Equine proliferative enteropathy (EPE) is an emerging intestinal disease primarily of recently weaned foals. Lawsonia intracellularis, the causative bacterium of EPE, is capable of inducing similar disease in many animal species, most notably swine. According to Dr. Alan Lynacham of the Livestock Disease Diagnostic Center at the University of Kentucky, comparatively little research has been undertaken into the disease in horses.
The emergence of EPE over the last 15 years has been puzzling. Transmission between horses occurs by the fecal-oral route through environmental contamination of feed and water.
Links have been proposed between the transmission of L. intracellularis from other domestic animals and wildlife to horses. Weaning, transportation, overcrowding, decreased colostral antibodies, dietary changes, and concurrent disease have been identified as predisposing factors associated with infection.
Development of the disease is usually sporadic; however, infection can become endemic on farms, and outbreaks have been described. The prevalence of L. intracellularis infection in the equine population is thought to be high, based on serologic and fecal polymerase chain reaction (PCR) data, but the incidence of disease is considered low.
EPE can be difficult to diagnose clinically due to vague signs and lack of definitive diagnostic assays. Affected horses may develop one or more of the following signs: ventral edema, depression, fever, weight loss, colic, and diarrhea.
Hypoproteinemia (low blood protein levels) remains the only consistent clinicopathologic finding. A presumptive diagnosis of EPE should be based on the combination of clinical signs, the presence of hypoproteinemia, ultrasonographic evidence of a thickened small intestine, detection of Lawsonia-specific serum antibodies, and the detection of the organism in the feces by PCR.
Neither serology nor PCR alone should be solely relied upon for diagnosis, because these tests cannot identify and differentiate subclinical infection from EPE. A definitive diagnosis of EPE can only be made by examination of biopsy or necropsy samples for characteristic lesions and identification of the organism within the lesion by silver stains, immunohistochemistry, or PCR . Infections can be efficiently resolved with antimicrobial agents.
Once L. intracellularis is ingested by a susceptible animal, the bacterium makes its way to the small intestine, where it enters the undifferentiated small intestinal crypt epithelium. Here the organism replicates unchecked and alters the cell cycle of the infected cells.
Infected cells remain immature and rapidly proliferate, which eventually results in a thickened and inefficient small intestinal mucosa that allows for increased protein and fluid loss with resultant clinical signs.
Retrospective studies have been performed to evaluate the long-term outcome for horses previously infected with L. intracellularis. Results indicate that previously infected yearlings sell for significantly less money but do not suffer from long-term health effects. Interestingly, lifetime earnings are not significantly different in comparison to uninfected horses.
At the University of Kentucky, 38 L. intracellularis- infected horses were identified at necropsy from 2004 to 2008. Infection was identified in the Thoroughbred, Standardbred, Quarter horse, American Miniature, and Mountain Pleasure breeds. Ages of infected horses ranged from 5 months to 18 years, but the majority of cases were identified in horses less than 1 year old.
Necropsy findings commonly included a thin body condition, edema, and proliferative microscopic lesions in the small intestine. Not all of the identified horses developed clinical signs or EPE lesions, which suggests that some horses were subclinically infected.