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Acta sci. vet. (Impr.); 41: Pub. 1165, 2013. graf, ilus, tab

Artigo em Inglês | VETINDEX | ID: biblio-1371086

Resumo

Background: Although the canine visceral leishmaniasis be characterized as a severe systemic disease, few studies have been conducted describing the main histopathological alterations found in the various organs of the host affected by the parasite. This paper evaluated the structural and immune-inflammatory changes of the spleen, liver, popliteal lymph nodes (PLN) and skin of naturally infected dogs in different clinical forms of canine visceral leishmaniasis. Material, Methods & Results: Forty seven adult dogs were used, varying in age and weight, selected by Immunofluorescence Assay (IFA), were considered positive IFA titres of ≥ 1:40 and the parasitological examination of L. infantum amastigotes forms in bone marrow smears. The dogs were grouped according to the clinical signs associated to the disease: negative dogs (ND = 7), subclinical dogs (SD = 20) and clinical dogs (CD = 20). After the euthanasia procedure, all animals were weighed, and then the spleen and liver were dissected for relative weights measurements. Fragments of spleen, liver, PLN and skin were collected and subjected to procedures for histology (H&E). The same samples were subjected to immunohistochemical analysis for detection of L. infantum amastigotes. The authors observed increased relative weight of spleen and liver of the CD and SD groups (P < 0.05). Discrete hypoplasia of red and white pulps and capsular thickening, moderate hypertrophy of red and white pulps and intense splenic congestion were observed in the spleen in group SD, whereas a slight thickening of the capsule and hypertrophy of red and white pulps, intense congestion and moderate subcapsular fibrosis and hypoplasia of the splenic red and white pulps were found in the CD group. Histological evaluation of the liver showed moderate periportal inflammatory infiltrate, hypertrophy/hyperplasia of Kupffer cells and congestion, slight thickening of the capsule and intralobular granulomas in the SD group, while moderate peri-portal inflammatory infiltrate, hypertrophy/hyperplasia of Kupffer cells, congestion, thickening of the capsule and intralobular granulomas were found in the CD group. The PLN histologic evaluation presented discrete capsular inflammation, congestion, hemosiderosis and hypertrophy/hyperplasia of lymphatic nodules and moderate hypertrophy/hyperplasia of cortical and medullar in the SD group, while slight capsular inflammation, congestion, hemosiderosis and hypertrophy/hyperplasia of lymphatic nodules and moderate hypertrophy/hyperplasia of cortical and medullar were found in the CD group. The main change observed in the skin was moderate histiolymphocyte inflammatory infiltrate in the SD group. The greatest parasite density of L. infantum amastigotes could be observed in the spleen. Discussion: The capsular thickening, subcapsular fi brosis and hypoplastic spleen can be explained by the disease chronicity. The liver infection caused by L. infantum has the ability to self-resolute through an immune response mediated by Th1 lymphocytes, mono-nuclear cells and involving the Kupffer cells, macrophages and subsequent granuloma formation. The hypertrophy/hyperplasia of cortical and medullary in lymph nodes is considered the most relevant change, because they suggest that the immunopathological status is a characteristic of chronic infection. In dogs infected by L. infantum, the ears are the skin areas where the lesions and inflammatory infiltrates are most evident. This unequal tropism doesn't occurs solely because of the area being the preferred location by transmitting insects, but also by the high incidence of lesions caused by ectoparasites and itchy reactions. It follows that organs and tissues of dogs naturally infected by L. infantum have histological changes consistent with immune-inflammatory response, demonstrating the functional impairment of the same.

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