Clinical importance of neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio and systemic immune-inflammation index in dogs with leishmaniasis.

Leishmaniasis is a zoonotic disease caused by Leishmania spp., impacts multiple systems and organs. While hematological and biochemical profiles aren't definitive for diagnosis, recent studies have identified the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and systemic immune-inflammation index (SII) as predictors of morbidity and mortality in critically ill human and dog patients. This study examined 100 dogs diagnosed with leishmaniasis, categorized by the International Renal Interest Society (IRIS) stages 1-4. Additionally, the dogs were divided based on whether they survived less or more than one year (L1Y and G1Y). Control group consisted of 43 dogs. The NLR increased as the disease progressed (IRIS 1-4), presenting statistically significant differences (P<0.05) when compared to the control group (2,37±2,08) IRIS 3 and 4 (4,59±13,39 and 6,99±12,86, respectively), and G1Y and L1Y (3,60±4,02 and 4,87±5,82, respectively). Significant changes in SII were only evident in short-term survivors (L1Y 951,93±1402) and advanced renal disease cases (IRIS 4 stage 1073,68±1901,09). Conversely, PLR remained largely unchanged. In conclusion, these results suggest that the neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII) may serve as potential markers for assessing disease progression and prognosis in dogs diagnosed with leishmaniasis.

Comparison of myocardial damage among dogs at different stages of clinical leishmaniasis and dogs with idiopathic chronic kidney disease.

Canine leishmaniasis (CanL) is a systemic disease caused by the protozoan parasite Leishmania infantum. Myocarditis in CanL has been described previously in CanL by histopathological analysis of post-mortem specimens and by evaluation of cardiac troponin I (cTnI) levels. However, the degree of myocardial damage at different stages of CanL and the role that concurrent azotaemia plays in this myocardial injury are unknown. The aim of this study was to prospectively evaluate and compare the presence of myocardial injury in dogs at different stages of clinical CanL and in dogs with severe idiopathic chronic kidney disease (CKD) by measuring cTnI. Forty-eight dogs were included in the study, divided into four groups: (1) group A (10 healthy dogs); (2) group B (17 dogs with CanL without renal azotaemia, classified as mild to severe in the LeishVet scheme); (3) group C (11 dogs with CanL and renal azotaemia, classified as very severe in the LeishVet scheme); and (4) group D (10 dogs with idiopathic CKD). Dogs in group C had significantly higher cTnI than dogs in groups B and D, although cTnI was also elevated in these groups. Dogs in group A had normal cTnI values. Dogs in groups D and C had similar renal IRIS classification scorers. Severe lymphoplasmocytic myocarditis and a positive real time PCR of L. infantum DNA were observed in all dogs in group C. Dogs with very severe CanL exhibit more myocardial injury than dogs with milder CanL or dogs with idiopathic CKD.