Advances in the pathogenesis of canine leishmaniosis: epidemiologic and diagnostic implications

Abstract

Canine leishmaniosis caused by Leishmania infantum (Syn. L. chagasi) is an important zoonosis with a complex pathogenesis. Parasite transmission occurs via female sandflies that inject promastigotes into the skin of the host. The interaction between the parasite and skin immune system is influenced by the repeated infectious bites and the simultaneous intradermal injection of sandfly saliva. Amastigotes are transported via infected macrophages to the regional lymph nodes and finally dissemination may occur. The outcome of the infection depends on host factors (genetic background, cell-mediated and humoral immune response, cytokine milieu, concurrent diseases) and parasite virulence. Resistance may be breed-associated; it is characterized by low to undetectable antibody production and effective cell-mediated immunity, and is orchestrated by cytokines such as interleukin-2, interferon-gamma and tumour necrosis factor-alpha. Susceptibility may be genetically determined or acquired (advanced age, concurrent diseases); in these dogs, parasite multiplication goes unrestricted and overproduction of specific and nonspecific antibodies occurs, leading to multiple organ pathology. Resistance or susceptibility is not an all-or-nothing phenomenon and many intermediate phenotypes may be found. From a diagnostic point of view, although clinical cases are readily identified using microscopy and serology, investigation should not stop at this point and an extensive search for underlying diseases is advised, especially in aged dogs. Conversely, microscopy and conventional serology are frequently negative in asymptomatic infected dogs; to identify such dogs, polymerase chain reaction, evaluation of cutaneous delayed-type hypersensitivity, in vitro lymphocyte proliferation test to Leishmania antigen, and Western blotting may be employed.