Guillain-Barre Syndrome - Association with Campylobacter jejuni

12/16/02 (Hewitt)

Question: What is known about the association between Campylobacter jenuni infection and Guillain-Barre syndrome?

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Unique Identifier:11274311

Authors: Hadden RD. Karch H. Hartung HP. Zielasek J. Weissbrich B. Schubert J. Weishaupt A. Cornblath DR. Swan AV. Hughes RA. Toyka KV. Plasma Exchange/Sandoglobulin Guillain-Barre Syndrome Trial Group.

Institution: Department of Neuroimmunology, Guy's, King's and St. Thomas' School of Medicine, Swan), London, UK. rob.hadden@doctors.org.uk

Title: Preceding infections, immune factors, and outcome in Guillain-Barre syndrome.

Source: Neurology. 56(6):758-65, 2001 Mar 27.

Abstract: OBJECTIVE: To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain-Barre syndrome (GBS). METHODS: We tested pretreatment sera, 7 +/- 3 (mean +/- SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features. RESULTS: Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein-Barr virus in four (2%). Patients with C. jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM(1) antibodies, pure motor GBS, lower CSF protein, and worse outcome. Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R). Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology. Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM(1) antibodies. CONCLUSIONS: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features. A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors. Most patients had no identified infection. CAS Registry/EC Number 0 (Antibodies). 0 (Cell Adhesion Molecules). 0 (Receptors, Cytokine). 37758-47-7 (G(M1) Ganglioside).

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Unique Identifier:9781538

Authors: Jacobs BC. Rothbarth PH. van der Meche FG. Herbrink P. Schmitz PI. de Klerk MA. van Doorn PA.

Institution: Department of Neurology, Erasmus University, Rotterdam, The Netherlands.

Title: The spectrum of antecedent infections in Guillain-Barre syndrome: a case-control study.

Source: Neurology. 51(4):1110-5, 1998 Oct.

Abstract: OBJECTIVE: To determine which antecedent infections are specifically associated with the Guillain-Barre 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. METHOD: 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. CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (Antibodies, Viral). 0 (Gangliosides).

 Link Directly to Fulltext Article at Science Direct

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Unique Identifier:9746040

Authors: Hahn AF.

Institution: Clinical Neurological Sciences, University of Western Ontario, London Health Sciences Centre, Canada. angelika.hahn@lhsc.on.ca

Title: Guillain-Barre syndrome. [Review] [74 refs]

Source: Lancet. 352(9128):635-41, 1998 Aug 22.

Abstract: Guillain-Barre syndrome (GBS) is viewed as a reactive, self-limited, autoimmune disease triggered by a preceding bacterial or viral infection. Campylobacter jejuni, a major cause of bacterial gastroenteritis worldwide, is the most frequent antecedent pathogen. It is likely that immune responses directed towards the infecting organisms are involved in the pathogenesis of GBS by cross-reaction with neural tissues. The infecting organism induces humoral and cellular immune responses that, because of the sharing of homologous epitopes (molecular mimicry), cross-react with ganglioside surface components of peripheral nerves. Immune reactions against target epitopes in Schwann-cell surface membrane or myelin result in acute inflammatory demyelinating neuropathy (85% of cases); reactions against epitopes contained in the axonal membrane cause the acute axonal forms of GBS (15% of cases). Care for such patients may be challenging, yet the prognosis overall is favourable. Optimal supportive care and anticipation and prevention of complications are the mainstay of therapy. Admission to the intensive-care unit is necessary in 33% of patients who require intubation and assisted ventilation. Immunomodulation with infusions of IgG or plasma exchange treatments foreshorten the disease course. [References: 74] CAS Registry/EC Number 0 (Epitopes).

See special issue [supplement] of Journal of Infectious Diseases devoted to this topic 

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Unique Identifier:9396695

Authors: Allos BM.

Institution: Division of Infectious Diseases, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Title: Association between Campylobacter infection and Guillain-Barre syndrome. [Review] [30 refs]

Source: Journal of Infectious Diseases. 176 Suppl 2:S125-8, 1997 Dec.

Abstract: Guillain-Barre syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illnesses precede 50%-75% of the GBS cases. Although many infectious agents have been associated with GBS, the strongest documented association is with Campylobacter infection. The first line of evidence supporting Campylobacter infection as a trigger of GBS is anecdotal reports. The second line of evidence is serologic surveys, which have demonstrated that sera from GBS patients contain anti-Campylobacter jejuni antibodies, consistent with recent infection. Finally, culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurologic symptoms. Neurologic symptoms are more severe and more likely to be irreversible when GBS is preceded by C. jejuni infection. One of every 1058 Campylobacter infections results in GBS, and 1 of 158 Campylobacter type O:19 infections results in GBS. [References: 30] CAS Registry/EC Number 0 (Antibodies, Bacterial). 0 (O Antigens).