Abstract

Dogs are the main reservoir of Leishmania infantum in endemic regions. Canine leishmaniasis, caused by L. infantum, can progress to a chronic disease resulting in death. Vaccines have been developed with a certain degree of success. The pathogenesis of this disease is not completely understood, especially in previously vaccinated dogs. We herein described clinical data, parasite load, serum levels of cytokines, and the reservoir potential in vdogs vaccinated with the fucose-mannose ligand (FML)/QuilA saponin vaccine (Leishmune™) naturally infected (Vi) and compared to vaccinated not infected dogs (Vn). Thirty-four dogs from private owners were divided into two groups: vaccinated/infected and vaccinated/uninfected. Clinical evaluation, hematological and biochemical parameters, and serum levels of cytokines were measured by conventional methods. The parasite burden in the bone marrow was measured by quantitative real-time PCR, and the transmissibility of parasites to sand flies was assessed by xenodiagnosis. Clinical, biochemical, and hematological parameters of vaccinated infected dogs were mostly normal. Vi dogs developed mild disease with low clinical scores. Serum levels of IL-10 were higher in Vi dogs, and a strong correlation was observed in IL-4 levels and the A/G ratio in Vi dogs. These results suggest a role of TH2 response in Vi dogs, although more data is needed to better understand the disease in vaccinated dogs.

Highlights

  • Zoonotic visceral leishmaniasis (VL) is a disease caused by the protozoa Leishmania infantum and is transmitted to mammalian hosts by the bites of female sand flies

  • All dogs were tested by different methods to determine the evidence of infection with L. infantum parasites

  • Bone marrow cytology was not performed in three dogs from the vaccinated infected (Vi) group due to rapid coagulation of the sample during collection, and xenodiagnosis was not performed in one dog

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Summary

Introduction

Zoonotic visceral leishmaniasis (VL) is a disease caused by the protozoa Leishmania infantum and is transmitted to mammalian hosts by the bites of female sand flies. While blood feeding on a vertebrate host, females ingest amastigote-infected macrophages in the tissue. Once in the insect gut, amastigotes develop into promastigotes and, a few days later, into the infective forms known as metacyclic promastigotes. During their blood meal, the female sand flies regurgitate the metacyclic promastigotes into the host’s skin, completing the cycle of the transmission [4, 5]. The parasites replicate inside macrophages and are disseminated throughout the body, infecting various tissues including the liver, spleen, and bone marrow [6]

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