Epidemiology

The epidemiology of type C disease in different animal species is poorly understood. Limited available data indicate that the prevalence of the disease varies among animal species, but the case fatality rate is usually high for all of them. In non-vaccinated swine populations, the incidence may be nearly 100%, while case fatality rates vary from 50 to 100%. Litters from non-immune sows are particularly at risk. Adequate herd immunity may significantly decrease the incidence of the disease. “Struck” of adult sheep occurs primarily in pastured, non-vaccinated animals; its prevalence may range from 5 to 15%. The prevalence of infections in foals is low, but the case fatality rate ranges from 80 to 100%.

C. perfringens type C disease is typically a condition of young animals but occurs occasionally in adults, as in ovine “struck.” In swine, the disease can occur as early as 12 hours of age but is more commonly seen in 1- to 3-day-old piglets. Type C disease is rare in piglets older than 1 week. In foals, type C infection occurs most commonly during the first week of life. Lambs, goats, and calves may develop type C disease as early as the second day of life.

Pathogenesis

C. perfringens type C is found in soil and in feces and the intestinal tracts of humans and other animals, and spores survive in the environment for long periods of time. However, this microorganism is not typically considered an important commensal in the intestinal tract of most animal species. Its presence is rare in the intestines of healthy horses, but it is commonly found in the feces of pigs on farms where the disease is endemic. In vitro studies have shown that type C strains may transfer the plasmid carrying the CPB-encoding gene to type A strains and, although not yet proven, it has been suggested that this might also happen in vivo.

Environmental contamination with feces from infected animals is an important source of infection. For instance, small numbers of C. perfringens type C may be detected in the feces of sows, exposing piglets to the microorganism shortly after birth. Although the main source of infection for piglets is sow feces, piglets may also be a source of infection for other piglets. In vitro studies have shown that a pH between 6.5 and 7.5 leads to high production of CPA, CPB, CPB2, and CPE toxins by C. perfringens. Therefore, gastrointestinal factors that increase the luminal pH in the stomach may increase intestinal colonization, growth, and toxin production by C. perfringens.

Dietary changes are also considered important predisposing factors for the disease. A sudden change in the diet and other factors may cause an imbalance of the normal intestinal flora, which favours overgrowth of C. perfringens. As noted previously, CPB is protease-labile and disease only occurs in situations where protease activity is very low or absent. In neonates, this occurs due to early failure to produce protective quantities of proteases and also because of the protease-inhibitor effect of colostrum. Human enteritis necroticans has often been associated with routine consumption of a protein-poor diet with occasional consumption of high-protein food rich in trypsin inhibitors and contaminated with type C. A classic scenario has been documented in the Highlands of Papua New Guinea over the past 60 years, although it seems likely that these cases have occurred there over a much longer period. The primary diet consisted of sweet potato, which contains a protease inhibitor, but is also low in protein, leading to a protease deficiency in the small intestine. Consumption of undercooked meat from pigs slaughtered without careful attention to sanitation provided the source of infection with C. perfringens type C. Under these conditions, production of CPB in the intestine was followed by fulminant disease. In Papua New Guinea, there remains a significant incidence of this disease, where it is known in the native dialect as “pigbel” (pig belly). Vaccination with a beta toxoid was quite effective in children, but that vaccine is no longer in production and the incidence has risen as a result.

On occasion, even when adequate levels of trypsin are present in the intestinal lumen, high levels of CPB may overpower the neutralizing effects of trypsin and cause disease, possibly explaining cases of type C disease in adult animals. The presence of foods with high levels of trypsin inhibitors, such as sweet potato and soybeans, may predispose domestic animals to type C enteritis and enterotoxemia.

Concurrent infection with other pathogens can change the intestinal environment, creating circumstances that favor the proliferation of type C in the intestine. There is speculation that coinfection of pigs with transmissible gastroenteritis virus, porcine epidemic diarrhea virus, rotavirus, or coccidia may predispose to type C disease. In calves, concurrent infections with rotavirus, Cryptosporidium spp., and Salmonella spp. have been described, but whether these really predispose to type C infection is not known. In horses, both C. perfringens type C and C. difficile have been identified in foals with hemorrhagic enteritis or enterocolitis.

Clinical signs

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