Humoral and Cell-mediated Immunity in Natural and Experimental Canine Leishmaniasis

This paper describes immunological and clinicopathological findings in dogs naturally and experimentally infected with progressive visceral leishmaniasis. Eight dogs were intravenously inoculated with 5 x 10(7) stationary phase promastigotes of Leishmania infantum (LEM 2002, ZMON-1). A further eight naturally infected dogs were diagnosed by parasitological and serological methods and selected according to their clinical and immunological condition. Clinical, hematological, pathological and parasitological examinations, including parasite burden and distribution, were included in the study. Antibody production was estimated by means of enzyme-linked immunosorbent assay and immunofluorescence assay techniques; the cellular immune response was studied by means of the skin test and the lymphocyte proliferation test. Experimentally infected dogs developed a chronic and progressive disease with the same clinical signs shown by naturally infected dogs. Both naturally and experimentally infected dogs developed the same histopathological reaction, but to differing degrees. Parasite burden and distribution were related to the extent of lesions, and were consequently less pronounced in experimentally infected dogs. The main feature of the immune response in experimental and natural infection was the lack of specific T-cell response to leishmanial antigen. Non-specific responses to mitogens were normal (i.e. as compared with healthy dogs) throughout the experimental infection, but were partially suppressed (65.3%) in naturally infected animals. A remarkable humoral response was evident in both natural and experimental infection: IgG-isotype antibodies were detected in experimental infection at 50-70 days post infection, and their production increased during the course of the infection. However, high titers were observed only in naturally infected dogs.