Guillain-Barre syndrome and Campylobacter jejuni: a serological study.

Kaldor, J.; Speed, Bryan

doi:10.1136/bmj.288.6434.1867

Cited by 200 publications

(93 citation statements)

References 21 publications

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“…Most of the data supporting the association of antecedent infections with GBS result from serological studies (2,6,8,10,14,18,19,21,23,25,29,31). Routinely used serological assays for the diagnosis of CMV and EBV infections are of high quality, with sensitivities and specificities of Ͼ90%.…”

Section: Vol 13 2006 Role Of C Jejuni In Triggering Guillain-barrémentioning

confidence: 99%

Improved Serological Diagnosis Stresses the Major Role of Campylobacter jejuni in Triggering Guillain-Barré Syndrome

Schmidt-Ott

Schmidt

Feldmann

et al. 2006

Clin Vaccine Immunol

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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.

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Section: Vol 13 2006 Role Of C Jejuni In Triggering Guillain-barrémentioning

confidence: 99%

Improved Serological Diagnosis Stresses the Major Role of Campylobacter jejuni in Triggering Guillain-Barré Syndrome

Schmidt-Ott

Schmidt

Feldmann

et al. 2006

Clin Vaccine Immunol

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“…This report was soon followed by a retrospective study of 56 patients with GBS, 38% of whom exhibited serological evidence of C.jejuni infection 49 . Numerous subsequent studies documented the prevalence of C.jejuni infection or seropositivity in patients with GBS, confirming the finding to be widespread and reproducible 50 .…”

Section: [H1] Molecular Mimicry In Pathogenesis [H2] Campylobacter Jementioning

confidence: 99%

Guillain–Barré syndrome: a century of progress

2016

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In 1916, Guillain, Barré and Strohl reported on two cases of acute flaccid paralysis with high cerebrospinal fluid protein levels and normal cell counts -novel findings that identified the disease we now know as Guillain-Barré syndrome (GBS).100 years on, we have made great progress with the clinical and pathological characterization of GBS. Early clinicopathological and animal studies indicated that GBS was an immune-mediated demyelinating disorder with secondary axonal injury if severe; the current treatments of plasma exchange and intravenous immunoglobulin, which were developed in the 1980s, are based on this premise. Subsequent work has, however, shown that the underlying disease can be an axonal injury. The association of Campylobacter jejuni strains has led to confirmation that anti-ganglioside antibodies are pathogenic and that axonal GBS involves an antibody and complement-mediated disruption of nodes of Ranvier, neuromuscular junctions and other neuronal and glial membranes. Now, ongoing clinical trials of the complement inhibitor eculizumab are the first of targeted immunotherapy in GBS.Guillain-Barré syndrome (GBS) is the commonest cause of acute flaccid paralysis and manifests as rapidly evolving weakness and sensory disturbance in arms, legs and in some patients, facial, bulbar and respiratory muscles. Many patients will make a good recovery over many months but in severe cases patients can require months of intensive care support and be left with permanent severe weakness, sensory disturbance and pain. Furthermore, around 5% die from complications including respiratory failure, pneumonia and arrhythmias, making it a medical emergency with a high morbidity and significant mortality.Descriptions of clinical cases that closely resemble the condition we now know as GBS were made at least as early as 1859, when Jean Baptiste Octave Landry reported on "acute ascending paralysis". His report led to use of the term "Landry's ascending paralysis" to describe subacute ascending peripheral sensory and motor dysfunction. He observed that:

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“…Additional evidence of the role of cell-mediated immunity in CBJ infection is provided by the possible linkage between Guillain-Barre syndrome and CBJ infection. An imbalance in cellmediated immunity during CBJ infection may lead to Guillain-Barre syndrome (9). Campylobacter found in homosexuals with cellular immunity imbalance provides further support for the importance of the cellular response.…”

Section: Methodsmentioning

confidence: 99%

The Immune System Response to Campylobacter Infection

Melamed

Zakuth

Schwartz

et al. 1988

Microbiology and Immunology

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Campylobacter may be one of the most common causes of bacterial gastroenteritis (GE) in children. It has recently been suggested that it is one of the bacterial pathogens most likely to infect immune-compromised children, and it may facilitate colonization of enteric pathogens. The immune system response was studied in 12 children with Campylobacter fetus subspecies jejuni (CBJ) infections. Serum concentrations of IgA, IgM, and IgG were analyzed using a Beckman autoanalyzer. Sera specific Ab to CBJ were tested with CBJ specific enzyme-linked immunosorbant assay (ELISA). Mitogen stimulation of lymphocytes was performed to three lectins : Con A, PWM, and PHA. The lymphocyte blast transformation to Campylobacter was studied using the Campylobacter antigen. T-cell subsets were studied using the monoclonal antibodies Leu 2, 3, and 4 (Becton Dickinson). Chemotaxis was measured in modified Boyden chambers; chemotactic stimulants were the Formyl Met Leu Phe, Campylobacter antigen virion, and E. coli 0111 B. Immunoglobulins were normal in nine cases and abnormal in two children previously diagnosed as agammaglobulinemic and one diagnosed as hypoagammaglobulinemic. Specific serum Ab level was significantly higher in the CBJ group, except in the agammaglobulinemic group. Stimulation indices to mitogens and monoclonal subset were in the normal range. The blastogenic transformation to CBJ Ag was decreased compared to normal lectins, and positive and high compared to controls. The chemotactic activity to campylobacter Ag was decreased in comparison to other stimulants. Most CBJ infections are self-limiting due to a normal immune response and collaboration of all cellular limbs. When, however, the immune response is disturbed, we may find a prolonged and complicated course of CBJ.

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Guillain-Barre syndrome and Campylobacter jejuni: a serological study.

Cited by 200 publications

References 21 publications

Improved Serological Diagnosis Stresses the Major Role of Campylobacter jejuni in Triggering Guillain-Barré Syndrome

Improved Serological Diagnosis Stresses the Major Role of Campylobacter jejuni in Triggering Guillain-Barré Syndrome

Guillain–Barré syndrome: a century of progress

The Immune System Response to Campylobacter Infection

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