Canine leishmaniasis is caused by Leishmania infantum (syn. L. chagasi, in America) and is transmitted by the bite of phlebotomine sand flies. Infected dogs constitute the main domestic reservoir of the parasite and play a key role in transmission to humans, in which the parasite produces visceral leishmaniasis. The increasing awareness that control of the human disease depends on effective control of canine leishmaniasis has promoted, in the last few years, research into leishmanial infection in dogs. Newly available specific reagents and molecular tools have been applied to the detailed investigation of canine leishmaniasis and important advances have been made in elucidating the epidemiology and pathology of the disease. These new findings have led to better understanding of the disease, and have also helped in the development of new diagnostic methods and control measures against the infection, such as insecticide-impregnated collars for dogs, new drugs and treatment protocols, and second generation vaccines, with the hope of not only reducing the heavy burden of the disease among dogs but also reducing the incidence of human visceral leishmaniasis.

Over 850 Leishmania-human immunodeficiency virus (HIV) coinfection cases have been recorded, the majority in Europe, where 7 to 17% of HIV-positive individuals with fever have amastigotes, suggesting that Leishmania-infected individuals without symptoms will express symptoms of leishmaniasis if they become immunosuppressed. However, there are indirect reasons and statistical data demonstrating that intravenous drug addiction plays a specific role in Leishmania infantum transmission: an anthroponotic cycle complementary to the zoonotic one has been suggested. Due to anergy in patients with coinfection, L. infantum dermotropic zymodemes are isolated from patient viscera and a higher L. infantum phenotypic variability is seen. Moreover, insect trypanosomatids that are currently considered nonpathogenic have been isolated from coinfected patients. HIV infection and Leishmania infection each induce important analogous immunological changes whose effects are multiplied if they occur concomitantly, such as a Th1-to-Th2 response switch; however, the consequences of the viral infection predominate. In fact, a large proportion of coinfected patients have no detectable anti-Leishmania antibodies. The microorganisms share target cells, and it has been demonstrated in vitro how L. infantum induces the expression of latent HIV-1. Bone marrow culture is the most useful diagnostic technique, but it is invasive. Blood smears and culture are good alternatives. PCR, xenodiagnosis, and circulating-antigen detection are available only in specialized laboratories. The relationship with low levels of CD4+ cells conditions the clinical presentation and evolution of disease. Most patients have visceral leishmaniasis, but asymptomatic, cutaneous, mucocutaneous, diffuse cutaneous, and post-kala-azar dermal leishmaniasis can be produced by L. infantum. The digestive and respiratory tracts are frequently parasitized. The course of coinfection is marked by a high relapse rate. There is a lack of randomized prospective treatment trials; therefore, coinfected patients are treated by conventional regimens. Prophylactic therapy is suggested to be helpful in preventing relapses.

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