Studies on the pathogenesis of Campylobacter jejuni show that for this organism to cause disease the susceptibility of the host and the relative virulence of the infecting strain are both important. Infection with C. jejuni results from the ingestion of contaminated food or water, and the infective dose can be as low as 800 organisms. To initiate infection the organism must penetrate the gastrointestinal mucus, which it does by using its high motility and spiral shape. The bacteria must then adhere to the gut enterocytes and once adhered can then induce diarrhoea by toxin release. C. jejuni releases several different toxins which vary from strain to strain, mainly enterotoxin and cytotoxins, and these correlate with the severity of the enteritis. During infection, levels of all immunoglobulin classes rise. Of these, IgA is the most important as it can cross the gut wall. IgA immobilises organisms, causing them to aggregate and activate complement, and also gives short-term immunity against the infecting strain of organism. The other immunoglobulin classes act on bacteria entering the blood stream, thus preventing bacteraemia. C. jejuni can also stimulate the cellular immune system, but this seems to play only a small role in preventing infection.