Further observations on clinical, histopathological, and immunological features of borderline disseminated cutaneous leishmaniasis caused by Leishmania (Leishmania) amazonensis

Sílveira, Fernando Tobias; Lainson, Ralph; Corbett, Carlos Eduardo Pereira

doi:10.1590/s0074-02762005000500013

Cited by 59 publications

(59 citation statements)

References 29 publications

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“…This finding may be an indication of the immune modulation of tissue inflammation. IFN-g and TNF-a in the inflamed tissue may lead to an inflammatory response that forms granulomas (Silveira et al 2005). Granulomas were present in nine out of 18 the biopsies analysed; these biopsies were also observed to be among the ones with more inflammation area.…”

Section: Discussionmentioning

confidence: 91%

Inflammation in disseminated lesions: an analysis of CD4+, CD20+, CD68+, CD31+ and vW+ cells in non-ulcerated lesions of disseminated leishmaniasis

Mendes

Dantas

Gomes

et al. 2013

Mem. Inst. Oswaldo Cruz

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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.

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Section: Discussionmentioning

confidence: 91%

Inflammation in disseminated lesions: an analysis of CD4+, CD20+, CD68+, CD31+ and vW+ cells in non-ulcerated lesions of disseminated leishmaniasis

Mendes

Dantas

Gomes

et al. 2013

Mem. Inst. Oswaldo Cruz

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“…Cutaneous leishmaniasis predominates, with 1.5 million new cases occurring per year (2). Lesions appear as papules that may progress to nodules and even severe forms characterized by ulcerated lesions (8,9). In Brazil, the most relevant species are Leishmania amazonensis, L. guyanensis, L. braziliensis, and L. chagasi, and approximately 30,000 cases were reported in 2010 alone (2,10).…”

mentioning

confidence: 99%

In Vitro and In Vivo Activities of 2,3-Diarylsubstituted Quinoxaline Derivatives against Leishmania amazonensis

Kaplum

Cogo

Sangi

et al. 2016

Antimicrob Agents Chemother

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Leishmaniasis is endemic in 98 countries and territories worldwide. The therapies available for leishmaniasis have serious side effects, thus prompting the search for new therapies. The present study investigated the antileishmanial activities of 2,3-diarylsubstituted quinoxaline derivatives against Leishmania amazonensis. The antiproliferative activities of 6,7-dichloro-2,3-diphenylquinoxaline (LSPN329) and 2,3-di-(4-methoxyphenyl)-quinoxaline (LSPN331) against promastigotes and intracellular amastigotes were assessed, and the cytotoxicities of LSPN329 and LSPN331 were determined. Morphological and ultrastructural alterations were examined by electron microscopy, and biochemical alterations, reflected by the mitochondrial membrane potential (⌬⌿m), mitochondrial superoxide anion (O 2 · ؊ ) concentration, the intracellular ATP concentration, cell volume, the level of phosphatidylserine exposure on the cell membrane, cell membrane integrity, and lipid inclusions, were evaluated. In vivo antileishmanial activity was evaluated in a murine cutaneous leishmaniasis model. Compounds LSPN329 and LSPN331 showed significant selectivity for promastigotes and intracellular amastigotes and low cytotoxicity. In promastigotes, ultrastructural alterations were observed, including an increase in lipid inclusions, concentric membranes, and intense mitochondrial swelling, which were associated with hyperpolarization of ⌬⌿m, an increase in the O 2 · ؊ concentration, decreased intracellular ATP levels, and a decrease in cell volume. Phosphatidylserine exposure and DNA fragmentation were not observed. The cellular membrane remained intact after treatment. Thus, the multifactorial response that was responsible for the cellular collapse of promastigotes was based on intense mitochondrial alterations. BALB/c mice treated with LSPN329 or LSPN331 showed a significant decrease in lesion thickness in the infected footpad. Therefore, the antileishmanial activity and mitochondrial mechanism of action of LSPN329 and LSPN331 and the decrease in lesion thickness in vivo brought about by LSPN329 and LSPN331 make them potential candidates for new drug development for the treatment of leishmaniasis.

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“…withmani and Lu. nuneztovari anglesi are suspected vectors of this parasite in the state of Mato Grosso do Sul, Brazil [231], and Bolivia [233,234], respectively. And L. (V.) amazonensis amastigotes developed normally to promastigotes in experimentally infected Lu.…”

Section: Infections By L (V) Braziliensis Are Also Encountered In Omentioning

confidence: 99%

“…Mammalian reservoirs of L. (L.) amazonensis are probably small rodents, marsupials, primates, and carnivores [226] including rice rats and grass mice in Bolivia [228,233,234], and in Brazil, domestic dogs [236]. The latter assumption is based on a case of canine leishmaniasis caused by L. (V.) amazonensis in the Brazilian state of Paraná which is considered endemic for CL in humans [2].…”

Section: Infections By L (V) Braziliensis Are Also Encountered In Omentioning

confidence: 99%

Epidemiological, Biological and Clinical Aspects of Leishmaniasis with Special Emphasis on Busi Yasi in Suriname

Mans¹,

Kent²,

Hu³

et al. 2017

J Clin Exp Dermatol Res

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The parasitic disease leishmaniasis is caused by protozoa of the genus Leishmania which are transmitted by sand fly vectors of the genus Phlebotomus in the Old World and Lutzomyia in the New World. Transmission can either be anthroponotic (human to human) or zoonotic through mammalian reservoirs such as dogs and rodents. Leishmaniasis has three principal clinical manifestations, namely cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis (MCL), and visceral leishmaniasis (VL). The cutaneous form characteristically causes skin ulcers, the mucocutaneous form manifests as lesions of skin, mouth, and nose, and the (potentially lethal) visceral form affects the internal organs such as spleen and liver and also invades the bone marrow. Leishmaniasis is endemic in about ninety-eight countries and the diverse types of the disease occur in different regions of the world. CL is most common in Afghanistan, Algeria, Pakistan, Iran, Brazil, and Colombia; MCL is mainly restricted to countries of the Amazon Basin; and VL is most frequently seen in the Indian sub-continent, the Horn of Africa (Sudan and Ethiopia), and Brazil. The current global prevalence is estimated at about 12 million, and each year, the disease in one of its forms makes about 2 million new victims and claims up to 50,000 fatalities. This paper presents epidemiological, biological, and clinical aspects of leishmaniasis throughout the world; then focuses on the disease in the Republic of Suriname (South America); addresses in more detail the species of Leishmania parasites in that country; and concludes with potential future directions to improve our understanding of leishmaniasis in Suriname.

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Further observations on clinical, histopathological, and immunological features of borderline disseminated cutaneous leishmaniasis caused by Leishmania (Leishmania) amazonensis

Cited by 59 publications

References 29 publications

Inflammation in disseminated lesions: an analysis of CD4+, CD20+, CD68+, CD31+ and vW+ cells in non-ulcerated lesions of disseminated leishmaniasis

Inflammation in disseminated lesions: an analysis of CD4+, CD20+, CD68+, CD31+ and vW+ cells in non-ulcerated lesions of disseminated leishmaniasis

In Vitro and In Vivo Activities of 2,3-Diarylsubstituted Quinoxaline Derivatives against Leishmania amazonensis

Epidemiological, Biological and Clinical Aspects of Leishmaniasis with Special Emphasis on Busi Yasi in Suriname

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