Enteritis caused by Campylobacter jejuni followed by acute motor axonal neuropathy: a case report (original) (raw)
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Guillain-Barré Syndrome Induced by Campylobacter jejuni
British Microbiology Research Journal, 2015
Purpose of Review: Guillain-Barré syndrome (GBS) is a neurologic disease that produces ascending paralysis that affects people all over the world. Several infectious agents have been associated with GBS and many reports suggest that infection with Campylobacter jejuni, a common enteric pathogen, may cause GBS by triggering demyelination of peripheral nerves. This review provides an update on the C. jejuni infections engaged in the developing of GBS. Summary and Results: Guillain-Barré syndrome is the most common cause of acute neuromuscular paralysis, yet its cause and pathogenesis are unknown. In approximately two thirds of patients, neuropathic symptoms follow an infection-often a mild, undiagnosed respiratory or gastrointestinal illness. The organism that has most frequently been described in association with GBS is C. jejuni, a gram-negative rod that is now the most common cause of bacterial gastroenteritis in developed countries. Although there has been a plethora of case reports and studies documenting the association, the specific clinical and epidemiologic features are not well Review Article Honarmand and Moghadam; BMRJ, 6(2): 71-83, 2015; Article no.BMRJ.2015.060 72 known. In addition, there is controversy about whether those with preceding C. jejuni infection have a more severe form of the GBS. C. jejuni can cause the disease by a mechanism called molecular mimicry. C. jejuni contains ganglioside-like epitopes in the lipopolysaccharide (LPS) moiety that elicit autoantibodies which can react with peripheral nerve targets. It seems that heterogeneity in the LPS structure determines the specificity of the antiglycolipid response and thereby the clinical features in patients with a post-campylobacter infection neuropathy.
Clinical Microbiology and Infection, 2003
We present a case of Guillain-Barré syndrome (GBS) following Campylobacter jejuni HS serotype O:19 infection in a child. Antibodies against C. jejuni and autoantibodies to the peripheral nerve gangliosides GM1 were positive, a pattern correlating well with the existence of an inflammatory neuropathy like GBS. The patient shared the HLA-B35 and HLA-DR8 antigens, which have been found to be increased in GBS patients with previous C. jejuni infection. As this is the first diagnosed C. jejuni-associated GBS case reported from Greece, further clinical and epidemiologic investigations are warranted.
Guillain-Barre syndrome subtypes related to Campylobacter infection
Journal of Neurology, Neurosurgery & Psychiatry, 2011
Background: In Guillain-Barré syndrome (GBS) the diversity in electrophysiological subtypes is unexplained, but may be determined by geographical factors and preceding infections. Acute motor axonal neuropathy (AMAN) is a frequent GBS variant in Japan and one study proposed that in Japan Campylobacter jejuni infections exclusively elicit AMAN. In the Netherlands C. jejuni is the predominant type of preceding infection, yet AMAN is rare. This may indicate that not all Dutch GBS patients with C. jejuni infections have AMAN. Objective: To determine if GBS patients with a preceding C. jejuni infection in the Netherlands exclusively have AMAN. Methods: Retrospective analysis of preceding infections in relation to serial electrophysiology and clinical data from 123 GBS patients. C. jejuni-related cases were defined as having preceding diarrhea and positive C. jejuni serology. Electrophysiological characteristics in C. jejuni-related cases were compared with those in viral-related GBS patients. In addition, eight GBS patients from another cohort with positive stool cultures for C. jejuni were analysed. Results: Seventeen (14%) of 123 patients had C. jejuni-related GBS. C. jejuni patients had lower motor and higher sensory action potentials compared to viral-related cases. Nine (53%) C. jejuni patients had either AMAN or inexcitable nerves. However, three (18%) patients fulfilled the criteria for acute inflammatory demyelinating polyneuropathy (AIDP). Also, two (25%) of eight additional patients with a C. jejuni-positive stool sample had AIDP. Conclusion: In the Netherlands C. jejuni infections are strongly, but not exclusively associated with axonal GBS. Some patients with these infections fulfil current criteria for demyelination.
Guillain-Barré Syndrome and Campylobacter jejuni Infection: A Review
Delta Medical College Journal, 2014
Guillain-Barre´ syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illness precedes 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 serological 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 neurological symptoms. One of every 1058 Campylobacter infections results in GBS. Sialic acid containing lipooligosaccharides (LOS) biosynthesis gene locus are associated with GBS and the expression of ganglioside mimicking structures. GM 1a was the most prevalent ganglioside mimic in GBS associated strains. Molecular mimicry between C. jejuni LOS and gangliosides in human peripheral nerves, and cross-reactive serum antibody precipitate the majority of GBS cases in Bangladesh, like worldwide.
Neurology India, 2011
Background: Guillain-Barré syndrome (GBS), is a common post-infectious polyradiculoneuropathy worldwide. The commonest implicated causative organism the world over is Campylobacter jejuni (C. jejuni). This study was carried out to determine the relationship between C. jejuni infection and GBS in an Indian setting. Materials and Methods: This prospective study was carried out on a cohort of 50 patients with GBS who were treated in a tertiary care hospital in India. Based on electrophysiological findings the patients were divided into various subtypes. Serology for C. jejuni (Immunoglogulin G, IgG and Immunoglogulin, IgM) using an enzyme-linked immunosorbent assay method (ELISA) was done both in patients and 40 age, sex and geographically matched controls. Results: Evidence of recent C. jejuni infection was present in 30% of GBS patients compared to 8% of controls (15/50 vs. 3/40 P<0.005). Eight (47%) C. jejuni-positive patients reported symptoms of gastroenteritis 4-30 days (mean 13 days) prior to onset of GBS. Of the 15 patients with evidence of C. jejuni infection, 10 (67%) patients had axonal type of GBS. Axonal variety of GBS presented in a younger age group compared to acute inflammatory demyelinating polyradiculoneuropathy (AIDP) patients (mean age: axonal vs. AIDP: 30.11 + 13.73 vs. 40.2 + 18.77). C. jejuni-positive patients presented mainly in spring and winter and had a similar age and sex incidence as compared to the rest of the GBS patients. Conclusions: Preceding C. jejuni infection is common among GBS patients and is often associated with the axonal variety of GBS. Axonal variety of GBS generally presents in a younger age group as compared to AIDP.
The risk of Guillain–Barré syndrome following infection with Campylobacter jejuni
Epidemiology and Infection, 1999
To estimate the incidence of Guillain-Barré syndrome (GBS) following Campylobacter jejuni infection (CI) we studied three populations where outbreaks of CI had occurred involving an estimated 8000 cases. No case of GBS was detected in the 6 months following the outbreaks in the local populations. The point estimate for the risk of GBS following CI estimated in this study was 0 in 8000 (95% confidence interval 0–3).
Serum Antibodies To Campylobacter Jejuni In Multifocal Motor Neuropathy
Journal of the Peripheral Nervous System, 2001
Multifocal motor neuropathy (MMN) has been frequently associated with high titers of anti‐ganglioside antibodies but the cause of this immune response is not known. Recently a possible association with an antecedent Campylobacter jejuni (CJ) infection has been reported in three patients who developed MMN and high titers of anti‐GM1 antibodies after CJ enteritis. Furthermore reactivity with the lipopolysaccharides (LPS) of CJ have been reported in some patients with chronic motor neuropathies and high anti‐ganglioside antibodies. To determine whether CJ may be involved in the pathogenesis of MMN we examined 22 patients with MMN, including 6 with anti‐ganglioside reactivity (2 GM1, 2 GD1a, 1 GM1+GD1a, 1 GM1+GM2), for the presence of anti‐CJ antibodies by Covalink ELISA and immunoblot, and correlated their presence with that of anti‐ganglioside antibodies. As controls we examined 17 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 23 with amyotrophic lateral scle...
Campylobacter Species and Guillain-Barré Syndrome
Clinical Microbiology Reviews, 1998
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 w...
Guillain-Barre syndrome and Campylobacter jejuni: a serological study
BMJ, 1984
The association between Campylobacter jejuni infection and Guillain-Barr6 syndrome was investigated serologically in a retrospective study of 56 patients admitted to this hospital over four years. Evidence of preceding C jejuni infection was found in 21 (38%) of these patients, indicating that C jejuni was the most common single identifiable pathogen precipitating the disease. Among those patients who had presented with preceding diarrhoea the serum antibody response was similar to that in uncomplicated C jejuni enteritis. Patients with serological evidence of preceding C jejuni infection manifested a significantly more severe form of the disease. In cerebrospinal fluid the predominant specific antibody class was IgG, and this was closely related to the serum titres of specific IgG. IgA and IgM specific antibodies were found only in the cerebrospinal fluid of patients with recent C jejuni infection. These findings support the possibility that humoral immune factors are responsible for the neural damage and demyelination seen in Guillain-Barre syndrome.