Diagnostic Features of Acute Chagas Myocarditis with Sudden Death in a Family of Boxer Dogs

A 10-week old, intact male, Boxer puppy was referred to the Texas A&M University Veterinary Medical Teaching Hospital (TAMU-VMTH) for emergency evaluation of ascites secondary to right-sided heart failure approximately 2 weeks after the owners purchased the dog from a breeder in south Texas. Clinical signs began 2 days before presentation, and included lethargy, acute inappetence, diarrhea, and vomiting that was nonresponsive to antiemetic therapy. At that time, the dog tested negative for parvovirus antigen. Abdominal and thoracic ultrasound examinations were performed and hepatomegaly, abdominal effusion, and enlarged right atrium and ventricle were reported. The dog presumptively was diagnosed with tricuspid valve dysplasia and was referred for further evaluation. On presentation to the TAMU-VMTH, the dog had dull mentation and was mildly tachypneic with a respiratory rate of 48 breaths/min, tachycardic with a heart rate of 240 beats/min, and had weak femoral pulses. Body condition score was 5/9 with a mildly distended abdomen that was soft on palpation. Brief abdominal ultrasound examination confirmed the presence of ascites. Indirect blood pressure measurement identified systemic hypotension with a systolic pressure of 43 mmHg and mean and diastolic pressures could not be obtained. Laboratory abnormalities included marked hyponatremia (127 mEq/L; reference range, 147–153 mEq/L), hyperkalemia (6.53 mEq/L; reference range, 3.91–4.4 mEq/L), hyperlactatemia (6.0 mmol/L; reference range, <2.5 mmol/L), mild hypocalcemia (1.16 mmol/L; reference range, 1.23–1.35 mmol/L), and a disproportionally increased BUN concentration (71 mg/dL; reference range, 7–32 mg/dL) compared to serum creatinine concentration (1.8 mg/dL; reference range, 0.2–2.5 mg/dL). An ECG disclosed a wide complex tachycardia that was unresponsive to several IV bolus injections of lidocaine. A standard transthoracic 2-dimensional and Doppler echocardiographic study was performed with a phased-array 2.7–8.0 MHz transducer. The right atrium and ventricle were severely dilated (Fig 1A, C) and ventricular systolic function was decreased (Video S1). The tricuspid valve leaflets were normal in appearance with mild tricuspid valve regurgitation noted. Mild pleural effusion was noted. Shortly after presentation, the dog died suddenly and a complete necropsy was performed. On gross evaluation of the heart, the right atrium was enlarged and there was marked, diffuse myocardial pallor of both ventricles (Fig 2A). The tricuspid valve was structurally normal. Histology of the heart disclosed severe lymphoplasmacytic and histiocytic necrotizing pancarditis affecting the atria (Fig 3A) and ventricles (Fig 3C, E) with resultant cardiomyocyte degeneration and necrosis. Numerous cardiomyocytes had protozoal pseudocysts containing amastigotes (Fig 4A) with parallel kinetoplasts. Based on the presence of severe myocarditis and amastigotes, a preliminary diagnosis of Chagas disease was made. Additional relevant findings included acute centrilobular hepatocellular necrosis, pulmonary edema, and mild meningoencephalitis with a single macrophage containing intracytoplasmic amastigotes. The breeder was contacted and reported that the remaining 6 littermates and dam were alive and had not exhibited any abnormal clinical signs. Three of the puppies from the litter and the dam were evaluated for Chagas disease at the TAMU-VMTH the following week. All 4 dogs had normal physical examination findings and body condition scores, and the puppies all were similar in size. Each dog had an indirect fluorescent antibody (IFA) test for Trypanosoma cruzi, serum cardiac troponin I (cTnI) concentration using a From the Department of Small Animal Clinical Sciences, (Vitt, Saunders); the Department of Veterinary Pathobiology, (O’Brien, Mansell, Ajithdoss); and the Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX (Hamer). Dr. Ajithdoss is presently affiliated with the Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA. All work performed at Texas A&M University. Corresponding author: J.P. Vitt, Department of Small Animal Clinical Sciences, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, 4474 TAMU, College Station, TX 77843-4474; e-mail: jvitt@cvm.tamu.edu. Submitted December 1, 2015; Revised March 11, 2016; Accepted April 21, 2016. Copyright © 2016 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. DOI: 10.1111/jvim.13967 Abbreviations: