Role of Infection Due to Campylobacter jejuni in the Initiation of Guillain-Barre Syndrome

Abstract

Recent reports suggest that infection with Campylobacter jejuni, a common enteric pathogen, may cause Guillain-Barré syndrome (GBS) by triggering demyelination of peripheral nerves. GBS is preceded by an acute infectious illness (due to a variety of agents) in 50%–75% of cases; the onset of neurological symptoms is preceded by diarrhea in 10%–30% of cases. In the last decade, more than 20 published anecdotal reports and case series have described patients with C. jejuni infection documented 1–3 weeks before onset of GBS. Cultures of fecal samples obtained at the onset of neurological symptoms from patients with GBS have yielded C. jejuni in more than 25% of cases. A relatively rare serotype, Penner type O19, is overrepresented among isolates of C. jejuni from Japanese patients with GBS. Serological studies suggest that 20%–40% of patients with GBS have evidence of recent C. jejuni infection. In summary, infection with C. jejuni is a common antecedent to GBS and probably plays a role in initiating demyelination; although several pathogenic mechanisms are possible, none has been proven.