Campylobacteriosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Campylobacter organisms are curved or spiral, motile, non–spore-forming, gram-negative rods. The known routes of transmission are fecal-oral, person-to-person sexual contact, raw milk and poultry ingestion, and waterborne (ie, through contaminated water supplies). Exposure to sick pets, especially puppies, has also been associated with outbreaks. The infectious dose is 1000-10,000 bacteria. Campylobacter species are sensitive to hydrochloric acid in the stomach, and acid reduction treatment can reduce the amount of inoculum needed to cause disease. Symptoms begin after an incubation period of one to seven days. The sites of tissue injury include the jejunum, the ileum, and the colon. C jejuni appears to invade and destroy epithelial cells. Some strains of C jejuni produce a cholera-like enterotoxin, which is important in the watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with hemolytic uremic syndrome and thrombotic thrombocytopenic purpura through a poorly understood mechanism. In patients with HIV, infections may be more frequent, may cause prolonged or recurrent diarrhea, and may be more commonly associated with bacteremia and antibiotic resistance. The severity and persistence of infection in patients with AIDS and hypogammaglobulinemia indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection.