Campylobacter is an important cause of foodborne gastroenteritis. We determined the occurrence of Campylobacter jejuni and Campylobacter coli, using culture-based methods and PCRs targeting virulence-associated genes (VAGs) among children aged ¡14 years who were treated for diarrhoea at emergency rooms in northeastern Brazil. Genomic DNA was extracted directly from stool samples collected from 366 children. A questionnaire was also applied to qualify the clinical conditions presented by each child at the time of admission. C. jejuni and C. coli were detected in 16.4 % (60/366) and 1.4 % (5/366) of the diarrhoeal samples, respectively, by PCR, a much higher proportion than that detected by conventional methods. C. jejuni VAGs were detected in the following proportions of hipO-positive samples: ciaB, 95 % (57/60); dnaJ, 86.7 % (52/60); racR, 98.3 % (59/60); flaA, 80 % (48/60); pldA, 45 % (27/60); cdtABC, 95 % (57/60); and pVir 0 % (0/ 60). Particular symptoms, such as blood in faeces, vomiting, fever, and/or abdominal pain, were not associated with detection of C. jejuni nor were they associated with any particular VAG or combination of VAGs (P.0.05). C. jejuni and its VAGs were detected in a substantial proportion of the children admitted. Further efforts shall be directed towards elucidating whether these genetic factors or their expressed proteins play a role in Campylobacter pathogenesis.
INTRODUCTIONThe genus Campylobacter, a group of thermotolerant, microaerophilic, Gram-negative bacteria, includes a number of pathogens that primarily cause gastrointestinal disease in humans, particularly Campylobacter jejuni and Campylobacter coli. Campylobacter-associated gastroenteritis is thought to occur through zoonotic transmission, being acquired from exposure to tainted food and/or contaminated drinking water (Sherman et al., 2010). Campylobacter infection frequently presents as self-limiting acute enteritis with diarrhoea, malaise, fever and abdominal pain, sometimes with vomiting and the presence of blood in faeces (Allos, 2001); disruption of epithelial cells and inflammation of the intestinal mucosa are hallmark features of severe cases (Beltinger et al., 2008). C. jejuni and C. coli cause significant morbidity worldwide, especially in children (Amieva, 2005;Tam et al., 2003;Wang et al., 2008; Fernández et al., 2008).Adherence and colonization are crucial steps in the pathogenesis of C. jejuni. Flagella have a major role in invasion; markedly reduced internalization in vitro has been reported with flaA 2 C. jejuni mutants (Wassenaar, 1997). The genes racR and dnaJ are determinants for C. jejuni colonization and are presumably expressed in response to conditions encountered in the intestinal microenviroment, such as differences in temperature between environmental reservoirs and human intestines (Konkel et al., 1998; Brás et al., 1999 antigen B protein, which confers invasive properties, as shown by C. jejuni ciaB null mutants which display a significant reduction in internalization (Konkel et al., 1999). Also, ...