Workshop Summary and Recommendations Regarding the Development of Guillain‐Barré Syndrome following<i>Campylobacter</i>Infection

Abstract

Although there is substantial immunologic evidence linking the development of Guillain-Barrd syndrome (GBS) with a preceding infection with Campylobacter jejuni, microbiologic evidence is less complete. This is likely due to the brief period of excretion of C. jejuni in stools (median, 16 days) after an acute infection. Symptoms of GBS typically occur 10 days to 3 weeks after C. jejuni infection, when many patients have already cleared their stools. As such, studies of C. jejuni serotypes associated with GBS are limited to a small number of strains. If diarrheal cases were more frequently screened for C. jejuni, and if more and better typing reagents were available, the epidemiologic link between preceding infection with particular strains and the development of GBS would become better established. In addition, antibiotic resistance is emerging among Campylobacter species in both developing and developed countries. This could lead to difficulties in the treatment of human disease, and resistance enhances the need for protective vaccination of animals raised for food or of humans (or both). The following recommendations can be made: * Diagnostic tests sensitive for detection of a variety of Campylobacter species are needed. It is likely that a large number of Campylobacter infections go unrecognized. * Standardized microbiologic laboratory procedures are needed to insure isolation of Campylobacter strains associated with GBS. In particular, C. jejuni and Campylobacter upsaliensis should be looked for, but other species also may play a role. The concept of viable but nonculturable Campylobacter should be examined.