No abstract

Summary The aim of this work was to study alterations in the extracellular matrix of liver in dogs naturally infected with Leishmania (Leishmania) chagasi that are correlated with clinical aspects and with histological, parasitological and immunological findings. The study was carried out on 30 dogs, 10 uninfected (control group) and 20 infected. The infected animals were further divided into two groups: an asymptomatic group of 10 dogs without clinical signs of the disease; and a symptomatic group of 10 dogs with classical clinical signs. All thirty animals were mongrel dogs of undefined age, obtained from the municipality of Belo Horizonte, MG, metropolitan area. During necropsy, liver fragments were collected and fixed in 10% buffered formaldehyde for histological examination. Paraffined sections of the tissues were stained with haematoxylin-eosin, Gomori's ammoniacal silver stain for reticular fibres and strepto-avidin peroxidase for immunohistochemical detection of Leishmania amastigotes. Frozen tissue sections were stained by immunofluorescence for fibronectin (FN) and laminin (LN). Liver collagen deposition was significantly greater in the infected than the control animals and differed significantly between the symptomatic and asymptomatic dogs. There was a positive correlation between the parasite load and liver collagen deposition. The increased collagen deposition in infected animal livers may be associated with the parasite burden. Adhesive FN and LN fibres were significantly more highly expressed in the livers of symptomatic than of asymptomatic dogs. Our results demonstrate that canine visceral leishmaniasis causes fibrogenesis in liver, associated with the parasite load and degenerative processes.

Factors related to positive testing of dogs for visceral leishmaniasis in endemic area

Leishmania amazonensis infection was studied in mice to evaluate the evolution of leishmaniasis. The association of different methods, such as lesion kinetics, limiting dilution analysis, and immunohistochemistry, established different levels of susceptibility and resistance. Mice were arranged in 3 groups: susceptible (C57BL/10 and CBA), relatively resistant (DBA/2), and resistant (C3H.He). The histopathological analysis of primary lesions and draining lymph nodes showed a predominance of eosinophils and mast cells in the initial phase of infection in all mice. However, the most susceptible mice presented a greater number of amastigotes and higher tissue damage. The immunoglobulin analysis showed that susceptible mice produced high levels of antibodies, whereas resistant and relatively resistant mice exhibited low production of antibodies. Resistant mice showed parasite persistency in the skin and lymph nodes, suggesting that the infection in these mice can be sustained through the infection of cells such as dendritic cells, fibroblasts, and other cells present in these organs.

Tegumentary leishmaniasis is an important public health problem in several countries. The capacity of the Leishmania species, at the initial moments of the infection, to invade and survive inside the host cells involves the interaction of surface molecules that are crucial in determining the evolution of the disease. Using C57BL/6 wild-type and TLR-2(-/-) mice infected with L. (L.) amazonensis, we demonstrated that TLR-2(-/-) mice presented eosinophilic granuloma in the ear dermis, different from C57BL/6 wild-type mice that presented a cellular profile characterized mainly by mononuclear cell infiltrates, besides neutrophils and eosinophils, during the two first week of infection. When the parasite load was evaluated, we found that the absence of TLR-2 lead to a significant reduction of the infection in deficient mice, when compared with C57BL/6 mice which were more susceptible to the infection. Using TLR-2 deficient mice, it was possible to show that the absence of this receptor determined the reduction of the parasite load and the recruitment of inflammatory cells during the two first weeks after L. (L.) amazonensis infection.