Chapter 59 - Infections as a Cause of Guillain–Barré Syndrome

Abstract

Guillain–Barré syndrome (GBS) is a rare autoimmune disorder, the incidence of which is estimated to be from 0.6 to 4 in 100,000 people per year worldwide. Often (around one-third of cases) GBS occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal microbial infection. The disorder is subacute, developing over the course of hours or days up to 3 to 4 weeks. Reflexes are usually lost. GBS is a classical autoimmune disease, because all four major Witebsky-Rose criteria for an autoimmune disease are fulfilled. Viral and bacterial infections are often associated with GBS. About a third of all cases of Guillain–Barré syndrome are preceded by Campylobacter jejuni infection. C. jejuni strains isolated from GBS patients have a lipooligosaccharide (LOS) with a GM1-like structure. Molecular mimicry between LOS and the peripheral nerves as a cause of GBS was demonstrated in animal models of human GBS. Infection with serotype HS:19 of C. jejuni and the class A locus were predictive of the development of GBS. Recent studies have found that influenza illness was associated with higher rates of GBS, and influenza viral structures can induce anti-GM1 (ganglioside) antibodies. Judging from the evidence presented in this chapter, the aetiology of GBS can be multifactorial, as it is in other autoimmune diseases. It involves genetic and environmental factors and may be triggered by infections or vaccinations, and predisposition can be predicted by analysing some of these factors.