Female weaner pigThis pig is from a group of weanling pigs purchased by an FFA group. All had loose stools and fair body condition. Swine dysentery was suspected.

Gross Description:  

On gross necropsy, the submitting veterinarian noted swollen mesenteric lymph nodes and liquid gut contents; small and large intestines were purple. 

Histopathologic Description:

In a section of ileum there is a diffuse, proliferative and necrotizing inflammatory lesion. Intestinal glands are long and lined by tall, amphophilic cells with a high mitotic rate. Goblet cells are decreased in number. Peyer's patch lymphoid follicles are necrotic and proliferative glands are herniated into those spaces. Histiocytes replace follicular centers and surround necrotic foci. Glands in these and other areas are often dilated and filled with necrotic debris. The lamina propria is mildly expanded by lymphocytes and plasma cells.

Steiner's silver technique shows numerous short, curved rods within the apical portions of glandular epithelial cells.

Morphologic Diagnosis:  

Proliferative ileitis (porcine proliferative enteropathy)

Lab Results:  

Dark field examination of colonic scrapings were negative for spirochetes. Moderate numbers of Campylobacter coli were isolated from the intestines. PCR for Lawsonia intracellularis was not performed in this case.


Lawsonia intracellulare

Contributor Comment:  

Porcine proliferative enteropathy (PE) is a collection of syndromes all caused by infection by the obligate intracellular organism Lawsonia intracellularis1. The organism is prevalent in swine worldwide and is shed by infected pigs for weeks. Clinical disease is seen most commonly in feeder pigs. Signs vary from mild, subclinical disease with decreased weight gain and unthriftiness to severe diarrhea, cachexia and death or to death from acute intestinal hemorrhage. Morbidity and mortality vary with the different syndromes.

As an obligate, intracellular pathogen, pathogenesis of L intracellularis related disease requires active uptake by intestinal epithelial cells. Localization of lesions to the ileum may be related to uptake of organisms by epithelium associated with Peyer's patches. Organism are initially taken up in membrane-bound vesicles and later released into the cytoplasm where they multiply. Cell division is required for bacterial proliferation. The mechanism by which L intracellularis stimulates proliferation and dedifferentiation of ileal epithelial cells are poorly understood. Studies have shown, however, that the organism suppresses the inflammatory response by decreasing both B cell and T cell numbers, while macrophage numbers increase 4. 

Gross lesions are characteristic of the various forms of the disease. Proliferative ileitis, also called intestinal adenomatosis, is characterized by ridge-like thickening of terminal portion of the ileum, occasionally extending cranially or caudally to involve the cecum and proximal spiral colon. The marked thickening can be observed from the serosal surface as accentuation of the normal reticular pattern of the ileum. Necrotic enteritis is characterized by coagulative necrosis of the adenomatous mucosa, likely the result of anaerobic bacterial proliferation. Chronic infection, ulceration and stricture may result in a lesion called regional ileitis, characterized by severe hypertrophy of the muscular layers of the ileum. Proliferative hemorrhagic enteropathy may occur when extensive necrosis and ulceration causes massive hemorrhage into the lumen of the ileum. Grossly, the typical adenomatosis lesion is overlain by clotted blood and fibrin. Animals affected by this form of the disease may die acutely from exanquination.

In all forms of the disease, the histologic features are similar. The characteristic morphology is that of marked hyperplasia of intestinal crypt epithelium with loss of goblet cells and minimal inflammation. Mitotic activity is high and glands become crowded, branched and dilated by accumulation of necrotic debris. Hyperplastic glands may protrude into the lymphoid follicles of the submucosa (a prominent feature in this case).

Differential diagnoses for diarrhea and weight loss in feeder pigs include swine dysentery and salmonellosis, both of which have distinct gross and histologic lesions centerd mainly on the cecum and colon. Porcine circovirus-2, the agent of postweaning multisystemic wasting disease PMWR), reportedly can cause similar histologic lesions in the absence of co-infection with L intracellularis2. That intestinal lesion is characterized by a necrotic, proliferative enteritis with marked replacement of Peyer's patches by histiocytes and multinucleate giant cells, which can also be a feature of PE. However, characterisitic botryoid cytoplasmic inclusions of PCV-2 infection should help differentiate the 2 diseases. No PCV-2 inclusions were seen in this case.

Although primarily a disease of pigs, L intracellularis can infect many species, most notably young horses, causing a similar proliferative enteropathy. The organism has also been investigated as an agent of inflammatory bowel disease in human beings 6.

JPC Diagnosis:  

Ileum: Ileitis, proliferative, diffuse, marked, with villar atrophy and fusion, lymphoid necrosis, crypt herniation and crypt abscesses, breed not specified, porcine.

Conference Comment:  

Lawsonia intracellularis has been identified as the causative agent of a proliferative enteropathy in a number of species. It primarily affects the ileum in horses, sheep, ostriches, guinea pigs, pigs, rabbits and hamsters; the cloaca in emus; and the colon in ferrets, foxes and rats. The numerous short curved rods can be visualized with a silver stain (e.g. Warthin-Starry) and are located in the apical portion of the intestinal epithelial cells.


1. Brown CC, Baker DC, Barker K: The Alimentary system IN Jubb, Kennedy and Palmer's Pathology of Domestic Animals, fifth edition, GM Maxie, ed. , Saunders, Edinburgh, 2007. Vol 2, pp 206-209.

2. Jensen TK, Vigre H, Svensmark B, Bille-Hansen V: Distinction between porcine circovirus type 2 enteritis and porcine proliferative enteropathy caused by Lawsonia intracellularis J Comp Path 135:176-182, 2006.

3. Lawson, GHK and Gebhart CJ: Proliferative enteropathy J. Comp. Pathol 122: 77- 100, 2000

4. MacIntyre N, Smith DGE, Shaw DJ, Thomson JR, Rhind SM: Immunopathogenesis of experimentally induced proliferative enteropathy in pigs. Vet Pathol 40:421-432, 2003

5. McOrist S, Gebhart CJ: Proliferative enteropathies. In: Diseases of Swine, eds. Straw BE, Zimmerman JJ, DAllaire S, Taylor DJ pp. 727-737. Blackwell Publishing, Ames, IA, 2006

6. Mickalski CW, Francesco Di Mola F, Kummel K, Wendt M, Koniger JS, Giese T, Giese NA, Friess H: Human inflammatory bowel disease does not associate with Lawsonia intracellularis infection. BMC Microbiology 6:81-88, 2006

7. Straw BE, Dewey CE, Wilson MR: Differential diagnosis of disease. In: Diseases of Swine, eds. Straw BE, Zimmerman JJ, DAllaire S, Taylor DJ pp. 727-737. Blackwell Publishing, Ames, IA, 2006

A virtual slide is not available for this case.

Ileum, pig

Back | VP Home | Contact Us |