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Abstract Background The protozoal parasite Trypanosoma cruzi causes myocarditis in dogs. Objectives To describe the cardiac diagnostic test results and outcomes of dogs naturally infected with T. cruzi. Animals Forty‐four client‐owned dogs. Methods Medical records were retrospectively reviewed to identify dogs with an indirect fluorescent antibody test result for T. cruzi ≥1 : 80. Data collected included signalment, cardiac diagnostic test results (ECG, echocardiography, cardiac troponin I) and outcome. Outcomes were categorized as alive, dead (cardiac or noncardiac) or lost to follow up. Results ECG abnormalities were present in 41 dogs with ventricular arrhythmias (n = 28) and atrioventricular block (AVB) (n = 15) most commonly identified. Echocardiographic chamber enlargement was present in 28 dogs and most often included the right ventricle (RV) (n = 15) and left atrium (n = 12). Troponin was ≥2 times the reference range in 20/36 (56%) dogs. In univariate analysis using nonparametric Kaplan‐Meier, ventricular arrhythmias with a modified Lown score ≥2 (P = .02), presence of AVB (P = .04), and RV enlargement (P = .006) were associated with decreased survival times. Right ventricular enlargement (HR 3.6; 95% confidence interval [CI] 1.4‐9.3; P = .007) and higher body weight at presentation (HR 1.0; 95% CI 1.0‐1.1; P = .04) were associated with decreased time to death in the final explanatory multivariable model. Conclusions and Clinical Importance Cardiac abnormalities were common and variable, and RV enlargement was associated with shorter survival time. A diagnostic evaluation that includes screening for arrhythmias, echocardiography, and cTnI can provide useful information related to the characterization of heart disease in dogs seropositive for T. cruzi.

Abstract Background Chagas disease is increasingly recognized in the southern U.S., where triatomine vectors transmit Trypanosoma cruzi among wildlife and domestic dogs with occasional vector spillover to humans. As in humans, clinical outcome in dogs is variable, ranging from acute death to asymptomatic infections or chronic heart disease. In order to characterize cardiac manifestations of T. cruzi infections, we tracked a cohort of naturally-infected dogs and a matched cohort of uninfected dogs. We hypothesized that selected measures of cardiac disease (abnormal rate, abnormal rhythm, and elevated cardiac troponin I (cTnI; a biomarker of cardiac injury)) would occur more commonly in infected than uninfected dogs matched by age, breed, sex and location. In addition to the clearly positive and negative dogs, we specifically tracked dogs with discordant test results across three independent serological assays to gather clinical data that might elucidate the infection status of these animals and inform the utility of the different testing approaches. Results We placed an ambulatory ECG monitor (Holter) on 48 government working dogs and analyzed 39 successful recordings that met length and quality criteria from 17 T. cruzi-infected, 18 uninfected dogs and 4 dogs with discordant results. Overall, 76.5% of positive, 100.0% of discordant, and 11.1% of negative dogs showed > 1 ECG abnormality (p

Abstract Background Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, causes sudden death and chronic heart disease with no currently approved treatment. Objective To report epidemiologic and select cardiac characteristics associated with T. cruzi infection in dogs presenting to a teaching hospital in Texas. Animals Three hundred seventy‐five client‐owned dogs. Methods A retrospective search of medical records identified dogs tested for T. cruzi antibodies or with histologic T. cruzi parasites. Data retrieved included signalment, location of residence, reported reason for testing, cardiac troponin I (cTnI) concentration, and ECG abnormalities. Results Trypanosoma cruzi‐infected dogs (N = 63, 16.8%) were significantly younger than negative dogs (N = 312) (mean, 5.9 ± 3.8 versus 7.4 ± 4.0 years; P = .007) with no difference by sex or breed. Ninety‐one breeds were tested; the highest percent infected were non‐sporting (10/35; 29%) and toy breed (10/42; 24%) groups. The odds of infection were 13 times greater among dogs with an infected housemate or littermate (95% confidence interval [CI], 3.94‐50.45; P < .001). Infected dogs were more likely to have ventricular arrhythmias (odds ratio [OR], 2.19; 95% CI, 1.15‐4.33, P = .02), combinations of ECG abnormalities (OR, 2.91; 95% CI, 1.37‐5.99; P = .004), and cTnI >0.129 ng/mL (ADVIA; OR, 10.71; 95% CI, 1.60‐212.21; P = .035). Conclusions and Clinical Importance Dogs infected with T. cruzi were identified in Texas in many breed groups including breeds affected by well‐described heart diseases that mimic Chagas disease suggesting a need for increased awareness, including knowledge of when to consider testing.

Abstract Trypanosoma cruzi infection in dogs can cause heart failure and sudden death with few treatment options available. A litter of 4 dogs living in a T cruzi endemic area were randomized to prophylaxis and nonprophylaxis groups as part of a study evaluating a modified benznidazole dosing regimen administered twice weekly to prevent T cruzi infection during a vector transmission season. The 2 dogs that received prophylaxis remained healthy without T cruzi infection or cardiac disease for >2 years. One dog that did not receive prophylaxis died unexpectedly with acute T cruzi–induced pancarditis, and the second dog tested positive for T cruzi and developed complex arrhythmias with markedly increased cardiac troponin I and improved with a higher benznidazole treatment dose. Although the small sample size precludes definitive conclusions, we describe the potential clinical benefit of prophylactic and early treatment with modified benznidazole dosing regimens for dogs with T cruzi infection.