Etiology

The family Campylobacteriaceae includes >20 species. Those known or considered pathogenic for humans include C. jejuni, C. fetus, C. coli, C. hyointestinalis, C. lari, C. upsaliensis, C. concisus, C. sputorum, C. rectus, C. mucosalis, C. jejuni subspecies doylei, C. curvus, C. gracilis, and C. cryaerophila. Additional Campylobacter species have been isolated from clinical specimens, but their roles as pathogens have not been established. C. jejuni and C. coli are the most important pathogens of the genus. More than 100 serotypes of C. jejuni have been identified.

Campylobacter organisms are thin (0.2-0.4 µm wide), curved, gram-negative, non–spore-forming rods (1.5-3.5 µm long) that usually have tapered ends. They are smaller than most other enteric bacterial pathogens and have variable morphology, including short comma- or S-shaped organisms and long, multispiraled, filamentous, seagull-shaped organisms. Individual organisms are usually motile with a flagellum at 1 or both poles. Growth on solid media results in small (0.5-1 mm), slightly raised, smooth colonies. Visible growth in blood cultures is often not apparent until 5-14 days after inoculation. Most Campylobacter organisms are microaerophilic and do not oxidize or ferment carbohydrates. Selective culture media developed to enhance isolation of C. jejuni may inhibit the growth of other Campylobacter species. C. jejuni has a circular chromosome of 1.64 million base pairs (30.6% G+C) that is predicted to encode 1,654 proteins and 54 stable RNA species. The genome is unusual in that there are virtually no insertion sequences or phage-associated sequences and very few repeat sequences.

Clinical presentations differ, in part, by species (Table 194-1). Intestinal disease is usually associated with C. jejuni and C. coli, and extraintestinal and systemic infections are most often associated with C. fetus. C. jejuni septicemia is increasingly recognized and can occur without gastrointestinal signs or symptoms. Less commonly, enteritis is recognized in association with isolation of C. lari, C. fetus, and other Campylobacter species.

Table 194-1 CAMPYLOBACTER SPECIES ASSOCIATED WITH HUMAN DISEASE

Epidemiology

Human campylobacterioses most commonly result from ingestion of contaminated poultry (chicken, turkey) or raw milk and less commonly from drinking water, pets (cats, dogs, hamsters), and farm animals. Infections are more common in resource-limited settings, are prevalent year-round in tropical areas, and can exhibit seasonal peaks in temperate regions (late summer and early fall in most of the USA). In industrialized countries, Campylobacter infections peak in early childhood and in persons 15-44 yr of age. Each year in the USA there are an estimated 2.4 million cases of Campylobacter infections, resulting in >100 deaths. Medical record keeping in the Netherlands has allowed analyses showing that each resident acquires asymptomatic Campylobacter infection every 2 years and that asymptomatic infection progresses to symptomatic infection in approximately 1% of colonized persons.

Although chickens are a classic source of Campylobacter, many animal sources of human food can harbor Campylobacter, including seafood. Additionally, many animals kept as pets carry Campylobacter, and insects inhabiting contaminated environments can acquire the organism. Direct or indirect exposure to this plethora of environmental sources is the origin of most human infections. Airborne transmission of Campylobacter can occur in farm workers. There is increasing evidence that the use of antimicrobials in animal foods increases the prevalence of antibiotic-resistant Campylobacter isolated from humans.

Human infection can result from exposure to as few as a few hundred colony-forming units. At times, C. jejuni and C. coli spread person to person, perinatally, and at child care centers where diapered toddlers are present. Persons infected with C. jejuni usually shed the organism for weeks but can shed for months.

Pathogenesis

The conceptual model for the pathogenesis of C. jejuni enteritis includes mechanisms to transit the stomach, adhere to intestinal mucosal cells, and initiate intestinal lumen fluid accumulation. Most Campylobacter