Host-Pathogen Interactions in Guillain-Barré Syndrome : the role of Campylobacter jejuni lipooligosaccharide sialylation

Campylobacter jejuni (C. jejuni) is a spiral, comma-shaped Gram-negative bacterium which is motile due to bipolar flagella. C. jejuni is frequently present in the intestines of poultry and birds, where it is considered to be part of the normal intestinal flora (1). During slaughter procedures, poultry meat products often become contaminated with fecal content containing C. jejuni (2, 3). As a consequence of the extensive consumption of chicken worldwide, the handling of raw chicken and ingestion of undercooked chicken meat are the main causes of C. jejuni infection in humans (3). Apart from poultry, other sources of C. jejuni infection include raw milk, (swimming) water and pets (4). Upon ingestion, C. jejuni can pass through the human gastrointestinal tract without clinical symptoms; however, infection with C. jejuni will often lead to a diarrheal illness (5). In the Netherlands, approximately 80,000 people per year (range, 30,000 – 160,000) are estimated to experience acute gastroenteritis caused by Campylobacter (6). The symptoms include fever, abdominal pain, and slimy or bloody diarrhea that lasts for several days (7). C. jejuni diarrhea is self-limiting, though complications such as bacteraemia, post-infectious reactive arthritis or Guillain-Barré syndrome (GBS) occasionally occur. In view of the broad spectrum of clinical disease presentations associated with C. jejuni infection, microbial as well as host factors are likely to contribute to C. jejuni pathogenesis.