof Yang.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja elisabet Pvm 07.05.2016 - 09:50:07

Hei,
en ole lukenut kaikkia viestejä tästä ketjusta, mutta jos ms:n taustalla on jatkuvasti kytevä bakteeri-infektio, niin eikö sen pitäisi ainakin ajoittain näkyä kohonneena crp-arvona?

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.05.2016 - 19:03:29

En osaa vastaa edelliseen kysymykseen, mutta katsoin kuinka usein itselläni CRP arvot on mitattu. Ei kovinkaan usein viimeisen 15 vuoden aikana. Vaikka diagnoosivuotena arvo oli normaalia korkeampi, samoin seuraavana vuonna, sitä ei minulle silloin mainittu. Enkä tiedä oliko lääkärille mitään merkitystä ko arvoilla. Terveyskirjaston mukaan: "Valitettavasti CRP ei ole kaikissa tilanteissa käyttökelpoinen bakteeri- ja virustulehdusten erottajana. Tällaisia ovat mm. pienelle alueelle rajoittuneet tulehdukset kuten välikorvan tulehdus ja virtsarakon tulehdus. Laskon tapaan CRP-arvo voi hieman suurentua monissa epämääräisissä tilanteissa ilman, että kyseessä on hoitoa vaativa sairaus." Ei siis kaikkein tarkin mittari. CRP-arvo voi nousta akuutissa tai kroonisessa bakteeri tai virusinfektiossa tai tulehduksessa ja sitä voidaan käyttää myös reuman tai autoimmuunisairauksien lääkityksen tehokkuuden seurannassa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.05.2016 - 16:26:17

The Correlation between the Virus- and Brain Antigen-Specific B Cell Response in the Blood of Patients with Multiple Sclerosis

Viruses. Published: 23 April 2016

Abstract: There is a largely divergent body of literature regarding the relationship between Epstein-Barr virus (EBV) infection and brain inflammation in multiple sclerosis (MS). Here, we tested MS patients during relapse (n = 11) and in remission (n = 19) in addition to n = 22 healthy controls to study the correlation between the EBV- and brain-specific B cell response in the blood by enzyme-linked immunospot (ELISPOT) and enzyme-linked immunosorbent assay (ELISA).
Cytomegalovirus (CMV) was used as a control antigen tested in n = 16 MS patients during relapse and in n = 35 patients in remission. Over the course of the study, n = 16 patients were untreated, while n = 33 patients received immunomodulatory therapy. The data show that there was a moderate correlation between the frequencies of EBV- and brain-reactive B cells in MS patients in remission. In addition we could detect a correlation between the B cell response to EBV and disease activity.
There was no evidence of an EBV reactivation. Interestingly, there was also a correlation between the frequencies of CMV- and brain-specific B cells in MS patients experiencing an acute relapse and an elevated B cell response to CMV was associated with higher disease activity. The trend remained when excluding seronegative subjects but was non-significant. These data underline that viral infections might impact the immunopathology of MS, but the exact link between the two entities remains subject of controversy.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.06.2016 - 23:50:40

Scientists unpack how Toxoplasma infection is linked to neurodegenerative disease
New research focused on glutamate, the most important neurotransmitter in the brain

https://www.sciencedaily.com/releases/2016/06/160609150841.htm

June 9, 2016
Toxoplasma gondii, a protozoan parasite about five microns long, infects a third of the world's population. Ingested via undercooked meat or unwashed vegetables, the parasite infects 15-30 percent of the US population. In France and Brazil, up to 80 percent of the population has the infection.

Particularly dangerous during pregnancy -- infection in pregnant women can cause serious congenital defects and even death of the fetus -- this chronic infection has two components: the unicellular parasite, and inflammation of tissues it causes.

Working on mice (like all mammals, a natural host for this parasite), a University of California, Riverside team of biomedical scientists reports in the journal PLOS Pathogens that Toxoplasma infection leads to a disruption of neurotransmitters in the brain and postulates that it triggers neurological disease in those already predisposed to such a disease.

They note that Toxoplasma infection leads to a significant increase in glutamate -- the primary and most important neurotransmitter in the brain, which transmits excitatory signals between neurons. This glutamate increase is "extracellular," meaning outside the cell, and is strictly controlled by specialized cells in the central nervous system (brain and spinal cord), called astrocytes. Glutamate buildup is seen in traumatic brain injury as well as highly pathological and neurodegenerating diseases such as epilepsy, multiple sclerosis and amyotrophic lateral sclerosis (ALS).

One role astrocytes play is to remove extracellular glutamate, lest it increase to pathological levels that could damage neurons. This is primarily achieved using a glutamate transporter, called GLT-1, tasked with regulating extracellular glutamate. GLT-1 soaks up glutamate released by neurons and converts it back into the safer substance glutamine, which can then be used by cells for energy.

"When a neuron fires it releases glutamate into the space between itself and a nearby neuron," explained lead researcher Emma H. Wilson, an associate professor in the Division of Biomedical Sciences in the School of Medicine, who has worked on toxoplasmosis for more than 15 years. "The nearby neuron detects this glutamate which triggers a firing of the neuron. If the glutamate isn't cleared by GLT-1 then the neurons can't fire properly the next time and they start to die."

Wilson and her team found that during toxoplasma infection, astrocytes swell and are not able to regulate extracellular glutamate concentrations. Further, GLT-1 is not expressed properly. This leads to a buildup of the glutamate released from neurons and the neurons misfire.

"These results suggest that in contrast to assuming chronic Toxoplasma infection as quiescent and benign, we should be aware of the potential risk to normal neurological pathways and changes in brain chemistry," Wilson said.

When the researchers treated the infected mice with ceftriaxone, an antibiotic known to produce beneficial results in mouse models of ALS as well as neuroprotection in a variety of central nervous system injuries, they found that GLT-1 was upregulated. This restoration of GLT-1 expression significantly reduced extracellular glutamate from pathological to normal concentrations, returning neuronal function to a normal state.

"We have shown for the first time the direct disruption of a major neurotransmitter in the brain resulting from this infection," Wilson said. "More direct and mechanistic research needs to be performed to understand the realities of this very common pathogen."

Next, Wilson and her colleagues will research what initiates the downregulation of GLT-1 during chronic Toxoplasma infection.

"Despite the importance of this transporter to maintaining glutamate homeostasis, there is little understanding of the mechanism that governs its expression," Wilson said. "We'd like to know how cells, including peripheral immune cells, control the parasite in the brain. Toxoplasma infection results in the lifelong presence of parasitic cysts within the neurons in the brain. We'd like to further develop a project focused on killing the cysts, which is where the parasite hides from the immune response for the rest of the infected person's life. Getting rid of the cyst removes the threat of reactivation of the parasite and the risk of encephalitis while also allowing us to minimize chronic inflammation in the brain."

Mysteriously, the parasite that causes toxoplasmosis can sexually reproduce only in cats. Asexually, it can replicate and live in any mammalian cell that has a nucleus. Indeed, the parasite has been found in every mammal ever tested.

Post-infection, a competent immune system is needed to prevent parasite reactivation and encephalitis. Infected people with compromised immune systems need to be on prophylactic drugs for life. Otherwise they are at risk of cyst reactivation and death. The parasite lives in areas of the brain that have the potential to disrupt certain behaviors such as risk-seeking (infected mice will run toward cat urine instead of away from it).

The parasite is not as latent or dormant as researchers once thought. Cases of congenital infection and retinal toxoplasmosis are on the rise (the brain and retina are closely linked). People who have schizophrenia are more likely to be infected with Toxoplasma. Infection shows some correlation with Alzheimer's disease, Parkinson's disease and epilepsy.

Nevertheless, Wilson notes that infection is no cause for major worry.

"We have been living with this parasite for a long time," she said. "It does not want to kill its host and lose its home. The best way to prevent infection is to cook your meat and wash your hands and vegetables. And if you are pregnant, don't change the cat litter."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 11.06.2016 - 23:56:11

Nerve-insulating cells more diverse than previously thought

https://www.sciencedaily.com/releases/2016/06/160609150823.htm

June 9, 2016
Oligodendrocytes, a type of brain cell that plays a crucial role in diseases such as multiple sclerosis, are more diverse than have previously been thought, according to a new study by researchers at Karolinska Institutet in Sweden. The findings, published in the journal Science, will help increase our understanding of diseases in which these cells are affected and possibly provide clues to future treatment strategies.

In multiple sclerosis and similar neurological diseases, the electrical signals in the brain propagate more slowly. The reduced speed of information flow contributes to symptoms such as numbness, balance and walking difficulties and blurred vision. Multiple sclerosis is characterised by the loss of myelin, a protective sheath that insulates nerve cells and allows rapid transmission of electrical signals in the brain. Myelin is produced by a specialized cell type, the oligodendrocyte. While oligodendrocytes have thus far been thought to be a homogenous population, a different view emerges from the current study.

The researchers, led by Dr. Gonçalo Castelo-Branco and Dr. Sten Linnarsson, used the recently developed technique of single cell RNA-sequencing. This method allows investigators to get a snapshot of gene activity in individual cells. In this way, they could reveal differences between cells that may not be visible using classical methods. The researchers analysed more than five thousand oligodendrocytes from several regions of the brain and spinal cord in adolescent and adult mice, which allowed them to see the diversity of these cells with unprecedented detail and clarity.

"We uncovered an unexpected diversity within the oligodendrocyte population," says Sten Linnarsson from the Department of Medical Biochemistry and Biophysics. "In this study, we have identified 12 subclasses of oligodendrocytes and a novel cell distinct from oligodendrocytes residing in the blood vessels"

They found that the initial stages of maturation in oligodendrocyte development were similar across the central nerve system in juvenile mice, whereas different subsets of mature oligodendrocytes were enriched in specific regions in adult brains.

"The uncovering of this unexpected oligodendrocyte diversity might bring new insights on mechanisms of degeneration and regeneration of diseases where myelin is lost, such as multiple sclerosis," says Gonçalo Castelo-Branco at the same department.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.06.2016 - 00:02:27

New biomarker for nerve cell damage
Blood test could help monitor treatment response

https://www.sciencedaily.com/releases/2016/06/160609134255.htm

June 9, 2016
Scientists at the German Center for Neurodegenerative Diseases, the Hertie Institute for Clinical Brain Research and the University of Tübingen have identified proteins in the blood and cerebrospinal fluid that reflect nerve cell damage. The results of the study, published in the journal Neuron, suggest that the concentration of these 'neurofilament light chain proteins' could provide information about the progression of neurodegenerative diseases and the effects of treatment. Such a biomarker would be valuable for developing therapies.

"The results of our research indicate that disease progression can be tracked by monitoring the concentration of neurofilament light chain proteins. According to our study this is possible in both animal models and humans," says Mathias Jucker, who leads a research group at the DZNE's Tübingen site and is also a director of the Hertie Institute. "We have also found that the measured levels react sensitively when pathological hallmarks in the brain are influenced experimentally. It may thus be possible to evaluate the effect of a treatment by measuring the concentration of light neurofilaments, both in preclinical laboratory studies and in clinical trials. Such a biomarker would be a major benefit for developing treatments."

Parts of the cytoskeleton

"Neurofilament light chain proteins" are parts of the cytoskeleton that gives nerve cells shape and stability. These thread-like molecules are therefore mainly located inside cells, but may be released due to damage.

Professor Jucker and his colleagues -- including Mehtap Bacioglu, first author of the current publication -- took this known fact as the basis for investigating the concentration of neurofilament light chains proteins in the blood and cerebrospinal fluid (liquor). For this, they looked at mice that showed the typical features of neurodegenerative diseases, namely deposits of aggregated "alpha-synuclein," "tau" or "beta-amyloid" protein in their brains. Such deposits are associated with nerve cell damage. Besides, the scientists examined biomaterials from patients with Alzheimer's, Parkinson's and other neurodegenerative diseases.

Sensitive measurements

In mice, a close association was found between the concentration of neurofilament proteins in the liquor and blood. Moreover, the more advanced the brain damage, the higher the measured levels. If the neurological lesions were induced or inhibited protein levels increased or dropped accordingly. In patients, blood and liquor readings also correlated strongly. Furthermore, levels were higher than in healthy people.

A tool for developing treatments

"The special potential of this biomarker comes from the fact that it is significant in both animals and humans. Therefore, the results from animal models can be translated into clinical studies and their findings may be directly compared. This is critical for the development of new treatments," says Jucker. "What's more, we don't have to rely on withdrawals of liquor. The lumbar puncture required to obtain cerebrospinal fluid can be stressful for the person undergoing it. Our study shows that blood levels also provide information about neurodegeneration in the brain, because the concentrations of the neurofilaments in the blood and cerebrospinal fluid are closely coupled. A simple blood sample may therefore be sufficient when performing clinical studies on humans."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.06.2016 - 00:11:52

Epstein-Barr virus and multiple sclerosis. From evidence to therapeutic strategies.

http://www.ncbi.nlm.nih.gov/pubmed/26810546

Abstract

Multiple sclerosis is caused by a complex interaction between genetic predisposition and environmental factors. Epstein-Barr virus (EBV) is an environmental risk factor that is strongly related to multiple sclerosis (MS), since EBV seropositivity is linked to a significant risk of developing MS. EBV may be involved in the pathogenesis of the disease and it is possibly a prerequisite for the development of MS. EBV infection persists in B-cells during the lifetime of the host and can modulate their function. In addition, MS patients might have a deficient capacity to eliminate latent EBV infection in the central nervous system and this would promote the accumulation of infected B cells. Several mechanisms of pathogenesis, including a direct and indirect function of infected B cells, have been postulated in inflammation and neurodegeneration. A relationship between EBV and human endogenous retroviruses in the pathogenesis of MS has also been reported. If EBV is important in the pathogenesis of MS, different therapeutic strategies seem possible for MS treatment.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.07.2016 - 23:55:53

The Lyme disease debate: Can the condition be chronic?

http://www.foxnews.com/health/2016/05/25/lyme-disease-debate-can-condition-be-chronic.html

With 300,000 new cases of Lyme disease in the U.S. each year, it's no surprise that the tick-borne illness has been a hotly debated topic among medical experts.

Dr. Manny recently sat down with New York Times best selling author of “Why Can’t I Get Better? Solving the Mystery of Lyme and Chronic Disease” to sort out the facts.
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Lyme is known as "The Great Imitator." And it's true, it's very difficult for doctors sometimes to make the diagnosis because as you said, it imitates chronic fatigue syndrome, fibromyalgia, autoimmune diseases like MS (multiple sclerosis). I have a lot of MS patients coming in [who] have Lyme. It can mimic arthritis, ALS, psychiatric [disorders].
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6 percent of the Chinese population had been diagnosed with Lyme.[eli noin 83 milj.?!]
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Fox News ei olisi minun kanavavalinta, mutta se, että konservatiivinen ilmaston muutoksen kieltävä kanava pohtii sitä, voiko borrelioosi olla krooninen sairaus, on hieman yllättävä. Ja Suomessahan ei esiinny kroonista borrelioosia..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.07.2016 - 20:37:31

Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain

http://jem.rupress.org/content/204/12/2899.short

2007
Epstein-Barr virus (EBV), a ubiquitous B-lymphotropic herpesvirus, has been associated with multiple sclerosis (MS), an inflammatory disease of the central nervous system (CNS), but direct proof of its involvement in the disease is still missing. To test the idea that MS might result from perturbed EBV infection in the CNS, we investigated expression of EBV markers in postmortem brain tissue from MS cases with different clinical courses. Contrary to previous studies, we found evidence of EBV infection in a substantial proportion of brain-infiltrating B cells and plasma cells in nearly 100% of the MS cases examined (21 of 22), but not in other inflammatory neurological diseases. Ectopic B cell follicles forming in the cerebral meninges of some cases with secondary progressive MS were identified as major sites of EBV persistence. Expression of viral latent proteins was regularly observed in MS brains, whereas viral reactivation appeared restricted to ectopic B cell follicles and acute lesions. Activation of CD8+ T cells with signs of cytotoxicity toward plasma cells was also noted at sites of major accumulations of EBV-infected cells. Whether homing of EBV-infected B cells to the CNS is a primary event in MS development or the consequence of a still unknown disease-related process, we interpret these findings as evidence that EBV persistence and reactivation in the CNS play an important role in MS immunopathology.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.08.2016 - 15:34:26

EBNA1 antigen-specific CD8+ T cells in cerebrospinal fluid of patients with multiple sclerosis

http://www.jni-journal.com/article/S0165-5728(16)30044-3/abstract?cc=y=

May 15, 2016

Highlights

   •CD8+ T cells specific for one EBNA1-derived epitope (HPVGEADYFEY) were detected in blood and CSF of MS patients.
   •Their frequency did not differ significantly in blood nor CSF in MS compared to other inflammatory neurological diseases.

   •Frequency of HPVGEADYFEY-specific CD8+ T cells was consistently higher in CSF compared to blood regardless of diagnosis.

Abstract

Epidemiological data suggests that Epstein–Barr virus may be involved in the pathogenesis of Multiple Sclerosis (MS). We aimed to determine the frequency of CD8+ T cells specific for one EBNA1-derived epitope (HPVGEADYFEY) in cerebrospinal fluid (CSF) and blood of patients with MS and other inflammatory neurological diseases (OIND). The frequency of specific CD8+ T cells was assessed by HLA-class-I-binding pentamers restricted to HLA-B35. The frequency of HPVGEADYFEY-specific CD8+ T cells did neither differ significantly in blood nor CSF in MS compared to OIND, but was consistently higher in CSF compared to blood regardless of diagnosis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.08.2016 - 15:44:12

Big step towards cure for HIV and other lifelong viral infections

https://www.sciencedaily.com/releases/2016/08/160803214858.htm

August 3, 2016

New research has taken us a step closer to finding a cure for human immunodeficiency virus (HIV), as well as other infections including the glandular fever virus, which is associated with the development of lymphoma. Some infections, such as HIV, cannot be cured with antiviral therapy because the virus effectively hides from the immune system.

An international team of scientists, led by Monash Biomedicine Discovery Institute researcher Dr Di Yu, and Dr Axel Kallies from the Walter and Eliza Hall Institute, have discovered that killer T cells, a specialised type of white blood cells, can find these "hidden" infected cells in tissue and destroy them. This discovery, published today in Nature Immunology, could provide new insights into finding a lifelong cure for chronic infections such as HIV.

Dr Yu said this type of killer T cell was naturally found in the body during infection, but their numbers and killing function needed to be boosted to allow them to eradicate chronic infections.

"We've shown for the first time that there are specialised killer T cells that can migrate into a part of the lymphoid tissue and control hidden infection," Dr Yu said.

Although treatments for HIV with antiretroviral drugs are highly effective, treatment is lifelong and there is no cure. Other infections such as Epstein-Barr virus, the cause of glandular fever, may also hide and persist for many years, but become active when the immune system is compromised.

The researchers discovered that these specialised killer T cells, called follicular cytotoxic T cells, can enter hiding spots inside lymphoid tissue, where viruses can hide on treatment. These hiding spots are called B cell follicles.

Dr Yu's PhD student Mr Yew Ann Leong, who conducted a large portion of the research, also from the Monash Biomedicine Discovery Institute, said that although some infections including HIV could hide within B cell follicles, these killer T cells are specialised to eradicate this hidden virus pool.

"This discovery will help us to design new therapies that could eventually treat many different infections, including HIV," Mr Leong said.

Dr Axel Kallies, fellow lead researcher on the study from the Walter and Eliza Hall Institute, said he was excited to have co-led this exciting piece of international research.

"The potential of this discovery is huge. It helps us to understand how we may be able to treat diseases that affect the immune system itself, such as HIV or B cell lymphoma," Dr Kallies said.

Professor Sharon Lewin, the Director of the Peter Doherty Institute for Infection and Immunity, a joint venture of the University of Melbourne and Royal Melbourne Hospital and a co-author on the study, said there were a few ways this discovery could be translated into a treatment for people with chronic infections.

"We could potentially transfer these specialised super potent killer T cells into patients, or we could treat patients with proteins that can drag these specialised killer T-cells into the right spots, specifically to the hot spots where HIV can hide on antiviral treatment," Professor Lewin said.

Dr Yu said he hoped human trials of such treatments would begin within the next five years.

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Wikipedia: Follicular B helper T cells (also known as just follicular helper T cells or TFH), are antigen-experienced CD4+ T cells found in the periphery within B cell follicles of secondary lymphoid organs such as lymph nodes, spleens and Peyer's patches, and are identified by their constitutive expression of the B cell follicle homing receptor CXCR5.[1] Upon cellular interaction and cross-signaling with their cognate follicular (Fo B) B cells, TFH cells trigger the formation and maintenance of germinal centers through the expression of CD40 ligand (CD40L) and the secretion of IL-21[2] and IL-4.[3] TFH cells also migrate into these seeded germinal centers, predominantly composed of rapidly dividing and mutating B cells. Within germinal centers, TFH cells play a critical role in mediating the selection and survival of B cells that go on to differentiate either into special plasma cells capable of producing high affinity antibodies against foreign antigen, and memory B cells capable of quick immune re-activation in the future if ever the same antigen is re-encountered. TFH cells are also thought to facilitate negative selection of potentially autoimmune-causing mutated B cells in the germinal center. However, the biomechanisms by which TFH cells mediate germinal center tolerance are yet to be fully understood.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 20.08.2016 - 20:57:43

Researchers find herpes strain in the nervous system

https://www.sciencedaily.com/releases/2016/08/160819153258.htm

There are a couple strains of herpes so common that researchers estimate 90% of the human population have them. These strains, human herpes 6 and human herpes 7, usually do not cause severe symptoms when people acquire them. But researchers know that under certain circumstances, dormant herpes viruses in the body can unexpectedly come roaring back and cause complications not typically associated with herpes virus.
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Dormant viruses can ramp up again

When a person acquires a herpes virus, the body initially mounts a response. However, some of the virus stays in the body and lies dormant.

"In a healthy child who gets chicken pox, a virus from the herpes family, the body fights the virus and the child gets better," Barcy said. "But dormant chicken pox virus remains in the body, and later in life something can trigger it and the person can develop shingles."

Researchers know when a person needs a bone marrow transplant, one potential dangerous side effect is encephalitis, or inflammation of the brain. When doctors test patients who develop encephalitis after bone marrow transplants, they often find that herpes 6b, a common herpes strain similar to herpes 7, has reactivated in the patient's body and is causing the encephalitis.

"It's a classic case where a person has been infected with a common, benign herpes strain and never had trouble with it before," Barcy said. "But then the person needs a bone marrow transplant for another medical condition, like leukemia. All of a sudden there is a risk that the herpes will reactivate after the bone marrow transplant and cause encephalitis."

Barcy says more research is needed to determine if and how herpes 7 can cause damage when reactivated. But researchers have found it to be a recurring theme in herpes viruses: Under normal circumstances most herpes viruses are benign, but if a person's immune system become vulnerable, the herpes viruses can create a deadly problem.

Understanding effects on nervous system


Barcy's next step is to understand what the herpes 7 virus could be doing in the nervous system. He wants to study if herpes 7 may interfere with myelin, a substance that surrounds and protects nerve cells.

Other viruses have been known to trigger nerve diseases by interfering with myelin. Zika virus has been associated with Guillain-Barre Syndrome, in which the body's immune system attacks part of the nervous system, decreases myelin and can lead to paralysis.

"More and more evidence is building that herpes viruses may use the nervous system as a highway to spread and could be interfering with normal nerve function under certain circumstances," Barcy said. "Our next step in the research is to investigate this possible link."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.09.2016 - 19:26:38

Lyme Bacteria Hides Inside Parasitic Worms, Causing Chronic Brain Diseases

http://www.prnewswire.com/news-releases/lyme-bacteria-hides-inside-parasitic-worms-causing-chronic-brain-diseases-300270742.html



WASHINGTON, May 19, 2016 /PRNewswire/ -- The examination of autopsied brain tissues from patients who died of serious neurological conditions has revealed that many tick-borne infections, such as Lyme disease, go undiagnosed and untreated. Board-certified pathologist, Alan B. MacDonald, MD, says his research shows "tick infections are not easily detected with routine tests, nor are they easily cured with short courses of antibiotics."

MacDonald will present his findings Thursday on Capitol Hill, in the Rayburn House Office Building, at a forum to explore the scientific, economic, and policy challenges posed by the epidemic of Lyme disease and associated tick-borne illnesses.

MacDonald found two Borrelia pathogens, including B. burgdorferi the causative agent of Lyme disease, thriving inside parasitic nematode worms, worm eggs or larvae in the brain tissue of nineteen deceased patients. These microscopic worms are endosymbionts, meaning the Borrelia bacteria dwell inside the worms. A tick bite delivers the nematode into the human body.

"Both the worms and the Borrelia pathogens can cause devastating brain damage," said MacDonald. "Current tests, like the ELISA and Western blot, do not adequately detect the presence of Borrelia bacteria." MacDonald says his discovery also shows "while patients are wrongly declared free of Lyme and other tick-borne infections, in reality, too often they contract serious neurodegenerative diseases which can kill them."

The Rocky Mountain Multiple Sclerosis Center Tissue Bank provided MacDonald with ten specimens from deceased MS patients; all ten specimens showed evidence of Borrelia infected nematodes. Infected worms were also found in five tissue specimens from patients who succumbed to the highly malignant brain tumor Glioblastoma multiforme, the same cancer which took the life of Senator Edward Kennedy (D-MA). Ironically, in 1993, Senator Kennedy chaired a hearing of the Labor and Human Resources committee titled: Lyme disease: A Diagnostic and Treatment Dilemma. Finally, four specimens from patients who died from Lewy Body dementia, the same illness which afflicted comedian Robin Williams, also showed the presence of infected nematodes.

MacDonald's work breaks new ground while building on previous studies. In 1984, Lyme pioneer Willy Burgdorfer, Ph.D. wrote of finding nematodes in tick guts. In 2014, University of New Haven researcher Eva Sapi, Ph.D., examined the guts of ticks gathered in southern Connecticut and found 22% of the nymphs and 30% of adult Ixodes ticks carried nematodes in their systems.

MacDonald identified the infected nematodes using a technique known as FISH: Fluorescent In Situ Hybridization which involves using molecular beacon DNA probes. FISH identifies pieces of Borrelia's genetic material which fluoresce under the microscope with a 100% DNA match. Dr. MacDonald, a fellow of the Academy of American Pathologists, conducts his research through the Dr. Paul Duray Research Fellowship Endowment Inc. MacDonald's presentation can be accessed here: https://vimeo.com/166688480.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.09.2016 - 19:30:04

Epstein–Barr virus and autoimmunity: the role of a latent viral infection in multiple sclerosis and systemic lupus erythematosus pathogenesis

http://www.futuremedicine.com/doi/abs/10.2217/fvl.12.136

February 2013
Multiple sclerosis (MS) and systemic lupus erythematosus (SLE) are both chronic autoimmune diseases with unknown etiology. To date, EBV is the most closely implicated infectious agent to be associated with both MS and SLE. Epidemiological findings show a strong correlation between EBV infection and the risk of developing these diseases. The type and magnitude of both EBV-specific antibodies and T-cell responses produced by MS or SLE patients are dysregulated when compared with healthy cohorts. Despite all these findings, it is still not clear if and how EBV triggers autoimmunity. EBV infects and establishes latency mainly in B cells, but it can also infect other cell types and indirectly influence the activation status of the immune system by stimulating the production of proinflammatory mediators. This could play a role in both MS and SLE pathogenesis. In this review we will summarize recent literature that links EBV infection to SLE and MS, and discuss possible new mechanisms that explain how EBV drives autoimmunity.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 09.09.2016 - 22:12:31

Whole genome sequence of an unusual Borrelia burgdorferi sensu lato isolate.

http://www.ncbi.nlm.nih.gov/pubmed/21217002

2011
Human Lyme disease is caused by a number of related Borrelia burgdorferi sensu lato species. We report here the complete genome sequence of Borrelia sp. isolate SV1 from Finland. This isolate is to date the closest known relative of B. burgdorferi sensu stricto, but it is sufficiently genetically distinct from that species that it and its close relatives warrant its candidacy for new-species status. We suggest that this isolate should be named "Borrelia finlandensis."


Borrelia burgdorferi sensu lato detected in skin of Norwegian mountain hare (Lepus timidus) without sign of dissemination


http://scandtick.com/publikasjoner/borrelia-bakterien/?pub=26

The mountain hare (Lepus timidus) population in southern Norway appears to be in decline. Necropsy and laboratory examinations of 36 hares found dead or diseased during 2007? 2009 in Vest- and Aust-Agder counties showed that disease and deaths were attributed to multiple causes, with no specific etiology emerging as a cause for population decline. To investigate whether Borrelia burgdorferi sensu lato (s.l.) infection is associated with mortality in mountain hares, tissues and ticks collected from hares were investigated for infection with the spirochete. Borrelia burgdorferi s.l. DNA was not detected in samples from internal organs, whereas Borrelia afzelii, B. burgdorferi sensu stricto (s.s.), and the not-yet-defined Borrelia sp. SV1 were found in skin samples from hares and in adult and nymphal Ixodes ricinus feeding on hares. Only B. burgdorferi s.s. and Borrelia sp. SV1 were detected in larvae feeding on hares. Our results indicate that disseminated Borrelia infection in hares rarely occurs and, presumably, does not play a central role in the suspected population decline. The results also suggest that the mountain hare to some degree functions as a transmission host for B. burgdorferi s.s. and Borrelia sp. SV1.

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Amerikkalaiset löysivät uuden borrelia kannan Suomesta 2011  ja se nimitettiin Borrelia finlandensiksi. Norjassa sama kanta on löydetty jäniksistä, jotka ovat siis tätä kantaa kantavien punkkien isäntiä.
Ja testataanko tätä meidän omaa kantaa labrakokeissa? Huslabissa "antigeenina Borrelia afzelii -kanta, johon on IgG-vasta- ainemittauksessa lisätty myös Borrelia burgdorferi ryhmän bakteerien VlsE- antigeenia".
Vaikka itsekin olen tutkinut oman infektioni takia borrelioosia, ei tätä meidän omaa kantaa ole tullut esiin aikaisemmin. Mielenkiintoista...

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.09.2016 - 15:12:41

Researchers’ discovery may explain difficulty in treating Lyme disease

http://www.northeastern.edu/cos/2015/06/researchers-discovery-may-explain-difficulty-in-treating-lyme-disease/

North­eastern Uni­ver­sity researchers have found that the bac­terium that causes Lyme dis­ease forms dor­mant per­sister cells, which are known to evade antibi­otics. This sig­nif­i­cant finding, they said, could help explain why it’s so dif­fi­cult to treat the infec­tion in some patients.

“It hasn’t been entirely clear why it’s dif­fi­cult to treat the pathogen with antibi­otics since there has been no resis­tance reported for the causative agent of the dis­ease,” explained Uni­ver­sity Dis­tin­guished Pro­fessor Kim Lewis, who led the North­eastern research team.

In other chronic infec­tions, Lewis’ lab has tracked the resis­tance to antibi­otic therapy to the pres­ence of per­sister cells—which are drug-​​tolerant, dor­mant vari­ants of reg­ular cells. These per­sister cells are exactly what they’ve iden­ti­fied here in Bor­relia burgdor­feri, the bac­terium that causes Lyme disease.

The researchers have also reported two approaches—one of them quite promising—to erad­i­cate Lyme dis­ease, as well as poten­tially other nasty infections.

Lewis and his col­leagues pre­sented their find­ings in a paper pub­lished online last week in the journal Antimi­cro­bial Agents and Chemotherapy. He co-​​authored the paper with North­eastern doc­toral stu­dents Bijaya Sharma and Autumn Brown, both PhD’16; recent grad­uate Nicole Matluck, S’15, who received her Bach­elor of Sci­ence in Behav­ioral Neu­ro­science; and Linden T. Hu, a pro­fessor of mol­e­c­ular biology and micro­bi­ology at Tufts University.

The research was sup­ported by grants from the Lyme Research Alliance and the National Insti­tutes of Health.

Lyme dis­ease affects 300,000 people annu­ally in the U.S., according to the Cen­ters for Dis­ease Con­trol and Pre­ven­tion, and is trans­mitted to people via bites from infected black­legged ticks. If caught early, patients treated with antibi­otics usu­ally recover quickly. How­ever, about 10 to 20 per­cent of patients, par­tic­u­larly those diag­nosed later, who have received antibi­otic treat­ment may have per­sis­tent and recur­ring symp­toms including arthritis, muscle pain, fatigue, and neu­ro­log­ical prob­lems. These patients are diag­nosed with Post-​​treatment Lyme Dis­ease Syndrome.

In addi­tion to iden­ti­fying the pres­ence of these per­sister cells, Lewis’ team also pre­sented two methods for wiping out the infection—both of which were suc­cessful in lab tests. One involved an anti-​​cancer agent called Mit­o­mycin C, which com­pletely erad­i­cated all cul­tures of the bac­terium in one fell swoop. How­ever, Lewis stressed that, given Mit­o­mycin C’s tox­i­city, it isn’t a rec­om­mended option for treating Lyme dis­ease, though his team’s find­ings are useful to helping to better under­stand the disease.

The second approach, which Lewis noted is much more prac­tical, involved pulse-​​dosing an antibi­otic to elim­i­nate per­sis­ters. The researchers intro­duced the antibi­otic a first time, which killed the growing cells but not the dor­mant per­sis­ters. But once the antibi­otic washed away, the per­sis­ters woke up, and before they had time to restore their pop­u­la­tion the researchers hit them with the antibi­otic again. Four rounds of antibi­otic treat­ments com­pletely erad­i­cated the per­sis­ters in a test tube.

“This is the first time, we think, that pulse-​​dosing has been pub­lished as a method for erad­i­cating the pop­u­la­tion of a pathogen with antibi­otics that don’t kill dor­mant cells,” Lewis said. “The trick to doing this is to allow the dor­mant cells to wake up.”

He added: “This gives you an idea that you could, in prin­ciple, estab­lish a sim­ilar reg­i­ment for treating patients for this and other chronic diseases.”

Lewis is a fac­ulty member in the biology depart­ment and directs Northeastern’s Antimi­cro­bial Dis­covery Center. Over the past decade he has led pio­neering work on this spe­cial­ized class of cells pro­duced by all pathogens known as per­sis­ters. Ear­lier this year, Lewis, biology pro­fessor Slava Epstein, and other col­leagues pub­lished ground­breaking research in Nature pre­senting a new antibi­otic that kills pathogens without encoun­tering any detectable resistance.

In pre­vious work, Lewis’ lab iden­ti­fied a com­pound called ADEP that causes dor­mant per­sister cells in MRSA to self-​​destruct. This com­pound was among the first options the researchers tried out to combat Lyme dis­ease. But it didn’t work, and nei­ther did com­bi­na­tions of stan­dard antibi­otics used to treat the dis­ease. The team thought it had hit a dead end yet remained vig­i­lant in its quest to iden­tify promising alter­na­tive options.

“What we came up with was the pulse-​​dosing reg­imen, which worked beau­ti­fully,” Lewis explained. “I think this could be very useful, espe­cially for antibi­otics for which resis­tance doesn’t rapidly develop.”


Though the researchers iden­ti­fied the pres­ence of these per­sister cells, they also note in their paper that the mech­a­nisms by which the per­sis­ters are able to sur­vive remain unknown. More work in this area will be required, they wrote.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.10.2016 - 21:58:37

Coronavirus and neurological disease: Direct link

https://www.sciencedaily.com/releases/2016/10/161003114804.htm

October 3, 2016

For the first time, researchers have found proof of a direct association between strain OC 43 of the human coronavirus (HCoV) and neurological disease in humans. This breakthrough was made by British and Quebec researchers, including Professor Pierre Talbot of the INRS-Institut Armand-Frappier Centre, who was the first not only to demonstrate the virus's ability to invade the human central nervous system, but also to suggest the neuropathological effects of this virus responsible for approximately 20% of common colds and more severe respiratory conditions in certain vulnerable individuals. The discovery was recently featured in the New England Journal of Medicine.

The researchers studied the case of a very young patient who died from encephalitis. The patient had presented severe immunodeficiency and received a stem cell transplant. Although most cases of encephalitis are caused by viruses or bacteria, it can be particularly difficult to pinpoint the cause in immunodeficient patients. As the case study shows, it was impossible to identify the pathogen using conventional techniques.

The researchers used various methods that allowed them to irrefutably identify the presence of strain OC-43 of the human coronavirus in the young patient's brain tissue. "Among the methods used, deep sequencing of biopsy materials provides an important tool for the diagnosis of unexplained encephalitis, particularly in immunodeficient patients who have undergone stem cell transplantation," said Professor Talbot. This breakthrough is significant because it will make it possible to use specific treatments that are better tailored to patient conditions.

The results obtained confirm Professor Talbot's hypothesis that the human respiratory coronavirus can cause certain neurological diseases of unknown origin, such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and encephalitis.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.10.2016 - 22:10:21

Respiratory tract bacterium uncovered as trigger for serious nervous system disease

https://www.sciencedaily.com/releases/2016/10/161003092441.htm

October 3, 2016
Guillain-Barré syndrome (GBS) is an acute life-threatening disease of the nervous system that leads to sensory disturbances and acute flaccid paralysis. A group of researchers involving the University of Zurich has now shown for the first time that bacteria, which often cause pneumonia, can trigger the autoimmune disease GBS. Antibodies that not only attack the bacteria but also the outer layer of the body's own nerve cells are a critical step in the pathogenesis of GBS after this respiratory infection.

The bacterium Mycoplasma pneumoniae has been under suspicion for quite a while. Now, researchers at the University of Zurich, the University Children's Hospital Zurich, and the Erasmus University in Rotterdam have proved without a doubt that it is the culprit. In fact, mycoplasma is not only responsible for respiratory tract infections such as pneumonia in children and adults, it can also trigger Guillain-Barré syndrome (GBS) in infected individuals. The scientists have succeeded for the first time in culturing mycoplasma from a GBS patient in a laboratory setting.

Antibodies attack not only the bacteria but also the nerve pathways

The reason for this is the similarity between structures on the surface of the bacteria and the body's own nerve-sheath structures (molecular mimicry). This leads to an immune reaction, which attacks both the mycoplasma and the surrounding myelin sheath of nerve pathways. "Antibodies recognize a certain glycolipid structure present at the cell membrane of the bacteria. These antibodies cross-react with and bind to galactocerebroside (GalC), one of the most common components of human myelin," explains Patrick Meyer Sauteur, the study's first author. This fatty substance ensures electrical conductivity of the nerve fibers. If it is destroyed, the patient experiences GBS, characterized by paralysis in arms and legs, weakness, and sensory disturbances.

Antibodies against GalC had already been described in patients with GBS. Such anti-GalC antibodies were also found in the aforementioned patient, and there was a correlation between their concentration in the blood and the progression of the illness. Immunological tests demonstrated that anti-GalC antibodies of the patient reacted most strongly with the cultured isolate, less strongly with other subtypes of mycoplasmas, but not with other bacteria. These results confirmed the cross-reactivity of the anti-GalC antibody.

Antibody isotype class switch may be responsible for GBS

The researchers investigated a total of 189 adults and 24 children with GBS for the presence of antibodies to mycoplasma (as an indication of a recent bacterial infection) and GalC (as the suspected trigger for GBS), and compared them with 677 healthy individuals as controls. Three percent of the adults and 21 percent of the children were found to have had a recent mycoplasma infection -- which was higher than in healthy control individuals. Anti-GalC antibodies were found in their blood with almost the same frequency: in three percent of the adults and 25 percent of the children. These anti-GalC antibodies also reacted to several mycoplasma strains.

Interestingly, the anti-GalC antibodies were also found in patients without GBS who had recently been infected with mycoplasma. However, these were all of the antibody isotype M (immunoglobulin M, IgM), the earliest antibody type elicited during an acute immune response. By contrast, the anti-GalC antibodies in the GBS patients were of the isotype IgG. "We therefore assume that this class switch of the antibody isotype may contribute to the pathogenesis of GBS," explains Meyer Sauteur. "In fact, this antibody isotype class switch is also assumed as a critical step in the development of other autoimmune diseases. Immunotherapies based on that premise may thus be a new possible treatment option for GBS."


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Kirjoittaja HopeSprings Pvm 19.10.2016 - 16:22:09

Coronavirus and neurological disease: Direct link

https://www.sciencedaily.com/releases/2016/10/161003114804.htm

October 3, 2016
For the first time, researchers have found proof of a direct association between strain OC 43 of the human coronavirus (HCoV) and neurological disease in humans. This breakthrough was made by British and Quebec researchers, including Professor Pierre Talbot of the INRS-Institut Armand-Frappier Centre, who was the first not only to demonstrate the virus's ability to invade the human central nervous system, but also to suggest the neuropathological effects of this virus responsible for approximately 20% of common colds and more severe respiratory conditions in certain vulnerable individuals. The discovery was recently featured in the New England Journal of Medicine.

The researchers studied the case of a very young patient who died from encephalitis. The patient had presented severe immunodeficiency and received a stem cell transplant. Although most cases of encephalitis are caused by viruses or bacteria, it can be particularly difficult to pinpoint the cause in immunodeficient patients. As the case study shows, it was impossible to identify the pathogen using conventional techniques.

The researchers used various methods that allowed them to irrefutably identify the presence of strain OC-43 of the human coronavirus in the young patient's brain tissue. "Among the methods used, deep sequencing of biopsy materials provides an important tool for the diagnosis of unexplained encephalitis, particularly in immunodeficient patients who have undergone stem cell transplantation," said Professor Talbot. This breakthrough is significant because it will make it possible to use specific treatments that are better tailored to patient conditions.

The results obtained confirm Professor Talbot's hypothesis that the human respiratory coronavirus can cause certain neurological diseases of unknown origin, such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and encephalitis.

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Kirjoittaja HopeSprings Pvm 04.11.2016 - 12:16:37

Validation of a multiplexing technique to determine the intrathecal, polyspecific antiviral immune response in multiple sclerosis.

https://www.ncbi.nlm.nih.gov/pubmed/27759441

Abstract
BACKGROUND:
Beside the determination of oligoclonal bands (OCBs) as a diagnostic biomarker in multiple sclerosis (MS), the presence of an intrathecal production of antibodies against the neurotropic viruses measles (M), rubella (R) and Varicella-Zoster (Z), the so called MRZ reaction (MRZR) is an even more specific diagnostic biomarker in MS.

METHODS:
We compared and validated the determination of the MRZR in 97 cerebrospinal fluid (CSF) and serum sample pairs of a bead-based multiplexing technique and a classical enzyme-linked immunosorbent assay (ELISA).

RESULTS:
Conformity of 94% (M), 94% (R), 94% (Z), 96% (H) and 97% for the interpretation of the MRZR was obtained.

CONCLUSION:
Based on our findings of high conformity between the multiplex technique and classical ELISA, as well as the time and cost savings multiplexing allows, we conclude that the multiplexing technique is applicable as a diagnostic tool for the determination of the MRZR.

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Kirjoittaja HopeSprings Pvm 04.11.2016 - 12:26:00

How autoimmune disease is prevented: Mechanism discovered

https://www.sciencedaily.com/releases/2016/11/161101093250.htm

November 1, 2016

A previously unknown safety mechanism in our immune system keeps the body free from autoimmune diseases. Researchers from Karolinska Institutet have discovered that a cell in our inherited immune system can prevent our adaptive (learned) immune system from reacting to the body's native cells, which can otherwise lead to autoimmune diseases such as SLE. The study is published in the academic journal Nature Immunology.

Autoimmune diseases and allergies, in which the immune system triggers an immunological reaction in sufferers, are becoming increasingly common. In some cases, such as the rheumatic disease SLE, the immune system reacts to the body's own cells. One of the most important components of our learned (adaptive) immune system is the white blood cells called B lymphocytes, which are one of the main causal factors of many autoimmune diseases, including SLE, since it is these cells that start to react to the body's native structures, giving rise to the symptoms.

"Our research group has been interested in B lymphocytes and what goes wrong in the regulation of different types of autoimmune disease," says Professor Mikael Karlsson at the Department of Microbiology, Cell and Tumour Biology.

It has long been known that a certain type of cell in the inherited immune system called a neutrophil plays an important part in wound healing and the early stages of the immune response. Through their studies on laboratory mice, the team from KI has now discovered that neutrophils have another crucial function in their interaction with B lymphocytes. What they found was a safety mechanism that prevents B lymphocytes from reacting to endogenous antigens.

"We have discovered a previously unknown mechanism in the immune system that prevents autoimmune disease and that could be lacking, we think, in people with autoimmune diseases such as SLE," says Professor Karlsson.

When an inflammation occurs in the body, the neutrophils cause the B lymphocytes in the spleen to start producing antibodies that retard an infection. At the same time, however, the neutrophils also communicate with a kind of immune cell called an NKT cell, instructing it to regulate the response to prevent over-reaction.

It is known that SLE patients do not have as many NKT cells as other people, which could be a contributing factor to the failure of the body to regulate B lymphocytes.

"Apart from our discovery being interesting in general terms of how the immune system works, it can also be very important for people with other autoimmune diseases," says Professor Karlsson. "We think that this mechanism could be used to regulate B lymphocytes in different morbid conditions and that it could be a way forward for stopping SLE."

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Kirjoittaja HopeSprings Pvm 09.12.2016 - 22:19:01

CD8+ T-Cell Deficiency, Epstein-Barr Virus Infection, Vitamin D Deficiency, and Steps to Autoimmunity: A Unifying Hypothesis

https://www.hindawi.com/journals/ad/2012/189096/

Epstein-Barr virus (EBV) has been suspected of involvement in the pathogenesis of various chronic autoimmune diseases since the finding of elevated levels of antibody to the virus in systemic lupus erythematosus (SLE) in 1971 [1]. Generally the effect of EBV infection has been attributed to immunological cross-reactivity between EBV and self-antigens [2–4]; however, in 2003 the EBV-infected autoreactive B-cell hypothesis of autoimmunity was proposed as the basis for human chronic autoimmune diseases [5]. This hypothesis proposes that, in genetically susceptible individuals, EBV-infected autoreactive B cells seed the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells which would otherwise die in the target organ by activation-induced apoptosis [5] (Figure 1). The present article presents a further development of this hypothesis, proposing that susceptibility to develop chronic autoimmune diseases after EBV infection is dependent on a genetically determined quantitative deficiency of the cytotoxic CD8+ T cells that normally keep EBV infection under tight control. It is postulated that autoimmunity evolves in the following steps: (1) CD8+ T-cell deficiency; (2) primary EBV infection; (3) decreased CD8+ T-cell control of EBV; (4) increased EBV load and increased anti-EBV antibodies; (5) EBV infection in the target organ; (6) clonal expansion of EBV-infected autoreactive B cells in the target organ; (7) infiltration of autoreactive T cells into the target organ; and (8) development of ectopic lymphoid follicles in the target organ (Figure 2).
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5.1.2. Treatment

There are potentially 3 ways to treat chronic autoimmune diseases by controlling EBV infection: (1) B-cell depletion with monoclonal antibodies; (2) boosting immunity to EBV; (3) antiviral drugs. B-cell depletion with rituximab eliminates not only EBV-infected B cells but also uninfected B cells, which normally confer protective immunity against infectious agents. Improvement of an autoimmune disease with rituximab therapy would be consistent with an essential role of EBV in the development of the disease but would not constitute proof because the beneficial effect could be mediated by the elimination of autoreactive B cells not infected with EBV. More convincing evidence for an essential role of EBV would be eradication of autoimmune diseases by boosting immunity to EBV or by treatment with antiviral drugs. Humoral immunity to EBV could be boosted by vaccination with gp350 or administration of humanized or human monoclonal antibody against gp350. CD8+ T-cell immunity could be boosted by the intravenous infusion of autologous EBV-specific cytotoxic CD8+ T cells after expansion in vitro [201] or by the administration of agents such as interleukin-7, which expands the population of functional virus-specific CD8+ T cells in chronic viral infection [202]. With regard to antiviral drugs, treatment with aciclovir and related drugs, which inhibit herpesvirus DNA polymerase, is likely to have only a limited beneficial effect in chronic autoimmune diseases because these drugs act on EBV only when it is using its own DNA polymerase to replicate its DNA. This will apply only to lytically infected cells but not to latently infected ones, which replicate EBV DNA through the use of EBV nuclear antigen 1 (EBNA1) to engage host cell DNA polymerase. One strategy to overcome this would be first to administer rituximab to eliminate as many EBV-infected B cells as possible and to follow this with long-term antiviral drug therapy. An alternative approach is to target LMP1 [203], LMP2A, or EBNA1 [204] to inhibit EBV in latently infected cells. It has also been suggested that retroviral integrase inhibitors might be effective against EBV in autoimmune diseases [205]. If EBV infection of B cells in the target organ underpins the development of autoimmune diseases, effective antiviral drugs have the potential to be curative.
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6. Conclusions

CD8+ T-cell deficiency is a general feature of chronic autoimmune diseases and also occurs in healthy blood relatives of patients with these diseases. It is proposed that this deficiency is genetically determined and underlies the development of chronic autoimmune diseases by impairing CD8+ T-cell control of EBV infection, with the result that EBV-infected autoreactive B cells accumulate in the target organ where they produce pathogenic autoantibodies and provide costimulatory survival signals to autoreactive T cells. Autoimmunity is postulated to evolve in a series of steps culminating in the development of ectopic lymphoid follicles containing EBV-infected autoreactive B cells in the target organ. It is also proposed that deprivation of sunlight and vitamin D facilitates the development of autoimmune diseases by aggravating the CD8+ T cell deficiency and thereby further impairing control of EBV. The hypothesis makes predictions which can be tested, including the prevention and successful treatment of chronic autoimmune diseases by controlling EBV infection.

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Kirjoittaja HopeSprings Pvm 09.12.2016 - 22:39:03

Understanding bacteria's slimy fortresses

https://www.sciencedaily.com/releases/2016/10/161021122614.htm

October 21, 2016
For the first time, scientists have revealed the mechanics of how bacteria build up slimy masses, called biofilms, cell by cell. When encased in biofilms in the human body, bacteria are a thousand times less susceptible to antibiotics, making certain infections, such as pneumonia, difficult to treat and potentially lethal. In a new study, engineers and biologists tracked a single bacterial cell as it grew into a mature biofilm of 10,000 cells with an ordered architecture. The findings should help scientists learn more about bacterial behavior and open up new ways of attacking biofilms with drugs.

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Kirjoittaja HopeSprings Pvm 09.12.2016 - 22:43:05

Inflammation triggers unsustainable immune response to chronic viral infection

https://www.sciencedaily.com/releases/2016/10/161021154906.htm

October 21, 2016
Scientists at the University of Basel discovered a fundamental new mechanism explaining the inadequate immune defense against chronic viral infection. These results may open up new avenues for vaccine development. They have been published in the journal Science Immunology.

In the course of an infection or upon vaccination, specialized cells of our immune system, so-called B cells, produce antibodies that bind viruses and inactivate them. In the context of chronic viral infections such as HIV or hepatitis C virus, however, antibody production by B cells is quantitatively inadequate and starts too late.

A team of scientists headed by Prof. Daniel Pinschewer at the Department of Biomedicine, University of Basel, reports that the inadequate antibody response to chronic viral diseases is due to the strong inflammatory reaction upon infection. While most pronounced at the onset of an infection, inflammation can persist for decades, especially in HIV/AIDS.

Hasty immune response lasts only short-term

Under the influence of inflammatory messengers, so called interferons, B cells produce as many antibodies as they possibly can. Unfortunately, this hasty response occurs at the expense of sustainability. B cells that turn on antibody production too quickly lose their potential to proliferate and die shortly thereafter. As a consequence, the immune response takes an impetuous start but subsides rapidly.

The scientists assume that this panic reaction of B cells reflects a mechanism ensuring an optimized response to acute life threatening infections. In the context of chronic infections, however, the battle is not decided within a matter of days, but rather only after months or years. Under these circumstances, the hasty reaction of our body seems inappropriate and may actually favor the virus.

Cornerstone for new vaccines
For viral diseases such as HIV or hepatitis C protective vaccines remain unavailable. The scientists are hopeful that the discovery of this fundamental mechanism may provide a basis to improve vaccination strategies against chronic viral diseases.

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Kirjoittaja HopeSprings Pvm 20.12.2016 - 15:58:58

Antivirus immune activity in multiple sclerosis correlates with MRI activity.

https://www.ncbi.nlm.nih.gov/pubmed/25939660

Jan 2016

OBJECTIVE:
The objective of this study was to determine whether reactivation of Epstein-Barr (EBV) or activation of the anti-EBV immune response correlates with MS disease activity on MR imaging.

METHODS:
Subjects with early, active relapsing-remitting MS were studied for 16 weeks with blood and saliva samples collected every 2 weeks and brain MRI performed every 4 weeks. We isolated peripheral blood mononuclear cells from each blood sample and tested the immune response to EBV, autologous EBV-infected lymphoblastoid cell lines (LCL), human herpesvirus 6 (HHV6), varicella zoster virus (VZV), tetanus, and mitogens. We measured the proliferative response and the number of interferon-γ secreting cells with ELISPOT. We measured the amounts of EBV, HHV6, and VZV DNA in blood and saliva with quantitative PCR. On MRI, we measured number and volume of contrast enhancing and T2 lesions. We tested for correlation between the immunologic assays and the MRI results, assessing different time intervals between the MRI and immunologic assays.

RESULTS:
We studied 20 subjects. Ten had enhancing lesions on one or more MRI scans and one had new T2 lesions without enhancement. The most significant correlation was between proliferation to autologous LCL and the number of combined unique active lesions on MRI 4 weeks later. Both proliferation and number of cells secreting interferon-γ in response to LCL correlated with the number of enhancing lesions 8 weeks later.

CONCLUSIONS:
We find evidence for correlation of antiviral immune responses in the blood with subsequent disease activity on MRI scans.

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Kirjoittaja HopeSprings Pvm 20.12.2016 - 16:09:50

Aetiology: Neighbourhood watch

http://www.nature.com/nature/journal/v540/n7631_supp/full/540S4a.html?cookies=accepted

Emerging evidence points to a viral infection, low levels of vitamin D and genetics as culprits in multiple sclerosis, but how they combine to cause the disease is unclear.
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Canada has the highest rate of MS in the world, with 291 cases per 100,000 people2. But rates vary widely from one region of Canada to another3, 4, 5. Several studies have concluded that something in the environment in Canada is contributing to MS — indeed, rates of MS in immigrants to Canada quickly rise to approach Canadian levels6, 7.

Differences between countries can suggest possible causes. Clusters in particular neighbourhoods, such as those in Ottawa and Winnipeg, raise suspicion about local environmental factors, including outbreaks of infectious disease or genetic differences in multicultural cities, says Mahmoud Torabi, a statistician at the University of Manitoba and an author of the Winnipeg study.

   “The body of evidence is difficult to get a grip on, it's so huge.”

Until recently, researchers could not pinpoint why Canada in general, and specific places in particular, are so rife with this neurodegenerative disease6, 7, 8. But an international research effort — including database analyses, epidemiology, microbiology, genetics and immunology — is now yielding a growing body of evidence on the causes of MS. “It's difficult to get a grip on, it's so huge,” says Egil Røsjø, a neurologist at Akershus University Hospital near Oslo, who is also completing a doctorate on MS aetiology. “There are lines of evidence that are pointing more or less in the same direction from all these different angles.”

And they are pointing to three main culprits: Epstein–Barr virus (EBV), which is a herpesvirus that causes mononucleosis (glandular fever); low levels of vitamin D; and genetic variants that increase susceptibility to MS.
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There are three broad theories to explain how EBV infection could result in MS, explains Bar-Or. One possibility is that the EBV infects the central nervous system (CNS), especially the brain. The virus may then kill oligodendrocytes, the cells that produce the myelin sheath — the insulating envelope that coats the nerve fibres (axons). Myelin speeds up the nerve impulses travelling through the axons and is essential for normal nerve function.

In the CNS, the infection may also trigger an immune response in which a type of immune cell known as CD8 tries to kill the virus but also damages oligodendrocytes and neurons. Bar-Or admits that this theory is controversial, because although some researchers have found the virus in the CNS, others have been unable to replicate the finding.

A second theory involves molecular mimicry, in which the immune system, Bar-Or says, may mistake myelin basic protein (MBP), which is important for the myelination process, for a similar piece of the invading EBV. The immune system's T cells have receptors that can recognize both the virus and MBP, and when the T cells are activated during the immune response to the virus, they could attack MBP as well as EBV in parts of the brain, resulting in a loss of myelin.

A third possible mechanism involves immune cells known as B cells. In normal immune responses, there are interactions between B cells, myeloid cells and T cells when responding to invading bacteria and viruses, and reversing the immune response when it is no longer needed. Any imbalance in this delicate dance can cause a strong or long-term response that goes beyond its original purpose and injures the body by interfering with basic cell functions, says Bar-Or. Perhaps EBV causes such an imbalance in MS by activating the B cells that they no longer perform their crucial regulatory functions, but instead start to promote inflammation. There is some support for this theory because MS treatments that remove B cells have succeeded in decreasing MS relapses, says Bar-Or.
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The mounting evidence of the link with vitamin D has sparked discussion about how low levels could lead to MS. Bar-Or points out that vitamin D has been shown to affect the immune response in many of the cell types involved in MS, including myeloid, B and T cells. “There's an enormous amount of literature that associates vitamin D deficiency with risk of disease,” adds Richards.
*******
“The genetic contribution doesn't explain even half the risk,” cautions Bar-Or, so it may be possible to prevent the disease by targeting the environmental factors involved.


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Kirjoittaja HopeSprings Pvm 24.12.2016 - 00:51:27

Role of Therapeutic Plasma Exchange in Treatment of Tumefactive Multiple Sclerosis-Associated Low CD4 and CD8 Levels

https://www.karger.com/Article/Pdf/448704

We  report  a  35-year-old  healthy  male  who  developed  central  nervous  system  inflammatory demyelinating  disease [ CNS IDD]  consistent  with  tumefactive  multiple  sclerosis.  About  2  weeks  after onset  of  symptoms  and  prior  to  initiation  of  therapy,  the  patient  had  lymphopenia  and  low CD4 and CD8 levels. His lymphocyte count was 400 cells/μl (850–3,900 cells/μl), CD4 was 193 cells/μl (490–1,740 cells/μl) and CD8 was 103 cells/μl (180–1,170 cells/μl). He was treated with intravenous methylprednisolone followed by therapeutic plasma exchange, the levels of CD4 and CD8 normalized, and ultimately, he recovered completely.
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A unique aspect of our investigation  of  this  patient  are  the  immunological  parameters tested  in  the  patient  upon  initial  presentation  and  not  on  any  treatment.  His  CD4  and  CD8 counts were low, and to our knowledge, this is the first time this laboratory abnormality has been  observed  in  a  patient  with  IDD.  There  have  been  studies  of  the  role  of  CD4  and  CD8 cells in MS, where the implications of low levels of both of these
cell types is not clear, although a low CD4 count has been described in a number of conditions such as HIV disease
and levels of CD8 cells are reduced in patients treated with dimethyl fumarate [10]. However, the combination of reduced values of both the CD4 and CD8 levels has not been reported in any disorder [9, 11]. In this patient, this abnormality could be due to a prior viral infection which may have initiated the process of CNS demyelination. Alternatively, it  may represent the response of the immune system to the beginning of the disease process.
Whether abnormally low CD4 and CD8 levels are involved in the pathophysiology of IDD will require further confirmation with studies investigating CD4 and CD8 parameters in patients  early  in  the  clinical  course  prior  to  initiation  of  any  therapy.  If  our  results  are  confirmed, levels of CD4 and CD8 could represent a biomarker for tumefactive CNS IDD. Regardless of the specific pathophysiology, therapeutic plasma exchange should be a consideration in atypical cases of IDD consistent with tumefactive MS.

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Kirjoittaja HopeSprings Pvm 07.01.2017 - 15:18:06

Autoimmunity and infections: When the body fights itself

https://www.sciencedaily.com/releases/2017/01/170106092354.htm

January 6, 2017
Basel-based doctors are on the trail of a possible connection between autoimmune diseases and infections: errors can occur when immune cells absorb certain proteins from pathogen cells. These findings were reported in the journal PNAS by researchers from the Department of Biomedicine at the University of Basel and University Hospital Basel, as well as colleagues in the USA.

It is already known that there is a connection between infections and autoimmunity -- the inability of an organism to recognize parts of its own body as "self." As a result, increasing hygiene is leading to a higher incidence of autoimmune diseases in the population. It is also apparent that some autoimmune diseases are triggered by infections. However, the mechanism behind these connections is still not fully understood. One possible explanation is that the immune system confuses protein structures from pathogens with the body's own proteins because they look structurally alike.

Errors in protein uptake

Together with colleagues from the Whitehead Institute in Cambridge (USA), the Basel-based team of researchers tested out a new hypothesis in experiments to investigate the special ability of immune cells to identify specific proteins on the surface of neighboring cells and capture them from the cell membrane. In certain cases, errors can occur in the uptake of these proteins, as the group led by Professor Tobias Derfuss has now demonstrated.

Their assumption is that certain immune cells, so-called B cells, capture not only the protein of an influenza virus for which they were specialized but also small quantities of other neighboring membrane proteins. One example of this is a protein known as an autoantigen that originates from the cell membrane layer in the central nervous system. An immune response to this membrane protein results in an autoimmune inflammation in the brain in the animal model and may well also contribute to inflammation of this kind in humans.

Harmful immune cells

B cells cultivated with cells that had incorporated both the influenza virus protein and the membrane protein were not only able to activate other immune cells, specifically certain T cells, in order to combat the virus; they also activated T cells that had recognized the body's own membrane protein -- which can trigger autoimmune inflammation in the brain. Consequently, a viral infection could lead to the activation of autoaggressive T cells through an error in the protein uptake of B cells.

The researchers discovered this mechanism after conducting experiments using cells from genetically modified mice. "The next step would now be to examine whether similar errors occur in protein uptake by human B cells. We also want to clarify whether a viral infection in an animal can, under certain circumstances, lead to autoimmune inflammation in the brain," says Derfuss. Corresponding follow-up projects are planned.

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Kirjoittaja HopeSprings Pvm 07.01.2017 - 15:25:24

Factors responsible for chronic nature of autoimmune disease identified

https://www.sciencedaily.com/releases/2017/01/170104114327.htm

January 4, 2017
Researchers from Schepens Eye Research Institute of Massachusetts Eye and Ear have uncovered two factors responsible for the chronic, lifelong nature of autoimmune disorders, which tend to "flare up" intermittently in affected patients. These two factors are cell-signaling proteins called cytokines -- specifically Interleukin-7 and -15 (IL-7 and IL-15) -- that are secreted by cells of the immune system and help modulate memory Th17 cells, a subset of T cells which are known to contribute to autoimmune disorders. Until now, it was unclear how Th17 cells maintained memory; the study results show that IL-7 and IL-15 signal the Th17 cells to chronically reside in the body. These findings, published online in the Journal of Autoimmunity, may lead to the development of new therapies to address a variety of chronic autoimmune disorders.

"We wanted to know the precise factors that maintain memory in Th17 cells so that we can better understand what is causing chronic autoimmune disorders," said senior author Reza Dana, M.D., M.Sc., MPH, Director of the Cornea and Refractive Surgery Service at Mass. Eye and Ear and the Claes H. Dohlman Professor of Ophthalmology at Harvard Medical School. "By selectively targeting the production and expression of IL-7 and IL-15, we may be able to prevent the development of chronic autoimmune disorders."

Affecting up to 50 million Americans, autoimmune disorders develop when the body's immune system attacks its own healthy tissue. Many autoimmune disorders are chronic, and patients may experience "flare-ups," in which symptoms worsen temporarily and then enter a period of remission.

Previous research studies have linked Th17 cells to a variety of autoimmune disorders, including multiple sclerosis,
rheumatoid arthritis, inflammatory bowel disease, and chronic inflammatory eye disorders such as uveitis and dry eye disease. When Th17 cells are activated, a subset of them become memory cells, causing them to reside in the body for long periods of time. These memory Th17 cells can become reactivated and cause flare-ups of the autoimmune condition. However, the underlying mechanisms that promote the maintenance of Th17 memory were previously unknown.

Using a mouse model for dry eye disease, an autoimmune condition affecting the surface of the eye, the study authors set out to determine what molecular factors are critical for the maintenance of Th17 memory. They identified IL-7 and -15 as playing a crucial role in the survival and homeostatic proliferation of memory Th17 cells, and when they neutralized IL-7 and IL-15, they saw a substantial reduction of memory Th17 cells.

While further studies are needed to determine ways to block these factors, the findings suggest that targeting IL-7 and IL-15 in order to remove the memory Th17 cells may be an effective treatment strategy for autoimmune diseases.

"In the case of dry eye disease, many of the treatments are showing limited efficacy in patients that do not have a highly inflamed eye," said Dr. Dana. "Targeting the chronic, immune nature of autoimmune diseases may be a better strategy for controlling these conditions."


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Kirjoittaja HopeSprings Pvm 29.01.2017 - 14:59:18

Defective T-cell control of Epstein–Barr virus infection in multiple sclerosis

http://www.nature.com/cti/journal/v6/n1/full/cti201687a.html

20 January 2017
Mounting evidence indicates that infection with Epstein–Barr virus (EBV) has a major role in the pathogenesis of multiple sclerosis (MS). Defective elimination of EBV-infected B cells by CD8+ T cells might cause MS by allowing EBV-infected autoreactive B cells to accumulate in the brain. Here we undertake a comprehensive analysis of the T-cell response to EBV in MS, using flow cytometry and intracellular IFN-γ staining to measure T-cell responses to EBV-infected autologous lymphoblastoid cell lines and pools of human leukocyte antigen (HLA)-class-I-restricted peptides from EBV lytic or latent proteins and cytomegalovirus (CMV), in 95 patients and 56 EBV-seropositive healthy subjects. In 20 HLA-A2+ healthy subjects and 20 HLA-A2+ patients we also analysed CD8+ T cells specific for individual peptides, measured by binding to HLA-peptide complexes and production of IFN-γ, TNF-α and IL-2. We found a decreased CD8+ T-cell response to EBV lytic, but not CMV lytic, antigens at the onset of MS and at all subsequent disease stages. CD8+ T cells directed against EBV latent antigens were increased but had reduced cytokine polyfunctionality indicating T-cell exhaustion. During attacks the EBV-specific CD4+ and CD8+ T-cell populations expanded, with increased functionality of latent-specific CD8+ T cells. With increasing disease duration, EBV-specific CD4+ and CD8+ T cells progressively declined, consistent with T-cell exhaustion. The anti-EBNA1 IgG titre correlated inversely with the EBV-specific CD8+ T-cell frequency. We postulate that defective CD8+ T-cell control of EBV reactivation leads to an expanded population of latently infected cells, including autoreactive B cells.
***********
In this comprehensive study of the T-cell response to EBV in MS, we have shown that there is a decreased CD8+ T-cell response to EBV lytic phase antigens at the onset of MS and at all subsequent stages of the disease. In contrast to the decreased response to the lytic antigens of EBV, the CD8+ T-cell response to the lytic antigens of CMV, another common human herpesvirus, was normal in patients with MS. Even in healthy EBV carriers, EBV is continuously being reactivated in the tonsil with shedding of virions into saliva,5 a process normally kept in check by lytic-specific cytotoxic CD8+ T cells (Figure 7a).7, 8 Thus the predicted consequence of defective CD8+ T-cell control of EBV reactivation is increased production of infectious virions with increased oral shedding, as occurs in children with MS,37 and increased infection of new naive B cells, which become blasts in a new cycle of infection (Figures 7b and d).6 Indeed the amplification of virus production in the tonsil wherein virus released from each bursting plasma cell infects epithelial cells which in turn generate enough virions to infect ~10 000 naive B cells6 means that impaired immune control of this critical stage of the EBV life cycle can have a major follow-on effect into the infected blast population. The crucial importance of controlling the lytic phase of infection is also supported by the study of Hopwood et al.38 who concluded that in healthy individuals viral loads are maintained within normal limits by cytotoxic CD8+ T cells directed against lytic rather than latent EBV proteins. According to the mathematical model of EBV infection proposed by Hawkins et al.,6 increased input into the EBV-infected blast pool from the lytic phase will increase the size of the blast population, in turn stimulating the expansion of CD8+ T cells specific for EBV latent antigens, as we found in patients with MS. If the increase in latent-specific cytotoxic CD8+ T cells suffices to counteract the increased input into the blast population, the size of the infected blast cell population remains at its pre-existing healthy size at the expense of a sustained increase in the latent-specific CD8+ T-cell population. However, if the persistently high EBV latent antigen load induces T-cell exhaustion of the latent-specific T cells, as occurs in high-grade chronic viral infections, the increased input into the blast pool from the lytic phase is no longer counterbalanced by the T-cell response, so that the blast population increases in size, as does its input into the germinal centre pool. We have shown that there is indeed T-cell exhaustion of CD8+ T cells recognizing EBV latent antigens in MS. Interestingly the T-cell exhaustion appears preferentially to affect CD8+ T cells responding to the EBNA3C-derived LLD peptide rather than the LMP2A-derived CLG and FLY peptides. Potential explanations for the predilection of EBNA3C-specific CD8+ T cells to exhaustion include their immunodominance and the earlier expression of EBNA3 proteins than LMP proteins after infection of naive B cells. Increased input of cells from the expanded EBV-infected blast pool into the germinal centre pool will enlarge the infected germinal centre B-cell population, which will continue to grow if inadequately controlled. Furthermore, unchecked growth of the EBV-infected germinal centre B-cell pool will increase the infected memory B-cell population and thus the number of latently infected cells available to reactivate the virus into the lytic stage, thereby further taxing the already impaired EBV-lytic-specific CD8+ T-cell response. This in turn leads to increased generation of virions which infect naive B cells, driving them into clonal expansion with further enlargement of the EBV-infected blast population—truly a vicious cycle. Progressive exhaustion of EBV-latent-specific T cells will permit unbridled proliferation of EBV-infected germinal centre B cells (Figure 7d), which might underlie the development of EBV-infected lymphoid follicles in the brain in secondary progressive MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2017 - 21:42:46

IL-17 increases in secondary progressive MS

http://multiple-sclerosis-research.blogspot.com/2014/09/il-7-increases-in-secondary-progressive.html


Sunday, 28 September 2014

OBJECTIVE:In the current exploratory study, we longitudinally measured immune parameters in the blood of individuals with relapsing-remitting multiple sclerosis (RRMS) and secondary progressive multiple sclerosis (SPMS), and investigated their relationship to disease duration and clinical and radiologic measures of CNS injury.
******
RESULTS: Frequencies of myelin basic protein-specific IL-17- and IFN-γ-producing PBMCs were higher in individuals with RRMS and SPMS compared to healthy controls. Patients with SPMS expressed elevated levels of IL-17-inducible chemokines that activate and recruit myeloid cells. In the cohort of patients with SPMS without inflammatory activity, upregulation of myeloid-related factors correlated directly with MRI T2 lesion burden and inversely with brain parenchymal tissue volume.
CONCLUSIONS: The results of this exploratory study raise the possibility that Th17 responses and IL-17-inducible myeloid factors are elevated during SPMS compared with RRMS, and correlate with lesion burden. Our data endorse further investigation of Th17- and myeloid-related factors as candidate therapeutic targets in SPMS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2017 - 21:54:26

The Antibody Response to Epstein-Barr Virus in Multiple Sclerosis Is Increased Only to Selected Antigens

http://www.neurology.org/content/86/16_Supplement/P5.344

Objective: The objective of this work was to identify Epstein-Barr virus (EBV) proteins that are the targets of an increased antibody response in multiple sclerosis (MS).
Background: EBV is associated with MS. One of the most consistent findings has been that antibodies to the EBV nuclear antigen-1 [b](EBNA-1) are increased in MS[/b]. Only a limited number of other EBV proteins have been investigated. Our previous work using Western blots demonstrated that most people have antibodies to many different EBV proteins, and suggested that antibodies were increased to some, but not all, EBV antigens in MS patients.
Methods: We immunoprecipitated EBV proteins using either MS or control IgG, and identified the bound proteins using iTRAQ quantitative mass spectrometry. We compared the amounts bound by MS or control IgG. We then selected and produced single EBV proteins, and used quantitative immunoassays to compare the antibody response in 80 MS patients and 80 matched controls.
Results: Mass spectrometry identified 28 EBV proteins that were immunoprecipitated by MS or control IgG. Fifteen of these proteins were more concentrated in the MS immunoprecipitate. We selected 8 individual EBV proteins for further study. The antibody response to EBNA-1 was significantly increased in MS (p<0.001), as was the antibody response to the small capsid protein BFRF3 (p=0.007) and the tegument protein BRRF2 (p=0.006). The antibody response to the other 5 antigens was not increased in MS.
Conclusions: The anti-EBV antibody response is increased only to selected EBV antigens in MS patients. This finding may be relevant to the pathogenesis of MS.

*******
Ts, jos EBV testataan, niin täytyy vaatia, että tutkitaan EBNA-1. Itselläni sitä ei ole Suomessa mitattu, kun taas Saksassa se  oli >600 (normaali <5).

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2017 - 22:01:08

The Interplay Between Epstein Barr Virus and B Lymphocytes: Implications for Infection, Immunity, and Disease

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4199828/

Human B cells are the primary targets of Epstein Barr virus (EBV) infection. In most cases EBV infection is asymptomatic because of a highly effective host immune response but some individuals develop self-limiting infectious mononucleosis, while others develop EBV-associated lymphoid or epithelial malignancies. The viral and immune factors that determine the outcome of infection are not understood. The EBV life cycle includes a lytic phase, culminating in the production of new viral particles, and a latent phase, during which the virus remains largely silent for the lifetime of the host in memory B cells. Thus, in healthy individuals there is a tightly orchestrated interplay between EBV and the host that allows the virus to persist. To promote viral persistence EBV has evolved a variety of strategies to modulate the host immune response including inhibition of immune cell function, blunting of apoptotic pathways, and interfering with antigen processing and presentation pathways. In this article we focus on mechanisms by which dysregulation of the host B cell, and immune modulation, by the virus can contribute to development of EBV+ B cell lymphomas.
*********
In conclusion, EBV infection initiates a complex, ongoing interplay between the virus, the host B cell and the immune response. EBV has successfully employed a variety of strategies to promote viral persistence in healthy individuals, however, dysregulation of these pathways, or perturbation of host immunity, may contribute to the development of EBV-associated malignancies. Future studies to elucidate the mechanisms by which EBV coopts B cell function, the immune response to EBV, and the significance of viral diversity will be important in understanding the outcome of EBV disease.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.02.2017 - 22:10:41

Identification of Epstein-Barr virus proteins as putative targets of the immune response in multiple sclerosis

http://www.direct-ms.org/pdf/InfectiousMS/Cepak%20EBV%20in%20MS.pdf

MS is a chronic inflammatory and demyelinating disease of the CNS with as yet unknown etiology. A hallmark
of this disease is the occurrence of oligoclonal IgG antibodies in the cerebrospinal fluid (CSF). To assess the
specificity of these antibodies, we screened protein expression arrays containing 37,000 tagged proteins. The 2
most frequent MS-specific reactivities were further mapped to identify the underlying high-affinity epitopes.
In both cases, we identified peptide sequences derived from EBV proteins expressed in latently infected cells.
Immunoreactivities to these EBV proteins, BRRF2 and EBNA-1, were significantly higher in the serum and
CSF of MS patients than in those of control donors. Oligoclonal CSF IgG from MS patients specifically bound
both EBV proteins.
Also, CD8+ T cell responses to latent EBV proteins were higher in MS patients than in controls. In summary, these findings demonstrate an increased immune response to EBV in MS patients, which
suggests that the virus plays an important role in the pathogenesis of disease

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Kirjoittaja HopeSprings Pvm 17.03.2017 - 17:57:42

CONTROVERSIES  IN  LATE  NEUROBORRELIOSIS  AND  MULTIPLE  SCLEROSIS  
CASE  SERIES

http://www.mms-seminar.com/wp-content/uploads/2015/08/2009-romanian-study-ms-is-lyme.pdf

2009
Abstract.
Introduction
The  etiology  of  MS  remains  uncertain,  bacterial  infection  with  B.  burgdorferi  is  most  frequently  incriminated.  Neuroimaging  criteria  considered  in  the  diagnosis  of  MS  can  also  be fulfilled  in  NB,  the  joint  feature  being  demyelinating  lesions.  We  present  the  diagnosis  and  treatment difficulties  in  NB  versus  MS  and  other  clinical  considerations.

Methods
We  retrospectively  studied  all  consecutive  cases  of  neuroborreliosis  hospitalized  in  the  University  Hospital  of  Infectious  Diseases  during  2006-2008.  The  diagnosis  was  established  through  clinical  criteria  (using  a  probability  score  for  Lyme  disease),  serological  criteria  (enzyme  immunoassay  for  IgM  and IgG antibodies followed by confirmatory Western blot) and MS diagnosis was stratified as confirmed or  possible  according  to  MacDonald’s  criteria.

Results
There were 36 cases of probable or highly probable neuroborreliosis (score ≥6), out of which ten cases  were  also  diagnosed  as  possible  (5)  or  confirmed  MS  (5).  The  age  range  was  19  to  43  years,  with  female  predominance  (7/10).  The  clinical  picture  was  marked  by  poor  stamina  and  fatigue,  paresthesia  mainly  in  the  lower  extremities,  palsies  (facial  or  in  the  limbs),  difficult  walking  and  vertigo.  In  all  cases  the  screening  enzyme  immunoassay  was  positive  for  IgM  antibodies,  confirmatory  Western  blots  were  positive  in  four  out  of  seven  tests  performed.  Tick  exposure  was  identified  in  5  cases  without  erythema  migrans.  In  all  patients  cerebral  imaging  examination  revealed  demyelinating  lesions  that  were  interpreted  as  late  NB  and/or  MS  (possible  or  confirmed).  Treatment  with  neurotropic  drugs  and  antibiotics  was  done  and  the  five  patients  with  confirmed  MS  received  beta  interferon  or  corticosteroids.  All  cases  demonstrated  improvement  after  6  weeks  of  sequential  treatment  (ceftriaxone  and  doxycycline).  In  one  case,  the  diagnosis  of  cerebral  lymphoma  was  considered  suggesting  the  association  between  NB  and  MS  or  neuroborreliosis  mimicking  primary  effusion lymphoma.

Conclusions.
The  diagnosis  of  MS  and  NB  are  difficult  showing  remarkable  clinical  and  neuroimaging  similarities.  The  infectious  etiology  of  MS  remains  probable  and  in  patients  with  possible  MS  it  is  reasonable  to  evaluate  B.  burgdorferi  infection  in  order  to  ensure  etiologic  treatment.  

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 07.04.2017 - 17:43:55

Massive intracerebral Epstein-Barr virus reactivation in lethal multiple sclerosis relapse after natalizumab withdrawal

http://www.jni-journal.com/article/S0165-5728(17)30055-3/abstract?cc=y=

March 2017

Abstract

Rebound of disease activity in multiple sclerosis patients after natalizumab withdrawal is a potentially life-threatening event. To verify whether highly destructive inflammation after natalizumab withdrawal is associated with Epstein-Barr virus (EBV) reactivation in central nervous system infiltrating B-lineage cells and cytotoxic immunity, we analyzed post-mortem brain tissue from a patient who died during a fulminating MS relapse following natalizumab withdrawal. Numerous EBV infected B cells/plasma cells and CD8+ T cells infiltrated all white matter lesions; the highest frequency of EBV lytically infected cells and granzyme B+ CD8+ T cells was observed in actively demyelinating lesions. These results may encourage switching to B-cell depleting therapy after natalizumab discontinuation.
*******
Kaksi seikkaa tästä artikkelista: Tysabrin lopettaminen voi olla hengenvaarallista ja toiseksi sen teho näyttää perustuvan siihen, että se pitää EBV:n kurissa.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 07.04.2017 - 17:59:00

Viimeisten testien mukaan minulla on aktiivinen EBV, yhä kaikkien vuosien jälkeen. Ja siihen liittyen CD8 arvo on normaalia pienempi, CD4 normaali, ja niiden suhde normaalia kaksinkertaisesti suurempi. CD8 T-solut tappavat solunsisäisiä bakteereita ja viruksia, ja niitähän minulla on riittänyt. Toisin sanoen immuunipuolustukseni on melko heikko. Mutta tulokset ovat aivan Penderin tutkimusten mukaisia. Sain teetettyä kokeet ulkomailla (Virossa), koska Suomessa en pääse neurologin vastaanotolle edes keskustelemaan.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 07.04.2017 - 19:15:10

Defective T cell control of EBV in MS

http://multiple-sclerosis-research.blogspot.com/2017/03/

Clin Transl Immunology. 2017;6(1):e126

Mounting evidence indicates that infection with Epstein-Barr virus (EBV) has a major role in the pathogenesis of multiple sclerosis (MS). Defective elimination of EBV-infected B cells by CD8+ T cells might cause MS by allowing EBV-infected autoreactive B cells to accumulate in the brain. Here we undertake a comprehensive analysis of the T-cell response to EBV in MS, using flow cytometry and intracellular IFN-γ staining to measure T-cell responses to EBV-infected autologous lymphoblastoid cell lines and pools of human leukocyte antigen (HLA)-class-I-restricted peptides from EBV lytic or latent proteins and cytomegalovirus (CMV), in 95 patients and 56 EBV-seropositive healthy subjects. In 20 HLA-A2+ healthy subjects and 20 HLA-A2+ patients we also analysed CD8+ T cells specific for individual peptides, measured by binding to HLA-peptide complexes and production of IFN-γ, TNF-α and IL-2. We found a decreased CD8+ T-cell response to EBV lytic, but not CMV lytic, antigens at the onset of MS and at all subsequent disease stages. CD8+ T cells directed against EBV latent antigens were increased but had reduced cytokine polyfunctionality indicating T-cell exhaustion. During attacks the EBV-specific CD4+ and CD8+ T-cell populations expanded, with increased functionality of latent-specific CD8+ T cells. With increasing disease duration, EBV-specific CD4+ and CD8+ T cells progressively declined, consistent with T-cell exhaustion. The anti-EBNA1 IgG titre correlated inversely with the EBV-specific CD8+ T-cell frequency. We postulate that defective CD8+ T-cell control of EBV reactivation leads to an expanded population of latently infected cells, including autoreactive B cells.
******
So what did this study find

   The T-cell response to EBV-infected B cells is reduced at all stages of MS except during clinical attacks

   The T-cell response to EBV-infected B cells progressively decreases with increasing duration of MS.

These results are consistent with progressive T-cell exhaustion of EBV-specific CD4+ T cells and CD8+ T cells during the course of MS although they could also be due to other factors, for example an age-related decline in the tendency of EBV to reactivate.

T cell exhaustion is a state of T cell dysfunction that arises during many chronic infections and cancer. It is defined by poor effector function, sustained expression of inhibitory receptors and a transcriptional state distinct from that of functional effector or memory T cells.

The CD8+ T-cell response to EBV lytic phase antigens is reduced at the onset of MS and throughout its course.
CD8+ T cells recognizing EBV latent phase antigens in MS show T-cell exhaustion.

To test this model they suggest that further studies are necessary to determine:
(i) the cause of CD8+ EM/EMRA T-cell deficiency in MS, whether it genetically determined, and related to decreased type I IFN production;
(ii) whether CD8+ T-cell deficiency precedes the onset of MS and is present in healthy first-degree relatives of people with MS,
(iii) whether sunlight deprivation and vitamin D deficiency aggravate the CD8+ T-cell deficiency
(iv) how and why the EBV-specific CD4+ T-cell response declines during the course of MS;
(v) whether oral shedding of EBV is increased during clinical attacks;
(vi) whether the frequency of EBV-infected memory B cells in the blood is increased in MS, as in rheumatoid arthritis and systemic lupus erythematosus;
(vii) whether EBV-infected B cells and plasma cells in the CNS in MS are autoreactive, and (viii) finally and most importantly, whether therapies aimed at controlling EBV infection, such as EBV-specific T-cell therapy,prevent and cure MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.04.2017 - 16:05:18

Preliminary study suggests possible new treatment for MS

https://www.sciencedaily.com/releases/2017/04/170420162236.htm

A small, preliminary study may show promise of a new type of treatment for progressive multiple sclerosis (MS). Results from the first six people enrolled in the phase 1 study, a study designed to enroll 10 people, are being presented at the American Academy of Neurology's 69th Annual Meeting in Boston, April 22 to 28, 2017.

Phase 1 studies are designed to evaluate the safety of a treatment and identify side effects, using a small number of participants. While it was not the goal of this study to measure how effective the treatment was, symptoms improved for three of the six participants.

"While these results are very preliminary and much more research is needed, we are excited there were no serious side effects," said study author Michael Pender, MD, PhD, of The University of Queensland in Brisbane, Australia.

The study investigates the relationship between MS and the Epstein-Barr virus (EBV), a herpes virus that is extremely common but causes no symptoms in most people. However, when a person contracts the virus as a teenager or adult, it often leads to mononucleosis. Previous research has shown a link between the virus and MS.

The study involved six people with progressive MS with moderate to severe disability. People with progressive MS have a severe condition with slow, steady worsening of symptoms.

In MS, the body's immune system attacks the nerves in the central nervous system. As part of the normal immune response, immune cells called T cells and B cells work together to protect the body against infectious agents. In some people with MS, the immune response may be altered and T cells may be unable to control EBV-infected B cells, which accumulate in the brain and produce antibodies that attack and destroy myelin, the protective layer that insulates nerves in the brain and spinal cord. This in turns leads to neurologic dysfunction and symptoms. Elimination of the EBV-infected B cells may reduce the destruction of myelin in MS.

For the study, researchers removed the participants' own T cells and stimulated them to boost their ability to recognize and destroy cells infected with Epstein-Barr virus. They then injected participants with infusions of escalating doses of T cells every two weeks for six weeks. They followed the patients through 26 weeks to look for evidence of side effects and possible improvement of symptoms.

Three of the participants showed improvement, starting two to eight weeks after the first infusion.

"One person with secondary progressive MS showed striking improvement," Pender said. "This participant had a significant increase in ambulation from 100 yards with a walker at the start of the study, and over the previous five years, to three quarters of a mile, and was now also able to walk shorter distances with only one sided assistance. Lower leg spasms that had persisted for 20 years resolved."

Pender said another participant with primary progressive MS showed improved color vision and visual acuity.

All three responding participants had improvements in fatigue and ability to perform daily activities.

"The best responses were seen in the two people who received T cells with the highest amount of reactivity to the Epstein-Barr virus," Pender said.

None of the six participants had serious side effects.

"Of course, much more research needs to be done with larger numbers of participants to confirm and further evaluate these findings," Pender said. "But the results add to the mounting evidence for a role of the Epstein-Barr virus infection in MS and set the stage for further clinical trials.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 21.04.2017 - 16:08:53

EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model.

https://www.ncbi.nlm.nih.gov/pubmed/27836419

Dec 2016

Abstract

Multiple sclerosis (MS) is thought to be initiated by the interaction of genetic and environmental factors, eliciting an autoimmune attack on the central nervous system. Epstein-Barr virus (EBV) is the strongest infectious risk factor, but an explanation for the paradox between high infection prevalence and low MS incidence remains elusive. We discuss new data using marmosets with experimental autoimmune encephalomyelitis (EAE) - a valid primate model of MS. The findings may help to explain how a common infection can contribute to the pathogenesis of MS. We propose that EBV infection induces citrullination of peptides in conjunction with autophagy during antigen processing, endowing B cells with the capacity to cross-present autoantigen to CD8+CD56+ T cells, thereby leading to MS progression.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.05.2017 - 16:35:34

Cancer-causing virus masters cell's replication, immortality
Epstein-Barr virus steers the B-cell to hide in plain sight


https://www.sciencedaily.com/releases/2017/05/170502204538.htm

May 2, 2017
Viruses are notorious for taking over their host's operations and using them to their own advantage. But few human viruses make themselves quite as cozy as the Epstein-Barr virus, which can be found in an estimated nine out of ten humans without causing any ill effects.

That is, until this virus causes mononucleosis in adolescents or various cancers of the lymph nodes, including Hodgkin's and non-Hodgkin's lymphomas, in immune compromised people.

In a paper appearing in the open access journal eLife, a team of researchers from Duke's School of Medicine details just how the Epstein-Barr virus manages to persist so well inside the immune system's B cells, a type of white blood cell that is normally responsible for recognizing and responding to foreign invaders.

"The challenge is that it's a really efficient pathogen," and evades the host's immune system well even when it's recognized as an invader, said Micah Luftig, an associate professor of molecular genetics and microbiology and co-author on the new study.

Luftig's team has found that with a few select chemical signals used early in the course of an infection, Epstein-Barr mimics the beginning of the B cell's normal response to an infectious agent. From within, the virus manages to ramp up the B-cell's reproduction of itself, while at the same time helping the cell resist its own self-destruct signals.

"The virus actually taps into the B cell's normal protection against apoptosis," the programmed cell death that takes B cells out of circulation, Luftig said.

Once the infection is established, Epstein-Barr prefers to hide out in what are known as "memory B cells," relatively slowly reproducing cells that circulate throughout the body. "All of this is about establishing latency," Luftig said, or the ability to hide quietly in plain sight.

Using a new technique developed elsewhere called BH3 profiling that allowed them to test the critical cellular pro- and anti-apoptosis proteins individually, the team was able to see which of these the virus was controlling and then watch the transition from an uninfected cell to the active early infection phase to the latent infection in an immortal cell. The key piece they've uncovered is a viral protein called EBNA3A which manages apoptosis resistance in infected B cells.

The risk for cancers "is largely an issue if you're immune suppressed," Luftig said. But, for example, a recent National Cancer Institute study found that children who receive organ transplants have a 200-times higher chance of getting Non-Hodgkin's Lymphoma, one of the cancers caused by Epstein-Barr.

The team thinks BH3 profiling could prove useful in guiding treatment decisions on Epstein-Barr associated cancers such as these.





Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 26.05.2017 - 18:22:39

Evaluation of reactive Epstein-Barr virus (EBV) in Iranian patients with different subtypes of multiple sclerosis (MS)

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702013000200007

March/April 2013

ABSTRACT

OBJECTIVES: Epstein-Barr virus has been recently associated with the onset of multiple sclerosis, yet understanding how it elicits autoimmunity remains elusive. We investigated the relation between Epstein-Barr virus reactivation and disease development in different subtypes of multiple sclerosis.

METHODS: In the present research, we have determined the Epstein-Barr virus-DNA load by quantitative real-time polymerase chain reaction and Epstein-Barr virus antibody levels by EIA technique in both multiple sclerosis patients (n = 78) and healthy controls (n = 123).

RESULTS: Our results demonstrated increased titer of both anti-Epstein-Barr virus-IgG and IgM antibodies in patients (91.02% vs 82.11% in controls, p < 0.001 and 14.1% vs 4.06% in controls, p < 0.001, respectively). Overall, Epstein-Barr virus reactivation was found in 68.75% of subtypes of multiple sclerosis, 4.54% of multiple sclerosis primary subtype, and in only 3.25% of healthy control subjects. Moreover, in samples of patients with disease relapse (exacerbation) cell free viral DNA was elevated in contrast to other patients (p < 0.001).

CONCLUSIONS: These findings provide further support for the detrimental effects of Epstein- Barr virus in the reactivation of multiple sclerosis attacks.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.06.2017 - 13:54:24

Time correlation between mononucleosis and initial symptoms of MS

http://nn.neurology.org/content/4/3/e308.full.pdf

ABSTRACT
Objective:
To determine the average age of MS onset vs the age at which Epstein-Barr infection has previously occurred and stratify this analysis by sex and the blood level of Epstein-Barr nuclear antigen 1 (EBNA1) antibody.

Methods:
Using infectious mononucleosis (IM) as a temporal marker in data from the Swedish epidemiologic investigation of MS, 259 adult IM/MS cases were identified and then augmented to account for “missing” childhood data so that the average age of MS onset could be determined for cases binned by age of IM (as stratified by sex and EBNA1 titer level).

Results:
Mean age of IM vs mean age of MS reveals a positive time correlation for all IM ages (from 5to 30 years), with IM-to-MS delay decreasing with increased age. When bifurcated by sex or EBNA1 blood titer levels, males and high-titer subpopulations show even stronger positive time correlation, while females and low-titer populations show negative time correlation in early childhood (long IM/MS delay). The correlation becomes positive in females beyond puberty.

Conclusions:
IM/MS time correlation implies causality if IM is time random. Alternative confounding models seem implausible, in light of constraints imposed by time-invariant delay observed here. Childhood infection with Epstein-Barr virus (EBV) in females and/or those genetically prone to low EBNA1 blood titers will develop MS slowly. Males and/or high EBNA1-prone develop MS more rapidly following IM infection at all ages. For all, postpubescent EBV infection is critical for the initiation and rapid development of MS.

Neurol Neuroimmunol Neuroinflamm 2017;4:e308; doi:10.1212/

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 16.06.2017 - 20:35:24

Suomessa, Jyväskylän yliopistossa, on kehitetty testi borrelioosin ja lisäinfektioiden testaamiseen EU:n tuella. Testi on ollut käytössä Saksassa Arminlabsissa toukokuun alusta. Yhdellä testillä voi selvitä onko borrelioosi, clamydia pneumonia jne. Maailmalla on tulossa monia samankaltaisia testejä, esimerkiksi sen tutkimiseen sairastaako viruksen tai bakteerin aiheuttamaa infektiota.Eli tämä on aika kehittynyttä teknologiaa. Olen kuullut että Suomessa ainakaan infektiolääkärit eivät hyväksy testin tuloksia. Itselläni on taas aika tutkituttaa infektiotilanne, ja  tämä on yksi vaihtoehto. Kokonaiskuvan saamiseen tämä on halvin, yhden tai kahden infektion tutkimiseen kallis (n. 500€)

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Our technology is intended to tests for both early and late Lyme Disease and other tick-borne diseases. Our tests facilitate healthcare providers to test up to 20 tick-borne disease microbes against multiple antibody types that aids in pinpointing not only the causative agent for a patient’s illness but also the stage of illness, thus our tests are a multiplex and multi-functional diagnostic kits. Furthermore, the kits are equipped very specific antigens to enable detection at a higher sensitivity than ever before. Lastly, Te?teds digital healthcare solution is intended to deliver processed results to clinicians in order to expedite convenience and ease. Our vision is to establish our products as the standard for diagnosing tick-borne diseases so that patients no longer need to compromise with their quality of life and living standards. We truly believe if the patient can be tested the patient can be treated.

http://tezted.com/#focus
https://www.arminlabs.com/en/news/tickplex

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.07.2017 - 17:31:02

Hidden herpes virus may play key role in MS, other brain disorders

https://www.sciencedaily.com/releases/2017/07/170710122959.htm

July 10, 2017

The ubiquitous human herpesvirus 6 (HHV-6) may play a critical role in impeding the brain's ability to repair itself in diseases like multiple sclerosis. The findings, which appear in the journal Scientific Reports, may help explain the differences in severity in symptoms that many people with the disease experience.

"While latent HHV-6 -- which can be found in cells throughout the brain -- has been associated with demyelinating disorders like multiple sclerosis it has not been clear what role, if any, it plays in these diseases," said Margot Mayer-Proschel, Ph.D., an associate professor at the University of Rochester Medical Center Department of Biomedical Genetics and co-author of the study. "These findings show that, while in the process of hiding from the immune system, the virus produces a protein that has the potential to impair the normal ability of cells in the brain to repair damaged myelin."

It is estimated that more than 80 percent of people have been exposed to HHV6 at some point during their early childhood. HHV-6 is the most common human herpesvirus and infections that occur during childhood often go unnoticed but the virus can cause roseola, which is characterized by a fever and rash in infants. A much smaller number -- one percent of people -have congenital HHV6 where a single copy of the virus is acquired through either the father's sperm or mother's egg and is passed on to the developing child.

While the immune system fights off the most active forms of the infection, the virus never truly leaves our bodies and can reactivate later in life. The herpesvirus 6 accomplishes this form of latency by integrating itself into our genetic code and thus hiding in cells and evading the immune system.

One of the first studies to show an association between latent HHV-6 infection and demyelinating disorders was conducted in 2003 by URMC researchers David Mock, M.D., who is a co-author of the current study, Andrew Goodman, M.D. and others. They noted that HHV6 genetic code could be found in the brain cells of individuals with severe forms of multiple sclerosis.

Viruses have long been suspected to contribute to multiple sclerosis, a disorder in which the body's own immune system attacks and destroys myelin -- the fatty tissue that insulates the connections between nerve cells. However, while the 2003 study indicated that the herpes virus played some role in multiple sclerosis, it has subsequently become clear that the virus is unlikely to trigger the disease.

The Rochester researchers in the current paper took a new approach and asked instead whether the virus could have an impact on a critical support cell found in the brain called oligodendrocyte progenitor cells (OPCs). These cells play an important role in maintaining the brain's supply of myelin. When myelin is lost to disease, age, or injury, OPCs are activated, migrate to where they are needed, and mature into myelin-producing cells which repair the damage.

The researchers examined the impact of the latent HHV-6 on the activity of human OPCs, which was possible through the work of Chris Proschel, a co-author of the manuscript with expertise in the generation of human OPCs. One of the ways the virus stays hidden in cells is by expressing a protein called U94 that helps it keep its place in the human DNA and remain undetected from the immune system. By studying human cells and transplanting human OPCs into animal models, the team discovered that when U94 was expressed in OPCs, the cells stopped migrating to where they were needed.

What is still not fully understood is the relationship between the extent of the viral infection in the brain and the severity of diseases like multiple sclerosis and other demyelinating diseases such as leukodystrophies and Vanishing White Matter disease. For example, do the number of infected cells need to reach a certain threshold before OPC function is impeded? Are individuals who have congenital HHV6 more vulnerable to severe forms of these diseases?

"More research is needed to understand by which mechanisms the virus impedes the function of OPCs and what impact this has on the progression of these diseases," said Mayer-Proschel. "But it is clear that HHV6, while not necessarily the cause of demyelinating diseases, is limiting the ability of the brain to repair damage to myelin thereby potentially accelerating the progression of these diseases."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 29.07.2017 - 19:34:01

Quantitative Detection of Epstein-Barr Virus DNA in Cerebrospinal Fluid and Blood Samples of Patients with Relapsing-Remitting Multiple Sclerosis

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0094497

April 10, 2014

Abstract

The presence of Epstein-Barr Virus (EBV) DNA in cerebrospinal fluid (CSF) and peripheral blood (PB) samples collected from 55 patients with clinical and radiologically-active relapsing-remitting MS (RRMS) and 51 subjects with other neurological diseases was determined using standardized commercially available kits for viral nucleic acid extraction and quantitative EBV DNA detection. Both cell-free and cell-associated CSF and PB fractions were analyzed, to distinguish latent from lytic EBV infection. EBV DNA was detected in 5.5% and 18.2% of cell-free and cell-associated CSF fractions of patients with RRMS as compared to 7.8% and 7.8% of controls; plasma and peripheral blood mononuclear cells (PBMC) positivity rates were 7.3% and 47.3% versus 5.8% and 31.4%, respectively. No significant difference in median EBV viral loads of positive samples was found between RRMS and control patients in all tested samples. Absence of statistically significant differences in EBV positivity rates between RRMS and control patients, despite the use of highly sensitive standardized methods, points to the lack of association between EBV and MS disease activity.
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Tämä tutkimus ei siis löytänyt yhteyttä EBV-viruksen ja MS:n välillä. Toiset tutkimukset ovat löytäneet yhteyden, joten potilaat vaan joutuvat odottamaan jonkinlaista selvyyttä.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 05.08.2017 - 16:36:33

Programmed death 1 is highly expressed on CD8+CD57+ T cells in patients with stable multiple sclerosis and inhibits their cytotoxic response to EBV.

Cencioni MT1, Magliozzi R1,2, Nicholas R1,3, Ali R1,3, Malik O1,3, Reynolds R1, Borsellino G4, Battistini L4, Muraro P1,3.

https://www.ncbi.nlm.nih.gov/pubmed/28767147


Abstract

Growing evidence points to a deregulated response to Epstein-Barr virus (EBV) in the CNS of patients with Multiple Sclerosis (pwMS) as a possible cause of disease. In this study, we have investigated the response of a subpopulation of effector CD8+ T cells to EBV in 36 healthy donors and in 35 pwMS in active and inactive disease. We have measured the expression of markers of degranulation, the release of cytokines, cytotoxicity and the regulation of effector functions by inhibitory receptors, such as programmed death-1 (PD-1) and human inhibitor receptor Ig-like transcript 2 (ILT2). We demonstrate that polyfunctional cytotoxic CD8+CD57+ T cells are able to kill EBV-infected cells in healthy donors. In contrast, an anergic exhaustion-like phenotype of CD8+CD57+ T cells with high expression of PD-1 was observed in inactive pwMS compared with active pwMS or healthy donors. Detection of CD8+CD57+ T cells in meningeal inflammatory infiltrates from post-mortem MS tissue confirmed the association of this cell phenotype with the disease pathological process. The overall results suggest that ineffective immune control of EBV in pwMS during remission may be one factor preceding and enabling the reactivation of the virus in the CNS and may cause exacerbation of the disease.
This article is protected by copyright. All rights reserved.
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Itselläni CD8+ testattiin keväällä pyynnöstäni Tallinnassa ja heinäkuussa testautin CD57+ arvot uudelleen, tällä kertaa myös Tallinnassa. Kuten oletin, testien mukaan CD8 on selvästi minimitason alapuolella. CD57 on testattu säännöllisesti Saksassa liittyen krooniseen borrelioosiin, ja se on ollut olematon kunnes viime vuonna ponnisti minimiin ja on pysynyt siellä. Aikoinaan MS-diagoosin yhteydessä tutkittiin paljon eri viruksia, muttei EBV:tä. Eikä otettu borrelioosi verikokeita, eikä borrelioosi DNA:ta selkäydinnesteestä. Itse asiassa borrelioosin diagnoosi on kliininen (koska verikokeet eivät ole täysin luotettavia), mutta minua ei tutkinut infektiolääkäri, joka olisi poissulkenut borrelioosin. Kliininen diagnoosi tapahtui vasta myöhemmin, kun lähdin asiaa itse selvittämään.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 22.09.2017 - 15:54:20

Epstein-Barr virus, cytomegalovirus, and multiple sclerosis susceptibility

http://www.neurology.org/content/early/2017/08/30/WNL.0000000000004412


Abstract

Objective: To determine whether Epstein-Barr virus (EBV) or cytomegalovirus (CMV) seropositivity is associated with multiple sclerosis (MS) in blacks and Hispanics and to what extent measures of the hygiene hypothesis or breastfeeding could explain these findings. EBV and CMV have been associated with MS risk in whites, and the timing and frequency of both viruses vary by factors implicated in the hygiene hypothesis.

Methods: Incident cases of MS or its precursor, clinically isolated syndrome (CIS), and matched controls (blacks, 111 cases/128 controls; Hispanics, 173/187; whites, 235/256) were recruited from the membership of Kaiser Permanente Southern California. Logistic regression models accounted for HLA-DRB1*1501 status, smoking, socioeconomic status, age, sex, genetic ancestry, and country of birth.

Results: Epstein-Barr nuclear antigen-1 (EBNA-1) seropositivity was independently associated with an increased odds of MS/CIS in all 3 racial/ethnic groups (p < 0.001 for blacks and whites, p = 0.02 for Hispanics). In contrast, CMV seropositivity was associated with a lower risk of MS/CIS in Hispanics (p = 0.004) but not in blacks (p = 0.95) or whites (p = 0.96). Being born in a low/middle-income country was associated with a lower risk of MS in Hispanics (p = 0.02) but not after accounting for EBNA-1 seropositivity. Accounting for breastfeeding did not diminish the association between CMV and MS in Hispanics.

Conclusions: The consistency of EBNA-1 seropositivity with MS across racial/ethnic groups and between studies points to a strong biological link between EBV infection and MS risk. The association between past CMV infection and MS risk supports the broader hygiene hypothesis, but the inconsistency of this association across racial/ethnic groups implies noncausal associations.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.10.2017 - 13:38:15

Multiple sclerosis: an example of pathogenic viral interaction?

https://virologyj.biomedcentral.com/articles/10.1186/s12985-017-0719-3

Abstract

A hypothesis is formulated on viral interaction between HHV-6A and EBV as a pathogenic mechanism in Multiple Sclerosis (MS). Evidence of molecular and genetic mechanisms suggests a link between HHV-6A infection and EBV activation in the brain of MS patients leading to intrathecal B-cell transformation. Consequent T-cell immune response against the EBV-infected cells is postulated as a pathogenic basis for inflammatory lesion formation in the brain of susceptible individuals. A further link between HHV-6A and EBV involves their induction of expression of the human endogenous retrovirus HERV-K18-encoded superantigen. Such virally induced T-cell responses might secondarily also lead to local autoimmune phenomena. Finally, research recommendations are formulated for substantiating the hypothesis on several levels: epidemiologically, genetically, and viral expression in the brain.
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Conclusion

A link is postulated between HHV-6A and EBV in the aetio-pathogenesis of MS.

In summary, the tenet is that infection with the neurotropic HHV-6A leads to transformation of latently EBV-infected B-cells in the CNS. Both viruses will elicit a T-cell response, either specific towards HHV-6A and EBV, or non-specific as a response to the HERV-K18-encoded superantigen. Such viral induced T-cell responses might secondarily also lead to autoimmune phenomena. Evidence for mechanisms for induction of autoimmunity by viral infections has recently been reviewed [56].

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.10.2017 - 13:44:43

How seemingly acute viral infections can persist

https://www.sciencedaily.com/releases/2017/10/171006085921.htm

October 6, 2017
Infections caused by viruses, such as respiratory syncytial virus, or RSV, measles, parainfluenza and Ebola, are typically considered acute. These viruses cause disease quickly and live within a host for a limited time. But in some cases the effects of the infection, and presence of the virus itself, can persist. RSV, for example, can lead to chronic respiratory problems, measles can lead to encephalitis and the Ebola virus can be transmitted by patients thought to be cured of the disease.

New findings from the University of Pennsylvania suggest a mechanism that may explain how viruses can linger. Products of viral infection called defective viral genomes, DVGs for short, which have been known to be involved in triggering an immune response, can also kick off a molecular pathway that keeps infected cells alive, the researchers discovered. The study used a novel technique to examine the presence of DVGs on a cell-by-cell basis to show that DVG-enriched cells had strategies to survive in the face of an immune-system attack.

"One of the things the field has known for a long time is that DVGs promote persistent infections in tissue culture," said Carolina B. López, an associate professor of microbiology and immunology in Penn's School of Veterinary Medicine. "But the question was, How do you reconcile that with the fact that they're also very immunostimulatory? How can they help clear virus at the same time as they promote persistence? Our work helps explain this apparent paradox."

López was senior author on the work, teaming with co-lead authors and lab members Jie Xu and Yan Sun. Fellow coauthors included Gordon Ruthel and Daniel Beiting of Penn Vet, Yize Li and Susan R. Weiss of Penn's Perelman School of Medicine and Arjun Raj of the School of Engineering and Applied Science. Their study was published in Nature Communications.

DVGs have been a major focus of López's lab for years. These partial viral genomes are produced in infected cells when a virus begins to replicate rapidly, leading to defective versions of itself that contain large deletions. Once thought not to have any biological function, DVGs are increasingly believed to be important components of viral infections.

In 2013, López and colleagues reported that DVGs were critical in stimulating an immune response to respiratory viruses in mice; when DVGs were depleted from a virus, mice had more severe infections. In 2015 they reported that DVGs are also critical for stimulating an immune response to the human virus RSV, also demonstrating for the first time that the presence of DVGs in human respiratory samples from infected patients correlates with enhanced antiviral immune responses.

In the current work, López's team used a sophisticated technique that allowed them to differentiate full-length genomes from the partial genomes of DVGs at the single-cell level. They studied cells in culture infected with the Sendai virus, or with RSV, a virus that often affects infants and can lead to chronic respiratory problems,

Labeling the full-length genomes in red and the partial DVGs in green, the researchers found differences from cell to cell. Some cells had hardly any DVGs, while others were highly enriched with DVGs, with only a small number of full-length genomes.

"We saw this in many different cell lines and even in infected lungs in mice," López said. "We hadn't appreciated before that there is a lot of heterogeneity in what is going on with these DVGs."

To dig deeper into how the DVGs were influencing the course of infection, the researchers infected cells either with a version of the Sendai virus that lacked DVGs or one enriched in DVGs. The cells infected with the virus high in DVGs survived more than twice as long as those infected with virus lacking DVGs. Adding purified DVGs boosted the cells' survival time, indicating a direct role for the DVGs in promoting cell survival.

The results were similar in parallel experiments with RSV, suggesting that the pro-survival role of DVGs held across viral types.

The researchers next were curious to know what molecular pathways might enable the DVG-rich cells to avoid apoptosis. An analysis of highly-expressed genes in DVG-enriched cells compared to the cells with full-length viral genomes revealed that a host of pro-survival genes were activated in the DVG-rich cells. Notably, these genes encoded signaling proteins of the TNF pathway, known to both boost immunity and cell survival, and IFN, known to play a role in antiviral immunity.

A final set of experiments elucidated the mechanism by which a subset of DVG-enriched cells persisted during viral infection. López and colleagues found that signaling through the proteins MAVS and TNF receptor 2 protects infected cells from apoptosis that is otherwise triggered by TNF?.

"We found this dual role for TNF during these infections," López said. "If TNF binds to a cell that doesn't have the MAVS pathway engaged but is infected, the cell is killed, but, if the cell does have this pathway engaged, then it is protected. MAVS is engaged during the antiviral response, and only cells that have a lot of DVGs activate this pathway. These data show that our cells are wired to survive if they are engaged in an antiviral response, explaining the paradoxical functions of DVGs. It seems that in order to persist, the virus is taking advantage of these host pathways that are there to promote the survival of cells working to eliminate the virus."

The results, though limited to in vitro studies in the current report, point to a way that DVGs could enable "acute" viral infections to linger.

López hopes to build on these findings to be sure they hold in vivo. She's also curious to learn more about the dual roles of TNF, which may help explain why the use of TNF-targeted therapies hasn't always turned out as expected.

"I want to see if there's a way we can harness this pathway to minimize and avoid the persistence of these viruses, which is really relevant if we think about the chronic diseases associated with some of these respiratory viruses," López said.

In addition, she would like to explore how generalizable this pathway is and if it could, perhaps, help explain the problems with viral persistence seen in such infections with the Ebola and Zika viruses.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 31.10.2017 - 16:21:01

Infectious Agents and Neurodegenerative Diseases: Exploring the Links

http://www.eurekaselect.com/148942/article

Volume 17 , Issue 12 , 2017

Abstract:

Recent studies have shown that bacterial and viral infections are risk factors for various neurodegenerative diseases such as Amyotrophic lateral sclerosis (ALS), Multiple Sclerosis (MS), Alzheimer’s disease (AD), and Lyme disease (LD). However, it is still controversial how the infections play a role in neurological diseases progression. Infections in central nervous system may lead multiple damages in infected and neighboring cells. The infection leads to the activation of inflammatory processes and host immune responses, which acts as defense mechanism and also causes damage to the host neuronal functions and viability. Several bacterial and viral pathogens have been reported for neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in combination with other factors, like aging, metabolic diseases and the genetic makeup of the host. We will focus in this review on the possible link between neurodegeneration and infections particularly Chlamydophila pneumoniae, Borrelia burgdorferi, Mycoplasma etc.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 31.10.2017 - 16:24:22

Cerebrovascular Manifestations of Lyme Neuroborreliosis—A Systematic Review of Published Cases

https://www.frontiersin.org/articles/10.3389/fneur.2017.00146/full

20 April 2017
Background: Lyme neuroborreliosis (LNB) is a disease caused by spirochete Borrelia burgdorferi, involving the nervous system. It usually manifests as lymphocytic meningoradiculitis, but in rare cases, it can also lead to cerebrovascular complications. We aimed to perform a systematic review of all reported cases of LNB complicated by central nervous system vasculitis and stroke or transient ischemic attack (TIA).

Materials and methods: We conducted a systematic review of literature between May 1987 and December 2016 with patients who presented with cerebrovascular course of LNB.

Results: This study included 88 patients with a median age of 46 years. The median interval from onset of symptoms suggesting Lyme disease to first symptoms of cerebrovascular manifestations of LNB was 3.5 months. The most common cerebrovascular manifestation of LNB was ischemic stroke (76.1%), followed by TIA (11.4%). The posterior circulation was affected alone in 37.8% of patients, the anterior circulation in 24.4% of patients, and in 37.8% of cases, posterior and anterior circulations were affected simultaneously. The most common affected vessels were middle cerebral artery—in 19 cases, basilar artery—in 17 cases, and anterior cerebral artery—in 16 cases. A good response to antibiotic treatment was achieved in the vast number of patients (75.3%). The overall mortality rate was 4.7%.

Conclusion: Cerebral vasculitis and stroke due to LNB should be considered, especially in patients who live in or have come from areas with high prevalence of tick-borne diseases, as well as in those without cardiovascular risk factors, but with stroke-like symptoms of unknown cause.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.11.2017 - 21:36:53

More Australian trials for a cutting edge treatment

https://msra.org.au/news/australian-trials-cutting-edge-treatment/

01 November, 2017

Earlier in the year we announced  some exciting preliminary results from a phase 1 clinical trial into a novel therapy for progressive MS. Professor Michael Pender from the University of Queensland and Professor Rajiv Khanna from QIMR Berghofer Medical Research Institute lead a study into a new therapy called autologous EBV-specific adoptive immunotherapy.

In this trial specific cells from the immune system (T cells) were isolated from an individual’s blood. These cells were then exposed to a vaccine for Epstein Barr Virus (EBV) which has been shown to re-target and focus the T cells so they can more effectively kill EBV infected cells. These newly fortified T cells were then injected back into the person.

This therapy is called autologous immunotherapy, because the immune cells are obtained from and returned to the same individual so it is considered autologous, whereas if the cells were donated from a different individual it would be called allogenic. The phrase immunotherapy indicates that it is a therapy that enables your own immune system to fight off its target, in this case EBV.

This trial has arisen out of Professors Pender’s extensive fundamental research into the role EBV plays in MS. Professor Pender’s work and the work of other scientists have shown that EBV plays an important role in the development of MS. While EBV is a common infection in the general public, with between 90-95% of people being infected, it is thought that 100% of people with MS are infected. While EBV is associated with glandular fever (also known as infectious mononucleosis) in most infections it causes just a general non-specific viral illness resulting in most people not realising they have been infected.

Professor Pender and his team have previously shown that there are differences in the immune system in people with MS compared to people without MS, especially when it comes to controlling EBV infection. They hypothesised that targeting EBV infected cells in people with MS might help combat the disease.

While the full results have not yet been released from the trial, it has been reported that six out of the ten people with progressive MS treated (both primary and secondary progressive MS) showed clinical improvement.  It is important to note that this was an early trial and it was primarily designed to test the safety of the treatment, and not the efficacy of the treatment. No serious side effects were reported. Whilst this was a very early clinical trial we are cautiously optimistic. Going forward this treatment will be referred to as ATA190.

Atara Biotherapeutics have just released a press release stating that they have initiated a new multinational, multicentre Phase 1 clinical study to evaluate allogeneic immunotherapy in patients with progressive or relapsing-remitting MS. This is a very similar treatment but is allogeneic immunotherapy where the retrained T cells infused into the person come from a different donor. The treatment is referred to as ATA188.

The primary objective of this clinical trial is to assess the safety of allogeneic immunotherapy for at least 1 year after the first dose. At the same time they will be examining improvement or halting of MS progression.

The trial is expected to enrol a total of 60 patients; 30 patients with progressive forms of MS, and 30 patients with relapsing-remitting MS (RRMS) across Australia, the USA, and Europe.  More information about the Australian arm of the study will be made available shortly on the www.mstrials.org.au website.

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https://globenewswire.com/news-release/2017/07/31/1064895/0/en/Atara-Biotherapeutics-Announces-Two-Presentations-at-MSParis2017-Including-Updated-Interim-Results-from-a-Phase-1-Study-of-Autologous-ATA188-in-Patients-with-Progressive-Multiple-S.html

https://globenewswire.com/news-release/2017/10/19/1150382/0/en/Atara-Biotherapeutics-Initiates-60-Patient-Global-Phase-1-Clinical-Study-to-Evaluate-Allogeneic-ATA188-in-Patients-with-Progressive-or-Relapsing-Remitting-Multiple-Sclerosis-MS.html

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 15.12.2017 - 20:49:03

Anti-Human Immunodeficiency Virus Agent 3'-Azido-3'- Deoxythymidine Inhibits Replication of Epstein-Barr Virus

https://pdfs.semanticscholar.org/946e/e84c9c9fea640cdcc777b38feed64d34e383.pdf

Feb. 1988

We show that the anti-human immunodeficiency virus agent, 3'-azido-3'-deoxythymidine (AZT), which suppresses
infectivity and cytopathic effects of human immunodeficiency virus, also effectively inhibits Epstein-Barr virus (EBV) DNA replication. However, AZT has no effect on four other human herpesviruses: cytomegalovirus, varicella-zoster virus, and herpes simplex virus types 1 and 2. The combination of acyclovir and  AZT, while it is not synergistic, has an additive effect against EBV replication. AZT may prove to be a useful drug for treatment of coinfections with human immunodeficiency virus and EBV.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 19.12.2017 - 22:15:11

Lyme bacteria survive 28-day course of antibiotics months after infection

https://www.sciencedaily.com/releases/2017/12/171213143613.htm

December 13, 2017

Bay Area Lyme Foundation, a leading sponsor of Lyme disease research in the US, today announced results of two papers published in the peer-reviewed journals PLOS ONE and American Journal of Pathology, that seem to support claims of lingering symptoms reported by many patients who have already received antibiotic treatment for the disease.

Based on a single, extensive study of Lyme disease designed by Tulane University researchers, the study employed multiple methods to evaluate the presence of Borrelia burgdorferi spirochetes, the bacteria that cause Lyme disease, before and after antibiotic treatment in primates. The study also measured the antibody immune response to the bacteria both pre- and post- treatment, as this is how current diagnostics typically evaluate Lyme disease in humans.

The data show that living B. burgdorferi spirochetes were found in ticks that fed upon the primates and in multiple organs after treatment with 28 days of oral doxycycline. The results also indicated that the immune response to the bacteria varied widely in both treated and untreated subjects.

"It is apparent from these data that B. burgdorferi bacteria, which have had time to adapt to their host, have the ability to escape immune recognition,tolerate the antibiotic doxycycline and invade vital organs such as the brain and heart," said lead author Monica Embers, PhD, assistant professor of microbiology and immunology at Tulane University School of Medicine.

"In this study, we were able to observe the existence of microscopic disease and low numbers of bacteria, which would be difficult to 'see' in humans but could possibly be the cause of the variable and nonspecific symptoms that are characteristic of post-treatment Lyme disease syndrome. Although current antibiotic regimens may cure most patients who are treated early, if the infection is allowed to progress, the 28-day treatment may be insufficient, based on these findings," Embers said.

The findings also demonstrated:

*  All subjects treated with antibiotics were found to have some level of infection 7 -- 12 months post treatment.
*  Despite testing negative by antibody tests for Lyme disease, two of 10 subjects were still infected with Lyme bacteria in heart and bladder.
*  Lyme bacteria which persist are still viable.

To better elucidate previous animal studies demonstrating that some B. burgdorferi bacteria survive antibiotics, the study explored Lyme disease infection in rhesus macaque primates treated with antibiotics and a control group who were also infected but not treated. This species has been shown to demonstrate a progression of Lyme disease most similar to humans, particularly related to erythema migrans, carditis, arthritis, and neuropathy of the peripheral and central nervous systems.

"Clearly, some medical practices governing diagnosis and treatment of Lyme disease should be reconsidered in light of this study. This study shows that we must reevaluate the current paradigm of antibody response tests for diagnosis and move away from the one size fits all approach to Lyme treatment," said Wendy Adams, Research Grant Director, Bay Area Lyme Foundation. "Every day, patients with Lyme disease are told their symptoms cannot be caused by Lyme, because they test negative on antibody tests or because they have received a single course of antibiotics. More research and funding are imperative."

In the study, ticks carrying B. burgdorferi spirochetes fed on ten primates. Four months post infection, half of the primates (five) received the antibiotic doxycycline orally for 28 days at a proportional dose to that used in human treatment. Five subjects were treated with placebo and all ten were evaluated by more than five different diagnostic methods to characterize any remaining infection. The researchers used several important techniques, including xenodiagnoses, to determine if the spirochete bacteria persisted.

The results show:

*  Few subjects displayed a rash. Although all subjects were infected, only one of the 10 displayed a rash with central clearing, the classical "bulls-eye" rash. The subject that developed this rash, interestingly, never mounted an immune response to five borrelia antigens throughout the study period, prior to and following treatment.
*  Organs may be infected even if antibody tests are negative. One subject which tested negative for B. burgdorferi by skin biopsy cultures, PCR and in vivo cultures, was found to have B. burgdorferi infecting the heart. Another untreated subject, who was ultimately shown to have residual Lyme bacteria in the bladder, showed a decrease in immune response over the course of infection, with a negative xenodiagnosis test in the late stage, which would signal that the animal self-cured.
*  Intact spirochetes were found in three of five treated and four of five untreated subjects based on xenodiagnosis results 12 months after the tick bite.
*  Immune responses to B. burgdorferi varied greatly post-treatment, with one subject's antibody levels dropping to pre-bite levels for three antigens while another subject experienced elevated antibodies for the same antigens throughout the study period. This is significant because it demonstrates that subjects infected with the same strain of B. burgdorferi may have different immune responses to the same antigen. And, because humans, like primates, are genetically diverse, it underscores that testing antibody responses may be inherently unreliable as a singular diagnostic modality for Lyme disease.
* Widespread and variable microscopic disease was observed in all infected subjects, despite antibiotic treatment. Compared to uninfected subjects of the same age, infected subjects in this study (treated and untreated) demonstrated Inflammation in and around the heart, in skeletal muscles, joints, and the protective sheath that covers the brain, and near peripheral nerves.
*   Rare, but intact B. burgdorferi spirochetes were found in the tissues of both the treated and untreated subjects. In two subjects treated with doxycycline, multiple Lyme bacteria were observed in the brain tissue. Others organs in which the spirochetes were observed included the heart, joints, bladder, skeletal muscle and adjacent to peripheral nerves.

*******
Ehkä vähitellen järki voittaa. Nykyisin jos potilaalla oireet jatkuvat, se on potilaan syy, sen päässä on vikaa, koska borrelioosi paranee kahden viikon doxy kuurilla..

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.02.2018 - 23:55:48

Transcriptional profile and Epstein-Barr virus infection status of laser-cut immune infiltrates from the brain of patients with progressive multiple sclerosis.

https://www.ncbi.nlm.nih.gov/pubmed/29338732

J Neuroinflammation. 2018 Jan 16

Abstract

BACKGROUND:
It is debated whether multiple sclerosis (MS) might result from an immunopathological response toward an active Epstein-Barr virus (EBV) infection brought into the central nervous system (CNS) by immigrating B cells. Based on this model, a relationship should exist between the local immune milieu and EBV infection status in the MS brain. To test this hypothesis, we analyzed expression of viral and cellular genes in brain-infiltrating immune cells.

METHODS:
Twenty-three postmortem snap-frozen brain tissue blocks from 11 patients with progressive MS were selected based on good RNA quality and prominent immune cell infiltration. White matter perivascular and intrameningeal immune infiltrates, including B cell follicle-like structures, were isolated from brain sections using laser capture microdissection. Enhanced PCR-based methods were used to investigate expression of 75 immune-related genes and 6 EBV genes associated with latent and lytic infection. Data were analyzed using univariate and multivariate statistical methods.

RESULTS:
Genes related to T cell activation, cytotoxic cell-mediated (or type 1) immunity, B cell growth and differentiation, pathogen recognition, myeloid cell function, type I interferon pathway activation, and leukocyte recruitment were found expressed at different levels in most or all MS brain immune infiltrates. EBV genes were detected in brain samples from 9 of 11 MS patients with expression patterns suggestive of in situ activation of latent infection and, less frequently, entry into the lytic cycle. Comparison of data obtained in meningeal and white matter infiltrates revealed higher expression of genes related to interferonγ production, B cell differentiation, cell proliferation, lipid antigen presentation, and T cell and myeloid cell recruitment, as well as more widespread EBV infection in the meningeal samples. Multivariate analysis grouped genes expressed in meningeal and white matter immune infiltrates into artificial factors that were characterized primarily by genes involved in type 1 immunity effector mechanisms and type I interferon pathway activation.

CONCLUSION:
These results confirm profound in situ EBV deregulation and suggest orchestration of local antiviral function in the MS brain, lending support to a model of MS pathogenesis that involves EBV as possible antigenic stimulus of the persistent immune response in the central nervous system.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 10.02.2018 - 22:47:13

Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells

https://www.ncbi.nlm.nih.gov/pubmed/29394264#

PLoS One. 2018 Feb 2

Abstract

Multiple sclerosis (MS) is a chronic neuroinflammatory condition of the central nervous system (CNS). It is a major cause of neurological disability in young adults, particularly women. What triggers the destruction of myelin sheaths covering nerve fibres is unknown. Both genetic and infectious agents have been implicated. Of the infectious agents, Epstein-Barr virus (EBV), a common herpesvirus, has the strongest epidemiological and serological evidence. However, the presence of EBV in the CNS and demonstration of the underlying mechanism(s) linking EBV to the pathogenesis of MS remain to be elucidated. We aimed at understanding the contribution of EBV infection in the pathology of MS. We examined 1055 specimens (440 DNA samples and 615 brain tissues) from 101 MS and 21 non-MS cases for the presence of EBV using PCR and EBER-in situ hybridization (EBER-ISH). EBV was detected by PCR and/or EBER-ISH in 91/101 (90%) of MS cases compared to only 5/21 (24%) of non-MS cases with other neuropathologies. None of the samples were PCR positive for other common herpesviruses (HSV-1, CMV, HHV-6). By quantitative PCR, EBV viral load in MS brain was mainly low to moderate in most cases. However, in 18/101 (18%) of MS cases, widespread but scattered presence of EBV infected cells was noted in the affected tissues by EBER-ISH. Immunohistochemical analysis of EBV gene expression in the 18 heavily infected cases, revealed that the EBV latent protein EBNA1, and to a lesser extent the early lytic protein BZLF1 were expressed. Furthermore, using double-staining we show for the first time that astrocytes and microglia, in addition to B-cells can also be infected. To the best of our knowledge, this is the most comprehensive study demonstrating that EBV is present and transcriptionally active in the brain of most cases of MS and supports a role for the virus in MS pathogenesis. Further studies are required to address the mechanism of EBV involvement in MS pathology.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 12.02.2018 - 21:32:24

How viruses disarm the immune system

https://www.sciencedaily.com/releases/2018/02/180205134245.htm

February 5, 2018
How do viruses that cause chronic infections, such as HIV or hepatitis c virus, manage to outsmart their hosts' immune systems?

The answer to that question has long eluded scientists, but new research from McGill University has uncovered a molecular mechanism that may be a key piece of the puzzle. The discovery could provide new targets for treating a wide range of diseases.

Fighting off infections depends largely on our bodies' capacity to quickly recognize infected cells and destroy them, a job carried out by a class of immune cells known as CD8+ T cells. These soldiers get some of their orders from chemical mediators known as cytokines that make them more or less responsive to outside threats. In most cases, CD8+ T cells quickly recognize and destroy infected cells to prevent the infection from spreading.

"When it comes to viruses that lead to chronic infection, immune cells receive the wrong set of marching orders, which makes them less responsive," says Martin Richer, an assistant professor at McGill's Department of Microbiology & Immunology and senior author of the study, published recently in the journal Immunity.

The research, conducted in Richer's lab by graduate student Logan Smith, revealed that certain viruses persist by driving the production of a cytokine that leads to modification of glycoproteins on the surface of the CD8+ T cells, making the cells less functional. That maneuver buys time for the pathogen to outpace the immune response and establish a chronic infection. Importantly, this pathway can be targeted to restore some functionality to the T cells and enhance the capacity to control infection.

The discovery of this regulatory pathway could help identify new therapeutic targets for a variety of diseases. "We might be able to take advantage of the pathways induced by these signals to fight chronic viral infections by making the immune system more responsive," Richer says. "The findings might also prove useful for diseases like cancer and autoimmunity, where T cells function is poorly regulated."

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.03.2018 - 20:22:00

New clues to Epstein-Barr virus

https://www.sciencedaily.com/releases/2013/02/130221152738.htm

February 21, 2013
Epstein-Barr virus (EBV) affects more than 90 percent of the population worldwide and was the first human virus found to be associated with cancer. Now, researchers from Beth Israel Deaconess Medical Center (BIDMC) have broadened the understanding of this widespread infection with their discovery of a second B-cell attachment receptor for EBV.

The new findings, which currently appear on-line in Cell Reports, reinforce current directions being taken in the development of a vaccine to guard against EBV, and raise important new questions regarding the virus's possible relationship to malaria and to autoimmune diseases.

"Our discovery that CD35 is an attachment receptor for EBV helps explain several previously unsolved observations," explains the study's senior author Joyce Fingeroth, MD, a member of the Division of Infectious Disease at BIDMC and Associate Professor of Medicine at Harvard Medical School.

First discovered in the early 1960s, EBV is one of eight viruses in the human herpesvirus family. The virus affects nine out of 10 people at some point in their lifetimes.

Infections in early childhood often cause no disease symptoms, but people infected during adolescence or young adulthood may develop infectious mononucleosis. EBV is also associated with several types of cancer, including Hodgkin's lymphoma, non-Hodgkin's lymphoma and nasopharyngeal carcinoma, and has been linked to certain autoimmune disorders.

"EBV was the first human virus that was discovered to be a tumor virus," explains Fingeroth. "In fact, individuals who have had infectious mononucleosis have a four times increased risk of developing Hodgkin's disease." After the initial infection, the EBV virus remains in a person's body for life.

To gain entry, viruses must first attach to their host cells. For herpesviruses, receptors on the viral envelope become connected to complementary receptors on the cell membrane. In the case of EBV, the virus gains access to the immune system by attaching to primary B cells.

Nearly 30 years ago, Fingeroth and her colleagues discovered that this attachment occurs via the CD21 protein, which until now was the only known B cell attachment receptor for EBV.
The recent finding that B cells from a patient lacking CD21 can be infected and immortalized by EBV had indicated that an alternative attachment receptor must exist. The identification of this second receptor -- CD35 -- by Fingeroth's team, led by first author Javier Ogembo, PhD, of BIDMC and the University of Massachusetts Medical School, not only underscores an important finding regarding primary infection but also underscores the importance of EBVgp350/220, (the virus protein that has been found to bind to both attachment receptors) for the development of a vaccine against EBV.

"The EBV glycoprotein gp350/220, is the most abundant surface glycoprotein on the virus," says Fingeroth, adding that these results further suggest the virus fusion apparatus is the same for both receptors. "An EBV vaccine might be able to prevent infection or, alternatively, greatly reduce a person's risk of developing infectious mononucleosis and EBV-associated cancers, without necessarily preventing the EBV infection itself," she explains.

Interestingly, whereas a human has now been identified to be lacking the CD21 receptor, no persons are known to lack CD35. "CD35 is a latecomer in evolution and in its current form, exists only in humans," says Fingeroth. "We know that it is often targeted in autoimmune diseases and was recently identified as a malaria receptor. Our new discovery may, therefore, reveal new avenues for the exploration of unexplained links between EBV, autoimmune disease, malaria, and cancer."

In addition to Fingeroth and Ogembo, study coauthors include BIDMC investigators Lakshmi Kannan, Ionita Ghiran, Anne Nicholson-Weller and George Tsokos; and UMass investigator Robert Finberg.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.03.2018 - 20:25:48

Could antiretrovirals be treating EBV in MS? A case report.

https://www.ncbi.nlm.nih.gov/pubmed/29510325

Mult Scler Relat Disord. 2018 Feb 27;

Abstract

We present the case of an HIV-negative patient clinically diagnosed with relapsing-remitting MS who achieved significant disease improvement on Combivir (zidovudine/lamivudine). Within months of treatment, the patient reported complete resolution of previously unremitting fatigue and paresthesiae, with simultaneous improvements in lesion burden detected by MRI. All improvements have been sustained for more than three years. This response may be related to the action of zidovudine as a known inhibitor of EBV lytic DNA replication, suggesting future directions for clinical investigation.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 18.03.2018 - 20:30:17

Experimental immunotherapy ATX-MS-1467 shows promising trial results

https://msra.org.au/news/experimental-immunotherapy-atx-ms-1467-shows-promising-trial-results/

08 March, 2018

   Unlike most available MS medications which suppress or modify the immune system, immunotherapies aim to ‘re-educate’ the cells of the immune system to prevent them responding to a specific target.
   Experimental immunotherapy ATX-MS-1467 aims to re-train the immune system’s response to myelin, and previously showed good results in laboratory models of MS
   A Phase 1b clinical trial tested the safety of ATX-MS-1467 and found it to be well tolerated
   A Phase 2a clinical trial showed that the treatment was able to reduce lesions on magnetic resonance imaging (MRI)

MS results from the immune system mistakenly attacking and destroying myelin, the protective layer that insulates nerves in the brain and spinal cord. Most current treatments available for MS act by suppressing or ‘resetting’ the immune system to stop this attack. Immunotherapy is a completely different approach to treating MS. Immunotherapy aims to ‘re-educate’ the cells of the immune system responsible for the MS attack to reduce the likelihood of a relapse.

Results of two clinical trials of an experimental new immunotherapy for people with MS have recently been published in the journal Neurology showing encouraging results.

Myelin is made up of a range of fat molecules and some proteins. In MS, the immune cells mistakenly target some of the protein components of the myelin, including parts of one protein known as myelin basic protein. The experimental immunotherapy, ATX-MS-1467, is made up of a cocktail of four different protein fragments from myelin basic protein. The protein fragments are injected under the skin and are able to ‘teach’ immune cells not to attack myelin basic protein.

This essentially re-trains the immune system to recognise myelin as ‘self’ with the hope of preventing the myelin damage seen in MS. Previous research had shown good results of ATX-MS-1467 in a laboratory model of MS. In the studies just published, the researchers conducted clinical trials in a small number of people with relapsing MS to test for safety (Phase 1b trial) and effectiveness (Phase 2a trial).

The Phase 1b clinical trial compared two routes of administration of the drug, intradermal injections (injections into the skin just below the outermost layer) and subcutaneous injections (deeper injections into the fat layer below the skin) and compared a range of doses in 43 people with relapsing MS. Participants were given an injection every two weeks for 16 weeks and then followed for a further 32 weeks. This study showed that while there were some mild and moderate side effects, ATX-MS-1467 was well tolerated and that the intradermal injections were a better way of delivering the immunotherapy.

Exploratory investigations of the effectiveness of the treatment in the Phase I study indicated that it may have some temporary effect in reducing the gadolinium enhancing lesions on magnetic resonance imaging (MRI), a marker of active disease but lesions returned to pre-treatment levels after the 32 weeks off the medication.

The Phase 2b clinical trial was then designed to more thoroughly examine the effectiveness of the treatment in 37 participants compared with baseline levels of disease. Participants were given treatment over 16 weeks and then followed-up for 16 weeks off treatment. As for the first trial, the Phase 2b trial showed that ATX-MS-1467 was able to reduce gadolinium enhancing lesions on MRI at the end of the treatment period but also showed that this reduction persisted over the shorter 16 weeks of follow-up. The Phase 2b trial also showed that ATX-MS-1467 reduced the number of new or enlarging lesions on MRI.

Participants did not have significant reductions in their expanded disability status scale (EDSS) or MS functional composite (MSFC) measurements, both of which assess levels of disability in the clinic, as a result of the treatment. However, the short duration of the trial would make it difficult to reliably detect any changes in disability.

These promising results imply re-training the immune system to prevent it’s attacks on myelin may be an effective strategy and further clinical trial testing of ATX-MS-1467 is warranted in larger groups of people with MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 31.03.2018 - 00:10:59

GeNeuro and Servier announce successful 12-month results in neuroprotection for Phase 2b CHANGE-MS Study with GNbAC1 in Multiple Sclerosis

https://servier.com/en/communique/geneuro-and-servier-announce-successful-12-month-results-in-neuroprotection-for-phase-2b-change-ms-study-with-gnbac1-in-multiple-sclerosis-2/


  Geneva, Switzerland, and Paris, France, March 26, 2018  – GeNeuro (Euronext Paris: CH0308403085 – GNRO) and Servier announced today positive results at 12 months from the CHANGE-MS Phase 2b study of GNbAC1, a novel and promising therapeutic approach for the treatment of multiple sclerosis (MS). The data showed that GNbAC1 administration had a significant, consistent positive impact on key neuroprotection markers known to be linked to disease progression. This is the first time that the benefit of a treatment targeting endogenous retrovirus protein is shown in a clinical trial.

In this 270-patient study, conducted in 12 European countries, MRI showed a coherent neuroprotective benefit on brain atrophy. Benefits were seen in cortical and thalamic atrophy, with relative volume loss reductions of 31% and 72% respectively between the highest dose of 18 mg/kg and control group[1], with a statistically significant dose-relationship[2] for both (p=0.045 and P=0.014 respectively). Whole brain atrophy revealed a 29% relative reduction in brain volume loss over 12 months for the highest dose versus the control group, with a trend in dose-relationship2 (p=0.079).

In addition, the number of T1 hypointense lesion (black holes, a marker of permanent tissue destruction in the brain) of at least 14mm3 volume was reduced by 63% (p=0.014) at the end of the study in the 18mg/kg versus control group.

The benefit in Magnetization Transfer Ratio (MTR) signal of 18mg/kg relative to the placebo at 6 months remained stable versus the control group over the second period of the trial, in both normal appearing white matter and cerebral cortical bands, consistent with a potential benefit on remyelination.

For most MRI measures of neuroinflammation, all groups improved from Month 6 to Month 12, however there was no significant separation between treatment groups. The trend seen in post-hoc analyses at 6 months on neuroinflammatory markers, after the primary endpoint of reducing the total number of cerebral Gadolinium-enhancing lesions as measured by MRI was not met, did not translate into a relevant result at 12 months.

No organ-class related toxicity and no dose dependent adverse events were observed. GNbAC1 continued to show an excellent tolerability profile throughout the study.

“What is impressive is the consistency of the effect already observed at one year across all these key markers of neurodegeneration, and that this effect appears to be independent from an anti-inflammatory action,” noted Prof Hans-Peter Hartung, chairman of the Department of Neurology of the University Hospital Düsseldorf and Lead Investigator of the study. “These positive effects are very promising, and may open new doors towards addressing the key unmet medical need of disease progression in MS.”

“The positive impact of GNbAC1 on neuroprotection markers opens a novel therapeutic perspective for MS, in line with Servier’s ongoing commitment to bringing new, safe and effective treatments to patients. Based on this joint achievement, we will now assess the next development steps with our partner to bring these benefits to patients,” stated Dr. Christian de Bodinat, Director of Servier’s Neuro-psychiatry Centre for Therapeutic Innovation.

“These results are a significant success for GeNeuro as they demonstrate the role played by pathogenic HERV-W protein in patients affected by MS. It supports the concept of altering the neurodegenerative course of MS by treating a causal factor of the disease, as suggested by preclinical research,” stated Jesús Martin-Garcia, CEO of GeNeuro. “These clinical results support GeNeuro’s efforts to develop this approach in other HERV-related diseases such as Type 1 Diabetes, CIDP[3] and Amyotrophic Lateral Sclerosis”.

GNbAC1 is a monoclonal antibody designed to neutralize a pathogenic protein encoded by a member of the Human endogenous retroviruses (HERV-W) family. HERVs are ancestral, retroviral DNA insertions in the human genome, thought to account for up to 8% of the total DNA. The pHERV-W protein is thought to be a causal factor in the development of multiple sclerosis, Type 1 diabetes and CIDP.

GeNeuro is presently conducting a 60-patient Phase IIa with GNbAC1 in T1D with expected top line results in September 2018, and has received an Orphan Drug Designation from the FDA for GNbAC1 in CIDP. In 2017, GeNeuro entered into a research agreement with the US NIH for developing new approaches against pHERV-K protein as a target in the treatment of Amyotrophic Lateral Sclerosis (ALS).

CHANGE-MS Phase 2b study was fully funded through a €362.5 million[4] partnership signed with Servier in 2014, in which Servier is involved in the development and potential commercialization of GNbAC1 in MS in territories ex USA and Japan.

Achieving these positive Phase 2b results through the neutralization of pathogenic HERV-W protein supports its causal role in the neurodegenerative mechanisms of MS. GNbAC1 may provide a safe treatment option against neurodegeneration unrelated to inflammation in all forms of the disease, a major objective that is not addressed by currently available MS treatments.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.04.2018 - 22:06:21

HLA alleles modulate EBV viral load in multiple sclerosis.

https://www.ncbi.nlm.nih.gov/pubmed/29587799

J Transl Med. 2018 Mar 27;

Abstract
BACKGROUND:

The etiopathology of multiple sclerosis (MS) is believed to include genetic and environmental factors. Human leukocyte antigen (HLA) alleles, in particular,  are associated with disease susceptibility, whereas Epstein Barr Virus (EBV) infection has long been suspected to play a role in disease pathogenesis. The aim of the present study is to evaluate correlations between HLA alleles and EBV infection in MS.

METHODS:

HLA alleles, EBV viral load (VL) and serum anti-EBV antibody titers were evaluated in EBV-seropositive MS patients (N = 117) and age- and sex-matched healthy controls (HC; N = 89).

RESULTS:

Significantly higher DNA viral loads (p = 0.048) and EBNA-1 antibody titer (p = 0.0004) were seen in MS compared to HC. EBV VL was higher in HLA-B*07+ (p = 0.02) and HLA-DRB1*15+ (p = 0.02) MS patients, whereas it was lower in HLA-A*02+ (p = 0.04) subjects. EBV VL was highest in HLA-A*02-/B*07+/DRB1*15+ patients and lowest in HLA-A*A02+/B*07-/DRB1*15- individuals (p < 0.0001). HLA-B*07 resulted the most associated allele to EBV VL after multiple regression analysis considering altogether the three alleles, (p = 0.0001). No differences were observed in anti-EBV antibody titers in relationship with HLA distribution.

CONCLUSIONS:

Host HLA-B*07 allele influence EBV VL in MS. As HLA-class I molecules present antigens to T lymphocytes and initiate immune response against viruses, these results could support a role for EBV in MS.

******
Eli, jos ymmärränn oikein, MS:ään liitetyt geenit ovat syyllisiä heikkoon immuunivastukseen EBV-virukselle.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 28.04.2018 - 02:08:11

Transcription Factors Operate Across Disease Loci, With EBNA2 Implicated in Autoimmunity

JB Harley et al. Nat Genet. 2018 Apr 16.

https://www.ncbi.nlm.nih.gov/labs/articles/29662164/

Abstract

Explaining the genetics of many diseases is challenging because most associations localize to incompletely characterized regulatory regions. Using new computational methods, we show that transcription factors (TFs) occupy multiple loci associated with individual complex genetic disorders. Application to 213 phenotypes and 1,544 TF binding datasets identified 2,264 relationships between hundreds of TFs and 94 phenotypes, including androgen receptor in prostate cancer and GATA3 in breast cancer. Strikingly, nearly half of systemic lupus erythematosus risk loci are occupied by the Epstein-Barr virus EBNA2 protein and many coclustering human TFs, showing gene-environment interaction. Similar EBNA2-anchored associations exist in multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease. Instances of allele-dependent DNA binding and downstream effects on gene expression at plausibly causal variants support genetic mechanisms dependent on EBNA2. Our results nominate mechanisms that operate across risk loci within disease phenotypes, suggesting new models for disease origins.

Lisää asiasta ja selitys:
http://multiple-sclerosis-research.blogspot.com/2018/04/ebv-and-not-so-magnificant-7-cause-of.html




Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 25.05.2018 - 18:16:36

Different diseases elicit distinct sets of exhausted T cells

https://www.sciencedaily.com/releases/2018/05/180515113754.htm

May 15, 2018
The battle between the human immune system and long-term, persisting infections and other chronic diseases such as cancer results in a prolonged stalemate. Over time battle-weary T cells become exhausted, giving germs or tumors an edge. Using data from multiple molecular databases, researchers from the Perelman School of Medicine at the University of Pennsylvania have found nine distinct types of exhausted T cells ("Tex"), which could have implications for fighting chronic infections, autoimmunity, and cancer. They published their findings in Immunity this week.

"Exhausted T cells are a discrete cell lineage that have become important immunotherapy targets for chronic infection and cancer," said senior author John Wherry, PhD, a professor of Microbiology and director of the Institute for Immunology. "Now, we know that exhausted T cells are a vastly diverse set of immune cells."

Wherry's lab has spent the last decade describing these populations of fatigued cells. Overall, when normal T cells become exhausted, they develop defects in their germ- and tumor-fighting capabilities. Tex also express inhibitory receptor proteins on their surface that stall key biochemical pathways, provoke changes in control of gene expression, alter metabolism for making energy to fight infections and tumors, and prevent development of optimal immune function.

New, highly effective immunotherapies that target these inhibitory receptors expressed by Tex such as PD-1 or CTLA-4 have shown dramatic effects among patients with melanoma and other diseases, with potential to also combat breast, ovarian and other cancers. Although Tex have been implicated in the response to checkpoint blockade drugs in animal models, the underlying immunological mechanisms of their therapeutic response or failure in people is only now being studied in earnest.

"Exhausted T cells are quite diverse, as are all types of T cells," Wherry said. "This sheer diversity is the hallmark of the human immune system that has to essentially have a way to respond to every germ an individual might encounter in a lifetime."

Knowing this, the Penn team asked what the diversity in the Tex pool reveals about a disease itself and its course in a patient. They developed an assay to investigate the molecules that control gene expression in Tex by comparing them to other types of T cells and within a Tex population in blood from HIV patients whose viral load is well-controlled.

Next, they defined core exhaustion-specific genes and identified disease-induced molecular changes in Tex populations in HIV with uncontrolled disease and in human lung cancer. Using this data, the Tex fell into nine distinct clusters of similar expression patterns with regard to transcription factors and inhibitory receptors.

Because of the clusters' relationships to specific disease type and progression, the team's aim is to use the signature of a Tex cluster to assess a patient's overall immune health and likelihood of responding to a certain therapy. "We want to be able to select and tailor immune therapies according to a patient's exhausted T cell pool and its individual characteristics," Wherry said.

Applying this type of assessment to exhausted T cells in the context of immunotherapy clinical trials might identify patients more likely to benefit from specific types of combination immunotherapies and may point to underlying mechanisms in the specific types of exhausted T cells responding to an infection or cancer.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 25.05.2018 - 18:23:13


How EBV might cause immune cells to go rogue in MS


https://msra.org.au/news/ebv-might-cause-immune-cells-go-rogue-ms/

08 May, 2018

   Epstein Barr Virus (EBV) infection can contribute to the development of autoimmune diseases including MS.
   The virus can make proteins which bind to DNA and these can interact with the parts of DNA that control MS risk genes.
   The variations in some genes that are associated with an increased risk of developing MS are more likely to interact with EBV.

Viruses are the ultimate pirates using cunning and deceit to evade our body’s defences and hijack our cells – once inside they can use our cells as a factory to manufacture and copy themselves, or they can just lie dormant until they are ready to jump ship and move on.

Different human viruses favour invading different types of cells in the body. The Epstein Barr Virus, which has been linked to the development of MS and some other autoimmune diseases, favours B cells which is a type of cell in the immune system.

When viruses commandeer our immune cells they can cause the cells to go rogue and steer off course a bit and this is thought play a role in the development of autoimmune diseases.

EBV is a very common infection most often acquired during early childhood, either without symptoms or just as a generic childhood upper respiratory tract infection. In adolescents and young adults it can also cause glandular fever. Between 90 and 95% of the general population will have been infected by the virus at some point in their life. In comparison, close to 100% of people with MS have been infected. So it is thought that, on its own EBV, can’t cause MS, but in susceptible people it contributes to the development of MS. Until now the exact reason for this was not clear.

When a virus enters a cell it starts controlling some of the genes in the cell and researchers have now found that EBV can interact specifically and directly with some of the genes that have been identified as risk genes for MS and other autoimmune disorders. Their work has been published in the prestigious scientific journal Nature Genetics.

To show this, the scientists took cells which were either infected or not with EBV, and then looked to see where proteins from the virus were bound to the DNA of the cells, as this is a key sign that the virus is using those specific genes. In the case of MS, they found that out of the 109 known MS risk genes the viral proteins where bound to 44 of these genes. Importantly, the virus appeared to do this more readily in B cells, and not other cells.

The scientists also looked at whether the specific variations in the DNA code that is linked to MS in these genes changed how strongly the virus proteins bound to the DNA. They found that the virus latched on to the version of the gene code linked to MS more readily than it did to the ‘standard’ version of the gene, suggesting a specific interaction between the MS risk gene variations and EBV.

This work reveals an important mechanism by which our genes and the virus might effectively conspire against us to cause MS only in some people and not everyone who has been infected with EBV. Ultimately, this type of work may help us to understand how we can prevent the changes that EBV makes to the immune system to help prevent or treat MS.

EBV has long been studied in relation to MS, and Australian researchers have been working on an early phase clinical trial of a therapy called EBV-specific adoptive immunotherapy. In this therapy the scientists remove some of the immune cells from people with MS, and prime them to hunt out and destroy EBV infected cells.

The results of this initial safety trial are still awaited but it represents an innovative new way to tackle the role of EBV in MS. You can read more about that study here.

By understanding the fundamental impacts of EBV on B cells and genes we will be much better placed to understand the causes of autoimmunity and discover molecular targets for future treatments.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 03.08.2018 - 17:05:57

Epstein Barr Virus found in lesions in the brains of people with MS

https://msra.org.au/news/epstein-barr-virus-found-lesions-brains-people-ms/

02 July, 2018

   Epstein Barr Virus (EBV) is the virus that causes glandular fever and is one of the known risk factors for developing MS.
   EBV infects B cells in the blood and new research has investigated EBV in the brains of people with MS.
   They identified that a higher proportion of MS brains showed evidence of EBV infected cells and that the cells moved from the bloodstream to the chronic lesions in the MS brain. Further strengthening the evidence for a role of EBV in MS.

Being infected by Epstein Barr Virus (EBV), the virus that causes glandular fever, is a known risk factor of developing MS. While the rate of EBV infection in the general population is very high, essentially everyone  with MS has had EBV at some point in their lives whether they realise or not. EBV infects immune cells called B cells in the blood, but whether EBV is found in the immune  cells that have entered in the brain during an MS attack is still not clear, as previous research was contradictory.

Now a new research paper, which includes some researchers from the Queensland Institute of Medical Research, has attempted to answer this question again and mapped EBV throughout the MS brain and in different types of MS lesions.

The study looked at brain tissue under the microscope from people with MS and compared it to brain tissue from people without MS. The people with MS had been diagnosed with different forms of the disease which meant the researchers could examine different types of lesions – both chronic lesions and chronic active lesions – in the brain tissue.

After infection, EBV can remain in the body in an inactive phase, which is known as ‘latent’ infection. A much higher proportion of the brains from people with MS contained a protein related to a latent EBV infection than the brains of those which did not have MS. In the brains of people with MS, the researchers could also see that the immune cells that respond to EBV infection had moved out of the blood and into the brain far more frequently. In the MS brains, these cells could be seen within the chronic MS lesions.

Another method was used to detect evidence of latent EBV infection within the brain, which tracks gene activity of the virus in a latent infection. This method showed that 6 of the 7 MS brains tested showed populations of these cells in different locations in the brain, but in brains without MS, they could only identify a single cell in 2 of the 4 brains tested.

This work has shown that B cells infected with EBV do enter travel to the brain and leave the blood circulatory system and enter the brain tissue. This happens in people with or without MS, but much more often in people who develop MS and this may suggest that people who go on to develop MS have a reduced capacity to deal with EBV infection. This idea that people with MS respond differently to EBV infection is not new and the immune response to EBV has been the subject of much research in the field of MS, particular by Professor Michael Pender and Professor Rajiv Khanna (an author on the study) from the University of Queensland. This research has led to a new approach to treatment of MS known as adoptive immunotherapy, which aims to boost person with MS’s immune response to infection with EBV using their own cells. This treatment is now in clinical trials for people with progressive MS and showing promising results . More recently, further trials were announced  that will test a similar treatment approach where cells are taken from donor rather than the person with MS.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.09.2018 - 01:24:13

Increasing Evidence Points to Inflammation as Source of Nervous System Manifestations of Lyme Disease

https://www.elsevier.com/about/press-releases/research-and-journals/increasing-evidence-points-to-inflammation-as-source-of-nervous-system-manifestations-of-lyme-disease

Philadelphia, PA, April 16, 2015
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Lyme disease in humans results from the bite of a tick infected with the spirochete Borrelia burgdorferi (Bb). As Bb disseminates throughout the body, it can cause arthritis, carditis, and neurologic deficits. When the nervous system is involved, it is called Lyme neuroborreliosis (LNB). Clinical symptoms of LNB of the peripheral nervous system may include facial nerve palsy, neurogenic pain radiating along the back into the legs and feet, limb pain, sensory loss, or muscle weakness. Central nervous system involvement can manifest as headache, fatigue, memory loss, learning disability, depression, meningitis, and encephalopathy.
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Some patients with Lyme disease also show evidence of demyelinating neuropathy and slowing nerve conduction. Nerve conduction studies in motor and sensory nerves of the macaques showed that the Bb infection resulted in specific electrophysiological abnormalities (increased F wave latencies and chronodispersion) that could be prevented with dexamethasone.
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“Importantly, we found necrotizing myelitis and degeneration in the spinal cord, neurodegeneration in the dorsal root ganglia, and demyelination in the nerve roots only when lymphocytic inflammatory lesions were also observed in both the central nervous system and peripheral nervous system,” stated Dr. Philipp. “Our results suggest that ongoing cytokine activation in the nervous system can contribute to the persistent symptoms of fatigue, pain, and cognitive dysfunction that patients sometimes experience despite having been treated for Lyme disease.”

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.09.2018 - 01:31:46

Scientists find a new way to attack herpesviruses

https://www.sciencedaily.com/releases/2018/08/180828121414.htm

August 28, 2018
Human cytomegalovirus is a leading cause of birth defects and transplant failures. As it's evolved over time, this virus from the herpes family has found a way to bypass the body's defense mechanisms that usually guards against viral infections. Until now, scientists couldn't understand how it manages to do so.

A team of scientists led by Leor S. Weinberger, PhD, the William and Ute Bowes Distinguished Professor and director of the Gladstone-UCSF Center for Cell Circuitry, uncovered the mechanism that allows the virus to replicate. Their study, published in the scientific journal PNAS, could open new therapeutic avenues to treat not only cytomegalovirus, but other viruses as well.

Normally, when a virus enters your cell, that cell blocks the virus's DNA and prevents it from performing any actions. The virus must overcome this barrier to effectively multiply.

To get around this obstacle, cytomegalovirus doesn't simply inject its own DNA into a human cell. Instead, it carries its viral DNA into the cell along with proteins called PP71. After entering the cell, it releases these PP71 proteins, which enables the viral DNA to replicate and the infection to spread.

"The way the virus operates is pretty cool, but it also presents a problem we couldn't solve," said Noam Vardi, PhD, postdoctoral scholar in Weinberger's laboratory and first author of the new study. "The PP71 proteins are needed for the virus to replicate. But they actually die after a few hours, while it takes days to create new virus. So how can the virus successfully multiply even after these proteins are gone?"

The researchers found that, while PP71 is still present in the cell, it activates another protein known as IE1. This happens within the first few hours of the virus entering the cell, allowing the IE1 protein to take over after PP71 dies and continue creating new virus.

To confirm their findings, the team created a synthetic version of the virus that allowed them to adjust the levels of the IE1 proteins using small molecules. With this technique, they could let the virus infect the cell while controlling how quickly the IE1 protein would break down in the cell.

"We noticed that when the IE1 protein degrades slowly, as it normally does, the virus can replicate very efficiently," said Vardi. "But if the protein breaks down faster, the virus can't multiply as well. So, we confirmed that the virus needs the IE1 protein to successfully replicate."

This study could have broad implications for the scientific community, which has been struggling to determine how cells maintain their identity over time. During development, for instance, stem cells choose a path based on the proteins that surround them. But even after these initial proteins disappear, the specialized cells don't change. So, stem cells that turn into neurons during development continue to be neurons long after those proteins are gone.

"The issue is similar for the virus," explained Weinberger, who is also a professor of pharmaceutical chemistry at UC San Francisco. "It was not clear what mechanisms allowed the virus to continue replicating long after the initial signal from the PP71 had decayed to a whisper. Our findings uncover a circuit encoded by the virus that controls its fate and indicate that such circuits may be quite common in viruses."

The new study could lead to a new therapeutic target to attack cytomegalovirus and other herpesviruses, such as Epstein-Barr virus that causes mononucleosis and herpes simplex virus 1 and 2 that produce most cold sores and genital herpes.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 08.09.2018 - 01:37:21

STAT3 can be a therapeutic target for chronic active EBV infection, a fatal disorder

https://www.sciencedaily.com/releases/2018/08/180820113117.htm

August 20, 2018
Tokyo Medical and Dental University(TMDU) study shows that ruxolitinib-induced inhibition of STAT3 activity blocks survival and reduces pro-inflammatory cytokine production in Epstein-Barr virus (EBV)-infected clonally proliferating T- or NK-cells in Chronic active Epstein-Barr virus infection.

Tokyo, Japan -- Chronic active Epstein-Barr virus infection (CAEBV) is an EBV-positive T- or NK-cell neoplasm accompanied by sustained systemic inflammation. Many studies have attempted to understand the case of CAEBV; none have provided a clear explanation, until now.

A research team, led by experts from Tokyo Medical and Dental University(TMDU), investigated the activity of STAT3, a factor that helps to control cell proliferation and survival, in EBV-infected T- or NK-cells in CAEBV. They found that STAT3 was constitutively activated in those cells, reported in Oncotarget, "STAT3 is constitutively activated in chronic active Epstein-Barr virus infection and can be a therapeutic target."

CAEBV is a disorder which has 2 aspects: an inflammatory disorder and a lymphoid neoplasm. During the course, it may progress to chemotherapy-resistant lymphoma or leukemia, or to a life-threatening disorder known as hemophagocytic lymphohistiocytosis. Despite a variety of efforts to control or cure CAEBV, the sole effective treatment has been stem cell transplantation from a HLA-matched donor. Unfortunately, some patients cannot be candidates for this therapy, and there are many side effects.

"Constitutively activated STAT3 has been observed in a variety of primary tumor cells, including other tumors associated with Epstein-Barr virus infection," says Ayoko Arai, corresponding author on the study. "We suspected that STAT3 may be similarly activated in cells from patients with CAEBV."

In the study, increased phosphorylation, an important modification of cellular proteins, was observed on STAT3 in EBV-infected T- or NK-cells from patients with CAEBV. In those same cells from health individuals, the phosphorylation was absent, suggesting that it may provide a useful drug target.

"Our analyses revealed no mutations in STAT3, so we tested whether inhibitors of STAT3 phosphorylation might modify its activity in laboratory-grown," says Erika Onozawa, lead author on the study. "We found that ruxolitinib, a drug that is currently used for treatment of myelofibrosis and polycythemia vera, could suppress the survival of the EBV-infected cells in a dose-dependent manner."

In addition to the ability of ruxolitinib to induce the death of virus-infected T- or NK-cells from patients with CAEBV, the researchers showed that it could block the production of several important inflammatory cytokines that play a role in the progression of CAEBV.

CAEBV is a neoplastic and inflammatory disease that can become extremely destructive for some patients. This study showed that STAT3 could be an important new target for treatment of this disorder, and that ruxolitinib may provide a readily available therapy that may be effectively used in clinical treatment.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.10.2018 - 18:42:50

Multiple sclerosis and mixed microbial infections. Direct identification of fungi and bacteria in nervous tissue.

https://www.ncbi.nlm.nih.gov/pubmed/29859870

Abstract

Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS), leading to multifocal demyelination and neurodegeneration. The etiology of this incurable disease is unknown and remains a matter of intensive research. The possibility that microbial infections, such as viruses or bacteria, can trigger an autoimmune reaction in CNS tissue has been suggested. However, the recent demonstration that bacteria are present in CNS tissue points to a direct involvement of microbial infections in the etiology of MS. In the present study, we provide the first evidence of fungal infection in CNS tissue of MS patients, and demonstrate that fungal DNA from different species can be detected in the CNS. We used, nested PCR assays together with next-generation sequencing to identify the fungal species in the nervous tissue of 10 patients with MS. Strikingly, Trichosporon mucoides was found in the majority of MS patients, and particularly high levels of this fungus were found in two patients. Importantly, T. mucoides was not detected in the CNS of control subjects. We were also able to visualize fungal structures in CNS tissue sections by immunohistochemistry using specific antifungal antibodies, which also revealed the accumulation of a number of microbial cells in microfoci. Again, microbial structures were not observed in CNS sections from controls. In addition to fungi, neural tissue from MS patients was also positive for bacteria. In conclusion, our present observations point to the novel concept that MS could be caused by polymicrobial infections. Thus, mycosis of the CNS may be accompanied by opportunistic bacterial infection, promoting neuroinflammation and directly causing focal lesions, followed by demyelination and axonal injury.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 13.11.2018 - 23:20:10


Molecular signature of Epstein-Barr virus infection in MS brain lesions


http://nn.neurology.org/content/nnn/5/4/e466.full.pdf

Neurol Neuroimmunol Neuroinflamm. 2018

Abstract

Objective
We sought to confirm the presence and frequency of B cells and Epstein-Barr virus
(EBV) (latent and lytic phase) antigens in archived MS and non-MS brain tissue by
immunohistochemistry.

Methods
We quantified the type and location of B-cell subsets within active and chronic MS brain lesions
in relation to viral antigen expression. The presence of EBV-infected cells was further confirmed
by in situ hybridization to detect the EBV RNA transcript, EBV-encoded RNA-1 (EBER-1).

Results
We report the presence of EBV latent membrane protein 1 (LMP-1) in 93% of MS and 78% of
control brains, with a greater percentage of MS brains containing CD138+plasma cells and
LMP-1–rich populations. Notably, 78% of chronic MS lesions and 33.3% of non-MS brains
contained parenchymal CD138+plasma cells. EBV early lytic protein, EBV immediate-early
lytic gene (BZLF1), was also observed in 46% of MS, primarily in association with chronic
lesions and 44% of non-MS brain tissue. Furthermore, 85% of MS brains revealed frequent
EBER-positive cells, whereas non-MS brains seldom contained EBER-positive cells. EBV in-
fection was detectable, by immunohistochemistry and by in situ hybridization, in both MS and
non-MS brains, although latent virus was more prevalent in MS brains, while lytic virus was
restricted to chronic MS lesions.

Conclusions
Together, our observations suggest an uncharacterized link between the EBV virus life cycle and
MS pathogenesis.


Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 23.11.2018 - 00:10:56

Epstein-Barr virus-specific T cell therapy for progressive multiple sclerosis.

https://www.ncbi.nlm.nih.gov/pubmed/30429369

JCI Insight. 2018 Nov 15

Abstract

BACKGROUND:
Increasing evidence indicates a role for EBV in the pathogenesis of multiple sclerosis (MS). EBV-infected autoreactive B cells might accumulate in the CNS because of defective cytotoxic CD8+ T cell immunity. We sought to determine the feasibility and safety of treating progressive MS patients with autologous EBV-specific T cell therapy.

METHODS:
An open-label phase I trial was designed to treat 5 patients with secondary progressive MS and 5 patients with primary progressive MS with 4 escalating doses of in vitro-expanded autologous EBV-specific T cells targeting EBV nuclear antigen 1, latent membrane protein 1 (LMP1), and LMP2A. Following adoptive immunotherapy, we monitored the patients for safety and clinical responses.

RESULTS:
Of the 13 recruited participants, 10 received the full course of T cell therapy. There were no serious adverse events. Seven patients showed improvement, with 6 experiencing both symptomatic and objective neurological improvement, together with a reduction in fatigue, improved quality of life, and, in 3 patients, reduced intrathecal IgG production. All 6 patients receiving T cells with strong EBV reactivity showed clinical improvement, whereas only 1 of the 4 patients receiving T cells with weak EBV reactivity showed improvement (P = 0.033, Fisher's exact test).

CONCLUSION:
EBV-specific adoptive T cell therapy was well tolerated. Clinical improvement following treatment was associated with the potency of EBV-specific reactivity of the administered T cells. Further clinical trials are warranted to determine the efficacy of EBV-specific T cell therapy in MS.

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Näiden kliinisten testien tarkoitus oli ainoastaan onko ATA-188 immunoterapia turvallinen. Eli on, ja seuraavaksi kliinisten testien kohteena on annostus. Toivottavasti myös eurooppalaiset osallistuisivat.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.12.2018 - 19:48:44

About the Anti-EBV clinical trial


https://msra.org.au/news/anti-ebv-trial-results-explained-by-professor-michael-pender/


A treatment to target EBV has been shown to improve symptoms in some people with progressive MS in a world-first clinical trial.

The small phase I safety trial used an ‘adoptive T cell immunotherapy’ treatment. This involves taking blood from patients, extracting their immune cells, and then ‘training’ these cells in the lab to recognise and destroy EBV. The cells are then reintroduced to the patient’s body and go to work in targeting the EBV hiding in the body.

The trial was carried out by Professor Michael Pender and Professor Rajiv Khanna and MS Research Australia is proud to have contributed to the funding of this project, as well as significantly supporting Professor Pender’s EBV research over the last decade.

In this video Professor Pender explains how the trial came about, what it involved and what the results may mean for the future.

About Professor Michael Pender

Professor Michael Pender is a neurologist and researcher from The University of Queensland and Royal Brisbane and Women’s Hospital. He has spent much of his career investigating EBV in MS with a great deal of support along the way from MS Research Australia.

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Katso video, jossa Dr Pender selittää kliinisen kokeen tuloksia.
Vaikka kukaan ei sano sitä, on tämä paras uutinen vuosiin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 02.12.2018 - 19:58:30


Anti-EBV trial shows promise in progressive MS

https://msra.org.au/news/anti-ebv-trial-shows-promise-in-progressive-ms/


20 November, 2018

   A treatment called ‘adoptive T cell immunotherapy’ – which targets the Epstein Barr virus (EBV) – was shown to be safe in a group of 10 patients with primary and secondary MS in a small phase I (safety) trial
   EBV infects B cells of the immune system and is a known risk factor for developing MS
   The treatment takes the patient’s own T cells from the immune system and primes them to recognise and kill EBV-infected B cells
   Seven of the 10 patients showed clinical improvements including some reduction in disability and improvements in fatigue
   Larger studies are now underway to test the safety and effectiveness of the treatment

Overview

A treatment to target EBV has been shown to improve symptoms in some people with progressive MS in a world-first clinical trial.

The small phase I safety trial used an ‘adoptive T cell immunotherapy’ treatment. This involves taking blood from patients, extracting their immune cells, and then ‘training’ these cells in the lab to recognise and destroy EBV. The cells are then reintroduced to the patient’s body and go to work in targeting the EBV hiding in the body.

The trial was carried out by Professor Michael Pender and Professor Rajiv Khanna and MS Research Australia is proud to have contributed to the funding of this project, as well as significantly supporting Professor Pender’s EBV research over the last decade.

What is EBV and its relationship with MS?

EBV is a virus which infects a subset of white blood cells in the body called B cells. Most people won’t know they have had it as it is a common childhood illness with non-specific symptoms, although in adolescents it can cause the more serious glandular fever (infectious mononucleosis).

Once a person becomes infected with EBV, they carry the virus in their B cells for the rest of their life, mostly without any symptoms or problems. The infected cells are usually kept under control by other cells of the immune system called T cells which recognise and kill virus-infected cells.

While we know that EBV is a risk factor for the development of MS, there has been intense research to understand exactly how the virus contributes to MS and how we might tackle it to prevent or treat MS.

How did this EBV trial come about?

Professor Michael Pender, a neurologist and researcher from The University of Queensland and Royal Brisbane and Women’s Hospital has spent much of his career investigating EBV in MS with a great deal of support along the way from MS Research Australia.

Previous studies by Professor Pender’s research group have shown that people with MS have a reduced number of T cells capable of killing EBV-infected B cells, compared with people who do not have MS. This led to the idea that boosting a person’s ability to kill EBV-infected cells might help treat MS.

In recent years Professor Pender has teamed up with Professor Rajiv Khanna from QIMR Berghofer Medical Research Institute to test a novel treatment that targets EBV infected cells in the body.

Professor Khanna had developed a technique where the T cells could be removed from a patient, grown in the laboratory and primed to recognise and destroy EBV infected cells. The T cells are then returned to the patient where they act like heat-seeking missiles to kill the problem cells. He has primarily been testing the type of treatment called ‘adoptive T cell immunotherapy’ on certain cancers that are associated with EBV.

After initially treating just one patient with secondary progressive MS with some success (reported in 2014), the pair set up a phase I clinical trial to test the safety of the therapy in a small group of five people with primary progressive MS and five with secondary progressive MS.

What did the trial involve?

13 people with progressive MS were enrolled into the study. The scientists were able to collect the EBV-targeting T cells from 11 of 13 people and grow them in the laboratory.

One patient had to drop out of the trial before being treated due to an unrelated health condition, leaving 10 patients still in the trial. 5 with primary progressive MS and 5 with secondary progressive MS. The T cells were primed against EBV and then infused back into their body in four doses.

The participants were then monitored for a period of 27 weeks with a range of tests including MRI scans, the EDSS neurological disability scoring system, fatigue, quality of life and thinking and memory skills.

Were there any improvements in MS symptoms?

This very small study was first and foremost designed to identify any safety issues with the treatment, however, it did appear to have some positive effects.

Seven of the 10 participants showed a clinical improvement on the tests of neurological disability. Of the three that did not improve, two remained stable and one experienced worsening of disability.

Overall for the whole group, fatigue was significantly improved across the 27 week period, this being a prominent feature in five of the seven patients who showed neurological improvements.

Thinking and memory skills, while not improved, did not worsen over the period of the study.

In general, the treatment did not appear to prevent the appearance of new or active lesions in the MRI scans of some of the participants, but these people were still among those who did show neurological improvement.

Were there any side-effects?

None of the 10 people experienced any serious side effects as a result of the treatment. Just one patient experienced a minor side effect of an alteration to their sense of taste. This was thought to be due to one of the chemicals used in the preparation of the cells.

What do the results tell us?

The results of the trial firstly show that it is possible to collect and identify the EBV-targeting T cells from the majority of people with progressive MS and grow them in the laboratory.

They also tell us that the treatment appears safe. The findings have been published in the scientific journal JCI Insight. It is a potentially encouraging results for people living with primary and secondary progressive MS. However, it is important to be mindful that this was a very small study that was first and foremost designed to identify any safety issues with the treatment. It is too small, and not designed with the gold-standard placebo controlled, blinded, design to identify whether the treatment was truly effective.

However, the clinical signs of improvement noted in this study are encouraging. In particular, one important observation was that the strength of the EBV-targeting response noted in the preparation of the cells in the laboratory prior to treatment did seem to match with the clinical outcomes. The six participants with a strong reaction to EBV showed clinical improvement, whereas only one of the four participants with a weak reaction to EBV showed clinical improvement of symptoms but not disability.

What’s next?

Professor Khanna is now collaborating with biotechnology company Atara Biotherapeutics to conduct a bigger, randomised controlled (double blind) trial of another ‘off-the-shelf’ version of this treatment – you can learn more about this trial here.

This phase I trial was funded through a grant to Professor Rajiv Khanna and Professor Michael Pender in a partnership between MS Research Australia and MS Queensland and other philanthropic support to QIMR Berghofer Medical Research Institute.

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Ilmoitin aikaisemmin, että tulokset olivat ATA-188 tutkmuksesta, mutta olivat adoptive immunotherapy tutkimuksesta, joka perustuu potilaan omiin soluihin.

Aihe: Re: Krooniset bakteeri-infektiot
Kirjoittaja HopeSprings Pvm 06.01.2019 - 00:38:44

Fungi cause brain infection and impair memory in mice

https://www.sciencedaily.com/releases/2019/01/190104104006.htm

January 4,