Pancarditis as the sole clinical manifestation of protothecosis in a Boxer dog.

A 4.2-year-old, male castrated Boxer was diagnosed with a dilated cardiomyopathy phenotype, complex arrhythmias and left-sided congestive heart failure, but died suddenly shortly after initial diagnostics were complete. Ultrasensitive cardiac troponin I was markedly elevated (9.345 ng/mL [reference range: 0-0.06 ng/mL]), and a Trypanosoma cruzi immunofluorescent antibody titer was positive at 1:80. Necropsy revealed a severe, necrotizing, histiocytic, lymphoplasmacytic pancarditis with intralesional algae consistent with protothecosis, as well as evidence of left-sided congestive heart failure. Algal organisms were found only in the heart. Acute Chagas disease was not thought to play a role given the lack of T. cruzi amastigotes on postmortem and negative reverse transcription polymerase chain reaction testing on formalin fixed, paraffin embedded myocardium, however a possible contribution of chronic Chagas disease to the clinical picture could not be ruled out. Canine protothecosis is typically a disseminated disease. This case represents the first report of canine protothecosis limited solely to the heart.

Prediction of clinically important acquired cardiac disease without an echocardiogram in large breed dogs using a combination of clinical, radiographic and electrocardiographic variables.

INTRODUCTION: Large breed (LB) dogs develop dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD). Echocardiography is required for a definitive diagnosis but is not always available. Our objective was to assess the clinical utility of thoracic radiographs alone and in combination with physical examination and electrocardiography findings for the prediction of clinically important DCM or MMVD in LB dogs. ANIMALS: Four hundred fifty-five client-owned dogs ≥20 kg with concurrent thoracic radiographs and echocardiogram. MATERIALS AND METHODS: Medical records were reviewed and stored thoracic radiographs and echocardiographic images were measured to classify dogs as normal heart size (NHS), preclinical DCM, clinical DCM, preclinical MMVD (with cardiomegaly), clinical MMVD, or equivocal. Dogs with preclinical MMVD, without cardiomegaly, were classified as NHS. Vertebral heart size (VHS) and vertebral left atrial size (VLAS) were measured. Receiver operating characteristic curves and prediction models were derived. RESULTS: Prevalence of MMVD (39.3%) was higher than the prevalence of DCM (24.8%), though most MMVD dogs (67.0%) lacked cardiomegaly and were classified as NHS for analysis. The area under the curve for VHS to discriminate between NHS and clinical DCM/MMVD or preclinical DCM/MMVD was 0.861 and 0.712, respectively, while for VLAS, it was 0.891 and 0.722, respectively. Predictive models incorporating physical examination and electrocardiography findings in addition to VHS/VLAS increased area under the curve to 0.978 (NHS vs. clinical DCM/MMVD) and 0.829 (NHS vs. preclinical DCM/MMVD). CONCLUSIONS: Thoracic radiographs were useful for predicting clinically important DCM or MMVD in LB dogs, with improved discriminatory ability when physical examination abnormalities and arrhythmias were accounted for.