Abstract
The aim of this study was to identify splenic immuno-inflammatory patterns associated with natural infection by Leishmania chagasi. Spleen samples were obtained from 72 stray dogs from an endemic area of visceral leishmaniasis. The animals were grouped into four categories as follows: (i) potentially resistant to visceral leishmaniasis, with a positive leishmanin skin test result, and negative splenic culture for Leishmania parasites (ii) potentially susceptible to visceral leishmaniasis, with a negative leishmanin skin test and positive splenic culture for Leishmania (iii) infected with undefined susceptibility status, with a positive leishmanin skin test and positive splenic culture for Leishmania, and (iv) noninfected, with a negative leishmanin skin test, negative splenic culture for Leishmania, and negative serology for anti-Leishmania antibodies. Histopathological analyses showed that there was a higher frequency of perisplenitis (18/25, P < 0·0001), granuloma (7/25, P = 0·0102), structural disorganization (14/25, P < 0·0001), and atrophy of the lymphoid follicles (20/25, P = 0·0036) and of the marginal zone (15/25, P = 0·0025) in the potentially susceptible group than in the other groups. The data presented here show changes in the white pulp of the spleen that are associated with naturally acquired visceral leishmaniasis.
Highlights
Visceral leishmaniasis is used to describe two clinically, parasitologically and epidemiologically different diseases: antroponotic visceral leishmaniasis, caused by Leishmania donovani, and zoonotic visceral leishmaniasis (VL), caused by L. chagasi/L. infantum
The presence of anti-Leishmania antibodies in the serum were investigated by ELISA, and a cellular immune response against L. chagasi antigens was detected by leishmanin skin test (LST)
We have shown that negative LST results were associated with high levels of serum antibody activity and emaciation in L. chagasi-infected dogs
Summary
Visceral leishmaniasis is used to describe two clinically, parasitologically and epidemiologically different diseases: antroponotic visceral leishmaniasis, caused by Leishmania donovani, and zoonotic visceral leishmaniasis (VL), caused by L. chagasi/L. infantum. We use the term VL to refer to this severe form of the disease In both humans and dogs, the disease proceeds with emaciation, enlargement of the liver and spleen, fever, anaemia, and an increased predisposition to bacterial infection [2,7,8,9,10]. Much that is known about the immune response to Leishmania parasites, and even the immune response in general has come from studies in murine models of leishmaniases [11,12,13] Most of these models, are intrinsically compromised by the artificial nature of the infective inocula. Canine VL, arising from natural infection by L. chagasi, is a disease worthy of study in its own right for veterinary and epidemiological reasons [15], and for consideration as an attractive animal model for the human disease, because
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