Acute deterioration and death with necrotizing enteritis associated with Lawsonia intracellularis in 4 weanling horses.

摘要

A n 8-month-old Thoroughbred colt was evaluated in October 2010 with a less than 1-day history of inappetence. Physical examination in the eld revealed throat latch edema, lethargy, and fever (103.8°F) (ref 99–101.5°F). A complete blood count revealed leukocytosis (18.0 × 10 3 /lL; ref 5.0–12.6 × 10 3 /lL) with a relative neutropenia (49%; ref 55–65%) and lymphopenia (26%; ref 35–45%), as well as a toxic left shift (25% bands; ref 0–5%). Serum biochemistry abnormalities included hypoproteinemia (3.3 g/dL; ref 6–7.9 g/dL), hypoalbuminemia (1.2 g/dL; ref 3.4–4.1 g/dL), and an increased BUN (45 mg/dL; ref 11–26 mg/dL), along with other abnormalities (Table S1). Lawsonia intracellularis-induced equine proliferative enteropathy (EPE) was suspected because of the combination of hypoproteinemia, hypoalbuminemia, inappetence, and the autumn presentation. Treatment consisted of intravenous oxytetracycline a (6.6 mg/kg IV q24hr), unixin meglumine b (1 mg/kg IV q12h), oral omeprazole c (1 mg/kg PO q24hr), dexamethasone d (0.1 mg/kg IV q24hr), intravenous crystalloid uids e (10 mL/kg IV bolus once), and intravenous colloids f (10 mL/kg IV bolus once). Despite treatment, the weanling was euthanized within 48 hours of presentation because of continued deterioration and signs of pulmonary disease characterized by nasal discharge, epistaxis, and tachypnea. Blood work submitted the morning of euthanasia revealed a worsening leukocytosis (35.4 9 10 3 /lL) with an unchanged dierential, as well as continued hypoproteinemia (3.5 g/dL), hypoalbuminemia (1.1 g/ dL), and an increased BUN (59 mg/dL).