Introduction: Canine visceral leishmaniasis (CVL) is a public health problem, and its prevalence is associated with the coexistence of vectors and reservoirs. CVL is a protozoonosis caused by Leishmania infantum that is endemic in the southeast region of Brazil. Thus, vector and canine reservoir control strategies are needed to reduce its burden. This study aimed to verify the CVL seroprevalence and epidemiology in a municipality in Southeast Brazil to initiate disease control strategies. Methods: A total of 833 dogs were subjected to Dual Path Platform (DPP) testing and enzyme-linked immunosorbent assays. For seropositive dogs, epidemiological aspects were investigated using a questionnaire and a global position system. The data were submitted to simple logistic regression, kernel estimation, and Bernoulli spatial scan statistical analysis. Results: The overall CVL-confirmed seroprevalence was 16.08%. The 28.93% in the DPP screening test was associated with dogs maintained in backyards with trees, shade, animal and/or bird feces, and contact with other dogs and cats, with sick dogs showing the highest chances of infection (odds ratio, 2.6; 95% confidence interval, 2.38-1.98), especially in residences with elderly people. A spatial analysis identified two hotspot regions and detected two clusters in the study area. Conclusions: Our results demonstrated that residences with elderly people and the presence of trees, shade, feces, and pet dogs and cats increased an individual's risk of developing CVL. The major regions where preventive strategies for leishmaniasis were to be initiated in the endemic area were identified in two clusters.
This study aimed to determine the amount of plasma nitric oxide in clinically stable dogs at different stages of chronic kidney disease (CKD). Five groups of dogs were studied, aged from 4 to 18, comprising of a control group composed of healthy animals (control n=17), group CKD stage 1 (DRC-1, n=12), group CKD stage 2 (CKD-2, n=10) group, CKD stages 3 (CRD-3, n=13) and Group CKD stage 4 (DRC-4, n=10). Dogs with CKD were clinically stable and received no treatment. Two blood samples were collected at 24 hours intervals (repeated measures) to obtain serum and plasma. The serum creatinine values were used to classify dogs as CG, CKD-1, CKD-2, CKD-3 and CKD-4, and were (1.02±0.02mg/dL), (1.07±0.04mg/dL), (1.81±0.03mg/dL), (3.40±0.15mg/dL) and (6.00±0.20mg/dL) respectively. The determination of nitric oxide (NO) was performed by dosing nitrate/nitrite indirectly, and used for measurement of nitrate according to the NO/ozone chemiluminescence. The data were submitted to ANOVA for nonparametric analysis(Kruskal-Wallis) (P<0.05). The concentration of plasmatic NO did not differ significantly among GC (10.81±0.51μM), CKD-1 (15.49±1.97μM) and CKD-2 (19.83±3.31μM) groups. The plasma concentration of CKD-3 (17.02±1.73μM) and CKD-4 (83.56±13.63μM) was significantly higher compared with healthy dogs. In conclusion, the NO plasma concentration can increase in dogs with CKD and become significantly higher in stage 3 and 4 dogs.
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