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Compendium April 2012 (Vol 34, No 4)

Clinical Snapshot: Lethargy, Fever, and Anorexia in a Thoroughbred Weanling

by Allen Page, DVM

    Case Presentation

    A 5-month-old Thoroughbred weanling filly presented in November with lethargy, fever, and partial anorexia. On physical examination, the filly was quiet and had a fever of 103.7°F (39.8°C), slightly decreased skin turgor, and dark pink mucous membranes with a capillary refill time of 2 to 3 seconds. The filly also had edema below the mandible, in the distal limbs, and in the ventral abdomen. A complete blood count revealed changes indicative of a stress leukogram, including a neutrophilia and lymphopenia. The fibrinogen level was within normal limits. Abnormalities on a chemistry panel included low concentrations of potassium (2.4 mEq/L; normal: 2.5 to 5.0 mEq/L), total protein (4.9 g/dL; normal: 6.0 to 7.9 g/dL), albumin (2.0 g/dL; normal: 3.4 to 4.1 g/dL), and calcium (10.0 mg/dL; normal: 11.6 to 13.2 mg/dL). Abdominal ultrasonography revealed several sections of thickened (6 mm; normal: <3 mm) small intestine wall (FIGURE 1).

    small intestine wall

    Figure 1. Thickened small intestine wall (6 mm; between the arrows).

    1. What is the top diagnostic differential?

    2. What confirmatory tests should be performed?

    3. What are the treatment options?

    Answers and Explanations

    1. Equine proliferative enteropathy (EPE) is the top diagnostic differential. Lawsonia intracellularis—a gram-negative, obligate intracellular, rod-shaped bacterium—causes this disease. L. intracellularis is an emerging pathogen of increasing significance to the equine industry, as yearlings previously hospitalized with EPE sell for an average of 68% less than unaffected yearlings by the same sire.1 The most common clinical signs in affected weanlings include dependent edema of the throat latch and ventral regions, depression, fever, anorexia, and weight loss, with diarrhea and colic noted less frequently. Affected foals often present between August and January, with the highest number of cases seen in November and December,1 although geographic variation is likely. Typical clinical pathologic findings include decreased plasma concentrations of total protein and albumin. Ultrasonographic changes, although inconsistent, include small intestine wall thickening (>3 mm) and small and large intestine wall edema secondary to hypoproteinemia. Other differentials for the clinical signs noted include salmonellosis, colitis, and the presence of intestinal parasites.

    2. Two commercial tests—the fecal polymerase chain reaction (PCR) test and the serum immunoperoxidase monolayer assay—are commonly used for antemortem diagnosis of proliferative enteropathy. In pigs, serologic testing is reported to be more sensitive than fecal PCR testing,2 but both methods have high specificity; similar data are not available for horses, but the same pattern is likely.3 When proliferative enteropathy is suspected in weanling foals, samples should be submitted for both tests1 to increase the likelihood of confirming the presence of L. intracellularis. When feces will be submitted for PCR testing, the sample should be obtained before an antimicrobial regimen is initiated, as treatment appears to reduce the sensitivity of PCR testing for detecting the organism.4

    3. The treatment goals are to eliminate the bacterial infection and provide supportive care. Because L. intracellularis is intracellular, choosing an appropriate antimicrobial is imperative. Typically, either a tetracycline (oxytetracycline [6.6 mg/kg IV bid diluted in 1 L of saline] or doxycycline [10 mg/kg PO bid]) or chloramphenicol (50 mg/kg PO tid) is used, sometimes for as long as 2 to 3 weeks. Because of potential adverse renal effects, care should be taken when administering tetracycline-class antimicrobials to hypovolemic horses; it is typically recommended that renal parameters be monitored closely in these patients. In addition to tetracyclines, macrolides with or without rifampin have been used to treat EPE.5,6

    Supportive care is often targeted toward oncotic support because clinically affected foals typically have hypoproteinemia. Options include intravenous (IV) administration of synthetic colloids or equine plasma at doses of 5 to 10 mL/kg. Other treatments include IV crystalloid fluids, IV NSAIDs, and oral gastroprotectants. Weanlings with severe anorexia may require partial or total parenteral nutrition in a hospital setting.

    The prognosis for recovery is typically good following proper diagnosis of EPE, although a small subset of affected weanlings succumb to the disease despite appropriate treatment. Weanlings with very low total protein and albumin levels may require multiple doses of synthetic colloids and/or plasma, and affected weanlings often take several months to regain the stature and appearance of their unaffected herd mates. Relapses of EPE have not been reported to date, and research in pigs has shown that previous infection protects against future disease.7

    The filly reported here was treated with one dose each of equine plasma and a synthetic colloid in addition to IV oxytetracycline, IV crystalloids, IV NSAIDs, and oral gastroprotectants. After this initial treatment over 5 days, the filly was discharged to the farm, where oral doxycycline was administered for an additional week. The farm reported that the filly remained smaller than her herd mates for 4 months after treatment but then began to appear like a typical Thoroughbred yearling.

    1. Frazer ML. Lawsonia intracellularis infection in horses: 2005–2007. J Vet Intern Med 2008;22:1243-1248.

    2. Guedes RM, Gebhart CJ, Winkelman NL, et al. Comparison of different methods for diagnosis of porcine proliferative enteropathy. Can J Vet Res 2002;66:99-107.

    3. Page AE, Loynachan AT, Bryant U, et al. Characterization of the interferon gamma response to Lawsonia intracellularis using an equine proliferative enteropathy challenge (EPE) model. Vet Immunol Immunopathol 2011;143:55-65.

    4. Dauvillier J, Picandet V, Harel J, et al. Diagnostic and epidemiological features of Lawsonia intracellularis enteropathy in 2 foals. Can Vet J 2006;47:689-691.

    5. Lavoie JP, Drolet R, Parsons D, et al. Equine proliferative enteropathy: a cause of weight loss, colic, diarrhoea and hypoproteinaemia in foals on three breeding farms in Canada. Equine Vet J 2000;32:418-425.

    6. Schumacher J, Rolsma M, Brock KV, et al. Surgical and medical treatment of an Arabian filly with proliferative enteropathy caused by Lawsonia intracellularis. J Vet Intern Med 2000;14:630-632.

    7. Collins AM, Love RJ. Re-challenge of pigs following recovery from proliferative enteropathy. Vet Microbiol 2007;120:381-386.

    References »

    NEXT: Editorial: An Invitation to “Excellence”


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