Reversible myocardial injury aggravated by complex arrhythmias in three <i>Toxoplasma gondii</i>-positive dogs

Abstract

Although Toxoplasma gondii represents an oft-cited cause of myocarditis in veterinary medicine, the existing literature on the pre-mortem demonstration of T. gondiiassociated 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.

Transient myocardial thickening associated with acute myocardial injury and congestive heart failure in two Toxoplasma gondii-positive cats

“…In the cats in this paper cats, the hypothesis of TMT eventually due to TM was based on: (1) the clinical presentation characterised by LVMT with CHF and elevated cTnI; (2) an aetiological diagnosis (ie, all cats had IgM titres ⩾1:64) 22 indicating ongoing toxoplasmosis; (3) the lack of other obvious causes of such a cardiac compromise; (4) a favourable disease course characterised by resolution of clinical signs, cTnI normalisation with concomitant decline of T gondii serology titres, cardiac reverse remodelling and a good long-term follow-up without cardiovascular medications; and (5) the fact that the aforementioned results were achieved only after antiprotozoal therapy administration. A similar diagnostic approach has been described for clinical diagnosis of human, 24,25 canine 26 and feline TM, 13 as well as for the diagnosis of feline TMT. 1 In TM, myocardial compromise is predominantly the result of tachyzoite replication within cardiomyocytes.…”