Vibrios are Gram-negative, curved, motile bacilli. There are more than eight species; V. cholerae and V. parahaemolyticus being the main human pathogens.
The organism is subdivided by the somatic O antigens; O1 and O139 being the main types associated with cholera. They are able to survive the gastric acidity, burrowing through the intestinal mucus to attach to intestinal epithelial cells via the GM1 ganglioside and produce a multimeric protein toxin (cholera toxin), which stimulates adenyl cyclase within the enteric cells, resulting in the secretion of water and electrolytes into the lumen of the bowel.
The clinical features of cholera include:
Where cholera is endemic, the diagnosis is based on clinical features. Immobilization of cholera bacteria in a diarrhoeal stool with specific antiserum yields a rapid diagnosis. The organism can be cultivated on specialist medium. Biochemical identification and serotyping should be performed to confirm the diagnosis.
Prevention and control
Campylobacter are associated with diarrhoeal disease and are the commonest cause of intestinal infection. Although there are more than 18 species of Campylobacter, C. jejuni is responsible for 90% of Campylobacter gastrointestinal infections. Infection follows ingestion of contaminated meat, poultry, unpasteurized milk or contaminated water. C. coli causes bacteraemia in immunocompromised patients.
Campylobacter jejuni invades and colonizes the mucosa of the small intestine. Antibodies to GM1 ganglioside are associated with Guillain-Barr� syndrome.
Diarrhoea is often self-limiting, but patients may be treated with erythromycin or fluoroquinolones. An aminoglycoside may be added for patients who have septicaemia.
Prevention and control
Prevention of campylobacteriosis depends on good animal husbandry and abattoir practices, and on good food hygiene in shops, dairies and the home.
Helicobacter pylori is a motile Gram-negative, spiral bacillus. H. cinaedi and H. fennelliae have been isolated from patients with HIV infection complicated by proctocolitis and bacteraemia.
Helicobacter pylori expresses urease, which raises the pH in the surrounding locality, therefore protecting the bacterium from the effects of gastric acid. The CagA pathogenicity island encodes a type IV secretion system that injects the CagA protein into the host cytoplasm, where subversion of a variety of cellular functions occurs that results in IL-8 secretion and inflammatory cell recruitment. VacA, a secreted protein that damages cells, is associated with severe disease.
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