| Host-pathogen interactions in campylobacter infections: the host perspective (2008) | |||||||||||||
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| Campylobacter is a major cause of acute bacterial diarrhea in humans worldwide (3). The incidence of human campylobacteriosis increased exponentially during the last decade of the 20th century (183), although part of this increase can be attributed to better detection of Campylobacter and better diagnosis. At the start of the 21st century, this increase has stopped, as shown by data for the total number of Campylobacter cases in the European Union until 2003 (Fig. 1). In humans, the clinical symptoms of campylobacteriosis are watery or bloody diarrhea, abdominal cramps, and nausea (151). In a small subgroup of patients, the acute phase is followed by serious sequelae: Guillain-Barre´ syndrome (GBS) and reactive arthritis (78, 86). Acute diarrhea, Campylobacter-related mortality, and residual effects of GBS are the main determinants contributing to this disease burden (79). Campylobacteriosis in humans is induced mainly by Campylobacter jejuni (about 90% of cases), and the remaining fraction is induced predominantly by Campylobacter coli. Campylobacter is part of the normal intestinal flora of birds, and humans are not the reservoir for infection. As a result, poultry is a major source of infection. The estimation of incidence of Campylobacter enteritis in the population is usually based on confirmed cases corrected for several factors like the proportion of patients consulting a physician and the number of this group submitting a stool sample for Campylobacter isolation. Because the infection is usually self-limiting, the true population incidence is estimated to be 8 to 30 times higher than confirmed cases, depending on the country (148, 166, 179). | |||||||||||||
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