Multiple Sclerosis and Infection
Could Multiple Sclerosis be caused by infection? These studies and articles offer compelling evidence. Contact Us for more information.
Multiple Sclerosis and Infection
Multiple Sclerosis and Fungus
Multiple Sclerosis and Lyme Disease
Multiple Sclerosis and Parasites
Multiple Sclerosis and Viruses
1. Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination.
Nature. 2011; 479(7374): 538-41. DOI: 10.1038/nature10554.
This study shows that microbes that live in the body (in particular the GI tract) are an essential factor in triggering the autoimmune response in MS and other diseases.
“Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. … The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. … We show that the commensal gut flora… is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease…“
2. Role of pathogens in multiple sclerosis.
International Reviews of Immunology. 2014; 33(4): 266-83. DOI: 10.3109/08830185.2013.823422.
This study states that “infectious pathogens (disease causing microbes) are the likely environmental factors involved in the development of MS.” It also identifies various microbes that are involved in the development of Multiple Sclerosis infection, which include various bacteria, parasites and viruses.
“Although the etiology of MS is unknown, genetic and environmental factors play a role. Infectious pathogens are the likely environmental factors involved in the development ofMultiple Sclerosis infection. Pathogens associated with the development or exacerbation of MS include bacteria, such as Mycoplasma pneumoniae and Chlamydia pneumoniae, the Staphylococcus aureus-produced enterotoxins that function as superantigens, viruses of the herpes virus (Epstein-Barr virus and human herpesvirus 6) and human endogenous retrovirus (HERV) families and the protozoa Acanthamoeba castellanii. Evidence, from studies with humans and animal models, supporting the association of these various pathogens with the development and/or exacerbation of MS will be discussed along with the potential mechanisms including molecular mimicry, epitope spreading and bystander activation. In contrast, infection with certain parasites such as helminthes (Schistosoma mansoni, Fasciola hepatica, Hymenolepis nana, Trichuris trichiura, Ascaris lumbricoides, Strongyloides stercolaris, Enterobius vermicularis) appears to protect against the development or exacerbation of MS… A complex interaction between the CNS (including the blood-brain barrier), multiple infections with various infectious agents (occurring in the periphery or within the CNS), and the immune response to those various infections may have to be deciphered before the etiology of MS can be fully understood.”
3. Could Multiple Sclerosis Begin in the Gut?
Scientific American. 2014
“MS researchers are focusing on the content of the gut’s microbiome as a possible contributor to the body’s autoimmune attack on its nervous system.
… 10 academic researcher centers across the U.S. and Canada, reported significantly altered gut flora in pediatric MS patients.”
4. The Gut Microbiome in Multiple Sclerosis
Current Treatment Options in Neurology. 2015. DOI: 10.1007/s11940-015-0344-7
Clinical trials aimed at modulating the gut microbiota (the microbes that live in the body – especially in the gut) in MS patients are currently being done and may prove to be an effective, safe way to treat Multiple Sclerosis infection.
“The gut microbiome is made up of a wide range of (chiefly) bacterial species that colonize the small and large intestine. The human gut microbiome contains a subset of thousands of bacterial species, with up to 1014 total bacteria. Studies examining this bacterial content have shown wide variations in which species are present between individuals. The gut microbiome has been shown to have profound effects on the development and maintenance of immune system in both animal models and in humans. A growing body of evidence has implicated the human gut microbiome in a range of disorders, including obesity, inflammatory bowel diseases, and cardiovascular disease. Animal studies present compelling evidence that the gut microbiome plays a significant role in the progression of demyelinating disease, and that modulation of the microbiome can lead to either exacerbation or amelioration of symptoms. Preliminary clinical trials aimed at modulating the gut microbiota in MS patients are underway and may prove to be a promising and lower-risk treatment option in the future.”
5. Gut Bacteria: Key to MS.
Multiple Sclerosis News Today. 2015.
“There has been a great deal of recent interest in the connection between nervous system function and the complex bacteria that are found in the gastrointestinal system, known as the gut microbiome. Some scientists believe that differences in the type of bacteria found in the gut may underlie neurological disease. In fact, it has been suggested by some that gut bacteria may interact with the immune system, in turn affecting autoimmune conditions like multiple sclerosis (MS).”
6. National MS Society Invests $28 Million in New Research.
The National MS Society. 2015
“Diet, gut bacteria, myelin repair trials and patient-centered wellness programs are among the new leads being explored to move us closer to a world free of MS.”
7. Multiple sclerosis patients have a distinct gut microbiota compared to healthy controls
Nature. Scientific Reports 6. Article number: 28484. 2016. DOI: 10.1038/srep28484
The conclusion of this study is consistent with the hypothesis that the microbes that live in the digestive tract of MS patients are out of balance compared to healthy people. They found that the types of microbes that live in the GI tract of MS patients was different from the microbes that live in healthy people and they feel that this may play an important role in the disease process ofMultiple Sclerosis infection.
“it’s hypothesized that gastrointestinal microbiota might play an important role in pathogenesis of MS. Therefore, this study was designed to investigate whether gut microbiota are altered in MS by comparing the fecal microbiota in relapsing remitting MS (RRMS) (n = 31) patients to that of age- and gender-matched healthy controls (n = 36). …Detailed fecal microbiome analyses revealed that MS patients had distinct microbial community profile compared to healthy controls. We observed an increased abundance of Psuedomonas, Mycoplana, Haemophilus, Blautia, and Dorea genera in MS patients, whereas control group showed increased abundance of Parabacteroides, Adlercreutzia and Prevotella genera. Thus our study is consistent with the hypothesis that MS patients have gut microbial dysbiosis and further study is needed to better understand their role in the etiopathogenesis of MS.”
8. Link between gut bacteria, MS discovered: MS patients show lower levels of good bacteria.
Science Daily. 2016
“Scientists say that MS patients have a distinct microbiome from their healthy peers.
… Researchers are now saying bad gut bacteria – or an insufficient amount of good bacteria – may have a direct link to multiple sclerosis as well.”
9. Gut microbiota composition and relapse risk in pediatric MS: A pilot study
Journal of Neurological Sciences. 2016; 363. Pages 153-157
This study found that the absence of a specific bacteria was associated with the higher risk of relapse of multiple sclerosis infection in pediatric MS patients.
“We explored the association between baseline gut microbiota (16S rRNA biomarker sequencing of stool samples) in 17 relapsing-remitting pediatric MS cases and risk of relapse over a mean 19.8 months follow-up. … After covariate adjustments for age and immunomodulatory drug exposure, only absence (vs. presence) of Fusobacteria was associated with relapse risk…”
10. From bugs to brains: the gut microbiome in paediatric multiple sclerosis.
Multiple Sclerosis and Related Disorders. 2017; 12. DOI: 10.1016/j.msard.2016.12.007
“Knowledge surrounding the trillions of microbes that inhabit the human gut has bloomed exponentially in recent years, and the emerging concept of a gut-brain axis represents a major shift in how we think about neurological health. A recent workshop at the University of British Columbia, Canada brought together multi-disciplinary leaders in the field of microbiomics and brain health and aimed to serve as a springboard for future combined endeavors in these areas. This article provides the motivation for, and overview of, the workshop, and the next steps in establishing a cross-disciplinary initiative on Brain Health and the Microbiome.”
11. Does the Gut Microbiota Influence Immunity and Inflammation in Multiple Sclerosis Pathophysiology? (2017)
- Recent studies have shown that changing some of the bacterial population in the gut can lead to a proinflammatory state, indicating a potential mechanism causingMultiple Sclerosis infection in humans.
- The intestinal microflora in MS patients has greater variability than that of healthy controls.
- Studies found a decrease in the percentage of bacteria called Bacteroides in the intestinal microflora in patients with MS.
- When certain bacteria are absent MS is more active.
- Intestinal flora may affect the pathogenesis of MS, as changes in the gut microbiome lead to an irregular immune response, in both the colon and distal regions of the immune system, that is, the CNS … indicating a substantial interaction between the GI tract and the brain. These observations suggest that the population of immune cells involved in the pathogenesis of MS in humans may be associated with the immune system located around the gut.
- These results indicate that the intestinal microflora in patients with Multiple Sclerosis infection is characterized by moderate dysbiosis.
Multiple Sclerosis and Fungus
1. Fungal infection in cerebrospinal fluid from some patients with multiple sclerosis
European Journal of Clinical Microbiology & Infectious Diseases. 2013; 32:795–801.
“… fungal infection can be demonstrated in CSF from some MS patients. This may constitute a risk factor in this disease and could also help in understanding the pathogenesis of MS.”
2. Fungal infection in a patient with multiple sclerosis
European Journal of Clinical Microbiology & Infectious Diseases. 2011; Vol 30, Issue 10.
“Antibodies against Candida spp. as well as C. famata-related antigens were also detected in cerebrospinal fluid (CSF). Our findings provide support for the notion that disseminated mycosis is present in this patient.”
3. Fungal toxins and multiple sclerosis: a compelling connection
The Brain Research Bulletin. 2010; 82(1-2):4-6.
“… a surprisingly coherent relationship can be made between multiple sclerosis and fungal toxins. Specifically, certain pathogenic fungi sequester in non-neuronal tissue and release toxins that target and destroy CNS astrocytes and oligodendrocytes. Without these glial support cells, myelin degrades triggering the onset of multiple sclerosis and its associated symptoms. We propose here that fungal toxins are the underlying cause of multiple sclerosis and thus may offer an avenue towards an effective cure.”
4. Association between multiple sclerosis and Candida species: evidence from a case-control study
European Journal of Clinical Microbiology & Infectious Diseases. 2010; Vol. 29, Issue 9.
“In this case-control study we found a significant association between elevated antibodies of four species of Candida and MS. … In summary, the results of this single study suggest that Candida species infection may be associated with increased odds of MS.”
5. Fungal Infection in Patients with Multiple Sclerosis
Open Mycology Journal. 2008, 2, 22-28
“Our results provide evidence that in all seven patients studied there are signs of fungal infection. Thus, some of these patients exhibit high antibody titers against several Candida spp.”
“In addition, quantitative PCR indicates that six out of seven patients contain fungal DNA in their blood. Four contain significant amounts of β-1,3 glucan in serum, while the presence of fungal antigens was evident in practically all of them, though to different extents. Yeast antibody and antigen analyses reveal the presence of both in cerebrospinal fluid.”
6. Multiple Sclerosis – Functional Approaches
Townsend Letter for Doctors & Patients. 2003. 66-74
“In our study, 100% of MS patients demonstrated an abnormally high Dysbiosis Index.”
- Frequent association of Candidiasis and MS
- Elevated anti-Candida antibodies in 70% of MS patients tested
- Shows the evidence supporting the relationship between gut abnormalities and brain pathology.”
7. Evaluation of APR1 Gene Expression in Candida albicans Strains Isolated From Patients With Multiple Sclerosis.
Jundishapur Journal of Microbiology. 2016; 9(5)
The expression of a specific gene (APR1) of Candida albicans is an important factor in the development of systemic candidiasis.
“Results from this study showed that “APR1 gene expression in Candida albicans strains isolated from MS patients may be an important factor for invasive Candida albicans strains in the progression of MS disease.”
8. The role of Candida albicans in the severity of multiple sclerosis.
Mycoses. 2016; 59(11): 697-704. doi: 10.1111/myc.12489.
This study compared the activity of a specific enzyme (SEA) in Candida albicans between multiple sclerosis infection patients and a healthy group. The study found that the level SEA of Candida albicans in MS patients was significantly more than in the healthy group. There was a positive relationship between higher levels of SEA and increased severity of MS. Their results found that SEA was the biggest factor (from all the factors they tested) in the severity of MS. Their results suggested that the level of SEA and perhaps the capacity of Candida albicans isolates to invade the tissue is associated with the severity of MS.
“The SEA of Candida albicans in MS patients (3466.95 ± 277.25 μmol min-1 mg-1 ) was significantly more than that of healthy controls … The SEA had a positive correlation with the severity of MS (P < 0.001, r = 0.65). Analytical models showed that SEA played the most important role (among all included factors that affect on EDSS) in the severity of MS. The SEA of C. albicans in MS patients was significantly more than the healthy controls. The results suggest that the level of SEA of proteinase A and probably the capacity of C. albicans isolates to invade the host tissue is associated with the severity of MS.”
9. Multiple sclerosis and mixed microbial infections. Direct identification of fungi and bacteria in nervous tissue. Neurobiol Dis. 2018 Sep;117:42-61. doi: 10.1016/j.nbd.2018.05.022. Epub 2018 Jun 1.
“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. … 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. … 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.”
Multiple Sclerosis and Lyme Disease
1. Excerpt from the book, “Why Can’t I Get Better?” by Dr. Horowitz. (2013)
“Multiple authors in the medical literature propose that MS is most likely caused by an infection with Borrelia burgdorferi, the agent of Lyme disease. There at least five reasons for the hypothesis that Lyme is the basis for some cases ofMultiple Sclerosis infection:
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 disease is also similar; they both can cause inflammation in 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 multiple sclerosis from neurological Lyme disease, they would find extremely similar results. As with multiple sclerosis infection, central nervous system infection with B. burgdorferi can cause an increased protein synthesis with IgG antibodies, lymphocytic pleocystosis (increased lymphocytes in the 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 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 (ie. 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.
One of the mysteries that has challenged my medical practice is that as more and more patients come for help, a large number present with symptoms of multiple sclerosis. Those coming for help said that the traditional medical establishment had failed to provide them with answers for their illnesses. Why is this the case?
Patients with multiple sclerosis infection often complain of intermittent tingling and numbness in different parts of their bodies, and MRIs of their brains can show varying amounts of white spots. Both of these symptoms and findings are seen in both Lyme disease and MS, and since some patients have negative serum Lyme ELISAs, they are often told by neurologists that they have MS and are given the ABC regimen, or Rebif. If these drugs don’t help, patients are told that they must have “relapsing remitting” form of the disease, in which the symptoms come and go, or a chronic, progressive form, and are told to remain on these drugs to stabilize their symptoms. However, just as with the patients diagnosed with lupus or with rheumatoid arthritis, the drugs may not help relieve their symptoms, or even if they do, we may be treating symptoms and not getting to the true, underlying cause of the disease process.
What is the link between Lyme disease and MS? Do Lyme disease and/or co-infections somehow provoke the MS autoimmune reaction, just as it can do with lupus, rheumatoid arthritis, and other inflammatory disorders? Dr. Stephen Phillips, past president of ILADS, has presented evidence at scientific conferences that there is an association between MS and Lyme disease. He also reported treating an abnormally high number of MS patients in his Lyme practice. Years earlier, Dr. Patricia Coyle of SUNY- Stony Brook presented research on how to differentiate between MS and Lyme at a Lyme Disease Foundation conference. Her work focused on the following:
- Both cause optic neuritis, inflammation of the optic nerve, and blindness.
- Both cause white spots or demyelinating lesions visible on an MRI scan of the brain.
- Both could cause paresthesias -tingling and numbness of the extremities.
- Both can cause bladder dysfunction.
- Both have relapsing, remitting nature.
- Both diseases can cause elevations of myelin basic protein (MBP) and oligoclonal bands (immunoglobulins) to appear in the spinal fluid.
The primary difference between the two diseases seemed to be that with MS there were more white matter lesions on an MRI and higher amounts of myelin basic protein and oligoclonal bands 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.”
2. Under Our Skin Documentary
CLICK HERE to watch Dr. Alan MacDonald
Quote from Dr. Alan MacDonald:
“Since spirochetes are the cause of neurodegenerative diseases in syphilis, could it be that the spirochetal infection in Lyme disease is partly or wholly responsible for some of the neurologic degenerative diseases we face in this century – Alzheimer’s disease, Lou Gehrig’s disease (ALS), Parkinson’s disease, multiple sclerosis (MS). Those are named conditions for which no cause is known.”
3. Under Our Skin Documentary
CLICK HERE to watch Dr. Klinghardt
Quote from Dr. Klinghardt:
“We never had…in the last five years a single MS patient…who did not test positive for Borrelia burgdorferi. Not a single one.”
4. Multiple Sclerosis is a Parasitosis, a Lecture by Dr. Alan MacDonald
Dr. Alan MacDonald presents powerful research showing that parasitic infections are present in the brains and spinal fluid of people who suffer with multiple sclerosis infection.
Dr. MacDonald explains one of the ways Borrelia is introduced into the central nervous system of MS patients in the following quote:
“It’s like a Trojan horse – the worm itself is an assault on the body and the Borrelia inside the worm, when they are released also assault the body and cause tissue injury. The two have a holy alliance and cause multiple sclerosis and other conditions of the brain.”
Why is this not studied more:
Quote from Dr. Alan MacDonald:
“Spinal fluid was not examined in animal autopsies or in human autopsies until 2016 by the Duray foundation – began its MS spinal fluid incentive.”
5. Lecture Notes of Tom Grier
Tom Grier (Microbiologist from Minnesota) spoke at Lac Court Oreilles Convention Center in Hayward, WI.
“There are more than 50 such MS-spirochete references prior to World War II and going back to as far as 1911, and published in such prestigious journals as the Lancet:
1911 Buzzard Spirochetes in MS Lancet
1913 Bullock MS Agent in Rabbits Lancet
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 Shhlossman MS Agent in Animal Model Rev Neuro
1924 Blacklock MS Agent in Animals J. 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 and Exp Med 11: No 4:343
1954 Steiner Morphology of Spirochaeta Myelophthora (Myelin Loving) In MS Journal of Neuropathology and Exp Neurol 11:4 343 1954
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 1957
1986 Gay D Dick 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 (Multiple Sclerosis 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
If you follow the European Medical Literature concerning Multiple Sclerosis from 1911 to 1939, you find that in France, Germany and England, there were independent researchers all observing similar things and coming to similar conclusions:
1) “Spirochetes are often found in conjunction with the lesions in the brains of patients who have died with MS.
2) These spirochetes can be isolated and can infect many mammalian animal models; including: mice, rats, hamsters, guinea pigs, rabbits, dogs, and primates.
3) The spirochetes could be re-isolated from the brains of the infected animals and be inoculated into more un-infected animals and re-isolated from their brains.”
6. Time Magazine (Monday June 24, 1957)
“Multiple sclerosis victims (about 250,000 in the U.S.) were anxiously wondering about a possible clue to their mysterious disease, which is marked by near-total loss of muscle control. (It happens when the myelin sheath, a fatty insulation around nerve pathways, degenerates for unknown reasons, thus short-circuiting nerve signals.) Philadelphia Bacteriologist Rose Ichelson, 59, reported success in cultivating an obscure microbe, Spirochaeta myelophthora, which she has found in the spinal fluid of MS victims. Inference: multiple sclerosis is caused by the spirochete, and early attack on it should lead to cure or alleviation…”
7. THE SPIROCHETE AND MULTIPLE SCLEROSIS
California Medicine. 1958; 89(6): 387–389.
“Cultures on anaerobic medium were made of the spinal fluids of 27 patients with multiple sclerosis and 13 controls after the method described recently by Ichelson. Where Ichelson found organisms resembling spirochetes in 78 per cent of patients with multiple sclerosis, we found some form of what appeared to be a living micro-organism in 18.5 per cent. The control fluids were all sterile. The work requires confirmation and amplification.”
8. Multiple sclerosis is a chronic central nervous system infection by a spirochetal agent.
Medical Hypothesis. 1988; 25(2):89-92.
“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.”
9. Borrelia burgdorferi antibodies in patients with relapsing/remitting form and chronic progressive form of multiple sclerosis.
Journal of Neurology, Neurosurgery, and Psychiatry. 1988; 51(9): 1215–1218.
“Sera of 106 multiple sclerosis patients and 103 closely matched controls were examined for Borrelia burgdorferi antibodies. The prevalence rate in multiple sclerosis patients was 14.2%, in controls 25.2%. Overall prevalence was 20.1%. Mean IgG antibody level was insignificantly higher in controls than in multiple sclerosis patients. Patients with a chronic progressive course of multiple sclerosis had an insignificantly higher mean Borrelia antibody level, when compared with those suffering from relapsing/remitting form of disease.”
10. Lyme Borreliosis and multiple sclerosis: any connection? A seroepidemic study.
The Annals of Agricultural and Environmental Medicine. 2000; 7(2):141-3
“A total of 769 adult neurological patients hospitalized 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.”
11. Book Cell Wall Deficient Forms, Third Edition: Stealth Pathogens by Lida H. Mattam (2000).
“Currently research is in the progress of growing spirochetes from MS cases, based on reports of early experimental work. From blood and spinal fluid of some MS cases it is possible to grow a Borrelia-like organism in serum-free autoclaved medium. Improvement in culture is the next step necessary to obtain a bulk of organisms for anti-body production. More research needs to be done to identify the biochemical signature of the organism. From blood and from more than 60 spinal fluids of MS cases, it is been possible to grow Borrelia like organisms in MPM medium. 14 cases of ALS have demonstrated in blood as spirochete which stains Lyme FA. In all instances pleomorphism is a constantly appearing phenomenon.”
12. Chronic Lyme borreliosis at the root of multiple sclerosis – is a cure with antibiotics attainable?
Medical Hypotheses. 2005; 64(3):438-48.
“… 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.”
13. Controversies in late neuroborreliosis and multiple sclerosis case series
Therapeutics, Pharmacology and Clinical Toxicology. Vol XIII, Number 1, March 2009
“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. … 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.”
14. Lyme disease in patients with multiple sclerosis: clinical, diagnostic and therapeutic features
Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova. 2012; 112(2 Pt 2):64-8.
“Lyme disease is one of the most frequent infections in the Russian Federation. In patients with multiple sclerosis, the Borrelia infection may act as a trigger in some cases and also worsens the clinical course of multiple sclerosis. One hundred patients with definite multiple sclerosis were examined including 19 patients with the combination of multiple sclerosis and Lyme disease. The difficulties of diagnosis, clinical features and treatment of Lyme disease in patients with multiple sclerosis are discussed.”
15. Unusual manifestation of neuroborreliosis (case report)
Georgian Medical News. 2017; (264): 72-75.
“A 44 year old man was diagnosed as MS …, who within two years developed typical clinical signs of Parkinsonism. Blood IgM, IgG detected to be negative against Chlamidia pneumonie, Micoplasma pneumonie, cytomegalovirus, Herpes simplex ½, while the blood IgG was strongly positive against Borrelia burgdorferi, confirmed by followed Western blot test. … MS and even Parkinsonism in suspicious cases should thoroughly be investigated for differentiation from chronic Neuroboreliosis.”
16. Infectious Agents and Neurodegenerative Diseases: Exploring the Links.
Current Topics in Medicinal Chemistry. 2017; 17(12):1390-1399.
“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)… Several bacterial and viral pathogens have been reported for neurodegeneration … We will focus in this review on the possible link between neurodegeneration and infections particularly Chlamydophila pneumoniae, Borrelia burgdorferi, Mycoplasma etc.”
Multiple Sclerosis and Parasites
1. Multiple Sclerosis is a Parasitosis, a Lecture by Dr. Alan MacDonald
“We have not found a case of multiple sclerosis that does not contain nematodes in the cerebral spinal fluid.”
2. MS: Parasitic Nematodes with Borrelia Endosymbionts Found in CSF
“In 2016, Dr. Alan B. MacDonald detected, for the first time ever, Borrelia endosymbionts inside parasitic nematode worms in the autopsy cerebrospinal fluid of patients who had died of multiple sclerosis.”
3. Nematodes, Nervous Disease and Neurotropic Virus Infection Observations in Animal Pathology or Probable Significance in Medical Neurology
British Medical Journal. 1952. pp 366
“It is generally accepted that ascarids, after the hatching of the eggs in the intestines, go on a tour to the lungs and that some larvae may wander into the general circulation and reach the nervous system or the eyes.”
4. Cerebrospinal Nematodiasis Focal Encephalomyelomalacia of Animals Caused by Nematodes (Setaria Digitata); A Disease Which May Occur in Man
Archives of Neurology & Psychiatry. 1953; 70(3): 325-349.
5. Epizootic cerebrospinal nematodiasis or setariasis. Focal encephalomyelomalacia in animals in the Orient caused by immature Setaria digitata: a disease which may occur in animals in other parts of the world
British Veterinary Journal. 1952. Vol.108 No.3 pp.71-88
6. Filarial Infections as Zoonoses
Journal of Helminthology. 1965. 39(2-3), 229-250.
“The paper summarizes existing information on the role of animals in the transmission of filarial infections to man.”
7. On the invasion of the central nervous system by nematodes I. The Incidence and pathological significance of nematodes in the central nervous system
Parasitology. 1955. 45(1-2), 31-40.
“A wide variety of nematode species have been observed to invade the central nervous system. They may be located in the meningeal spaces or may penetrate into the tissues of the brain and spinal cord.”
8. Cerebrospinal nematodiasis caused by Parelaphostrongylus tenuis in angora goats in Texas
Journal of Wildlife Diseases. 1979; Vol. 15
9. Cerebrospinal nematodiasis in seven goats
Schweizer Archiv Fur Tierheilkunde. 1997; 139(6):282-7.
“The animals were admitted to the clinic because of progressive pelvic limb ataxia, recumbency, vestibular disease and circling. Clinical findings were complete or incomplete posterior paresis, pelvic limb ataxia, circling, reduced cutaneous sensation and proprioceptive deficits as well as cranial nerve reflexes deficits. … In three goats predominance of mononuclear and eosinophilic cells in the cerebrospinal fluid was interpreted as typical findings for parasite infestation in the central nervous system. Histopathological changes and the finding of a nematode in cross sections in two affected animals confirmed the diagnosis.”
10. Zoonotic Filariasis
Clinical Microbiology Reviews. 1998; 11(2): 366–381.
“Filariae of animals, especially those of mammals, often infect humans and typically produce cryptic infections. These “zoonotic” infections have been reported from virtually all parts of the world including temperate zones. Infections may be symptomatic or not, and the parasites are found in surgical tissue biopsy specimens or, more rarely, are removed intact from superficial sites such as the orbit or conjunctivae. Typically, these worms tend to occupy tissue sites similar to those occupied in the natural animal host … Many kinds of filariae have been isolated from humans, including species of Dirofilaria, Brugia, Onchocerca, Dipetalonema, Loaina and Meningonema. Worms have been found in subcutaneous tissues, the heart and lungs, lymphatics, the eye, and the central nervous system. Specific identification of these filariae is based on their morphological features in histologic sections. Unfortunately, some of these worms cannot be identified even at the generic level. There are other species of filariae, presumed to be zoonotic, which produce patent infections in humans but are poorly and incompletely known. These include Microfilaria semiclarum and Microfilaria bolivarensis. It is probable that almost any filaria parasitizing animals can, under proper circumstances, infect humans and undergo some degree of development. Undoubtedly, additional species of filariae will continue to be isolated from humans in the future.”
Multiple Sclerosis and Viruses
1. Association of human herpes virus 6 (HHV-6) with multiple sclerosis: increased IgM response to HHV-6 early antigen and detection of serum HHV-6 DNA.
Nature Medicine. 1997; 3(12): 1394-7.
“… Recently, human herpes virus 6 (HHV-6) … has been reported to be present in active MS plaques. … Given the ubiquitous nature of this virus and the challenging precedent of correlating antiviral antibodies with disease association, these antibody studies have been supported by the detection of HHV-6 DNA from samples of MS serum as a marker of active viral infection.”
2. Human endogenous retroviruses and multiple sclerosis: innocent bystanders or disease determinants?
Biochimica et Biophysica Acta. 2011; 1812(2):162-76.
“Human endogenous retroviruses (HERVs) constitute 5-8% of human genomic DNA and are replication incompetent despite expression of individual HERV genes from different chromosomal loci depending on the specific tissue. … The HERV-W family has received substantial attention in large part because of associations with diverse syndromes including multiple sclerosis (MS) and several psychiatric disorders. HERV-H and HERV-K have also been implicated in MS and other neurological diseases but await delineation of their contributions to disease. …”
3. Activation of MSRV-type endogenous retroviruses during infectious mononucleosis and Epstein-Barr virus latency: the missing link with multiple sclerosis?
PLOS One. 2013; 8(11): e78474.
“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. … 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.”
4. A case of presumed herpes keratouveitis in a patient treated with fingolimod.
Multiple Sclerosis Journal – Experimental, Translational and Clinical. 2016; 2: 2055217316652907.
“… Fingolimod (Gilenya) treatment appears to increase the risk of herpes virus infections, including with herpes simplex virus and varicella zoster virus. This case report reviews the potential immunology behind this risk, and identifies the need for further research …”
5. Association between human herpesvirus & human endogenous retrovirus and MS onset & progression.
The Journal of the Neurological Sciences. 2017; 372: 239-249.
“This review discusses the role of Epstein-Barr virus (EBV), human herpesvirus 6 (HHV6) and human endogenous retroviruses (HERVs) in the onset and progression of multiple sclerosis (MS). … HHV6 has also been implicated in the pathogenesis of MS; moreover, it showed a closer connection with the disease activity. Recent studies found that HERVs were associated with the development and progression of MS.”
“If viral infection, principally EBV infection, was an essential part of MS pathogenesis, prevention of EBV infection by vaccination could be a feasible approach.”
“Similarly, novel studies assessing the role of immunomodulation of the complex EBV induced changes within the MS patient may provide another avenue for treatment. The exciting finding of the success of B-cell depletion in RRMS and PPMS adds further weight to the role of B-cell dysregulation possibly from HHV infection as a major driver of MS clinical course. Future studies aimed at understanding the mechanism and role of viral infection on the MS onset and progression will hopefully identify advanced methods for the prevention and treatment of MS.”
6. Extratemporal herpes encephalitis during natalizumab treatment: A case report.
Multiple Sclerosis and Related Disorders. 2016; 10: 134-136.
“… Herpes simplex virus encephalitis (HSE) is a rare but often fatal disease if left untreated. … We report a MS patient under natalizumab (Tysabri) treatment with HSE, who presented with MRI lesions exclusively in the right parietal lobe. The patient was timely started on acyclovir resulting in marked improvement. A high index of suspicion for HSE should be maintained when a patient presents with fever and extratemporal lesions, even more in immunocompromised subjects.”
7. EBV Infection and Multiple Sclerosis: Lessons from a Marmoset Model.
Trends in Molecular Medicine. 2016; 22(12): 1012-1024.
“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 (demyelination) 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.”
8. Trials of antivirals in the treatment of multiple sclerosis.
Acta Neurologica Scandinavica. 2017; 136 Suppl 201:45-48.
“There is increasing evidence that human herpes viruses and human endogenous retroviruses (HERV) are involved in the aetiology and pathogenesis of multiple sclerosis (MS). In order to acquire the ultimate evidence to confirm such a relationship, it is probably required to use specific antiviral drugs in clinical trials of MS. The results of published antiviral clinical trials in patients with MS are summarized in this review. None of them showed statistically significant effects on primary outcomes of disease activity or on disability development …”
9. Multiple sclerosis: an example of pathogenic viral interaction?
Virology Journal. 2017; 14(1):42.
“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.
10. The aliens inside us: HERV-W endogenous retroviruses and multiple sclerosis.
Multiple Sclerosis. 2018; 24(1):42-47.
“Two human endogenous retroviruses of the HERV-W family are proposed as multiple sclerosis (MS) co-factors: MS-associated retrovirus (MSRV) and ERVWE1, whose env proteins showed several potentially neuropathogenic features, in vitro and in animal models. Phase II clinical trials against HERV-Wenv are ongoing. HERV-W/MSRV was repeatedly found in MS patients, in striking parallel with MS stages, active/remission phases, and therapy outcome. The HERV-Wenv protein is highly expressed in active MS plaques. Early MSRV presence in spinal fluids predicted worst MS progression 10 years in advance. Effective anti-MS therapies strongly reduced MSRV/Syncytin-1/HERV-W expression. The Epstein-Barr virus (EBV) activates HERV-W/MSRV in vitro and in vivo, in patients with infectious mononucleosis and controls with high anti-EBNA1-IgG titers. Thus, the two main EBV/MS links (infectious mononucleosis and high anti-EBNA1-IgG titers) are paralleled by activation of HERV-W/MSRV. It is hypothesized that EBV may act as initial trigger of future MS, years later, by activating MSRV, which would act as direct neuropathogenic effector, before and during MS.
11. Low intrathecal antibody production despite high seroprevalence of Epstein-Barr virus in multiple sclerosis: a review of the literature.
Journal of Neurology. 2018; 265(2):239-252.
“Given the very high seroprevalence of EBV in MS, the frequency of intrathecally produced antibodies to EBV in patients with MS is paradoxically low compared to that of other common viruses. These findings are compatible with the recently proposed hypothesis that in individuals going on to develop MS antiviral antibody-producing cells may invade the brain predominantly at the time of and triggered by acute primary EBV infection, before anti-EBV IgG producing cells have yet occurred.”
12. Epstein-Barr virus is present in the brain of most cases of multiple sclerosis and may engage more than just B cells.
PLOS One. 2018; 13(2): e0192109.
“… 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 EBVusing PCR and EBER-in situ hybridization (EBER-ISH). EBV was detected by PCR and/or EBER-ISH in 91/101 (90%) … 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. … 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.”