Proliferative Enteropathy in Horses

Lawsonia intracellularis, a well-known pathogen of swine and hamsters, is now frequently recognized within the equine species. It is an obligate, intracellular, curved, gram-negative bacterium that resides freely within the apical

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Lawsonia intracellularis, a well-known pathogen of swine and hamsters, is now frequently recognized within the equine species. It is an obligate, intracellular, curved, gram-negative bacterium that resides freely within the apical cytoplasm of infected intestinal enterocytes, resulting in a proliferative enteropathy. L. intracellularis has been reported to infect several species, including the pig, hamster, rabbit, non-human primate, dog, guinea pig, rat, mouse, fox, white-tailed deer, ferret, and selected birds.


L. intracellularis most commonly causes proliferative enteropathy (which means a spreading disease involving the intestines) in foals three to seven months of age, with a higher incidence in those recently weaned. Older horses also can be affected. A wide range of clinical signs can be associated with the disease, including diarrhea, dehydration, lethargy, colic, progressive weight loss, rough hair coat, poor body condition, and pendulous abdomen (potbelly appearance). Clinical abnormalities encountered with proliferative enteropathy include hypoproteinemia, hypoalbunemia, increased serum creatine kinase, anemia, and transient leukocytosis.


Gross lesions caused by L. intracellularis usually involve the distal jejunum, ileum, and proximal colon, although any portion of the intestinal tract can be affected. Pathologic lesions range from multifocal to confluent regions of mucosal hyperplasia. These hyperplastic mucosal regions can form circumferential areas as well as coalescing prominent folds or rugae (corrugated appearance). The affected mucosal surface might demonstrate variable degrees of erosion and/or ulceration. Ulcerated lesions can often lead to intestinal perforation and peritonitis.


Microscopic lesions observed in horses with proliferative enteropathy include epithelial hyperplasia of crypt glands, with increased numbers of mitotic figures and decreased numbers of goblet cells. Variable numbers of small and curved bacteria are located within the apical cytoplasm of hyperplastic enterocytes and are readily discernible when silver stains (Warthinstarry and Steiner’s) are applied to affected tissues. Minimal to no inflammation involving mononuclear cells is associated with proliferative enteropathy unless concurrent ulceration is present

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