posted
I have an MS dx, but am now wondering if it could be Lyme even though I tested neg. Lyme is prevelant in our area and I did have a treated tick bite a couple of yrs ago.
I did not have OBands (which they say is common in MS). I did have mildly elevated Myelin Basic Protein(MBP). I'm wondering if it is possible to have MBP with Lyme.
I couldn't find anything in a search here.
Any advise is appreciated. Thanks, Darwin
Posts: 1 | From MA | Registered: Nov 2005
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posted
I have the dx of LD and MS. Only treating for LD at this point. LD mimics MS. If I were you I would see a LLMD in your area and be tested with IGNEX. Keep us posted.
Posts: 128 | From Brick, NJ, USA | Registered: Dec 2003
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posted
I am pretty sure the answer is yes. Can't remember where I read this right now.
Anything that causes a loss of myelin could cause MBP to be elevated -- this basically means anything that attacks the nerves.
Hubby has elevated antibodies to myelin from several blood tests, but his spinal taps show normal MBP. These tests are all at least 2 years old and at that time he had very little obvious nerve symptoms -- just a Parkinsonian tremor.
Nervous symptoms are currently much more severe -- transient Bell's Palsy and some numbness, tingling and burning in arms and legs -- but don't have the money to repeat any of these tests.
In my opinion you are already ahead of the game if you had a known tickbite -- at least you have something to go on where there are many here including hubby who searched years for a diagnosis and treatment because they never knew about a tickbite.
What have you got to lose??? Go see an LLMD.
At least Lyme and the coinfections can be treated. Anything that suppresses the immune system (such as standard MS treatment) will make Lyme disease worse.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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Chronic Lyme borreliosis at the root of multiple sclerosis - is a cure with antibiotics attainable?
*Fritzsche M.*
Clinic for Internal and Geographical Medicine, Soodstrasse 13, 8134 Adliswil, Switzerland.
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.
Bacterial infection as a cause of multiple sclerosis
Multiple sclerosis is an inflammatory demyelinating disease in which the immune system of genetically susceptible individuals is inexplicably activated to attack the central nervous system.
*Christina Wolfson, Pierre Talbot
*Department of Epidemiology and Biostatistics, McGill University, and Centre for Clinical Epidemiology and Community Studies, Lady Davis Institute for Medical Research, Montreal, Quebec, Canada; and Institut National de la Recherche Scientifique, Institut Armand-Frappier, University of Quebec, Laval, Quebec
Multiple sclerosis is an inflammatory demyelinating disease in which the immune system of genetically susceptible individuals is inexplicably activated to attack the central nervous system. Epidemiological studies strongly suggest that environmental factors are involved on a background of genetic susceptibility. (1) The possible involvement of infectious pathogens, most often viruses, has been much studied. (2,3)
Multiple sclerosis has a unique geographic distribution--temperate zones have a low prevalence and more northerly areas have a prevalence more than ten times that in warmer climates. (4) Sanitation, climate, ultraviolet radiation, hours of sunshine, socioeconomic status, and other environmental factors have been examined with little success. (1) Much early research used case-control designs with potential recall bias. (5) More recently, seroepidemiological research has suggested the involvement of infectious pathogens in multiple sclerosis: specific antibody responses in cerebrospinal fluid and blood, isolation of the pathogen from tissue of patients with multiple sclerosis, or in-situ or ex-vivo pathogen detection. The results have rarely been harmonious. Laboratory markers cannot be easily studied at the population level because infection by some agents (eg, with human herpesvirus 6 or Chlamydia pneumoniae) does not result in identifiable clinical disease, or infection occurs in childhood and is not reliably reported by study subjects.
The convergence of epidemiology and seroepidemiology of research, however, is seen with Epstein-Barr virus. (6,7) Data from the Nurses' Health study, (8) for example, show a moderately increased risk of multiple sclerosis in nurses with a history of infectious mononucleosis (odds ratio 2.1, 95% CI 1.5-2.9). Taking only those nurses whose report of infectious mononucleosis was confirmed by a positive heterophil-antibody-test, the risk remained (2.3, 1.6-3.5). Although there was no association found between multiple sclerosis and reports of other common viral diseases before disease onset, there was an association with mumps after 15 years of age and with late age at measles infection. Whether Epstein-Barr virus is a necessary cause requiring additional triggers to produce disease or merely a marker for a true cause is unresolved. (9)
Infection with Borrelia burgdorferi, the spirochaete responsible for Lyme disease, can involve the central nervous system and the later stages of the disease may mimic the clinical symptoms of multiple sclerosis. (10) Seroepidemiological studies of B burgdorferi and multiple sclerosis have produced conflicting results. Chmielewska-Badora and colleagues (11) reported that ten of 26 (38%) patients with multiple sclerosis were seropositive for B burgdorferi compared with 149 of 743 (20%) patients with other neurological disorders (p=0.042). Yet others reported negative findings. (12,13) More recently, O Brorson and colleagues (14) studied the presence of the infectious agent, or at least its cystic structure, in the cerebrospinal fluid of ten patients with multiple sclerosis, in five controls who had lower back pain, and in one patient infected with B burgdorferi. Cystic structures were found in eight of the ten with multiple sclerosis with use of immuofluorescence before culture and in all the multiple sclerosis patients by transmission electron microscopy and acridine-orange staining. No cystic structures were found in the controls with any method. The investigators also reported a positive reaction to antispirochaetal antiserum, a similarity between the cystic structures with known cystic forms of spirochaetes, and the similarity between the cysts found in the multiple sclerosis patients and the patient with B burgdorferi infection. These results led the team to suggest that the multiple sclerosis patients were infected with a spirochaete, most likely B burgdorferi. Whether this infection really was B burgdorferi and whether it occurred before or after the onset of multiple sclerosis cannot be determined from this study and indeed, given current methodology, it is difficult to imagine how this could be determined.
Whether infection with B burgdorferi is a cause of multiple sclerosis or whether it is merely a result of heightened susceptibility of multiple sclerosis patients to infection due to damage to the blood-brain barrier remains one of the enigmas of multiple sclerosis research. Indeed, this caveat applies to all infectious pathogens that have been associated with multiple sclerosis. Current thinking on how infections could trigger the autoimmune/immunopathological manifestations of multiple sclerosis target the following mechanisms: molecular mimicry between the pathogen and myelin antigens, determinant spreading after injury to the central nervous system by the pathogen, and bystander inflammation caused by central nervous system infection. (3) It needs to be explained how a ubiquitous infection, such as that with Epstein-Barr virus, could be involved in the pathogenesis of multiple sclerosis. Moreover, several pathogens could be associated with multiple sclerosis and their presence in the central nervous system may not be a necessary requirement for disease initiation or perpetuation.
(1) Granieri E, Casetta I, Tola MR, Ferrante P. Multiple sclerosis: infectious hypothesis. Neurol Sci 2001; 22: 179-85.
(2) Alvarez-Lafuente R, Martin-Estefania C, de Las Heras V, et al. Active human herpesvirus 6 infection in patients with multiple sclerosis. Arch Neurol 2002; 59: 929-33.
(3) Talbot PJ, Arnold D, Antel JP. Virus-induced autoimmune reactions in the CNS. Curr Top Microbiol Immunol 2001; 253: 247-71.
(4) Rosati G. The prevalence of multiple sclerosis in the world: an update. Neurol Sci 2001; 22: 117-39.
(5) Wolfson C, Granieri E, Lauer K. Case-control studies in multiple sclerosis. Neurology 1997; 49 (suppl 2): S5-S14.
(6) Ascherio A, Munch M. Epstein-Barr virus and multiple sclerosis. Epidemiology 2000; 11: 220-24.
(7) Marrie R, Wolfson C. Multiple sclerosis and Epstein-Barr virus. Can J Infect Dis 2002; 13: 111-18.
(8) Hernan MA, Zhang SM, Lipworth L, Olek MJ, Ascherio A. Multiple sclerosis and age at infection with common viruses. Epidemiology 2001; 12: 301-06.
(9) Wolfson C. Multiple sclerosis and antecedent infections. Epidemiology 2001; 12: 298-99.
(10) Karussis D, Weiner HL, Abramsky O. Multiple sclerosis vs Lyme disease: a case presentation to a discussant and a review of the literature. Mult Scler 1999; 5: 395-402.
(11) Chmielewska-Badora J, Cisak E, Dutkiewicz J. Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study. Ann Agric Environ Med 2000; 7: 141-43.
(13) Schmutzhard E, Pohl P, Stanek G. Borrelia burgdorferi antibodies in patients with relapsing/remitting form and chronic progressive form of multiple sclerosis. J Neurol Neurosurg Psychiatry 1988; 51: 1215-18.
(14) Brorson O, Brorson S-H, Henriksen T-H, Skogen PR, Schoyen R. Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection 2001; 29: 315-19.
* Christina Wolfson, Pierre Talbot
* Department of Epidemiology and Biostatistics, McGill University, and Centre for Clinical Epidemiology and Community Studies,
Lady Davis Institute for Medical Research, Montreal, Quebec, Canada; and Institut National de la Recherche Scientifique, Institut Armand-Frappier, University of Quebec, Laval, Quebec
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination. In Miklossy's study above, senile plaques stained avidly for Bb spirochetes. Vincent Marshall reviewed the MD literature in Medical Hypothesis (Vol 25: 89-92, 1988) and advances the notion that LD is causing MS! His survey revealed that multiple studies prior to 1951 were able to demonstrate spirochetes in the spinal fluid of MS patients (by inoculation into animals and on silver stain of CNS tissues). Dr. Coyle has documented the presence of antibodies to Bb in MS patients (Neurology Vol. 39:760-763, 1989). The encephalopathy attributed to MS is very reminiscent of LD. Both MS and LD are associated with sinusitis (Lancet, 1986). Dr. Leigner has reported a case of LD which fulfilled all criteria for MS. The epidemiology of MS and the geographic distribution parallels that of LD. The symptoms of both LD and MS can be aggravated if the patient takes a hot bath. Anecdotally, patients with LD, who previously had been identified as MS, responded to antibiotic therapy.
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent.
Marshall V.
Animal Vaccine Laboratory, Council Bluffs, Iowa 51501.
Multiple Sclerosis (MS) is a chronic central nervous system (CNS) infection similar to Lyme Disease or Neurosyphilis in its latency period, pathogenesis, symptoms, histopathology and chronic CNS involvement. It does not have as yet a fully identified spirochetal etiological agent. Much research and clinical support for this hypothesis was published before 1954 and is based on silver staining of neural lesions, animal isolation of the etiologic agent and the characteristic symptoms and pathogenesis of the disease. If this hypothesis is correct, the disease should be treatable with antibacterial agents that penetrate the CNS (such as high dose antibiotics), diagnosible by specific immunological tests, and preventable by early treatment or by the use of vaccines in high risk populations.
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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