Comparison of the Severity of Myocardial Damage with the Quantitative Estimation of the Myocardial Parasitic Load by Real-Time PCR in Dogs with Canine Visceral Leishmaniosis
27th ECVIM-CA Congress, 2017
J. Duque1; D. Casamian-Sorrosal2; S. Belinchón-Lorenzo1; J. Salado-Tato1; L. Gómez-Gordo1; J.J. Real-Ríos1; L. Martínez-Hernández1; R. Barrera-Chacón1
1Veterinary Teaching Hospital, Cáceres, Spain; 2Dick White Referrals, UK

It has been previously shown that canine leishmaniasis (CanL) causes severe myocardial damage which leads to elevation of troponin I (cTnI). It has also been previously shown that this myocardial damage is likely to be primarily associated with the severity of the protozoal disease and not with the degree of azotaemia, anaemia or systemic arterial hypertension. It remains to be determined, however, whether this myocardial damage is directly correlated with the cardiac parasitic load or the damage is primarily indirect through other mechanisms such as systemic inflammation.

The aim of this study was to evaluate and compare the concentration of cTnI, histopathology severity and plasma creatinine concentration (Cr) with the parasitic load within cardiac tissue samples in a cohort of dogs with CanL.

Ethical approval was granted by the University of Extremadura committee. Five dogs without previous history of cardiac disease and severe CanL and renal azotaemia (Stage IV, LeishVet scheme) were included in the study. All dogs underwent full physical examination, haematology, biochemistry, and urinalysis including protein-creatinine ratio, ELISA serology for L. infantum, cTnI measurement, blood pressure, abdominal ultrasound, electrocardiography, thoracic radiographs and echocardiographic examination. All dogs were euthanased due to the severity of the disease and underwent postmortem examination. Myocardial samples were taken for histopathology and were tested for L. infantum by real-time PCR (RT-PCR) by detection and quantification of Kinetoplast minicircle DNA.

Elevation of cTnI (dog 1: 0.36 ng/ml; dog 2: 0,59 ng/ml; dog 3: 4.56 ng/ml; dog 4: 7.69 ng/ml; dog 5: 9.23 ng/ml; median 4.56 ng/ml; IQR 0.59–7.56 ng/ml; normal <0.06 ng/ml) and Cr (dog 1: 2.7 mg/dL; dog 2: 4.3 mg/dL; dog 3: 15.5 mg/dL; dog 4: 3.8 mg/dL; dog 5: 7 mg/dL; median 4.3 mg/dl; IQR 3.8–7 mg/dl; normal 0.7–1.2 mg/dL) was detected in all dogs. Severe lymphoplasmacytic myocarditis was observed in all myocardial samples. L. infantum DNA was detected in the myocardial tissue of all five dogs and RT-PCR assay was performed in the samples to estimate the parasite load (dog 1: 20,72 parasites/mg; dog 2: 25.57 parasites/mg; dog 3: 146.19 parasites/mg; dog 4: 284.88 parasites/mg; dog 5: 290 parasites/mg; median 146.19 parasites/mg; IQR 25.57–258.88 parasites/mg). A positive strong correlation was observed between cTnI and the parasitic load (p<0.001), but no correlation (p>0.05) was observed between cTnI and Cr concentrations.

The results of this study show for first time an association between the severity of myocardial damage in canine leishmaniasis and the severity of myocardial parasitic load.

Disclosures

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Speaker Information
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J. Duque
Veterinary Teaching Hospital
Cáceres, Spain


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