3-Bromopyruvate: A new strategy for inhibition of glycolytic enzymes in Leishmania amazonensis.

The compound 3-bromopyruvate (3-BrPA) is well-known and studies from several researchers have demonstrated its involvement in tumorigenesis. It is an analogue of pyruvic acid that inhibits ATP synthesis by inhibiting enzymes from the glycolytic pathway and oxidative phosphorylation. In this work, we investigated the effect of 3-BrPA on energy metabolism of L. amazonensis. In order to verify the effect of 3-BrPA on L. amazonensis glycolysis, we measured the activity level of three glycolytic enzymes located at different points of the pathway: (i) glucose kinases, step 1, (ii) glyceraldehyde 3-phosphate dehydrogenase (GAPDH), step 6, and (iii) enolase, step 9. 3-BrPA, in a dose-dependent manner, significantly reduced the activity levels of all the enzymes. In addition, 3-BrPA treatment led to a reduction in the levels of phosphofruto-1-kinase (PFK) protein, suggesting that the mode of action of 3-BrPA involves the downregulation of some glycolytic enzymes. Measurement of ATP levels in promastigotes of L. amazonensis showed a significant reduction in ATP generation. The O2 consumption was also significantly inhibited in promastigotes, confirming the energy depletion effect of 3-BrPA. When 3-BrPA was added to the cells at the beginning of growth cycle, it significantly inhibited L. amazonensis proliferation in a dose-dependent manner. Furthermore, the ability to infect macrophages was reduced by approximately 50% when promastigotes were treated with 3-BrPA. Taken together, these studies corroborate with previous reports which suggest 3-BrPA as a potential drug against pathogenic microorganisms that are reliant on glucose catabolism for ATP supply.

Isolation of intact Leishmania amazonensis large parasitophorous vacuoles from infected macrophages by density gradient fractionation.

As the causative agent of hard-to-treat diffuse cutaneous leishmaniasis, Leishmania (L.) amazonensis persists in the host organism sheltered within large Parasitophorous Vacuoles (PVs) formed mainly in macrophages. In the present study, I present a simple and efficient method for L. amazonensis PV isolation. Isolated PVs are intact as demonstrated by the conservation of lysosomal probes loaded into PVs before the procedure. The method is useful for studies aiming at a complete and accurate molecular profile of these structures, to better understand the biogenesis of this pathogen-containing vacuole and its implication in parasite persistence and in leishmaniasis pathogenesis.

Differential Regulation of l-Arginine Metabolism through Arginase 1 during Infection with Leishmania mexicana Isolates Obtained from Patients with Localized and Diffuse Cutaneous Leishmaniasis.

l-Arginine metabolism through arginase 1 (Arg-1) and inducible nitric oxide synthase (NOS2) constitutes a fundamental axis for the resolution or progression of leishmaniasis. Infection with Leishmania mexicana can cause two distinct clinical manifestations: localized cutaneous leishmaniasis (LCL) and diffuse cutaneous leishmaniasis (DCL). In this work, we analyzed in an in vivo model the capacity of two L. mexicana isolates, one obtained from a patient with LCL and the other from a patient with DCL, to regulate the metabolism of l-arginine through Arg-1 and NOS2. Susceptible BALB/c mice were infected with L. mexicana isolates from both clinical manifestations, and the evolution of the infection as well as protein presence and activity of Arg-1 and NOS2 were evaluated. The lesions of mice infected with the DCL isolate were bigger, had higher parasite loads, and showed greater protein presence and enzymatic activity of Arg-1 than the lesions of mice infected with the LCL isolate. In contrast, NOS2 protein synthesis was poorly or not induced in the lesions of mice infected with the LCL or DCL isolate. The immunochemistry analysis of the lesions allowed the identification of highly parasitized macrophages positive for Arg-1, while no staining for NOS2 was found. In addition, we observed in lesions of patients with DCL macrophages with higher parasite loads and stronger Arg-1 staining than those in lesions of patients with LCL. Our results suggest that L. mexicana isolates obtained from patients with LCL or DCL exhibit different virulence or pathogenicity degrees and differentially regulate l-arginine metabolism through Arg-1.

Host and parasite responses in human diffuse cutaneous leishmaniasis caused by L. amazonensis.

Diffuse cutaneous leishmaniasis (DCL) is a rare form of leishmaniasis where parasites grow uncontrolled in diffuse lesions across the skin. Meta-transcriptomic analysis of biopsies from DCL patients infected with Leishmania amazonensis demonstrated an infiltration of atypical B cells producing a surprising preponderance of the IgG4 isotype. DCL lesions contained minimal CD8+ T cell transcripts and no evidence of persistent TH2 responses. Whereas localized disease exhibited activated (so-called M1) macrophage presence, transcripts in DCL suggested a regulatory macrophage (R-Mϕ) phenotype with higher levels of ABCB5, DCSTAMP, SPP1, SLAMF9, PPARG, MMPs, and TM4SF19. The high levels of parasite transcripts in DCL and the remarkable uniformity among patients afforded a unique opportunity to study parasite gene expression in this disease. Patterns of parasite gene expression in DCL more closely resembled in vitro parasite growth in resting macrophages, in the absence of T cells. In contrast, parasite gene expression in LCL revealed 336 parasite genes that were differently upregulated, relative to DCL and in vitro macrophage growth, and these transcripts may represent transcripts that are produced by the parasite in response to host immune pressure.

Case Report: Diffuse Cutaneous Leishmaniasis by Leishmania infantum in a Patient Undergoing Immunosuppressive Therapy: Risk Status in an Endemic Mediterranean Area.

This case report highlights the risk of severe cutaneous leishmaniasis (CL) by Leishmania infantum in patients undergoing immunosuppressant therapy who either live in an endemic area or are visiting in the transmission season. The case patient, resident in Majorca (Balearic Islands), presented 12 disseminated erythematous skin lesions, 1-6 cm in diameter, located on the scalp, cheek, umbilical region, and lower extremities 8 years after undergoing anti-tumor necrosis factor (TNF) therapy. Parasite presence in peripheral blood and high levels of specific antibodies were also observed, indicating a possible risk of CL shifting toward a visceral infection. However, once CL was diagnosed, anti-TNF therapy was discontinued and liposomal amphotericin B was administered, resulting in a complete healing of lesions, no Leishmania DNA detection in blood, and an important serological decrease in antibodies. The lack of data on the supposed epidemiological association between leishmaniasis and immunosuppressive therapy highlights the importance of implementing surveillance systems in endemic areas. No obvious relationship was found based on the data provided by the Balearic Islands Epidemiological System, in contrast with data reported in nearby endemic areas. This indicates that if the suspected association is to be clarified, greater efforts are needed to report information about concomitant diseases and therapies in leishmaniasis patients.

Disseminated Autochthonous Dermal Leishmaniasis Caused by Leishmania siamensis (PCM2 Trang) in a Patient from Central Thailand Infected with Human Immunodeficiency Virus.

AbstractSeveral case reports of autochthonous leishmaniasis in Thailand have been published since 1996. Most of the previous cases presented with visceral leishmaniasis (VL) and were mostly reported in southern part of Thailand. Recently, it has been evident that Leishmania martiniquensis is the main cause of Leishmania infection in Thailand. However, Leishmania siamensis (PCM2 Trang isolate) was found to be of a separate lineage with restricted distribution in southern Thailand and also a cause of disseminated dermal and visceral leishmaniasis in one published case. Here we report the first patient from central Thailand with human immunodeficiency virus infection presenting with disseminated dermal leishmaniasis. Polymerase chain reaction and DNA sequencing analysis (large subunit of RNA polymerase II and 18S ribosomal RNA internal transcribed spacer 1) from the tissue biopsy sample revealed the pathogen sequences to be highly homologous to PCM2 Trang strain previously reported from southern Thailand.

Coinfection of Leishmania guyanensis and Human Immunodeficiency Virus-Acquired Immune Deficiency Syndrome: Report of a Case of Disseminated Cutaneous Leishmaniasis in Ecuador.

AbstractReported herein is the first case of Leishmania-human immunodeficiency virus (HIV) coinfection in Ecuador. In Ecuador, HIV infections overlap endemic areas of leishmaniasis. Immunosuppression is a well-established risk factor for developing severe disease. This is a severe case of a 32-year-old man presenting with disseminated pleomorphic ulcers, papules, and cutaneous plaque-like lesions over his whole body. Numerous amastigotes were observed in both skin scrapings and biopsies. The sequence of the cytochrome b gene confirmed the presence of Leishmania guyanensis. The patient was treated but failed to respond to meglumine antimoniate and amphotericin B. Six months later, the patient died due to bacterial septic shock.

Importância da resolvinas na infecção por Leishmania Amazonensis / Importance of resolvins in Leishmania Amazonensis infection

A Leishmaniose Cutânea Difusa (LCD) é uma manifestação clínica. rara causada pela Leishmania amazonensis que é caracterizada por uma resposta celular. parasitária ineficiente e macrófagos intensamente parasitados nas lesões cutâneas.. Mediadores lipídicos e seus precursores desempenham um papel crucial durante a. infecção por Leishmania. Estudos prévios demonstram que pacientes com leishmaniose. tegumentar, exibem um distinto balanço de eicosanoides in situ e sistêmico.. Recentemente, demonstrou-se que mediadores lipídicos especializados na pró-resolução. desempenham um papel crítico na redução de processos inflamatórios patológicos. induzindo a restauração da homeostasia em diferentes modelos experimentais. Entre. esses mediadores, as resolvinas da série D exibem potente atividade anti-inflamatória e. imuno-regulatória que inclui a inibição da quimiotaxia leucocitária e bloqueio na. produção de citocinas pró-inflamatórias. No entanto, ainda é desconhecido se as. resolvinas desempenham um papel significativo no estabelecimento e persistência da. infecção por Leishmania. OBJETIVO: Nesse estudo, avaliamos os níveis circulantes. de Resolvina D1 (RvD1) em pacientes com leishmaniose tegumentar apresentando a. forma clínica cutânea localizada (LCL) ou difusa. RESULTADOS: Nossos resultados. demonstram que pacientes com LCD apresentam maiores níveis plasmáticos de RvD1. quando comparados a LCL ou controles endêmicos. Além disso, os níveis séricos de. RvD1 em pacientes com LCD se correlacionam positivamente com a Arginase I e TGF-. β, enquanto que inversamente com os níveis sistêmicos de TNF-α. Experimentos. adicionais in vitro utilizando macrófagos humanos revelaram que a RvD1 promove a. replicação intracelular da L. amazonensis por um mecanismo associado a indução da. enzima heme oxigenase-1. CONCLUSÃO: Os resultados sugerem que a via de. produção da RvD1 pode servir como uma potencial estratégia terapêutica para os. pacientes com LCD.

INTRODUCTION: Diffuse Cutaneous Leishmaniasis (DCL) is a rare clinical manifestation caused by Leishmania amazonensis that is characterized by an inefficient parasite-specific cellular responses and heavily parasitized macrophages in skin lesions. Lipid mediators and their precursors play a crucial role during Leishmania infection. Previous works have shown that patients with cutaneous leishmaniasis exhibit a distinct in situ and systemic balance of this eicosanoids. Recently, pro-resolution lipid mediators have been shown to play critical role in dampening pathological inflammatory processes to reestablish homeostasis in a diverse range of experimental settings. Among these mediators, resolvins from D series have been described to exhibit potent antiinflammatory and immune-regulatory activities that include inhibition of leukocyte chemotaxis and blockage on the production of proinflammatory cytokines. However, whether resolvins play significant roles in establishment and persistence of Leishmania infection is currently unknown. AIM: We addressed this question by assessing circulating levels of resolvin D1 (RvD1) in tegumentary leishmaniasis patients presenting localized cutaneous leishmaniasis (LCL) or diffuse disease. RESULTS: We found that DCL patients have higher plasma levels of RvD1 when compared with LCL patients or endemic controls. In addition, the levels of this mediator were positively correlated with arginase-I and TGF-β and were negatively correlated with TNF-α levels. Additional in vitro experiments using primary human macrophages revealed that resolvin D1 promotes the intracellular L. amazonensis replication for a mechanism dependent on induction of heme oxygenase-1 enzyme. CONCLUSION: These results indicate that targeting RvD1 could serve as potential strategy for DCL patients.

The antifungal compound butenafine eliminates promastigote and amastigote forms of Leishmania (Leishmania) amazonensis and Leishmania (Viannia) braziliensis.

The production of ergosterol lipid, important for the Leishmania membrane homeostasis, involves different enzymes. This pathway can be blocked to azoles and allylamines drugs, such as Butenafine. The aim of the present work was to evaluate the anti-leishmanicidal activity of this drug in 2 major species of Leishmania responsible for causing the American tegumentar leishmaniasis (L. (L.) amazonensis and L. (V.) braziliensis). Butenafine eliminated promastigote forms of L. amazonensis and L. braziliensis with efficacy similar to miltefosine, a standard anti-leishmania drug. In addition, butenafine induced alterations in promastigote forms of L. amazonensis that resemble programmed cell death. Butenafine as well as miltefosine presented mild toxicity in peritoneal macrophages, however, butenafine was more effective to eliminate intracellular amastigotes of both L. amazonensis and L. braziliensis, and this effect was not associated with elevated levels of nitric oxide or hydrogen peroxide. Taken together, data presented herein suggests that butenafine can be considered as a prototype drug able to eliminate L. amazonensis and L. braziliensis, etiological agents of anergic diffuse and mucocutaneous leishmaniasis, respectively.

In vitro and in vivo antileishmania activity of sesquiterpene lactone-rich dichloromethane fraction obtained from Tanacetum parthenium (L.) Schultz-Bip.

The discovery of new treatments for neglected diseases, including leishmaniasis, is a substantial challenge for scientific research. Plant extracts have shown potential in the selective treatment of tropical diseases. The present study evaluated the in vitro and in vivo antileishmania effects of a sesquiterpene lactone-rich dichloromethane fraction (DF) obtained from the aerial parts of Tanacetum parthenium (L.) Schultz-Bip. In vitro studies of the DF indicated an IC50 of 2.40±0.76 µg mL(-1) against the promastigote form and 1.76±0.25 µg mL(-1) against the axenic amastigote form of Leishmania amazonensis. In vivo intramuscular treatment with DF decreased the growth and size of footpad lesions in mice. The DF also significantly decreased the parasite population compared with animals that were treated with the reference drug. Plasma malondialdehyde levels were increased slightly by the DF, attributable to its parthenolide-rich composition that causes cellular apoptosis, compared with the control group, demonstrating treatment efficacy without toxicity or genotoxicity. Because the isolation and purification of plant compounds are costly and time-consuming and generate low yields, extract fractions, such as the DF studied herein, represent a promising alternative for the treatment of leishmaniasis.

Comparison of conventional, molecular, and immunohistochemical methods in diagnosis of typical and atypical cutaneous leishmaniasis.

CONTEXT: Localized cutaneous leishmaniasis (CL) typically presents as papules, crusted nodules, plaques, or noduloulcerative lesions. Atypical CL does not show these features or mimic malignant lesion. In atypical forms, CL may be overlooked because of its similarity to other dermal diseases. OBJECTIVE: To compare conventional, molecular, and immunohistochemical methods in the diagnosis of typical and atypical CL. DESIGN: The kinetoplast DNA, nested, polymerase chain reaction assay and immunohistochemical methods were compared and validated against conventional methods, including cytology and pathology, using 100 specimens of typical and atypical lesions of suspected CL. RESULTS: Compared with other methods, polymerase chain reaction of the kinetoplast DNA showed the highest sensitivity (typical positive, 100%, 67 of 67; atypical positive, 94%, 31 of 33) and specificity (100%), followed by immunohistochemistry (typical positive, 97%, 65 of 67, with 100% specificity; atypical positives, 94%, 31 of 33, with 100% specificity), and cytology (typical positive, 79%, 53 of 67, with 100% specificity; atypical positive, 58%, 19 of 33, with 100% specificity), followed by pathology (typical positive, 70%, 47 of 67, with 100% specificity; atypical positive, 42%, 14 of 33, with 100% specificity). In addition, polymerase chain reaction enabled identification of 98% (98 of 100) of the positive samples that included strains of Leishmania major (99% [99 of 100] cases) and Leishmania tropica (1% [1 of 100] cases). CONCLUSIONS: Because cytology is cheap and easy to perform with high sensitivity, it is the preferred, primary approach for typical CL, but cytology and pathology do not have sufficient sensitivity for diagnosis of atypical CL cases. Nested polymerase chain reaction and immunohistochemistry are sensitive tests for diagnosis of both typical and atypical CL and are recommended as complementary tests in suspected CL with negative conventional microscopy results.

PPAR activation induces M1 macrophage polarization via cPLA2-COX-2 inhibition, activating ROS production against Leishmania mexicana.

Defence against Leishmania depends upon Th1 inflammatory response and, a major problem in susceptible models, is the turnoff of the leishmanicidal activity of macrophages with IL-10, IL-4, and COX-2 upregulation, as well as immunosuppressive PGE2, all together inhibiting the respiratory burst. Peroxisome proliferator-activated receptors (PPAR) activation is responsible for macrophages polarization on Leishmania susceptible models where microbicide functions are deactivated. In this paper, we demonstrated that, at least for L. mexicana, PPAR activation, mainly PPAR γ , induced macrophage activation through their polarization towards M1 profile with the increase of microbicide activity against intracellular pathogen L. mexicana. PPAR activation induced IL-10 downregulation, whereas the production of proinflammatory cytokines such as TNF- α , IL-1 ß , and IL-6 remained high. Moreover, PPAR agonists treatment induced the deactivation of cPLA2-COX-2-prostaglandins pathway together with an increase in TLR4 expression, all of whose criteria meet the M1 macrophage profile. Finally, parasite burden, in treated macrophages, was lower than that in infected nontreated macrophages, most probably associated with the increase of respiratory burst in these treated cells. Based on the above data, we conclude that PPAR agonists used in this work induces M1 macrophages polarization via inhibition of cPLA2 and the increase of aggressive microbicidal activity via reactive oxygen species (ROS) production.

Leishmaniose tegumentar americana em cão errante da região noroeste do estado do Paraná - relato de caso / Cutaneous leishmaniasis in a stray dog in the northwestern region of the state of Paraná - a case report / Leishmaniose tegumentaria americana en perros callejeros de la región noroeste del estado de Paraná - relato de caso

A Leishmaniose Tegumentar (LT) é uma doença parasitária cosmopolita provocada por um protozoário pertencente à Ordem Kinetoplastida, família Trypanossomatidea e Gênero Leishmania e é transmitida por insetos dípteros hematófagos pertencentes à subfamília Phlebotominae. Nos cães a forma tegumentar se manifesta com lesões mucocutâneas, formação de úlceras de fundo granulomatoso e bordas salientes de difícil cicatrização. O objetivo deste trabalho foi relatar a presença de anticorpos anti-Leishmania spp. em um cão errante com sintomatologia clínica sugestiva para LTA na região noroeste do estado do Paraná. O resultado positivo no exame sorológico encontrado no presente trabalho sugere que houve a circulação do agente etiológico e, consequentemente, a exposição deste animal ao parasito, porém novos estudos com cães errantes e domiciliados com ou sem sintomatologia característica para LTA devem ser realizados para esclarecer melhor a participação do cão na epidemiologia da LTA no município local.

Cutaneous Leishmaniasis (CL) is a cosmopolitan parasitic disease caused by a protozoan belonging to the Kinetoplastida order, Trypanossomatidea family and Leishmania genus, and is transmitted by blood-sucking flies belonging to the Phlebotominae subfamily. In dogs, the cutaneous form manifests with mucocutaneous lesions, granulomatous bottom ulcers and difficult to heal flanges. This study aimed to report the presence of anti-Leishmania spp. in a stray dog with clinical symptoms suggesting LTA in the northwestern region of the state of Paraná. The positive serology found in the present study suggests that there was a movement of the etiological agent and, therefore, this animal’s exposure to the parasite, but further studies with stray and and domestic dogs with or without characteristic symptoms of LTA should be done to understand the role of a dog in the leishmaniasis epidemiology in the local municipality.

La Leishmaniosis Tegumentaria (LT) es una enfermedad parasitaria cosmopolita provocada por un protozoario perteneciente al Orden Kinetoplastida, familia Trypanosomatidae, Género Leishmania y es transmitida por insectos dípteros hematófagos pertenecientes a la subfamilia Phlebotominae. En perros, la forma tegumentaria se manifiesta con lesiones mucocutáneas, formación de úlceras de fondo granulo matoso y bordas salientes de difícil cicatrización. El objetivo de esta investigación fue relatar la presencia de anticuerpos anti-Leishmania spp. en un perro callejero con sintomatología clínica sugestiva para LTA en la región noroeste del estado de Paraná. El resultado positivo encontrado en el examen serológico, en la investigación, sugiere que hubo circulación del agente etiológico y, consecuentemente, la exposición de este animal al parasito, pero nuevos estudios con perros callejeros y domiciliados con o sin sintomatología característica para LTA deben ser realizados, para aclarar mejor la participación del perro en la epidemiología de LTA en el municipio local.

Exposure of phosphatidylserine on Leishmania amazonensis isolates is associated with diffuse cutaneous leishmaniasis and parasite infectivity.

Diffuse cutaneous leishmaniasis (DCL) is a rare clinical manifestation of leishmaniasis, characterized by an inefficient parasite-specific cellular response and heavily parasitized macrophages. In Brazil, Leishmania (Leishmania) amazonensis is the main species involved in DCL cases. In the experimental model, recognition of phosphatidylserine (PS) molecules exposed on the surface of amastigotes forms of L. amazonensis inhibits the inflammatory response of infected macrophages as a strategy to evade the host immune surveillance. In this study, we examined whether PS exposure on L. amazonensis isolates from DCL patients operated as a parasite pathogenic factor and as a putative suppression mechanism of immune response during the infection. Peritoneal macrophages from F1 mice (BALB/c×C57BL/6) were infected with different L. amazonensis isolates from patients with localized cutaneous leishmaniasis (LCL) or DCL. DCL isolates showed higher PS exposure than their counterparts from LCL patients. In addition, PS exposure was positively correlated with clinical parameters of the human infection (number of lesions and time of disease) and with characteristics of the experimental infection (macrophage infection and anti-inflammatory cytokine induction). Furthermore, parasites isolated from DCL patients displayed an increased area in parasitophorous vacuoles (PV) when compared to those isolated from LCL patients. Thus, this study shows for the first time that a parasite factor (exposed PS) might be associated with parasite survival/persistence in macrophages and lesion exacerbation during the course of DCL, providing new insights regarding pathogenic mechanism in this rare chronic disease.

Leishmania mexicana lipophosphoglycan differentially regulates PKCalpha-induced oxidative burst in macrophages of BALB/c and C57BL/6 mice.

Leishmania are protozoan parasites that infect macrophages and their survival is partially achieved through inhibition of the cellular oxidative burst by parasite lipophosphoglycan (LPG). PKCalpha is the predominant PKC isoenzyme required for macrophage oxidative burst, yet it is not known if different susceptibility of BALB/c and C57BL/6 mice to Leishmania mexicana could be related to PKCalpha. We analysed the effect of L. mexicana promastigotes and parasite LPG on expression of PKCalpha and on its activity in macrophages of both mouse strains. Our data show that expression of the isoenzyme was not altered either by LPG or by L. mexicana promastigotes. Yet LPG exerted opposing effects on PKCalpha activity of macrophages between both strains: in susceptible BALB/c cells, it inhibited PKCalpha activity, whereas in the more resistant strain it augmented enzymatic activity 2.8 times. In addition, LPG inhibited oxidative burst only in susceptible BALB/c macrophages and the degree of inhibition correlated with parasite survival. Promastigotes also inhibited PKCalpha activity and oxidative burst in macrophages of BALB/c mice, whereas in C57BL/6, they enhanced PKCalpha activity and oxidative burst inhibition was less severe. Our data indicate that control of PKCalpha-induced oxidative burst by L. mexicana LPG relates with its success to infect murine macrophages.

Leishsmania (Leishmania) amazonensis infection: Muscular involvement in BALB/c and C3H.HeN mice.

Recent studies have provided some insights into Leishsmania (Leishmania) amazonensis muscular infection in dogs, although, muscular disease due to leishmaniasis has been poorly documented. The aim of our study was to evaluate involvement of Leishmania in muscular infection of two distinct mouse strains (BALB/c and C3H.He), with different genetic backgrounds. BALB/c mice, susceptible to Leishmania infection, showed, at the beginning of infection, a great number of infected macrophages among muscle fibers; however, in C3H.He resistant mice, muscle fibers were less damaged than in BALB/c mice, but some parasitized macrophages could be seen among them. A follow up of the infection showed an intense inflammatory infiltrate mainly composed of infected macrophages in BALB/c muscles and the presence of amastigotes within muscle fibers; while C3H.He mice exhibited a moderate inflammatory infiltrate among skeletal muscle fibers and an absence of amastigotes. Total destruction of muscles was observed in BALB/c mice in the late phase of infection (day 90) while C3H.He mice showed a process of muscle repair. We concluded that: (1) the muscles of BALB/c mice were more affected by leishmaniasis than those of C3/H.He mice; (2) Leishmania amastigotes are capable of infecting muscular fibers, as observed in BALB/c mice; (3) as inflammatory infiltrate is less intense in C3H.He mice these animals are capable of restoring muscular fibers.

Diffuse cutaneous leishmaniasis in HIV.

Cutaneous leishmaniasis is caused by the intracellular protozoan parasite belonging to the genus leishmania and is characterized by a myriad of clinical lesions including papules, nodules, and ulcers. Diffuse cutaneous forms of leishmaniasis are rare. We report a rare case from South India of diffuse cutaneous leishmaniasis masquerading as lepromatous leprosy in the context of HIV infection.