Campylobacter jejuni is a major cause of the Guillain-Barre syndrome (GBS) and related diseases. These autoimmune diseases are caused by antibodies cross-reacting with the peripheral (GBS) and central neural tissue (Miller Fisher syndrome -MFS, Bickerstaff's brainstem encephalitis -BBE), leading to acute polyneuropathy. Recently, specific gene loci in C. jejuni have been distinguished which are associated with the onset of GBS, despite a molecular or phenotypic clustering. In this study, we used PCR to analyse C. jejuni isolates of different origin (i. e. bovine, poultry, human) for these genes. A total of 196 isolates were tested for cst-II and neuA. Of these, 101 isolates harboured the cst-II locus and 102 the neuA locus. Eighty-six isolates (44%) hold both genes. The frequency of cst-II in different sources of isolates of bovine, poultry and human isolates did not vary significantly (52, 50 and 52%, respectively). In contrast, the neuA locus was less often found in poultry isolates. Two human strains -from a family outbreak of campylobacteriosis (in 1989 in Austria) in which one person developed MFS -harboured both genes. Thus, although only one in more than 3000 patients with Campylobacter-associated enteritis develop GBS, about half of Campylobacter jejuni strains found in different environments are possibly able to cause GBS. These strains almost equally distributed in bovine, poultry and human isolates. Our results suggest that isolates associated with GBS are not selected by environmental or host-specific factors. Accordingly, this study indicates that host factors such as humoral and cellular immunity are possibly responsible for the development of these autoimmune diseases.