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Clostridium perfringens Type C Enteritis in Pigs


D. L. Hank Harris

, DVM, PhD, Department of Animal Science, Department of Veterinary Diagnostics and Production Animal Medicine, Iowa State University

Last full review/revision Sep 2013 | Content last modified Sep 2013
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Infection of the small intestine by type C strains of C perfringens causes a highly fatal, necrohemorrhagic enteritis. It most commonly affects piglets 1–5 days old but may be seen in pigs up to 3 wk old (and in other species, see Enterotoxemia Caused by Clostridium perfringens Types B and C).

Etiology and Pathogenesis:

The organism penetrates between the absorptive cells of the upper jejunum and elaborates β toxin, a potent, heat-labile, trypsin-sensitive exotoxin that causes necrosis of all structural components of the villi. Necrotizing inflammation usually extends to the mucosal crypts. The infection may continue caudally and involve the ileum, but it rarely affects the colon. Necrosis of the mucosa is accompanied by blood loss into the intestinal wall and lumen.

Clinical Findings:

Sudden onset of hemorrhagic diarrhea followed by collapse and death is characteristic in piglets 1–3 days old. In less acute cases, brownish liquid feces develop at 3–5 days. Infrequently, pigs develop a persistent, pasty, gray diarrhea and become progressively emaciated. In peracute cases, the perineal region is blood stained.


The small intestines are dark red, hemorrhagic, and filled with hemorrhagic liquid. Less acute cases at 3–5 days may have gas bubbles in the wall of the jejunum and necrosis of the mucosa of the jejunum and ileum. More chronic cases have a thickened small intestine lined by a pale yellow or gray necrotic membrane tightly adhered to the submucosa.


Necropsy is usually sufficient to establish the diagnosis in the peracute hemorrhagic form and in the acute form with jejunal emphysema. A rapid presumptive diagnosis can be made by demonstrating large rod-shaped bacteria in gram-stained mucosal impression smears. Histologic demonstration of villous necrosis with mucosal colonization by numerous large gram-positive rods is adequate for confirmation. Subacute and chronic forms of the disease in piglets 6–14 days old are easily confused at necropsy with Isospora suis enteritis, but diagnosis is usually possible by histologic examination of the jejunum and ileum or by observation of clostridia in mucosal smears (Gram or Giemsa stain). Isolates of C perfringens may be genotyped for the presence of genes that code for β toxin.

Treatment and Control:

Treatment of pigs with clinical signs is of little benefit because lesions usually are irreversible at the onset of diarrhea. In an acute outbreak, prophylactic administration of type C antitoxin or antibiotic (or both) parenterally or PO is protective if given to piglets within 2 hr of birth. The disease tends to recur on infected premises. Vaccination of gestating sows at 6 and 3 wk before parturition with type C bacterin-toxoid confers some passive lactogenic immunity to subsequent litters, if piglets consume colostrum soon after birth. Once immunized with two doses of bacterin-toxoid, sows should receive one dose ~3 wk before each subsequent farrowing.

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