A century ago when Guillain, Barré, and Strohl described the acute inflammatory polyneuropathic syndrome (Guillain-Barré syndrome [GBS]) for which they are still eponymously remembered, they noted that, “The pathogenesis of this radiculoneuropathic syndrome cannot be precisely defined. Although an infection or toxic insult should be considered, we have found no supporting evidence for either.”(p316) Many patients with GBS have signs or symptoms consistent with an antecedent infection, generally involving the respiratory and/or gastrointestinal tracts. In about 50% of cases of GBS with a suspected infectious precipitant, a specific pathogen can be identified as a potential trigger of a presumably postinfectious immune-mediated process leading to disease. The strongest associations, based on epidemiological studies, involve bacteria (Camplylobacter jejuni and Haemophilus influenzae), mycoplasma (Mycoplasma pneumoniae), and viruses (cytomegalovirus [CMV] and Epstein-Barr virus [EBV]). A far larger list of pathogens may be involved in the pathogenesis of sporadic cases or produce clusters of GBS during outbreaks or epidemics, as recently suggested for the Zika virus.
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