BALB/c, C57BL/6, and DBA/2 mice were subcutaneously infected in the left footpad 
by injecting 10(4) Leishmania (Leishmania) amazonensis amastigotes. Mice were 
sacrificed 20, 30, 40, 60 and 90 days post-infection. Fragments of liver, 
kidney, spleen, skin, and draining lymph node were collected for histological 
examination. Light microscopy showed that at 20 days after infection BALB/c mice 
presented discrete inflammatory infiltrates in the skin made up of eosinophils, 
lymphocytes, and rare parasitized macrophages. Ninety days post-infection, the 
dermis showed necrotic tissue, large numbers of mononuclear cells and vacuolated 
macrophages filled with amastigotes. Forty days post-infection, the draining 
lymph nodes showed hyperplastic germinal centers, increase of high endothelial 
venules and apoptosis in germinal center cells. After the first 3 months 
post-infection, the involvement of spleen, kidney and liver was discreet, being 
characterized by multifocal inflammatory infiltrates. Eight months after 
infection, the animals presented metastatic lesions in the contralateral footpad 
and nose. In deep dermis, there was remarkable proliferation of fibroblasts 
associated with collagen fibers. The liver showed multifocal granulomas and 
mononuclear infiltrate around the blood vessels, but no parasites were observed, 
except in one animal. In some mice there were immature cells of the 
hematopoietic lineage. Both BALB/c and C57BL/6 mice presented osteonecrosis, 
which is characterized by pycnotic osteocytes and empty lacunae at the point of 
inoculation and subsequently, replacement of this tissue by fibrous connective 
tissue and colonization of the bone marrow. A diffuse inflammatory process 
composed of mononuclear cells and rare parasites were seen in the kidneys. In 
one mouse, bone marrow cells were observed in the renal medulla along with where 
free amastigotes. DBA/2 mice developed a mild infection and they did not 
visceralize. In conclusion, our data demonstrates that in susceptible mice L. 
(L.) amazonensis, a causative agent of tegumentary leishmaniasis, causes 
pathological changes similar to those produced by Leishmania (L.) infantum in 
both humans and canids.