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(searched for: doi:10.1002/ana.410090709)
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, Bruno Fernandes de Sousa, Nathaly M. Coelho da Costa,
Published: 1 July 2021
by SciELO
Arquivos de Neuro-Psiquiatria, Volume 79, pp 607-611;

Background: Guillain-Barré syndrome (GBS) is currently the most common cause of acute flaccid paralysis worldwide. Risk factors for GBS include previous viral or bacterial infections or vaccination. Recently, an outbreak of Zika virus led to an outbreak of GBS in Latin America, mostly in Brazil, concomitant to continuous circulation of dengue virus serotypes. However, there is no study about cytomegalovirus (CMV) infection as a risk for GBS in Brazil. Objectives: In this study, we report a series of cases of GBS with the aim of determining the prevalence of CMV and the characteristics associated with the infection. Methods: A cohort of 111 GBS cases diagnosed between 2011 and 2017 in Natal, northeastern Brazil, was studied. Presence of CMV IgM antibodies was determined by means of electrochemiluminescence. The analysis was performed considering CMV infection status and the clinical outcome. Results: We found seroprevalence of 15.3% (n = 17) for CMV. CMV patients were younger (26 vs. 40; p = 0.016), with no apparent gastrointestinal (p = 0.762) or upper respiratory infections (p = 0.779) or sensory loss (p = 0.03). They presented more often with a classic GBS sensorimotor variant (p = 0.02) and with a demyelinating pattern in electrophysiological studies (p < 0.001). Conclusion: In Brazil, the clinical-epidemiological profile of GBS associated with CMV infection is similar to that described in other countries. Better understanding of the relationship between infectious processes and GBS is a key component of the research agenda and assistance strategy for global health initiatives relating to peripheral neuropathic conditions.
, W. Gu, M.E. Wise, J. J. Sejvar, , B. E. Mahon
Epidemiology and Infection, Volume 146, pp 1740-1745;

Guillain Barré syndrome (GBS), which is triggered by autoantibodies produced in response to antigenic stimuli such as certain infections and vaccinations, is the most common cause of acute flaccid paralysis worldwide. Campylobacter, the most common bacterial enteric infection in the USA, is reported to be the most commonly diagnosed antecedent of GBS, yet little information is available about the risk of post-Campylobacter GBS. Data collected through active, population-based surveillance in the Emerging Infections Program during the 2009–2010 novel Influenza A (H1N1) vaccination campaign allowed us to compare confirmed and probable GBS cases to non-cases to determine whether antecedent Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis) was more common among cases and to assess the risk of GBS following Campylobacter infection. We estimate that 8–12% of GBS cases in the USA are attributable to Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis), with 434–650 cases of post-diarrhoeal GBS annually and about 49 cases of GBS per 100 000 Campylobacter infections. These results provide updated estimates for post-Campylobacter GBS incidence in the USA and highlight an important benefit of effective measures to prevent Campylobacter infections.
Helmar C. Lehmann,
Published: 23 December 2016
The publisher has not yet granted permission to display this abstract.
Kate T. Brizzi,
Published: 20 June 2014
The Neurohospitalist, Volume 4, pp 230-240;

Infectious causes of peripheral nervous system (PNS) disease are underrecognized but potentially treatable. Heightened awareness educed by advanced understanding of the presentations and management of these infections can aid diagnosis and facilitate treatment. In this review, we discuss the clinical manifestations, diagnosis, and treatment of common bacterial, viral, and parasitic infections that affect the PNS. We additionally detail PNS side effects of some frequently used antimicrobial agents.
, Aparna R. Pai, Ullas Kamath,
International Journal of Neuroscience, Volume 125, pp 235-240;

Guillain-Barré syndrome (GBS) is an autoimmune polyneuropathy which presents with acute onset and rapid progression of flaccid, hyporeflexi quadriparesis. Both sensory and autonomic nerve involvement is seen. GBS has various subtypes that vary in their pathophysiology. The pathogenesis involves an immune response triggered by a preceding event which may be an infection, immunisation or surgical procedure. Clinical diagnosis has been largely the primary diagnosing criterion for GBS along with electrodiagnosis, which has several pitfalls and is supported by ancillary testing of cerebrospinal fluid (CSF) analysis and Nerve Conduction Studies. Measurement of anti-ganglioside antibodies is also an effective tool in its diagnosis. Further understanding of pathophysiology and better diagnostic methods are required for better management of GBS.
Published: 1 January 2013
Among the human herpes viruses, three are neurotropic and capable of producing severe neurological abnormalities: herpes simplex virus type 1 and 2 (HSV-1 and HSV-2) and varicella-zoster virus (VZV). Both the acute, primary infection and the reactivation from the site of latent infection, the dorsal sensory ganglia, are associated with severe human morbidity and mortality. The peripheral nervous system is one of the major loci affected by these viruses. The present review details the virology and molecular biology underlying the human infection. This is followed by detailed description of the symtomatology, clinical presentation, diagnosis, course, therapy, and prognosis of disorders of the peripheral nervous system caused by these viruses.
Yajuan Gu, Zi-Wei Chen, Allan Siegel, Ranie Koshy, Cristhian Ramirez, Timothy D. Raabe, George H. DeVries, Amjad A. Ilyas
Published: 15 May 2012
Journal of Neuroimmunology, Volume 246, pp 58-64;

Guillain-Barré syndrome (GBS) is an autoimmune-mediated disease triggered by a preceding infection. A substantial body of evidence implicates antibodies to various gangliosides in subtypes of GBS. A significant proportion of patients with acute demyelinating subset of GBS have IgG antibodies against peripheral nervous system myelin specific neolactogangliosides such as LM1 and Hex-LM1. Although anti-neolactoganglioside antibodies in GBS were described more than two decades ago, their pathogenic role in neuropathy remains unknown due to the lack of suitable experimental models. In this study, we immunized ten guinea pigs with purified LM1 ganglioside mixed with keyhole limpet hemocyanin (KLH) and emulsified in complete Freund's adjuvant (CFA). Control guinea pigs were injected with KLH emulsified in CFA only. The animals were bled every four week intervals. The animals were boosted 3 times every four weeks. Experiments were terminated four months after initial immunization. Nine of 10 guinea pigs immunized with LM1 exhibited antibody responses to LM1. Anti-LM1 IgG titers in nine guinea pigs ranged from 1:400 to 1:12,800 at 16-weeks after initial immunization. Anti-LM1 antibodies were predominantly of IgG2 subclass. One guinea pig with the highest levels of IgG antibodies exhibited mild signs of neuropathy. There was no evidence of demyelination or inflammation in the sciatic nerves of LM1-immunized guinea pigs. Anti-LM1 antibodies bound to rat sciatic nerve myelin and to isolated rat Schwann cells. In summary, our findings suggest that relatively high levels of anti-LM1 IgG antibodies can be induced in guinea pigs and that LM1 is localized in peripheral nerve myelin and in Schwann cells. Further studies are needed to determine the pathogenic potential of anti-neolactoganglioside antibodies in neuropathy.
John T. Sladky, Stephen Ashwal
Published: 1 January 2012
The publisher has not yet granted permission to display this abstract.
Neuropsychiatric Disease and Treatment, Volume 6, pp 119-122;

Role of anti-GQ1B antibody in differential diagnosis of acute ophthalmoparesis E Ece Boylu, R Erdem Togrol, Mehmet Güney Şenol, M Fatih Özdag, Mehmet SaraçogluGATA Hadarpaşa Educational and Research Hospital, Department of Neurology, Istanbul, Turkey Miller Fisher syndrome (MFS) is a triad of total external ophthalmoplegia, ataxia, and areflexia, while botulism has the usual clinical presentation of involvement of cranial muscles and palsies with blurred vision, diplopia, ptosis, dilated pupils, and facial paralysis, caused by a bacterial neurotoxin which attacks proteins involved in presynaptic vesicle release. In this report, we needed to make the differential diagnosis between MFS and botulism in a patient who presented with acute ophthalmoparesis and a history of diarrhea three days before, which started two days after consuming tinned food. Routine laboratory, neurophysiologic, and imaging investigations were normal. A clinical diagnosis of Miller Fisher syndrome was reached by anti-ganglioside GQ1B and GM1 Ig G and M antibody investigations which proved positive. The patient was treated with intravenous immunoglobulin two weeks after (in the late period) the symptoms started and he has recovered completely. Systemic autoimmune diseases should be considered in patients with bilateral ophthalmoparesis. As in the present patient, the evaluation of specific antibodies helps in the diagnosis and thus early effective treatment is possible.Keywords: anti-ganglioside antibody, botulism, Miller Fisher syndrome, ophthalmoparesis
Published: 28 January 2010
Journal of Neuroinflammation, Volume 7, pp 7-7;

Background Sudden limb paresis is a common problem in White Leghorn flocks, affecting about 1% of the chicken population before achievement of sexual maturity. Previously, a similar clinical syndrome has been reported as being caused by inflammatory demyelination of peripheral nerve fibres. Here, we investigated in detail the immunopathology of this paretic syndrome and its possible resemblance to human neuropathies. Methods Neurologically affected chickens and control animals from one single flock underwent clinical and neuropathological examination. Peripheral nervous system (PNS) alterations were characterised using standard morphological techniques, including nerve fibre teasing and transmission electron microscopy. Infiltrating cells were phenotyped immunohistologically and quantified by flow cytometry. The cytokine expression pattern was assessed by quantitative real-time PCR (qRT-PCR). These investigations were accomplished by MHC genotyping and a PCR screen for Marek's disease virus (MDV). Results Spontaneous paresis of White Leghorns is caused by cell-mediated, inflammatory demyelination affecting multiple cranial and spinal nerves and nerve roots with a proximodistal tapering. Clinical manifestation coincides with the employment of humoral immune mechanisms, enrolling plasma cell recruitment, deposition of myelin-bound IgG and antibody-dependent macrophageal myelin-stripping. Disease development was significantly linked to a 539 bp microsatellite in MHC locus LEI0258. An aetiological role for MDV was excluded. Conclusions The paretic phase of avian inflammatory demyelinating polyradiculoneuritis immunobiologically resembles the late-acute disease stages of human acute inflammatory demyelinating polyneuropathy, and is characterised by a Th1-to-Th2 shift.
E. Merelli, P. Sola, P. Faglioni, M. Poggi, M. Montorsi, G. Torelli
Published: 29 January 2009
Acta Neurologica Scandinavica, Volume 85, pp 334-336;

To investigate the presence of human herpesvirus-6 (HHV-6) in patients affected by Guillain-Barré syndrome (GBS) and by other neurological diseases (OND), we examined by indirect immunofluorescence analysis (IFA) the sera and cerebrospinal fluid (CSF) from 28 GBS and 63 OND. Moreover, we tested 150 blood donors (BD) to appreciate the diffusion of HHV-6 infection in the Italian adult healthy population. We found a significantly higher titre of antibody to HHV-6 in the GBS patients compared with OND and BD, although the pathogenicity of the virus is not known.
V. Ravi, A. B. Taly, S. K. Shankar, P. K. Shenoy, A. Desai, D. Nagaraja, M. Gourie-Devi, A. Chandramuki
Published: 29 January 2009
Acta Neurologica Scandinavica, Volume 90, pp 67-72;

This study is a report of 34 cases of Guillain-Barré syndrome (GBS) observed in Bangalore (South India), an endemic area for Japanese encephalitis virus (JEV) infection. Virological and immunological findings suggested an antecedent and recent JEV infection in 21/34 patients. Nineteen patients among them showed high levels of JEV-specific IgM antibodies in serum and/or CSF, while the viral antigen could be demonstrated in one case and virus isolation from the CSF was successful in one patient. EMG studies revealed features of predominantly demyelinating neuropathy in 18/25 cases. Comparison of clinical findings, duration of illness and outcome in GBS patients with evidence of JEV infection and those without did not reveal any differences. Pathological findings in one patient corroborated the association of JEV with GBS. We conclude that, JEV infection may predispose to Guillain-Barré syndrome in endemic areas.
S Agrawal, D Peake,
Archives of disease in childhood - Education & practice edition, Volume 92, pp 161-168;

We consider the pathophysiology, diagnostic features, assessment, differential diagnoses and management of GBS. This article will also outline the spectrum of the disease. Most of the research on GBS has been based on adult or predominantly adult studies, so there has been unavoidable extrapolation with respect to GBS in children and young people.
Clinical Microbiology and Infection, Volume 13, pp 953-963;

Cytomegalovirus (CMV) infection is one of the most important infectious complications of solid-organ transplantation, and is also responsible for serious, life-threatening diseases in patients infected with human immunodeficiency virus (HIV). Tremendous progress has been made with respect to prevention and treatment of CMV disease in such patients. The use of anti-CMV drugs and the immune reconstitution achieved by use of anti-retroviral drugs has reduced the incidence of CMV disease dramatically. Nevertheless, problems of clinical relevance remain (e.g., drug toxicity, drug–drug interactions, antiviral resistance) and new problems have emerged. Intragenic recombination among different CMV strains has been identified as a possible source of novel CMV strains in patients with advanced HIV infection. Development of a protective CMV vaccine remains elusive, perhaps, in part, because of strain-specific variation in immunodominant epitopes. Late-onset CMV disease, which occurs several months or years after transplantation, has been recognised as a clinically relevant complication in transplant recipients. The most effective strategy for the prevention of CMV disease in transplant recipients (i.e., prophylaxis or pre-emptive therapy) remains a matter of debate. A link between CMV infection and Guillain–Barré syndrome, a neurological disease characterised by flaccid paralysis, has been substantiated, but the efficacy of antiviral therapy in such patients remains to be determined. This review summarises the current status of CMV disease in immunocompromised patients, and discusses some of the emerging issues of clinical relevance with regard to CMV infection in patients with disorders of the immune system
, Andreas Seiser, Nevzat Gueler, Elisabeth Puchhammer-Stöckl, Stephan W. Aberle, Gerold Stanek, Theresia Popow-Kraupp
Published: 28 February 2007
Journal of Neuroimmunology, Volume 183, pp 214-219;

Guillain-Barré syndrome (GBS) is frequently associated with the presence of CMV-specific IgM-antibodies or CMV-DNA in serum. Detection of IgM-antibodies or viremia may indicate primary infection, but also reactivation or reinfection. We identified 46 GBS patients with detectable CMV-specific IgM- or IgG-antibodies, or both. Sera from these patients were tested for the presence of CMV-specific, low-avidity IgG-antibodies, which indicate primary infection that occurred <6 months before sample collection, and for the presence of CMV-DNA by polymerase chain reaction (PCR). Primary infection was identified by the presence of low-avidity IgG-antibodies in 9/46 (20%) or by detection of IgM-antibodies in the absence of IgG-antibodies in 1/46 (2%) patients. CMV-DNA was detectable in 17/46 (37%) sera. In contrast, CMV-DNA was detected in only 2% of sera from 46 age-matched patients with neuroborreliosis. The likelihood of viremia decreased in GBS patients significantly with increasing antibody-avidity (P=0.041). Detection of IgM-antibodies correlated with that of CMV-DNA in patients with low-avidity IgG-antibodies (P=0.048) but not in those with high-avidity IgG-antibodies (P=0.543). In 45 age-matched healthy controls, low-avidity IgG-antibodies and CMV-DNA were detected in only 2% and 0% of sera, respectively. Our findings further strengthen evidence for an association between CMV infection and GBS. Primary CMV infection was identified in almost one-fourth of patients with detectable CMV-specific antibodies. Nevertheless, endogenous reactivation and reinfection have to be considered also as relevant events associated with GBS.
Ruprecht Schmidt-Ott, Holger Schmidt, Sylvia Feldmann, Felicitas Brass, Bernd Krone, Uwe Gross
Clinical and Vaccine Immunology, Volume 13, pp 779-783;

Guillain-Barré syndrome (GBS) is a postinfectious autoimmune polyradiculoneuropathy. The most frequent antecedent pathogen is Campylobacter jejuni , followed by cytomegalovirus. However, more than 40% of GBS cases currently cannot be attributed to triggering events. This might be due to the shortcomings of the serological assays used for diagnosing infections, in particular for C. jejuni . In our study investigating 36 patients with acute GBS, standard serological methods identified the triggering viral or bacterial etiology in only 25% of cases. However, using a highly specific enzyme-linked immunosorbent assay based on two recombinant outer antigens encoded by C. jejuni genes Cj0017 (P39) and Cj0113 (P18), we found serological evidence of a preceding C. jejuni infection in 80.6% of the patients but in only 3.5% of the controls. We conclude that the role of C. jejuni in triggering GBS has been greatly underestimated.
, Hessam Nowzari
Journal of Periodontology, Volume 76, pp 2306-2311;

Guillain-Barré syndrome (GBS), an autoimmune disorder of the peripheral nervous system, is characterized by rapidly ascending neural paralysis, hyporeflexia, and areflexia. The polyneuropathy of the GBS affects one to four humans per 100,000 of the population annually throughout the world (adults and children). The pathogenesis of GBS remains unclear. However, there are increasing indications that the disease is triggered by a preceding well-established febrile infection by cytomegalovirus (CMV). The present report describes active CMV within the periodontium of a 37-year-old patient affected by GBS. Real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR) was performed to detect CMV, Epstein-Barr virus-1 (EBV-1), herpes simplex 1 (HSV-1) and 2 (HSV-2) virus, and enteroviruses (polio-, coxsackie-, echo-, and enteroviruses 68 and 71) from periodontal sites demonstrating advanced attachment loss. Healthy sites and sites with inflamed gingival tissue were not included in the study. Anaerobic bacterial culture determined the occurrence of potential major periodontal pathogens. Real-time RT-PCR and microbiologic analysis revealed the presence of a dual infection of CMV and specific bacterial plaque. CMV, Porphyromonas gingivalis, Tannerella forsythensis, and Campylobacter species were associated with periodontitis active sites, loss of attachment, and gingival bleeding. Furthermore, periodontal sites infected by active CMV had no visible radiographic crestal lamina dura. The periodontium may serve as a reservoir for CMV and a source of viral replication. However, further research is needed to test whether viral replication in the periodontium precedes the GBS symptoms.
G. Nakos, E. Tziakou, L. Maneta-Peyret, C. Nassis,
Published: 26 July 2005
Intensive Care Medicine, Volume 31, pp 1401-1408;

The publisher has not yet granted permission to display this abstract.
, Chitra Krishnan, Deepa M. Deshpande, ,
The Neurologist, Volume 11, pp 2-18;

Acute myelopathies represent a heterogeneous group of disorders with distinct etiologies, clinical and radiologic features, and prognoses. Transverse myelitis (TM) is a prototype member of this group in which an immune-mediated process causes neural injury to the spinal cord, resulting in varying degrees of weakness, sensory alterations, and autonomic dysfunction. TM may exist as part of a multifocal CNS disease (eg, MS), multisystemic disease (eg, systemic lupus erythematosus), or as an isolated, idiopathic entity. In this article, we summarize recent classification and diagnostic schemes, which provide a framework for the diagnosis and management of patients with acute myelopathy. Additionally, we review the state of current knowledge about the epidemiology, natural history, immunopathogenesis, and treatment strategies for patients with TM. Our understanding of the classification, diagnosis, pathogenesis, and treatment of TM has recently begun to expand dramatically. With more rigorous criteria applied to distinguish acute myelopathies and with an emerging understanding of immunopathogenic events that underlie TM, it may now be possible to effectively initiate treatments in many of these disorders. Through the investigation of TM, we are also gaining a broader appreciation of the mechanisms that lead to autoimmune neurologic diseases in general.
John W. Griffin, KaziM Sheikh
Published: 1 January 2004
The publisher has not yet granted permission to display this abstract.
, , Rosita Galli, Floriano Mugnaini, Cristina Lenzi
Published: 15 September 2003
Journal of the Neurological Sciences, Volume 213, pp 55-60;

Few reports exist on the influence of humoral immune responses, against microorganisms involved in infections preceding Guillain-Barré syndrome (GBS) and GM1, on clinical outcome. Nor is there any data on the relation between anti-Helicobacter pylori antibodies and prognosis in patients with GBS. To address these questions, we assayed and correlated serum anti-GM1 IgG and IgM and anti-H. pylori, anti-Campylobacter jejuni and anti-cytomegalovirus (CMV) IgG with duration of hospitalization of GBS patients and prognosis at discharge. Patients with anti-GM1 alone or associated with anti-H. pylori antibodies had significant longer hospitalization to reach a low clinical score at discharge than those without (P=0.004). A significant difference was also found for the association of anti-GM1 with anti-CMV antibodies (P=0.019). A weak but significant association of anti-GM1 and anti-C. jejuni antibodies with long hospitalization and worse prognosis at discharge was also found (P=0.02). The statistical significance increased when patients with anti-GM1 and anti-microorganism antibodies were compared with those displaying anti-H. pylori or anti-CMV only. These findings provide further evidence that the level of circulating anti-GM1 IgG plays a role in determining recovery from disability in GBS patients irrespective of other IgG against microorganisms causing infections preceding GBS.
, A.P Tio-Gillen, J Groen, P Herbrink, B.C Jacobs, R Van Koningsveld, A.D.M.E Osterhaus, F.G.A Van der Meché, P.A van Doorn
Published: 30 September 2002
Journal of Neuroimmunology, Volume 130, pp 179-183;

Anti-galactocerebroside (GalC) antibodies are reported to be present in GBS patients with preceding Mycoplasma pneumoniae (MP) infection. We investigated the presence of anti-GalC reactivity in serum of a large group of GBS patients using ELISA and compared this with healthy controls and individuals with an uncomplicated MP infection. Anti-GalC antibody reactivity was present in 12% of the GBS patients. Furthermore, anti-GalC antibodies were associated with MP infections, a relatively mild form of the disease and demyelinating features. Anti-GalC antibodies cross-reacted with MP antigen. In conclusion, anti-GalC antibodies in GBS patients may be induced by molecular mimicry with MP.
Published: 1 December 2001
Molecular Pathology, Volume 54, pp 381-5

Guillain Barré syndrome is one of the best examples of a post infectious immune disease and offers insights into the mechanism of tissue damage in other more common autoimmune diseases. Controlled epidemiological studies have linked it to infection with Campylobacter jejuni in addition to other viruses including cytomegalovirus and Epstein Barr virus. The syndrome includes several pathological subtypes, of which the most common is a multifocal demyelinating disorder of the peripheral nerves in close association with macrophages. Evidence from histological examination of peripheral nerve biopsy and postmortem samples suggests that both cell mediated and humoral mechanisms are involved in the pathogenesis. Immunological studies suggest that at least one third of patients have antibodies against nerve gangliosides, which in some cases also react with constituents of the liposaccharide of C jejuni. In the Miller Fisher variant of the disease, these antiganglioside antibodies have been shown to produce neuromuscular block, and may in part explain the clinical signs of that disorder. Treatment with both intravenous immunoglobulin and plasma exchange reduces the time taken for recovery to occur, although mortality remains around 8%, with about 20% of patients remaining disabled.
, Gilles Morali, Yoram Finkelstein, Jonathan Halevy
Journal of Clinical Gastroenterology, Volume 32, pp 179-180;

Guillain–Barré syndrome (GBS) is often preceded by an infectious disease. A case of GBS after hepatitis A in a pregnant woman is described. The patient was treated with intravenous immunoglobulin and had full recovery with no neurologic sequelae. She gave birth in term to a healthy baby. This is the first reported case in the English literature of a triple condition of hepatitis A, GBS, and pregnancy.
Shoenfeld Y, Aron-Maor A
Published: 29 February 2000
Journal of Autoimmunity, Volume 14, pp 1-10;

The question of a connection between vaccination and autoimmune illness (or phenomena) is surrounded by controversy. A heated debate is going on regarding the causality between vaccines, such as measles and anti-hepatitis B virus (HBV), and multiple sclerosis (MS). Brain antibodies as well as clinical symptoms have been found in patients vaccinated against those diseases. Other autoimmune illnesses have been associated with vaccinations. Tetanus toxoid, influenza vaccines, polio vaccine, and others, have been related to phenomena ranging from autoantibodies production to full-blown illness (such as rheumatoid arthritis (RA)). Conflicting data exists regarding also the connection between autism and vaccination with measles vaccine. So far only one controlled study of an experimental animal model has been published, in which the possible causal relation between vaccines and autoimmune findings has been examined: in healthy puppies immunized with a variety of commonly given vaccines, a variety of autoantibodies have been documented but no frank autoimmune illness was recorded. The findings could also represent a polyclonal activation (adjuvant reaction). The mechanism (or mechanisms) of autoimmune reactions following immunization has not yet been elucidated. One of the possibilities is molecular mimicry; when a structural similarity exists between some viral antigen (or other component of the vaccine) and a self-antigen. This similarity may be the trigger to the autoimmune reaction. Other possible mechanisms are discussed. Even though the data regarding the relation between vaccination and autoimmune disease is conflicting, it seems that some autoimmune phenomena are clearly related to immunization (e.g. Guillain-Barre syndrome). The issue of the risk of vaccination remains a philosophical one, since to date the advantages of this policy have not been refuted, while the risk for autoimmune disease has not been irrevocably proved. We discuss the pros and cons of this issue (although the temporal relationship (i.e. always 2-3 months following immunization) is impressive).
, R.D.M Hadden, N.A Gregson,
Published: 31 December 1999
Journal of Neuroimmunology, Volume 100, pp 74-97;

Recent neurophysiological and pathological studies have led to a reclassification of the diseases that underlie Guillain-Barré syndrome (GBS) into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor and sensory axonal neuropathy (AMSAN) and acute motor axonal neuropathy (AMAN). The Fisher syndrome of ophthalmoplegia, ataxia and areflexia is the most striking of several related conditions. Significant antecedent events include Campylobacter jejuni (4-66%), cytomegalovirus (5-15%), Epstein-Barr virus (2-10%), and Mycoplasma pneumoniae (1-5%) infections. These infections are not uniquely associated with any clinical subtype but severe axonal degeneration is more common following C. jejuni and severe sensory impairment following cytomegalovirus. Strong evidence supports an important role for antibodies to gangliosides in pathogenesis. In particular antibodies to ganglioside GM1 are present in 14-50% of patients with GBS, and are more common in cases with severe axonal degeneration associated with any subtype. Antibodies to ganglioside GQ1b are very closely associated with Fisher syndrome, its formes frustes and related syndromes. Ganglioside-like epitopes exist in the bacterial wall of C. jejuni. Infection by this and other organisms triggers an antibody response in patients with GBS but not in those with uncomplicated enteritis. The development of GBS is likely to be a consequence of special properties of the infecting organism, since some strains such as Penner 0:19 and 0:41 are particularly associated with GBS but not with enteritis. It is also likely to be a consequence of the immunogenetic background of the patient since few patients develop GBS after infection even with one of these strains. Attempts to match the subtypes of GBS to the fine specificity of anti-ganglioside antibodies and to functional effects in experimental models continue but have not yet fully explained the pathogenesis. T cells are also involved in the pathogenesis of most or perhaps all forms of GBS. T cell responses to any of three myelin proteins, P2, PO and PMP22, are sufficient to induce experimental autoimmune neuritis. Activated T cells are present in the circulation in the acute stage, up-regulate matrix metalloproteinases, cross the blood-nerve barrier and encounter their cognate antigens. Identification of the specificity of these T cell responses is still at a preliminary stage. The invasion of intact myelin sheaths by activated macrophages is difficult to explain according to a purely T cell mediated mechanism. The different patterns of GBS are probably due to the diverse interplay between antibodies and T cells of differing specificities.
James F. Bale
Published: 1 December 1999
Seminars in Pediatric Neurology, Volume 6, pp 278-287;

The human herpesviruses, a group of DNA viruses that includes herpes simplex viruses types 1 and 2, varicella zoster virus, cytomegalovirus, Epstein-Barr virus, and human herpes viruses types 6, 7, and 8, cause substantial neurological morbidity among infants and children. This review describes the biology of these viruses and summarizes the clinical manifestations and therapy of the diseases that result from childhood infection with these important pathogens.
, Stojanka Aleksic, Jan Kassubek, Miroslav M. Vrvic, Manfred Kist, Bernhard Steinbrückner, Marija Mitova
Published: 31 October 1999
Zentralblatt für Bakteriologie, Volume 289, pp 429-444;

C.jejuni serogroup PEN 0:19 was isolated from a stool specimen from a patient with Guillain-Barre syndrome (GBS). Flagellar protein was isolated and purified from reference strain C. jejuni PEN 0:19, ATCC 43446, as well as from a homologous patient strain. Antibodies against flagellar protein were detected by means of immunoblotting, enzyme-linked immunosorbent assay (ELISA) and tube agglutination test. The antibody titres were found to be directly correlated at the beginning and in the recovery phase of GBS. Antibodies of IgG and IgA classes were present from the very onset of the disease as well as 5 months later, but with a lower titre population. However, antibodies of the IgM class were persistent only at the onset of the infection and disappeared during the following 5 months. Our results strongly support the hypothesis that in GBS patients, antiflagellar antibodies are induced during C. jejuni infection and can be used in the diagnosis of C. jejuni associated GBS.
, A Neisser, H Bernheimer
Published: 1 May 1999
Infection and Immunity, Volume 67, pp 2414-20

We studied serum antibodies against gangliosides GQ1b and GM1 in 13 patients with Miller Fisher syndrome (MFS) and in 18 patients with Guillain-Barré syndrome (GBS) with cranial nerve involvement. Anti-GQ1b titers were elevated in all patients with MFS cases (immunoglobulin G [IgG] > IgA, IgM), and in 8 of the 18 with GBS. Lower frequencies of increased anti-GM1 titers were observed in MFS patients (3 of 13), as well as in GBS patients (5 of 18). During the course of MFS, anti-GQ1b titers of all Ig classes decreased within 3 weeks after onset. By contrast, anti-GM1 titers (mainly IgM) transiently increased during the course of MFS in five of six patients, suggesting a nonspecific secondary immune response. In patients with MFS following respiratory infections, IgG was the major anti-GQ1b Ig class (six of six patients) and IgG3 was the major subclass (five of six). In contrast, four of five patients with MFS following gastrointestinal infections showed predominance of anti-GQ1b IgA or IgM over IgG and predominance of the IgG2 subclass; anti-GQ1b IgG (IgG3) prevailed in one patient only. These distinct Ig patterns strongly suggest that different infections may trigger different mechanisms of anti-GQ1b production, such as via T-cell-dependent as opposed to T-cell-independent pathways. Thus, the origin of antibodies against GQ1b in MFS may be determined by the type of infectious agent that precipitates the disease.
Beatrix Schwerer, Andrea Neisser, Hanno Bernheimer
Infection and Immunity, Volume 67, pp 2414-2420;

We studied serum antibodies against gangliosides GQ1b and GM1 in 13 patients with Miller Fisher syndrome (MFS) and in 18 patients with Guillain-Barré syndrome (GBS) with cranial nerve involvement. Anti-GQ1b titers were elevated in all patients with MFS cases (immunoglobulin G [IgG] > IgA, IgM), and in 8 of the 18 with GBS. Lower frequencies of increased anti-GM1 titers were observed in MFS patients (3 of 13), as well as in GBS patients (5 of 18). During the course of MFS, anti-GQ1b titers of all Ig classes decreased within 3 weeks after onset. By contrast, anti-GM1 titers (mainly IgM) transiently increased during the course of MFS in five of six patients, suggesting a nonspecific secondary immune response. In patients with MFS following respiratory infections, IgG was the major anti-GQ1b Ig class (six of six patients) and IgG3 was the major subclass (five of six). In contrast, four of five patients with MFS following gastrointestinal infections showed predominance of anti-GQ1b IgA or IgM over IgG and predominance of the IgG2 subclass; anti-GQ1b IgG (IgG3) prevailed in one patient only. These distinct Ig patterns strongly suggest that different infections may trigger different mechanisms of anti-GQ1b production, such as via T-cell-dependent as opposed to T-cell-independent pathways. Thus, the origin of antibodies against GQ1b in MFS may be determined by the type of infectious agent that precipitates the disease.
G. Comi, Luisa Roveri
Published: 1 January 1999
The publisher has not yet granted permission to display this abstract.
B. C. Jacobs, P. H. Rothbarth, F.G.A. van der Meché, P. Herbrink, P. I.M. Schmitz, M. A. de Klerk, P. A. van Doorn
Neurology, Volume 51, pp 1110-1115;

Objectives: To determine which antecedent infections are specifically associated with the Guillain-Barré syndrome (GBS).Background: Infections with many agents have been reported preceding GBS. Some infections are related to specific clinical and immunologic subgroups in GBS. Most agents were reported in case reports and uncontrolled small series of GBS patients only, and their relation to GBS and its subgroups remains unclear.Methods: A serologic study for 16 infectious agents in 154 GBS patients and 154 sex- and age-matched controls with other neurologic diseases. Acute phase, pretreatment samples were used from clinically well-defined GBS patients. The seasonal distribution of serum sampling in the GBS and control group was the same.Results: Multivariate analysis showed that in GBS patients, infections with Campylobacter jejuni (32%), cytomegalovirus (13%), and Epstein-Barr virus (10%) were significantly more frequent than in controls. Mycoplasma pneumoniae infections occurred more often in GBS patients (5%) than in controls in univariate analysis. Infections with Haemophilus influenzae (1%), parainfluenza 1 virus (1%), influenza A virus (1%), influenza B virus (1%), adenovirus (1%), herpes simplex virus (1%), and varicella zoster virus (1%) were also demonstrated in GBS patients, but not more frequently than in controls. C. jejuni infections were associated with antibodies to the gangliosides GM1 and GD1b and with a severe pure motor form of GBS. Cytomegalovirus infections were associated with antibodies to the ganglioside GM2 and with severe motor sensory deficits. Other infections were not related to specific antiganglioside antibodies and neurologic patterns.Conclusions: Recent infections with C. jejuni, cytomegalovirus, Epstein-Barr virus, and M. pneumoniae are specifically related to GBS. The variety of infections may contribute to the clinical and immunologic heterogeneity of GBS.
, Ban Mishu Allos, Tony Ho
Clinical Microbiology Reviews, Volume 11, pp 555-567;

SUMMARY: Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.
Andrew Grigg, Brian Tait, Stephen Davis, Lyn Kiers
Published: 1 April 1998
Journal of Clinical Neuroscience, Volume 5, pp 169-171;

The publisher has not yet granted permission to display this abstract.
Ban Mishu Allos
Infectious Disease Clinics of North America, Volume 12, pp 173-184;

A previously unrecognized sequelum of infection with Campylobacter jejuni, a common cause of gastroenteritis, is Guillain-Barré syndrome (GBS). GBS is the most common cause of acute neuromuscular paralysis; 30% to 40% of cases are preceded by C. jejuni infection. Both patient and bacterial characteristics likely play a role in the pathogenesis of C. jejuni-induced GBS. Molecular mimicry between the LPS of some campylobacters and structures present on the gangliosides of the peripheral nerve may explain how this acute infectious diarrheal illness triggers GBS.
Qi Hao, Takahiko Saida, Shigekazu Kuroki, Masataka Nishimura, Masafumi Nukina, Hiroshi Obayashi, Kyoko Saida
Published: 31 January 1998
Journal of Neuroimmunology, Volume 81, pp 116-126;

The relationship between preceding infections and antibodies to glycolipids was investigated in 205 Japanese patients with Guillain–Barré syndrome (GBS). Serological evidence of recent Campylobacter jejuni (C. jejuni) infection was found in 45% of the patients, compared with 1% in healthy controls. In contrast, recent infection of cytomegalovirus (CMV), Mycoplasma pneumoniae (M. pneumoniae) and Epstein–Barr virus (EBV) was detected in only 5%, 2% and none of the patients, respectively. C. jejuni-associated GBS was more frequent in early spring than in other seasons. All stool specimens positive for C. jejuni isolation were obtained within 10 days after the onset of GBS symptoms. Of 13 C. jejuni isolates from GBS patients, 10 (77%) belonged to Penner serotype 19 (heat-stable, HS-19). Elevated titers of anti-GM1 antibody were found in 8 (80%) of 10 GBS patients whose C. jejuni isolates belonged to HS-19 and in none of those infected with non-HS-19 C. jejuni (P=0.04), and in 49% of 92 patients with C. jejuni infection and 25% of patients without infection of C. jejuni, CMV, EBV, or M. pneumoniae (P=0.0007). The frequencies of elevated antibody titers to GD1a, GD1b and GQ1b were also significantly higher in GBS patients associated with C. jejuni than those not associated with C. jejuni, CMV, EBV, and M. pneumoniae. GBS in Japan seems to be associated more frequently with C. jejuni and less frequently with CMV than in Europe and North America.
A Linde, , P Monteyne, J.M Echevarria, , F Rozenberg, B.F Vestergaard, , P Lebon, G.M Cleator
Published: 31 August 1997
Clinical and Diagnostic Virology, Volume 8, pp 83-104;

The publisher has not yet granted permission to display this abstract.
J.R. Fulgham, Eelco F.M. Wijdicks
Published: 1 January 1997
Critical Care Clinics, Volume 13, pp 1-15;

The leading cause of acute neuromuscular weakness in the developed world is Guillain-Barré syndrome (GBS). Mortality rates vary widely. This article discusses the care and management of patients with GBS, with an emphasis on those patients who require admission to an intensive care unit.
L. H. Visser, F.G.A. van der Meche, J. Meulstee, P. Rothbarth, B. C. Jacobs, P. I.M. Schmitz, P. A. van Doorn
Neurology, Volume 47, pp 668-673;

Guillain-Barre syndrome (GBS) is usually preceded by infections, in particular cytomegalovirus (CMV) and Campylobacter jejuni infection. We studied the clinical and electrophysiologic features of 20 CMV-associated GBS patients and compared the findings with earlier established data of C. jejuni-related GBS patients (n = 43) and of GBS patients without these infections (n = 71). The patients all participated in the Dutch GBS trial in which we compared the effect of intravenous immune globulins and plasma exchange. We demonstrate that CMV-related GBS patients have a different clinical pattern in comparison with the other two GBS groups. They are significantly younger, initially have a severe course indicated by a high frequency of respiratory insufficiency, and often develop cranial nerve involvement and severe sensory loss. This is in contrast to C. jejuni infection, which is associated with motor GBS. Both infections are associated with delayed recovery compared with the GBS patients without these infections.NEUROLOGY 1996;47: 668-673
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