Abstract

Disseminated leishmaniasis (DL) differs from other clinical forms of the disease due to the presence of many non-ulcerated lesions (papules and nodules) in non-contiguous areas of the body. We describe the histopathology of DL non-ulcerated lesions and the presence of CD4-, CD20-, CD68-, CD31- and von Willebrand factor (vW)-positive cells in the inflamed area. We analysed eighteen biopsies from non-ulcerated lesions and quantified the inflamed areas and the expression of CD4, CD20, CD68, CD31 and vW using Image-Pro software (Media Cybernetics). Diffuse lymphoplasmacytic perivascular infiltrates were found in dermal skin. Inflammation was observed in 3-73% of the total biopsy area and showed a significant linear correlation with the number of vW+ vessels. The most common cells were CD68+ macrophages, CD20+ B-cells and CD4+ T-cells. A significant linear correlation between CD4+ and CD20+ cells and the size of the inflamed area was also found. Our findings show chronic inflammation in all DL non-ulcerated lesions predominantly formed by macrophages, plasmacytes and T and B-cells. As the inflamed area expanded, the number of granulomas and extent of the vascular framework increased. Thus, we demonstrate that vessels may have an important role in the clinical evolution of DL lesions.

Highlights

  • Skin infection by Leishmania braziliensis promastigotes results in different forms of cutaneous lesions that include, but are not limited to localised (CL), disseminated (DL) and mucocutaneous forms

  • Histopathological analysis of the CL ulcer reveals a chronic perivascular infiltrate of lymphocytes, plasmocytes, macrophages, epithelioid and giant cells, all of which eventually arrange in granulomas with or without necrosis

  • Secondary skin lesions emerged after L. braziliensis dissemination

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Summary

Introduction

Skin infection by Leishmania braziliensis promastigotes results in different forms of cutaneous lesions that include, but are not limited to localised (CL), disseminated (DL) and mucocutaneous forms. Histopathological analysis of the CL ulcer reveals a chronic perivascular infiltrate of lymphocytes, plasmocytes, macrophages, epithelioid and giant cells, all of which eventually arrange in granulomas with or without necrosis In this study we have analysed non-ulcerated lesions from DL patients in attempting to better understand the nonulcerated cutaneous lesion present in DL and in early CL.

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