Guillain-Barré Syndrome Induced by Campylobacter jejuni

Abstract

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. jejuniinfections 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 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.