Disseminated mucocutaneous leishmaniasis resulting from chronic use of corticosteroid

Motta, Ana Carolina Fragoso; Arruda, Darlene; Souza, Cacilda da Silva; Foss, Norma T.

doi:10.1046/j.1365-4362.2003.01730.x

Cited by 31 publications

(25 citation statements)

References 10 publications

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“…For the human, however, it has been suggested that quiescent or slow-growing parasites could be reactivated and metastasize to mucocutaneous sites following immuno-suppressive treatment (Motta et al, 2003) or during in stress situations (Travi et al, 1988, 1996) which are perhaps not encountered in the laboratory model.…”

Section: Experimental Animal Models Of MCLmentioning

confidence: 99%

Leishmania RNA virus: when the host pays the toll

Hartley

Ronet

Zangger

et al. 2012

Front. Cell. Inf. Microbio.

124

143

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The presence of an RNA virus in a South American subgenus of the Leishmania parasite, L. (Viannia), was detected several decades ago but its role in leishmanial virulence and metastasis was only recently described. In Leishmania guyanensis, the nucleic acid of Leishmania RNA virus (LRV1) acts as a potent innate immunogen, eliciting a hyper-inflammatory immune response through toll-like receptor 3 (TLR3). The resultant inflammatory cascade has been shown to increase disease severity, parasite persistence, and perhaps even resistance to anti-leishmanial drugs. Curiously, LRVs were found mostly in clinical isolates prone to infectious metastasis in both their human source and experimental animal model, suggesting an association between the viral hyperpathogen and metastatic complications such as mucocutaneous leishmaniasis (MCL). MCL presents as chronic secondary lesions in the mucosa of the mouth and nose, debilitatingly inflamed and notoriously refractory to treatment. Immunologically, this outcome has many of the same hallmarks associated with the reaction to LRV: production of type 1 interferons, bias toward a chronic Th1 inflammatory state and an impaired ability of host cells to eliminate parasites through oxidative stress. More intriguing, is that the risk of developing MCL is found almost exclusively in infections of the L. (Viannia) subtype, further indication that leishmanial metastasis is caused, at least in part, by a parasitic component. LRV present in this subgenus may contribute to the destructive inflammation of metastatic disease either by acting in concert with other intrinsic “metastatic factors” or by independently preying on host TLR3 hypersensitivity. Because LRV amplifies parasite virulence, its presence may provide a unique target for diagnostic and clinical intervention of metastatic leishmaniasis. Taking examples from other members of the Totiviridae virus family, this paper reviews the benefits and costs of endosymbiosis, specifically for the maintenance of LRV infection in Leishmania parasites, which is often at the expense of its human host.

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Section: Experimental Animal Models Of MCLmentioning

confidence: 99%

Leishmania RNA virus: when the host pays the toll

Hartley

Ronet

Zangger

et al. 2012

Front. Cell. Inf. Microbio.

124

143

View full text Add to dashboard Cite

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“…As a result of immunosuppression of human immunodeficiency virus-positive patients, kidney and heart recipients, and chronic users of corticosteroids, a serious risk of reactivation of CL in MCL form is present. [19][20][21][22][23] On account of such complications, treatments should be started promptly after its diagnosis, so as to prevent mucosal metastasis.…”

Section: Introductionmentioning

confidence: 99%

Enhanced photodynamic leishmanicidal activity of hydrophobic zinc phthalocyanine within archaeolipids containing liposomes

Perez

Casasco

Schilrreff

et al. 2014

IJN

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In this work, the in vitro anti-Leishmania activity of photodynamic liposomes made of soybean phosphatidylcholine, sodium cholate, total polar archaeolipids (TPAs) extracted from the hyperhalophile archaea Halorubrum tebenquichense and the photosensitizer zinc phthalocyanine (ZnPcAL) was compared to that of ultradeformable photodynamic liposomes lacking TPAs (ZnPcUDLs). We found that while ZnPcUDLs and ZnPcALs (130 nm mean diameter and −35 mV zeta potential) were innocuous against promastigotes, a low concentration (0.01 µM ZnPc and 7.6 µM phospholipids) of ZnPcALs irradiated at a very low-energy density (0.2 J/cm 2 ) eliminated L. braziliensis amastigotes from J774 macrophages, without reducing the viability of the host cells. In such conditions, ZnPcALs were harmless for J774 macrophages, HaCaT keratinocytes, and bone marrow-derived dendritic cells. Therefore, topical photodynamic treatment would not likely affect skin-associated lymphoid tissue. ZnPcALs were extensively captured by macrophages, but ZnPcUDLs were not, leading to 2.5-fold increased intracellular delivery of ZnPc than with ZnPcUDLs. Despite mediating low levels of reactive oxygen species, the higher delivery of ZnPc and the multiple (caveolin-and clathrin-dependent plus phagocytic) intracellular pathway followed by ZnPc would have been the reason for the higher antiamastigote activity of ZnPcALs. The leishmanicidal activity of photodynamic liposomal ZnPc was improved by TPA-containing liposomes.

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“…However, there are only few case reports describing that systemic corticosteroid treatment may worsen mucocutaneous leishmaniasis or lead to a recurrence of the disease. 10,11 This is the first description of ML caused by L. major in a traveler as opposed to patients residing in endemic areas. The place of exposure in this patient was most likely North Africa, where he had traveled to Tunisia, Morocco, and Egypt 2 years before the occurrence of the disease.…”

Section: Discussionmentioning

confidence: 93%

Progressive Perforation of the Nasal Septum Due to Leishmania major: A Case of Mucosal Leishmaniasis in a Traveler

Harrison

Walochnik

Ramsebner

et al. 2017

The American Society of Tropical Medicine and Hygiene

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Abstract. This report describes a case of mucosal leishmaniasis caused by Leishmania major with destructive perforation of the nasal septum illustrating the diagnostic challenges of a rare clinical presentation of L. major infection in a traveler. The atypical presentation may have been associated with the use of cortisone as a potential trigger for the progressive destruction of the nasal septum.

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Disseminated mucocutaneous leishmaniasis resulting from chronic use of corticosteroid

Cited by 31 publications

References 10 publications

Leishmania RNA virus: when the host pays the toll

Leishmania RNA virus: when the host pays the toll

Enhanced photodynamic leishmanicidal activity of hydrophobic zinc phthalocyanine within archaeolipids containing liposomes

Progressive Perforation of the Nasal Septum Due to Leishmania major: A Case of Mucosal Leishmaniasis in a Traveler

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