Lawsonia Intracellularis Infections in Foals on the Rise

Lawsonia intracellularis is an obligate intracellular gram-negative bacterium causing equine proliferative enteropathy (EPE) in mostly young horses. It causes proliferation of the affected enterocytes, resulting in thickening segments of small intestines, sometimes large intestines as well (Lawson and Gebhart, 2000). L. intracellularis does not grow in routine aerobic/anaerobic culture and can only be grown in vitro in cell culture

which is not practical. Therefore several quick and reliable PCR tests have been developed for direct detection of bacteria. Besides horses, L. intracellularis infects pigs and many other domestic and wild animals, including hamsters, rabbits, foxes, deer, ferrets, ostriches, and non-human primates. Previous studies have shown that a variety of wild and domestic animals, including dogs, cats, rabbits, opossums, skunks, mice and coyote, shed L. intracellularis on farms with diagnosed EPE cases. Fecal-oral transmission of L. intracellularis has been documented in naïve foals housed with clinically infected foals experimentally challenged with an equine isolate of L. intracellularis (Pusterla et al 2010).

Clinical signs include depression, anorexia, fever, peripheral edema, hypoproteinemia, hypoalbuminemia, weight loss, colic and diarrhea in affected foals. Early clinical signs are generally unspecific and include mild depression, partial anorexia and fever. Signs of EPE may resemble those of other gastrointestinal disorders such as parasitism, bacterial infections (Clostridium spp., Salmonella spp., Neorickettsia risticii), rotavirus, coronavirus, ulcerations, sand accumulation, intestinal obstruction and intoxication with plants, chemicals and pharmacologic agents such as nonsteroidal anti-inflammatory drugs or antimicrobials (Pusterla and Gebhart, 2013). Therefore other diseases should be ruled out with diagnostic tests.

A presumptive diagnosis of EPE generally is made based on age of the affected animal, hypoproteinemia/hypoalbuminemia, fever and presence of thickened small intestinal loops on ultrasonographic evaluation. Laboratory diagnosis is through PCR detection of L. intracellularis in feces or rectal swab. Samples should be obtained before the antimicrobial treatment. Post mortem diagnosis is by PCR combined with thickening of the mucosa of the ileum and cecum grossly and compatible histopathologic lesions (adenomatous proliferation, curved bacteria in enterocytes et al).

EPE in horses are treated by macrolides (such as erythromycin) alone or in combination with rifampin, chloramphenicol, oxytetracycline, doxycycline or minocycline administered for 2–3 weeks. (Page et al, 2012; Pusterla and Gebhart, 2013). Separating horses showing clinical symptoms from the rest of the animals until full recovery or cessation of fecal shedding is a good practice to prevent spread and environmental contamination. Shedding can be monitored by PCR. The monitoring of a herd with endemic EPE status includes the regular physical evaluation of foals and regular assessment of total protein concentrations. Suspected animals in high risk areas can be monitored with a PCR test as well. Maintaining good pest control and preventing non-equine domestic and wild animals access to feed and feeding areas can minimize the risk of disease spread. An attenuated L. intracellularis vaccine has been shown to be safe and the administration well tolerated by the foals (Nogradi et al., 2012). However, no vaccine is labeled for use in horses. The extra-label use of the L. intracellularis vaccine is sometimes used on naïve and endemic farms in an attempt to reduce or prevent EPE (Pusterla and Gebhart, 2013).

Figure 1 below depicts the total number of cases submitted to UKVDL between 2010 and 2013. We are seeing an increasing trend of positive cases submitted this year as compared to recent years. This may be explained by a higher number of ante-mortem cases being submitted for diagnosis.

Figure 1. Positive PCR Equine Lawsonia Cases – 2010-2013

Please read the article by Pusterla and Gebhard at this link: http://ac.els-cdn.com/S0378113513003313/1-s2.0-S0378113513003313-main.pdf?_tid=42dea2c8-7c6c-11e3-af00-00000aab0f02&acdnat=1389629201_b5f98bd3b6d159f500c41a5c0d7e8560

Dr. Erdal Erol
Head, Diagnostic Microbiology, UKVDL
Dr. Jackie Smith
Head, Epidemiology, UKVDL
CRAIG N. CARTER, DVM PhD Dipl. ACVPM
Director & Professor, Epidemiology