Porcine proliferative enteritis is a common diarrheal disease of growing-finishing and young breeding pigs characterized by hyperplasia and inflammation of the ileum and colon. It often is mild and self-limiting but sometimes causes persistent diarrhea, severe necrotic enteritis, or hemorrhagic enteritis with high mortality.
The etiology is Lawsonia intracellularis, an intracellular, gram-negative, small rod-shaped bacterium. The organism has been cultivated only in cell cultures, and attempts to propagate it in cell-free medium have failed. Koch’s postulates have been fulfilled by inoculation of pure cultures of L intracellularis into conventionally reared pigs; typical lesions of the disease were produced, and L intracellularis was reisolated from the lesions. Inoculation of L intracellularis into gnotobiotic pigs does not cause the disease; therefore, other factors in the conventionally reared pig may contribute to development of lesions.
The more common, nonhemorrhagic form of the disease often affects 40- to 80-lb (18- to 36-kg) pigs and is characterized by sudden onset of diarrhea. The feces are watery to pasty, brownish, or faintly blood stained. After ~2 days, pigs may pass yellow fibrinonecrotic casts that have formed in the ileum. Most affected pigs recover spontaneously, but a significant number develop chronic necrotic enteritis with progressive emaciation. The hemorrhagic form is characterized by cutaneous pallor, weakness, and passage of hemorrhagic or black, tarry feces. Pregnant gilts may abort.
Lesions may be seen anywhere in the lower half of the small intestine, cecum, or colon but are most frequent and obvious in the ileum. The wall of the intestine is thickened, and the mesentery may be edematous. The mesenteric lymph nodes are enlarged. The intestinal mucosa appears thickened and rugose, may be covered with a brownish or yellow fibrinonecrotic membrane, and sometimes has petechial hemorrhages. Yellow necrotic casts may be found in the ileum or passing through the colon. Diffuse, complete mucosal necrosis in chronic cases causes the intestine to be rigid, resembling a garden hose. Proliferative mucosal lesions often are in the colon but are detected only by careful inspection at necropsy. In the profusely hemorrhagic form, there are red or black, tarry feces in the colon and clotted blood in the ileum.
Confirmation is based on histologic observation of characteristic proliferation and inflammation of mucosal crypts. L intracellularis (comma-shaped, resembling Campylobacter) can usually be demonstrated by silver stains. A PCR test has been developed and is useful for confirmation of the presence of L intracellularis in lesions. Bacterial culture of intestine and lymph nodes to exclude Salmonella infection, together with histologic examination and culture of cecum and colon to exclude swine dysentery, are essential additional procedures. The colon also should be examined for whipworms. L intracellularis is present in most swine herds, so demonstration of the organism in feces by PCR or the presence of antibody in clinically normal pigs is of little diagnostic value.
Various antibacterials administered parenterally to acutely affected pigs and by feed or water to the remainder of the group help reduce severity of the enteritis and prevent development of chronic, irreversible, necrotic enteritis. Porcine proliferative enteritis is one of the first diseases to be seen in new herds established by surgical derivation. A live avirulent vaccine administered via the water is highly effective. It should be administered to gilts and boars during acclimatization before introduction into a herd.