g(m1)-ganglioside and Infections

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder, the incidence of which is estimated to be 0.6-4/100,000 person/year worldwide. Often, GBS occurs a few days or weeks after the patient has had symptoms of a respiratory or gastrointestinal microbial infection. The disorder is sub-acute developing over the course of hours or days up to 3 to 4 weeks. 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. Following the "swine flu" virus vaccine program in the USA in 1976, an increase in incidence of GBS was observed and the calculated relative risk was 6.2. Later studies have found that influenza vaccines contained structures that can induce anti-GM1 (ganglioside) antibodies after inoculation into mice. More recent information has suggested that the occurrence of GBS after currently used influenza and other vaccines is rare. GBS involves genetic and environmental factors, may be triggered by infections or vaccinations, and predisposition can be predicted by analyzing some of these factors.

Topics: Adverse Drug Reaction Reporting Systems; Animals; Autoantibodies; Centers for Disease Control and Prevention, U.S.; Disease Models, Animal; G(M1) Ganglioside; Guillain-Barre Syndrome; Humans; Infections; Influenza Vaccines; Lipopolysaccharides; Mice; Molecular Mimicry; Peripheral Nerves; United States; United States Food and Drug Administration; Vaccination

The clinical spectrum of Guillain-Barré syndrome (GBS) is summarized in relation to antecedent infections and anti-ganglioside antibodies. Associations exist between a pure motor form of GBS, diarrhea, Campylobacter jejuni infection, and anti-GM1 antibodies; between cranial nerve involvement and Miller Fisher syndrome, C. jejuni infection, and anti-GQ1b antibodies; and between variants, such as severe sensory involvement and cytomegalovirus infection. These three clinical variants are suggested to form the extremes of a continuous spectrum; they are discussed in relation to the more pathologically defined patterns of acute motor axonal neuropathy and acute motor-sensory axonal neuropathy. In particular, patients with a clinically pure motor variant of GBS, diarrhea, anti-GM1 antibodies, or C. jejuni infection seem to respond better to early treatment with high-dose immunoglobulins than to plasma exchange.

Topics: Autoantibodies; Campylobacter Infections; Campylobacter jejuni; Cytomegalovirus Infections; G(M1) Ganglioside; Humans; Immunoglobulins, Intravenous; Infections; Plasma Exchange; Polyradiculoneuropathy

Topics: Catheterization, Central Venous; Double-Blind Method; G(M1) Ganglioside; Humans; Infections; Quadriplegia; Spinal Cord Injuries