After its successful isolation from stools in the 1970s, Campylobacter jejuni has rapidly become the most commonly recognised cause of bacterial gastroenteritis in man. Reported cases of human campylobacteriosis represent only a small fraction of the actual number. In industrialised countries, the incidence of C. jejuni/Campylobacter coli infections peaks during infancy, and again in young adults aged 15-44 years. Acute self-limited gastrointestinal illness, characterised by diarrhoea, fever and abdominal cramps, is the most common presentation of C. jejuni/C. coli infection. The introduction of selective media has made the diagnosis of Campylobacter enteritis a simple procedure. In general, Campylobacter enteritis is a self-limiting disease which seldom requires antimicrobial therapy, although one in 1000 infections may lead to the Guillain-Barré syndrome. In industrialised countries, most infections are acquired through the handling and consumption of poultry meat. In developing countries, where the disease is confined to young children, inadequately treated water and contact with farm animals are the most important risk factors. Many infections are acquired during travel. Fluoroquinolone resistance has been reported in C. jejuni since the late 1980s in Europe and Asia, and since 1995 in the USA. The use of fluoroquinolones to treat animals used for food has accelerated this trend of resistance. In Australia, where fluoroquinolones have not been licensed for use in food production animals, C. jejuni remains susceptible to fluoroquinolones. The public health burden of Campylobacter spp. other than C. jejuni/C. coli remains unmeasured. Better diagnostic methods may reveal the true health burden of these organisms.

The relationships of 77 aerotolerant Arcobacter strains that were originally identified as Campylobacter cryaerophila (now Arcobacter cryaerophilus [P.

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Summary.A collection of 44 Campylobacter isolates (37 C. jejuni and seven C. coli) from children with colitis (21 strains) or watery diarrhoea (23 strains) was analysed for toxin production, association with HeLa cells, and invasion of differentiated Caco-2 cell cultures. There was no obvious association of clinical symptoms with species, biotype or enterotoxin production. All colitis strains and most of the isolates from watery diarrhoea were cytotoxic for Chinese hamster ovary cells. Measurements of bacterial association indices with HeLa cells varied with time, and were considered to be unreliable for discriminating between isolates from the two diagnostic groups. Statistically significant differences were observed between the two groups (all colitis strains and 65% of strains from non-inflammatory diarrhoea) with respect to invasion of both HeLa and Caco-2 cell monolayers. However, among the strains from non-inflammatory diarrhoea that did invade, numbers of internalised bacteria were similar to the range observed for colitis strains. Of the colitis strains, 86 % were able to transcytose through polarised Caco-2 monolayers grown on filters, compared with 48% of isolates from non-inflammatory disease. We propose the use of Caco-2 cells as a model for studying invasion of intestinal epithelia by C. jejuni and C. coli.

Community-acquired bacteremia caused by multiresistant Enterobacteriacea is an important problem of hospitalized well-nourished and malnourished children in central Africa. Fever on admission is a sensitive diagnostic sign, even in malnourished children.