Extraintestinal Infection

In addition to typical bacterial enteritis, Campylobacter can cause extraintestinal infections. Extraintestinal infections are usually the result of systemic spread.

1. Bacteremia

C. jejuni bacteriemia occurs in approximately 1.5 per 1000 intestinal infections (Skirrow et al., 1993). The rate is higher in elderly individuals and in immunodeficient persons (Ladron de Guevara et al., 1994) and nearly twice as high in males as in females. Transient bacteremia might occur in many cases of C. jejuni enteritis but is not detected because blood cultures are not routinely conducted. Clinically significant bacteremia is infrequent because most C. jejuni strains are susceptible to killing by normal human serum. In contrast, C. fetus is serum-resistant because it is covered with a capsule-like protein (i.e., S layer) that prevents complement-mediated killing in serum. C. fetus infections easily induce bacteremia and systemic spread. However, C. jejuni still accounts for most (89%) Campylobacter isolated from blood. C. jejuni Penner serotypes O4 and O18 are more frequently isolated from blood than feces (Skirrow et al., 1993).

2. Other Infections

Secondary complications resulting from primary Campylobacter enteritis are relatively rare. These complications include cholecysitis, pancreatitis, peridontitis, gastrointestinal hemorrhage, meningitis, endocarditis, anthritis, peritonitis, cellulitis, hepatitis, and septic abortion. With improved methods for identification of Campylobacter, more species are now recognized to be important in causing human infections, especially when they infect immunocompromised persons. For example, C. fetus subsp. fetus is primarily associated with infectious abortion in cattle and sheep and is an infrequent cause of human infections. C. fetus can cause fetal death or septicemia in debilitated persons with chronic disease or in immunosuppressed patients (Blaser, 2000). C. jejuni and C. coli can also cause human abortion. Other Campylobacter spp., C. concisus, C. rectus, and C. curvus are known to be implicated in human periodontal disease (Tanner et al., 1987).

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