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Krooniset bakteeri-infektiot (Luettu 281798 kertaa)
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Re: Krooniset bakteeri-infektiot
Vastaus #30 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #31 - 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
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Re: Krooniset bakteeri-infektiot
Vastaus #32 - 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%20T...

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.
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Re: Krooniset bakteeri-infektiot
Vastaus #33 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #34 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #35 - 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_cl...

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.
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Re: Krooniset bakteeri-infektiot
Vastaus #36 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #37 - 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...

siinä Perttu J. Lindsberg, Jari Koistinaho ja Pentti Tienari
spekuloivat minosykliinillä ja MS:llä ihan mielenkiintoisella tavalla, myös hintanäkökulma tulee mukaan..
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Re: Krooniset bakteeri-infektiot
Vastaus #38 - 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
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Re: Krooniset bakteeri-infektiot
Vastaus #39 - 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..
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Re: Krooniset bakteeri-infektiot
Vastaus #40 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #41 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #42 - 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.

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Re: Krooniset bakteeri-infektiot
Vastaus #43 - 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.
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Re: Krooniset bakteeri-infektiot
Vastaus #44 - 18.10.2012 - 13:59:44
 
Inflammation and central nervous system Lyme disease

http://www.lymenet.de/literatur/Fallon_Inflammation-and-central-nervous-system-L...

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).

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