Clinical, hematological and biochemical alterations in hamster (Mesocricetus auratus) experimentally infected with Leishmania infantum through different routes of inoculation.

Nádia Das Dores Moreira,Jamille Mirelle De Oliveira Cardoso,Bruno Mendes Roatt,Henrique Gama Ker,Claudia Martins Carneiro,Wendel Coura-Vital,Juliana Vitoriano-Souza,Mariana Trevisan Rezende,Paula Melo De Abreu Vieira,Alexandre Barbosa Reis,Rodolfo Cordeiro Giunchetti

doi:10.1186/s13071-016-1464-y

Nádia Das Dores Moreira, Jamille Mirelle De Oliveira Cardoso + Show 9 more

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https://doi.org/10.1186/s13071-016-1464-y

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Abstract

BackgroundLeishmaniasis remains among the most important parasitic diseases in the developing world and visceral leishmaniasis (VL) is the most fatal. The hamster Mesocricetus auratus is a susceptible model for the characterization of the disease, since infection of hamsters with L. infantum reproduces the clinical and pathological features of human VL. In this context, it provides a unique opportunity to study VL in its active form. The main goal of this study was to evaluate the clinical, biochemical, and hematological changes in male hamsters infected through different routes and strains of L. infantum.MethodsIn the current study, hamsters (Mesocricetus auratus) were infected with the L. infantum strains (WHO/MHOM/BR/74/PP75 and MCAN/BR/2008/OP46) by intradermal, intraperitoneal and intracardiac routes. The animals were monitored for a nine month follow-up period.ResultsThe hamsters showed clinical signs similar to those observed in classical canine and human symptomatic VL, including splenomegaly, severe weight loss, anemia, and leucopenia. Therefore the OP46 strain was more infective, clinical signs were more frequent and more exacerbated in IC group with 80 to 100 % of the animals showing splenomegaly, in the last month infection. Additionally, desquamation, hair loss and external mucocutaneous lesions and ulcers localized in the snout, accompanied by swelling of the paws in all animals, were observed. Consequently, the animals presented severe weight loss/cachexia, hunched posture, an inability to eat or drink, and non-responsiveness to external stimuli. Furthermore, regardless of strain, route of inoculum and time assessed, the animals showed renal and hepatic alterations, with increased serum levels of urea and creatinine as well as elevated serum levels of aspartate aminotransferase and alanine aminotransferase.ConclusionsThese results strongly suggest that the inoculation through the intracardiac route resulted in a higher severity among infections, especially in the sixth and ninth month after infection via intracardiac, exhibited clinical manifestations and biochemical/hematological findings similar to human visceral leishmaniasis. Therefore, we suggest that this route must be preferentially used in experimental infections for pathogenesis studies of VL in the hamster model.

Highlights

Leishmaniasis remains among the most important parasitic diseases in the developing world and visceral leishmaniasis (VL) is the most fatal
Moreira et al Parasites & Vectors (2016) 9:181 (Continued from previous page). These results strongly suggest that the inoculation through the intracardiac route resulted in a higher severity among infections, especially in the sixth and ninth month after infection via intracardiac, exhibited clinical manifestations and biochemical/hematological findings similar to human visceral leishmaniasis
We suggest that this route must be preferentially used in experimental infections for pathogenesis studies of VL in the hamster model

Summary

Introduction

Leishmaniasis remains among the most important parasitic diseases in the developing world and visceral leishmaniasis (VL) is the most fatal. The hamster (Mesocricetus auratus) represents a good model for VL as it has a unique susceptibility to a variety of intracellular pathogens [14, 23] It develops the majority of immunopathological alterations characteristic of the human disease, with growth of parasites in the bone marrow, spleen and liver; clinical and hematological symptoms such as hepatosplenomegaly, depressed lymphocyte proliferation, anemia, leucopenia and glomerulonephritis; death by 9–10 weeks after visceral infection [7, 14]. This model has been extensively used for studies on disease pathogenesis and immunosuppression [14, 24,25,26] and to test efficacy of drugs and vaccines [26,27,28,29,30,31,32]

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