EPSTEIN-BARR VIRUS AND GUILLAIN-BARRE SYNDROME
Abstract
Five patients with Guillain-Barré (G.B.) syndrome, aged from 18 months to 27 years, had very high levels of antibodies to Epstein-Barr (E.B.) virus. All five had higher titres of E.B.-virus antibody than age-matched control groups. Two of the five patients had infectious mononucleosis (I.M.) but three had neither clinical nor laboratory evidence of this disease. These findings strongly suggest an association of E.B. virus with G.B. syndrome even without the signs of I.M.
credits to https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(72)92654-2/fulltext
Most now know that many people developed Guillain-Barre Syndrome after being vaccinated.
A study of 200 patients with Epstein-Barr Virus (often called Yuppie disease) is scheduled for publication this spring in the journal Medical Hypothesis. In an advance report in the San Diego Tribune (September 30. 1987). the study’s researchers have linked EBV syndrome to exposure to the weakened. but live, rubella virus found in the vaccine. Given to young children, the vaccine can linger in their systems for years and can be passed to adults through casual contact.
Biomedical researcher Allen D. Allen of Algorithms. Inc. of Northridge. California, blames EBV syndrome on Merck Sharp and Dohme’s Biavax and Meruvax vaccines which were introduced in the late 1970’s. Allen says. ‘I can say all this attention to the (Epstein-Barr) syndrome. the public awareness. started in the early 1980’s. right after these vaccines came out. Young adults. the ones most likely to be in contact with young children, are the primary targets. It’s too much of a coincidence to ignore."
In a similar study. Dr. Hugh Fudenberg http://members.aol.com/nitrf, professor of immunology at the Medical University in Charleston. South Carolina. found the same linkage in 24 patients.
Doctors have long struggled to find the cause of lupus. a chronic disease of the immune system that mainly affects women. Now , new research on children shows that it may be linked to Epstein- Barr, the virus that causes mononucleosis. In a recent study, researchers found that 99 percent of lupus patients had been exposed to the Epstein-Barr virus compared to 70 percent of those without the disease. " It may be that lupus patients are extremely susceptible to Epstein-Barr." or that the virus is a precursor to the disease, explains researcher John Harley, M.D. at the University of Oklahoma Medical Research Foundation, University of Oklahoma Health Sciences Center in Oklahoma City. Doctors hope this new discovery will aid in their efforts to find a cure for lupus.
Multiple Sclerosis May be Linked to Infection
Despite decades of research, the cause of multiple sclerosis remains unknown. In the past it was suggested that the disease might be immunological, though more recently it is thought that it could be a genetic disease.
One theory that has remained strong over the years is that of viral infections as a cause. Infections most under suspicion include 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.
Scientists have also focused on chlamydia pneumonia and the Epstein-Barr virus as it was found that patients with multiple sclerosis had an increase in respiratory infections before the onset of the disease. However, it is unknown whether the Epstein-Barr virus plays a specific role in multiple sclerosis or is an indication of an immune system response in patients with the disease.
A vascular theory for multiple sclerosis has also been discussed, along with dietary therapies, which have a vascular defect as part of the rationale. It has been suggested that vascular changes may precede the inflammation and demyelination in a multiple sclerosis plaque. Those that advocate the infection theory believe that an infection could be the initial event that brings on this process.
In terms of the genetic factor of the disease, research has shown that siblings and fraternal twins have a greater risk, by about two to five percent, than the general population. In identical twins, this risk is about 30 percent higher. While this seems to support the genetic proponent, the question has been raised of why all genetically disposed individuals do not get the disease. To explain this, researchers say that multiple sclerosis may be determined by multiple genes and an environmental factor, possibly infection.
One common theory holds that genetics, viral infections, and immune reactions all play a role in multiple sclerosis.
British Medical Journal 2002;325:1128
http://www.docguide.com/news/content.nsf/news/8525697700573E1885256D020062D3F4?
OpenDocument&id=03E05ADF052F2F3E852568C000807CA5&c=Paediatrics&count=10
AAN: Child-Onset Multiple Sclerosis More Likely to Have epstein-barr virus Antibodies than Controls
By Paula Moyer
HONOLULU, HI -- April 8, 2003 -- Children who have multiple sclerosis (MS) are more likely than healthy children to be seropositive for Epstein-Barr virus (EBV), according to researchers. "EBV seropositive status is significantly associated with paediatric MS," said Brenda L. Banwell, MD, the director of the paediatric MS unit at the Hospital for Sick Children in Toronto, Ontario, Canada. Because of EBV's lifelong effects on B cell proliferation and T cell surveillance, it "may play a pivotal role in the autoimmune milieu that fosters MS." She presented findings of her team's study here at the 55th Annual Meeting of the American Academy of Neurology.
Dr. Banwell and her colleagues wanted to compare the seropositive status for common viruses in patients with paediatric multiple sclerosis and in controls. Their rationale was that several investigators have postulated that infection by a common virus such as EBV in a genetically pre-disposed host may be a pathobiological mechanism for MS.
The literature has also shown that adults with MS have higher seropositivity for EBV than controls do and that EBV infection has been associated with other demyelinating disorders, including optic neuritis and central nervous system demyelination. Further, research has shown that infection with acute mononucleosis in adulthood increases the risk of MS several times over.
One complication to testing the theory in adults is that EBV seropositivity is nearly universal by adulthood, with 90% of adults having EBV antibodies. Therefore, comparative analysis is limited between adult MS patients and controls. It was necessary to study paediatric patients, instead, she said, since fewer children are EBV-positive than are adults. Dr. Banwell and her colleagues theorised that MS patients might be EBV-positive before their healthy peers have had exposure to the virus.
The investigative team obtained serum samples from 25 children with clinically diagnosed MS and 75 age-matched controls, who were matched at a 3:1 ratio for birth year for each MS patient. Control samples were obtained from previously healthy children for whom serology had been drawn previously due to acute symptoms of abdominal pain, pharyngitis, or rash.
All 100 samples were analysed for EBV capsid antigen (EBV-VCA), EBV nuclear antigen (EBV-EBNA), and EBV early antigen (EBV-EA). The researchers also analysed all 25 MS samples and a random sampling of 15 of the age-matched control samples for parvovirus B19 (parvo B19), cytomegalovirus (CMV), and varicella zoster (VZV). The investigators coded and analysed all samples in a uniform manner by the ELISA technique (as per manufacturer s instructions). The study virologist then interpreted results in a blinded manner.
Dr. Bandwell and her co-investigators found that EBV seropositivity differed markedly between paediatric MS patients and age-matched controls. Although 89% of paediatric MS patients were positive for EBV-VCA and EBV-EBNA, which indicated a temporally remote infection, 31% of controls had such infections (p 0.0004). Among the MS patients, 3 (12%) were negative for all three EBV antigens.
The investigators found no statistical significance regarding seropositivity for the other viruses between MS patients and controls. For parvovirus B19 the infection rates were 49% and 64%, respectively (p=NS). For CMV the rates were 42% and 64%, respectively (p=NS). For VZV those rates were 88% and 92%, respectively (p=NS).
This discrepancy in EBV seropositivity between paediatric MS patients and controls is "considerably more robust" than similar studies of EBV in adult MS patients, Dr. Banwell said. The finding demonstrates the advantage of comparative studies in which healthy subjects are relatively naïve to common infections.
Because exposure to other common viruses does not differ between paediatric MS patients and controls, the findings suggest that the association between MS and EBV may be specific, Dr. Banwell said.
The study was supported by a grant from The Hospital for Sick Children Foundation.
[Study title: Viral Studies in Pediatric Multiple Sclerosis. Abstract: S41.002]
http://www.medscape.com/viewarticle/451540_2
Infectious Diseases, April 2003 Journal Scan From JAMA
March 26, 2003 (Volume 289, Number 12)
Multiple Sclerosis and Epstein-Barr VirusLevin LI, Munger KL, Rubertone MV,
et al. JAMA. 2003;289(12):1533-1536
The Epstein-Barr virus (EBV) would win the prize for most versatile virus if Academy Awards were given to microbes. Both acute and chronic infections produce a wide variety of symptoms from minor illness to fulminant malignancy. The repertoire of the virus is extended to chronic neurologic disease in this brief report by investigators at the Walter Reed Army Institute of Research and collaborators at the Harvard School of Public Health and Virolab Inc. (Berkeley, California). The investigators showed a relationship between titer of serum IgG antibodies to viral capsid antigen (VCA) or EBV nuclear antigen (EBNA) complex and subsequent diagnosis of multiple sclerosis (MS). The relative risk is plausible, graded, and substantial. Although not proving causation, this study suggests the possibility of new ideas to prevent and treat multiple sclerosis.
The investigators used the extensive US Defense Department serum bank, which contains samples from more than 3 million persons collected at entry into service and approximately every 2 years starting in 1988. They identified cases of MS (defined as certain or probable on the basis of diagnostic criteria that included MRI and examination by a neurologist) from records of the US Army Disability Agency. Cases were each matched to 2 controls by age, sex, race/ethnicity, and date of blood draw. Samples were subjected to IgG and IgA antibody tests for VCA, anti-early antigen complex (EA-D and EA-R), and IgG antibodies against EBNA complex and EBNA-1 and EBNA-2. IgG antibodies to cytomegalovirus (CMV) were also measured in all cases and controls. Finally, cases and controls were compared
using geometric mean antibody titers against all of the antigens.
There were 83 cases and 166 controls. All cases and 98% of the controls had evidence of exposure to EBV at entry into the service. Mean age of onset of MS was 27 years, with diagnosis considered certain in 64% and probable in 36%. A mean of 4 years elapsed between first blood draw and onset of illness. The baseline geometric VCA and EBNA complex IgG antibody levels were significantly higher in cases than in controls. Additionally, the risk of MS rose significantly as the titer increased. The relative MS risk of subjects with highest compared to lowest VCA and EBNA IgG titers were 19.7 and 33.9, respectively. There was no association of risk to CMV antibodies, race, age, or sex. Using simultaneous regression analysis, only high EBNA complex antibody and EBNA-1 antibody correlated to risk. Interestingly, the VCA and EBNA antibody levels remained stable across time, even after the onset of disease.
The investigators state that the pattern of high VCA, high EBNA seen in the patients with MS suggests recent EBV infection or reactivation with vigorous cellular immune response. They also suggest that this pattern has been associated with greater risk of Hodgkin's disease and nasopharyngeal cancer. Could the high titer represent continued viral replication in the central nervous system? With new anti-herpes medications potentially achieving sufficient activity against EBV in the central nervous system, it might be time to see whether anti-EBV therapy is beneficial for this dreaded disease. On the other hand, it increasingly looks like a vaccine against EBV given early in childhood might be a good thing.
Here is my thought and it's a radical one......Don't inject people with it in the first place! Or another thought....take EBV out of the polio vaccine to begin with!
Epstein-Barr Virus Linked to Multiple Sclerosis
Laurie Barclay, MD
March 25, 2003 — Epstein-Barr virus (EBV) is associated with increased risk of multiple sclerosis (MS), according to the results of a large, nested, case-control study published in the March 26 issue of The Journal of the American Medical Association.
"The baseline geometric mean serum antibody titers to EBV were consistently higher among individuals who later developed MS than among their matched controls," write Lynn I. Levin, PhD, MPH, from the U.S. Army Physical Disability Agency in Washington, D.C., and colleagues. "Similarly strong positive associations between EBV antibodies and risk of MS were already present in samples collected five or more years before MS onset."
Using the Department of Defense Serum Repository of blood samples collected between 1988 and 2000 from more than 3 million U.S. military personnel, the investigators identified 83 individuals granted temporary or permanent disability because of MS. Two controls for each of these cases were matched by age, sex, race, ethnicity, and dates of blood sample collection. The mean length of time between blood collection and onset of MS was four years.
The strongest predictors of MS were serum levels of IgG antibodies to EBV viral capsid antigen (VCA) or nuclear antigen (EBNA) complex. Rising levels of these antibodies correlated linearly with increasing risk of MS. Compared with those in the group of lowest VCA titers (/= 2,560) was 19.7 (95% confidence interval [CI], 2.2 - 174; P for trend = .004). Compared with those who had EBNA complex titers /= 1,280 was 33.9 (95% CI, 4.1 - 283; P for trend <.001.
Samples collected five years or more before MS onset also showed strong positive associations between EBV antibodies and risk of MS. No relationship was detected between cytomegalovirus antibodies and risk of MS.
Samples collected five years or more before MS onset also showed strong positive associations between EBV antibodies and risk of MS. No relationship was detected between cytomegalovirus antibodies and risk of MS.
According to the authors, these findings suggest that "the increased antibody response to EBV occurs early in relation to the pathological process that leads to demyelination and clinical disease," and that "there is a long lag time between infection with EBV and occurrence of MS.... These results support a role for EBV in the etiology of MS."
JAMA. 2003;289:1533-1536
Reviewed by Gary D. Vogin, MD
Rheumatology, March 2003 Journal Scan
From
Journal of Rheumatology
March 2003 (Volume 30, Number 3)
Infections Preceding Early Arthritis in Southern Sweden: A Prospective Population-Based Study Soderlin MK, Kautiainen H, Puolakkainen M, et al.
Journal of Rheumatology. 2003;30(3):459-464
Soderlin and coworkers in this publication and previously[1] report an epidemiologic study of infections preceding arthritis in Southern Sweden. Among a population of 132,000 adults living in the study region, 71 were identified as developing arthritis during the 1999-2000 time period. These patients were systematically screened for infections caused by Salmonella typhimurium and Salmonella enteritidis, Yersinia enterocolitica, Campylobacter jejuni, Borrelia burgdorferi, Chlamydia trachomatis, Chlamydia pneumoniae, and parvovirus B19. Twenty-seven (38%) patients had reactive arthritis (ReA), 17 (24%) undifferentiated arthritis, 15 (21%) rheumatoid arthritis (RA), 4 (6%) psoriatic arthritis, and the rest (11%) other diagnoses. Forty-five percent had evidence of infection recently preceding the arthritis, as indicated by laboratory tests and/or disease history. C jejuni dominated the ReA group. Recent C trachomatis, B burgdorferi, C pneumoniae, and parvovirus B19 infections occurred infrequently. This study is important to rheumatologists because environmental factors have long been considered to have a causative role in reactive arthritis, but a long search for infectious agents in RA has not turned up any clear single candidate for RA. However, the dramatic success of TNF inhibitors in RA has led to renewed interest in the "innate" immune system (discussed below) , which has a major role in response to infectious agents.
The latest study by Soderlin and colleagues extends prior studies looking for specific infective triggers for RA based on serological methods to detect prior exposure, culture or molecular methods to detect the organism or its genetic material in blood or synovial tissue.[2] However, the study by Soderlin and coworkers has limitations that the author and the accompanying editorial point out.[1] In particular, the study examines subjects with established disease. The authors note that results of their study need to be treated with caution. First, their study lacks appropriate controls. Second, the disease itself or its treatment might increase the likelihood of infection. Third, the detection of an organism in synovium (even in viable, replicating form) is not necessarily indicative of an active role in pathogenesis: there is evidence that synovial tissue may nonspecifically trap bacteria and viruses,[3,4] and others may enter the inflamed synovium because they are parasitic residents of cells entering the joint (such as Epstein-Barr virus in B cells).[2] Nevertheless, the study by Soderlin and coworkers provides an interesting link between studies on pathogenesis and current trends in therapy of RA.
Although genetic factors are important in the development of RA, not all those who are genetically susceptible develop the disease. Twin studies in the United Kingdom and Australia have shown disease concordance rates in monozygotic twins of between 15% and 21%.[5,6] Earlier studies also showed only modest concordance for autoantibody and immunoglobulin production within twin pairs.[7,8] There is weak evidence, also, of an increased concordance of RA, rheumatoid factor, and other autoantibodies within spouse pairs.[9] There is also the intriguing observation that skeletons with characteristic findings of RA were not detected in Europe before the 1500s, suggesting that RA may be partly an "infectious" disease that developed as new gene pools came into contact with new organisms as a result of increased movement of populations in Europe.[10]
No single specific self-antigen or environmental antigen has been identified as responsible for inducing or perpetuating RA. Many investigators believe that RA develops in 2 stages in which an initial response induced by a foreign antigen (most likely an infectious organism) subsequently develops into a self-sustaining autoimmune process. Because the specific genetic and environmental agents are not known, rheumatologists increasingly look at pathogenesis in terms of sites for therapeutic action. One class of drugs is similar to those developed in assays for transplant rejection, namely HLA-D linked presentation of antigens to T cells (ie, hydroxychloroquine, cyclosporine, leflunomide, mycophenolic acid, and probably methotrexate). These drugs target the "acquired" immune system that is regulated by activated T cells. Although these drugs have been effective, the dramatic (and perhaps unexpected) success of TNF inhibitors has focused attention on the "innate" immune response, which is parallel but distinct from the "acquired" immune response.[11] Therapies originally developed for therapy of septic shock (ie, targeting the release of endotoxin by the innate immune system) later proved to be dramatically effective in RA.[12,13] Although the innate and acquired immune systems have distinct characteristics they are also interactive through a series of cytokines and second signals, which are designed to help the immune system to distinguish self from nonself.[14,15]
Recognition of pathogens by the innate immune system is mediated by a set of germline-encoded receptors that are referred to as pattern-recognition receptors (PRRs).[11] These receptors recognize conserved molecular patterns (pathogen-associated molecular patterns), which are shared by large groups of microorganisms.[12] Toll-like receptors (TLRs) function as the PRRs in mammals and play an essential role in the recognition of microbial components.[13] The TLRs may also recognize endogenous ligands induced during the inflammatory response.[16]
TLRs are type I transmembrane proteins that contain leucine-rich repeats in the extracellular domain and a cytoplasmic Toll/interleukin-1 (IL-1) receptor homology domain.[17] This receptor family has been phylogenetically conserved, from insects through vertebrates.[11] Signaling through TLR is a multistep process. Initially, TLRs interact with the MyD88 adapter molecule, initiating a signaling cascade that involves members of the IL-1 receptor-associated kinase family and TNF receptor-associated factor 6, the activation of downstream kinases, and the translocation of nuclear factor B (NF-B) from the cytoplasm to the nucleus.[18] NF-B up-regulates the transcription of genes encoding cytokines, chemokines, and other immunomodulatory factors.[12,13]
The TLRs recognize determinants that have been conserved at high frequency in prokaryotes but are rare in eukaryotes. Ten TLR family members have been identified in mammals.[18] For example, TLR-2 mediates recognition of bacterial lipoproteins and peptidoglycans, TLR-3 binds to viral double-stranded RNA, TLR-4 recognizes the bacterial cell membrane components lipopolysaccharide and lipoteichoic acid, TLR-5 recognizes flagellin, and TLR-9 interacts with unmethylated CpG motifs present in bacterial DNA. This pattern of innate immune response has been shown to improve the host's ability to limit the proliferation and spread of infectious pathogens in the period before development of acquired antigen-specific immunity.[11,14,15,19]
In summary, as rheumatologists, we use therapies for arthritis that were originally detected in screens for transplant rejection based on the cyclosporin A model (namely the HLA-DR-linked T-cell activation that defined the acquired immune response). More recently, we have used therapies originally designed for treatment of septic shock due to endotoxin, a process that has led to recognition of Toll receptors and the innate immune system. This study by Soderlin and colleagues points out that arthritis patients are frequently challenged by environmental infections just before onset of their arthritis and reminds us that a mistake in distinguishing self from nonself may have the pathogenetic consequences of arthritis.
References
Soderlin MK, Borjesson O, Kautiainen H, Skogh T, Leirisalo-Repo M. Annual incidence of inflammatory joint diseases in a population based study in southern Sweden. Ann Rheum Dis. 2002;61:911-915.
Carty SM, Snowden N, Silman AJ. Should infection still be considered as the most likely triggering factor for rheumatoid arthritis? J Rheumatol. 2003;30:425-429.
Wilkinson NZ, Kingsley GH, Jones HW, Sieper J, Braun J, Ward ME. The detection of DNA from a range of bacterial species in the joints of patients with a variety of arthritides using a nested, broad-range polymerase chain reaction. Rheumatology (Oxford). 1999;38:260-266.
Stahl HD, Hubner B, Seidl B, et al. Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis. Ann Rheum Dis. 2000;59:342-346.
Silman AJ, MacGregor AJ, Thomson W, et al. Twin concordance rates for rheumatoid arthritis: results from a nationwide study. Br J Rheumatol. 1993;32:903-907.
Bellamy N, Duffy D, Martin N, Mathews J. Rheumatoid arthritis in twins: a study of aetiopathogenesis based on the Australian Twin Registry. Ann Rheum Dis. 1992;51:588-593.
Buchanan WW, Boyle JA, Greig WR, et al. Occurrence of autoantibodies in healthy twins. Clin Exp Immunol. 1967;(suppl 2):803-811.
Rowe DS, Boyle JA, Buchanan WW. Plasma immunoglobulin concentrations in twins. Clin Exp Immunol. 1968;3:233-
Dalakos TG, MacSween RN, Whaley K, et al. Conjugal prevalence of rheumatoid arthritis, rheumatoid factor and other autoantibodies in rheumatoid arthritis. Clin Exp Immunol. 1968;3:761-769.
Buchanan WW. Rheumatoid arthritis: another New World disease? Semin Arthritis Rheum. 1994;23:289-294.
Medzhitov R, Janeway C, Jr. Innate immunity. N Engl J Med. 2000;343:338-344.
Ulevitch RJ. Toll gates for pathogen selection. Nature. 1999;401:755-756.
Ulevitch RJ. Endotoxin opens the Tollgates to innate immunity. Nat Med. 1999;5:144-145.
Medzhitov R, Janeway C, Jr. Innate immune recognition: mechanisms and pathways. Immunol Rev. 2000;173:89-97.
Medzhitov R, Janeway CA, Jr. Decoding the patterns of self and nonself by the innate immune system. Science. 12 2002;296:298-300.
Takeda K, Kaisho T, Akira S. Toll-like receptors. Annu Rev Immunol. 2003;21:335-376.
Aderem A, Ulevitch RJ. Toll-like receptors in the induction of the innate immune response. Nature. 2000;406:782-787.
Akira S, Takeda K, Kaisho T. Toll-like receptors: critical proteins linking innate and acquired immunity. Nat Immunol. 2001;2:675-680.
Medzhitov R, Janeway CA, Jr. An ancient system of host defense. Curr Opin Immunol. 1998;10:12-15.
[By Jennifer Warner. For more information on how it may apply to autism, reference the NIDS site and Center for Complex Infectious Disease www.ccid.org. Thanks to Tashia Berman.]
http://sar.c.tclk.net/maabn17aaZ41aa4JiD8b/rs81766&src=webmd < - - Address ends here.
Certain viral infections may increase the likelihood of mental decline and dementia, especially among older adults with heart disease. A new study shows that elderly people with evidence of infection with three common viruses -- viruses that cause cold sores, genital herpes, and a mono-like illness -- were more than twice as likely to suffer from dementia. Researchers say the study adds new evidence to the theory that inflammation, which is part of the body's natural response to infection, plays an important role in the development of several health problems, such as heart disease, stroke, and dementia.
Viruses May Trigger Dementia “Inflammation has been implicated in dementia, and viral infections could be a triggering factor,” says researcher Timo E. Strandberg, MD, PhD, of the University of Helsinki in Finland, in a news release. “Our findings should be tested in other studies, but if these viruses are involved, there are existing therapies such as vaccination and antiviral drugs that could be used to prevent or treat dementia.”
In the study, which appears in Stroke: Journal of the American Heart Association, researchers tested 383 elderly men and women with heart disease for the antibodies that are produced in response to infection with three common viruses: herpes simplex 1 (HSV1), herpes simplex type 2 (HSV2) and cytomegalovirus (CMV), and followed them for 12 months. HSV1 causes cold sores, and HSV2 causes genital herpes. CMV is a virus that infects between 50% to 85% of American adults by age 40, but it causes few symptoms and no long-term health problems in most people. The mental function of the participants was also assessed at the beginning and end of the study.
After testing for the viruses multiple times, researchers found that up to 60% of the participants tested positive for one or more or the viruses. And the more viral exposure, the higher the risk of dementia. Those who had evidence of infection with all three viruses were 2.5 times more likely to have mental impairment than those with antibodies for less than three of the viruses.
Dementia was found in about 5% of people who were infected with one or none of the viruses, but those numbers grew dramatically with additional infections. Sixteen percent of those infected with two viruses had dementia and 27% of those exposed to all three had dementia.
The researchers also looked at whether infection with two common bacteria was related to dementia risk but found no association between bacterial infections and mental decline. Because all of the participants also had heart disease, researchers say further studies should examine whether similar results are found in otherwise healthy individuals.
SOURCES: Stroke: Journal of the American Heart Association, Aug. 15,
- News release, American Heart Association.
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Epstein-Barr Virus-Associated Lymphadenitis: The Differential Diagnosis of
Diffuse Paracortical Lymphoid Hyperplasia. Pathology Case Reviews. 9(5):192-198, September/October 2004. Abbondanzo, Susan L. MD
Abstract:
The diagnosis of infectious mononucleosis associated with Epstein-Barrvirus (EBV) is usually based on a constellation of clinical signs and symptoms and a correlation with laboratory findings. In classic cases,there is a triad that includes sore throat, fever, and cervical (orgeneralized) lymphadenopathy. In some cases, however, the only presenting features may be fever and malaise, with or without lymphadenopathy. Important laboratory findings include leukocytosis with circulating atypical lymphocytes, a positive Monospot test, and characteristic serologic antibodies that are subsequently produced as an immunologic response to the virus. A lymph node biopsy is usually not necessary to make the diagnosis of EBV-related infectious mononucleosis and is actually discouraged because the histologic features may be worrisome and may mimic a malignant lymphoma. In rare cases, however, especially those with atypical clinical presentations,an excisional lymph node biopsy is performed as part of the routine clinical workup. It is important to be familiar with the characteristic histologic features, including diffuse paracortical lymphoid hyperplasia, and to be aware of the differential diagnosis that includes reactive entities as well as malignant lymphomas. Important benign entities that characteristically show diffuse paracortical lymphoid hyperplasia include other viral lymphadenitides such as herpes simplex, cytomegalovirus, postvaccinial and measles lymphadenitis, and drug-related lymphadenopathy, especially Dilantin. Malignant neoplasms,such as diffuse large B-cell-, Hodgkin-, and CD30-positive anaplasticlarge-cell lymphoma, are also in the differential diagnosis of EBV-associated lymphadenitis.(C) 2004 Lippincott Williams & Wilkins, Inc.
http://jama.ama-assn.org/cgi/content/full/293/4/463
JAMA, 2005;293:463-469.
Vol. 293 No. 4, January 26, 2005
Exposure to Infant Siblings During Early Life and Risk of Multiple Sclerosis
Anne-Louise Ponsonby, PhD; Ingrid van der Mei, PhD; Terence Dwyer, MD; Leigh Blizzard, PhD; Bruce Taylor, MD; Andrew Kemp, PhD; Rex Simmons, PhD; Trevor Kilpatrick, PhD
ABSTRACT
Context The "hygiene hypothesis" has implicated sibship as a marker of infection load during early life and suggests that exposure or reexposure to infections can influence the developing immune system. Viral infection has also been implicated in the pathogenesis of multiple sclerosis (MS). Objectives To evaluate whether exposure to infant siblings in early life is associated with the risk of MS, and to explore the possible mechanism for any apparent protective effect, including altered Epstein-Barr virus (EBV) infection patterns.
Design, Setting, and Patients Population-based case-control study in Tasmania, Australia, from 1999 to 2001 based on 136 cases of magnetic resonance imaging-confirmed MS and 272 community controls, matched on sex and year of birth. Main Outcome Measure Risk of MS by duration of contact with younger siblings aged less than 2 years in the first 6 years of life.
Results Increasing duration of contact with a younger sibling aged less than 2 years in the first 6 years of life was associated with reduced MS risk (adjusted odds ratios [AORs]: <1 infant-year, 1.00 [reference]; 1 to <3 infant-years, 0.57 [95% confidence interval {CI}, 0.33-0.98]; 3 to <5 infant-years, 0.40 [95% CI, 0.19-0.92]; 5 infant-years, 0.12 [95% CI, 0.02-0.88]; test for trend, P = .002). A history of exposure to infant siblings was associated with a reduced IgG response to EBV among controls. Controls with at least 1 infant-year contact had a reduced risk of infectious mononucleosis and a reduced risk of very high composite EBV IgG titers (AOR, 0.33; 95% CI, 0.11-0.98) compared with other controls. The inverse association between higher infant contact and MS was independent of EBV IgG titer.