Although Toxoplasma gondii represents an oft-cited cause of myocarditis in veterinary medicine, the existing literature on the pre-mortem demonstration of T. gondii-associated myocardial injury (MI) in dogs is scant. In this case series, we provide detailed clinical, laboratory, echocardiographic and electrocardiographic description of three T. gondii-positive dogs diagnosed with MI. In all cases, etiological diagnosis was based on the antibody screening test (all dogs had IgM titres ≥1:64) and MI was demonstrated by a concomitant increase of the serum concentration of cardiac troponin I (0.25-9.6 ng/ml, upper hospital limit <0.15 ng/ml). In all dogs, MI was aggravated by complex arrhythmias (ventricular in t... More
Although Toxoplasma gondii represents an oft-cited cause of myocarditis in veterinary medicine, the existing literature on the pre-mortem demonstration of T. gondii-associated myocardial injury (MI) in dogs is scant. In this case series, we provide detailed clinical, laboratory, echocardiographic and electrocardiographic description of three T. gondii-positive dogs diagnosed with MI. In all cases, etiological diagnosis was based on the antibody screening test (all dogs had IgM titres ≥1:64) and MI was demonstrated by a concomitant increase of the serum concentration of cardiac troponin I (0.25-9.6 ng/ml, upper hospital limit <0.15 ng/ml). In all dogs, MI was aggravated by complex arrhythmias (ventricular in two dogs, and either ventricular and supraventricular in the remaining dog). In one case, left ventricular systolic dysfunction was also present. All dogs underwent an extensive diagnostic work-up aimed at excluding additional comorbidities, either cardiac and extra-cardiac, possibly able to contribute to MI, arrhythmias and systolic dysfunction. All dogs received appropriate antiprotozoal (i.e., clindamycin) and antiarrhythmic (i.e., amiodarone, sotalol) therapy. This was systematically followed by a simultaneous decline in T. gondii serology titres, normalisation of troponin level and left ventricular systolic function, and the resolution of clinical and electrocardiographic abnormalities. In light of this result, therapies were interrupted and subsequent controls ruled out any disease relapse. In these cases, the clinical and instrumental findings obtained at admission and rechecks strongly supported the clinical suspicion of toxoplasmic myocarditis.
