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 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.

Few diagnostic techniques are available to diagnose proliferative enteropathy. Ultrasonographic evaluations of the intestinal tract might reveal segmental to diffuse thickening of intestinal loops, depending on the severity and stage of the disease process. Additional antemortem diagnostic procedures include serology via ELISA and immunoperoxidase monolayer antigen assay, immunohistochemistry and polymerase chain reaction (PCR) testing of fecal smears, mucosal scraping, and/or biopsies. Postmortem diagnostics include close gross evaluation of the entire intestinal tract during necropsy, silver staining of intestinal segments examined histologically, and PCR testing on mucosal scrapings of affected/diseased intestinal segments. PCR testing of mucosal scrapings is considered the most sensitive and specific of all aforementioned diagnostic procedures. L. intracellularis cannot be cultured using conventional media, although it can be cultured on cell cultures under microaerophilic conditions.

The incidence of young equids acquiring an infection with L. intracellularis has increased over the past five years within Central Kentucky. A total of 354 samples were submitted to the University of Kentucky Livestock Disease Diagnostic Center for PCR testing for Lawsonia between December of 2000 and June of 2006. Samples were received from several counties throughout Kentucky. Seventy-four of the 354 submitted samples had positive PCR results (21%). These positive PCR results were obtained from horses residing on 157 farms within six Kentucky counties. Twenty-six out of the 74 positive PCR results were accompanied by necropsy specimens that demonstrated characteristic histologic lesions suggestive of an infection with Lawsonia.

The preferred location for L. intracellularis is within the apical cytoplasm of enterocytes. Using antimicrobials that have the ability to penetrate cellular membranes is strongly recommended. Reports concerning Lawsonia infections in horses consider an Erythromycin-Rifampin combination to be the preferred and most effective treatment regimen. Additional antimicrobials reported efficacious for treatment include chlortetracycline, penicillin, enrofloxacin, chloramphenicol, and ampicillin.

The epidemiology and exact pathophysiologic mechanisms of this disease in horses remains unclear and is the subject of ongoing research efforts.

For more information contact Dr. Uneeda K. Bryant, 859/253-0571,, at the Livestock Disease Diagnostic Center, University of Kentucky.

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Equine Disease Quarterly

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