Clostridium perfringens type C necrotic enteritis in pigs: diagnosis, pathogenesis, and prevention

Abstract

Clostridium perfringens type C causes severe and lethal necrotic enteritis (NE) in newborn piglets. NE is diagnosed through a combination of pathology and bacteriologic investigations. The hallmark lesion of NE is deep, segmental mucosal necrosis with marked hemorrhage of the small intestine. C. perfringens can be isolated from intestinal samples in acute cases but it is more challenging to identify pathogenic strains in subacute-to-chronic cases. Toxinotyping or genotyping is required to differentiate C. perfringens type C from commensal type A strains. Recent research has extended our knowledge about the pathogenesis of the disease, although important aspects remain to be determined. The pathogenesis involves rapid overgrowth of C. perfringens type C in the small intestine, inhibition of beta-toxin (CPB) degradation by trypsin inhibitors in the colostrum of sows, and most likely initial damage to the small intestinal epithelial barrier. CPB itself acts primarily on vascular endothelial cells in the mucosa and can also inhibit platelet function. Prevention of the disease is achieved by immunization of pregnant sows with C. perfringens type C toxoid vaccines, combined with proper sanitation on farms. For the implementation of prevention strategies, it is important to differentiate between disease-free and pathogen-free status of a herd. The latter is more challenging to maintain, given that C. perfringens type C can persist for a long time in the environment and in the intestinal tract of adult animals and thus can be distributed via clinically and bacteriologically inapparent carrier animals.

CD31 (PECAM-1) Serves as the Endothelial Cell-Specific Receptor of Clostridium perfringens β-Toxin

“…Targeting this membrane molecule makes sense for pathogens like C. perfringens type C, which profit from a disturbed tissue perfusion at the site of infection. The targeting of endothelial cells via this specific CPB-CD31 interaction fits to the early vascular damage we described in an intestinal porcine infection model (Schumacher et al, 2013) and the massive intestinal hemorrhage observed in spontaneous C. perfringens type C enteritis (Posthaus et al, 2020). In our study, we confirmed the in vivo role of CD31 using a mouse toxemia model.…”

“…This model does not reflect the intestinal pathology induced in the natural disease. However, it can be used to determine the systemic effects of CPB toxemia, which have been suggested to occur also in the natural disease (Posthaus et al, 2020). We could clearly show that CD31-deficient mice are protected against the systemic and lethal effects of CPB.…”

In vitro protective effects of Lactobacillus plantarum Lac16 on Clostridium perfringens infection-associated intestinal injury in IPEC-J2 cells

“…Symptoms of its infection in piglets include severe diarrhoea, accompanied by necrotic mucosa and intestinal villi atrophy [7,8]. Currently, C. perfringens infections has become an important problem hindering the development of the pig industry [9,10]. Probiotics are de ned as "live microorganisms that, when administered in adequate amounts, confer a health bene t on the host" [11].…”

Pathogenicity and virulence of Clostridium perfringens

“…Similar lesions are frequently observed in foals and calves naturally diseased with type C strains [ 208 , 210 , 216 ]. CPB inhibition of platelet function may be responsible for systemic hemorrhages [ 291 ].…”