Leishmaniasis cutanea epub download


    Leishmaniasis is caused by an intracellular parasite transmitted to humans by the bite Albertos-Alpuche N: Vectores de la leishmaniasis cutánea en México. PAROLE CHIAVE: Leishmaniosi cutanea; Leishmania infantum; leishmaniosi correlata al lavoro; cambiamento climatico. SUMMARY. Background: Leishmaniasis is a widespread infectious disease, but there is not much .. Epub Malaria y leishmaniasis cutánea en Ecuador pdf epub ebooks download free, download more free pdf, epub ebooks of 0, pdf, epub ebooks free download.

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    Leishmaniasis Cutanea Epub Download

    COM in simple step and you can Download Now it now. [Free DOWNLOAD] Alice The than , free saicumspecsacont.cf library catalog is an Liposomas ultradeformables fotodinamicos contra leishmaniasis cutanea. Back to Top. ALICE THE. Leishmania amastigotes were also revealed by electron microscopy. Mazza, S : Leishmaniosis cutanea en el caballo y nueva observacion de la misma en el. such as Leishmaniasis, Chagas disease, Toxocariasis, Brucellosis in Latin America. (Rodriguez-Morales .. Impacto de Los Eventos de El Niño Southern Oscillation (ENSO) sobre la Leishmaniosis Cutánea .. Epub Apr 7. Liverman, D.

    Abstract Background Several controlled and uncontrolled studies addressing azole antifungal drugs for cutaneous and mucosal leishmaniasis have been published with inconclusive results. We conducted a systematic literature review of studies evaluating the efficacy and toxicity associated with azole therapy for tegumentary leishmaniasis. Additional resources such as Google Scholar and clinicaltrials. We included all studies reporting cure rate after cutaneous or mucosal leishmaniasis treatment with systemic azole drugs, regardless of their design. R software was used to estimate global rates of success and adverse events with each drug. The main outcome of interest was clinical cure, defined as complete re-epithelialization of all lesions. Results A total of 37 studies involving patients that reported outcomes after fluconazole 9 , ketoconazole 14 and itraconazole 15 treatments were included. Twenty-four studies were conducted in the Old World and 13 studies in the Americas. This systematic review included studies with small samples and both non-comparative and non-randomized studies and the main limitation was the low quality of the available studies. Conclusions Available evidence suggests that fluconazole, ketoconazole and itraconazole have similar and modest efficacy rates for tegumentary leishmaniasis treatment. There is insufficient evidence to support the exclusive use of azole therapy as a single agent for leishmaniasis treatment. This is an open access article distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: All relevant data are within the paper and its Supporting Information files. ELG is a Ph. The authors received no specific funding for this work.

    The inclusion criteria were treatment-naive patients with localized CL diagnosis primary involvement of the skin with one to fewer than 20 ulcerous lesions, usually with good response to treatment on the basis of clinical signs suggestive cutaneous lesions , immunological criteria Leishmania serology using indirect immunofluorescence reaction IIF and enzyme-linked immunosorbent assay ELISA , and parasitological criteria positive culture for Leishmania in suitable media , and patients whose samples were identified as L.

    Exclusion criteria were patients with clinical forms other than localized CL, lack of post-treatment follow-up for at least 2 years, or those presenting comorbidities. Clinical and laboratory data Clinical and laboratory data were collected directly from the records of the selected patients. The populations being studied were classified by therapeutic outcome. The R group included patients who presented clinical healing defined as complete epithelization of the cutaneous lesions up to 3 months after the conclusion of one course of treatment, and subsequent total regression of crusts, desquamation, infiltration, and erythema, without any sign of reactivation and absence of mucosal lesions over a 1 year observation period.

    The NR group included patients experiencing therapeutic failure absence of complete skin-lesion epithelization up to 3 months after the end of one treatment or lesion recurrence reappearance of skin or mucosal lesions up to 1 year after clinical healing requiring new courses of treatment. Sample preparation Leishmania promastigotes isolated from biopsies of cutaneous lesions were immediately stored in liquid nitrogen and subsequently recovered after two passages in Schneider's Drosophila medium Sigma-Aldrich, St.

    The L. The isolated parasites were previously characterized as Leishmania V. The reference strains L. Purified products underwent a second amplification using primer B1 under low-stringency conditions and using high concentrations of Taq DNA polymerase according to the protocol described by Oliveira et al. LSSP-PCR bands varying from to bp were scored and compared using the simple matching coefficient of similarity to determine the proportion of mismatched bands between pairs of isolates.

    A total of 14 characteristics bands were evaluated see Table 2 and Figure 2. The association between categorical variables with clusters and therapeutic outcome was verified by Pearson's chi-squared test, Fisher's exact test, and the Shapiro-Wilk normality test. The Mann-Whitney U test was used to compare the median of number of treatments, MST mm , number of lesions, and evolution time days , whereas Student's t-test was used to compare mean age by cluster and by therapeutic outcome.

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    Results Patient clinical and geographical data Forty-four patient samples were included in this study, with 26 Thirty-five patients Twenty-three patients Abstract Leishmaniasis is caused by an intracellular parasite transmitted to humans by the bite of a sand fly. It is endemic in Asia, Africa, the Americas, and the Mediterranean region. Worldwide, 1. Clinical features depend on the species of Leishmania involved and the immune response of the host. Manifestations range from the localized cutaneous to the visceral form with potentially fatal outcomes.

    Many drugs are used in its treatment, but the only effective treatment is achieved with current pentavalent antimonials. Keywords: Leishmaniasis, Leishmania, cutaneous-chondral, chicleros ulcer Introduction Leishmaniasis is a tropical and subtropical disease caused by an intracellular parasite transmitted to humans by the bite of a sand fly, mainly Phlebotomus and Lutzomyia Europe, Northern Africa, the Middle East, Asia, and part of South America ; exceptionally, transmission has also been reported as a laboratory accident 1.

    According to the World Health Organization WHO , leishmaniasis is one of the seven most important tropical diseases and it represents a serious world health problem that presents a broad spectrum of clinical manifestations with a potentially fatal outcome 2 , 3.

    Leishmaniasis: a review

    The clinical features include a broad range of manifestations with different degrees of severity that depend on the species of Leishmania involved and the immune response of the host 3. Epidemiology Leishmaniasis is a disease with a worldwide distribution; it is found in about 89 countries 4 , 5.

    In the American continent, it is mainly a jungle zoonosis but it can be acquired in semi-desert or cold regions transmitted by sand flies mainly of the genera Phlebotomus and Lutzomyia.

    It is important to note that, in parallel to treatment failure, the literature has also evidenced the possibility of an early spontaneous healing without treatment Oliveira-Ribeiro et al.

    In this context, understanding why leishmaniasis is becoming difficult to treat and control can help to develop new approaches to improve the healing of this infection. Unfortunately, despite an impressive amount of information, a conclusive understanding is still under construction.

    Our objective is to introduce and discuss some of the information already published regarding the factors that could influence the treatment response in humans with TL. Table 2 summarizes some findings regarding treatment response. Summary of the aspects involved in human TL treatment. The Healing Process in TL The presence of a balanced immune response mainly produced by cellular immunity is pointed out as necessary to control parasites and promote wound healing.

    Due to difficulties in obtaining tissue smears, many studies have been focused on analyzing the peripheral blood immune response. It is important to note that relevant information has been described correlating the results of the evolution and severity of the lesions, as well as in the therapeutic response. Despite this, in the last years various results were obtained by the evaluation of tissue damages and the organization and activity of the inflammatory process, which brought valuable information.

    The involvement of the in situ inflammatory response in the formation and maintenance of the lesions has previously been demonstrated in the murine model. In this context, Belkaid et al. In addition, in patients, the balance between types 1 and 2 responses has been identified as a determinant in the evolution of TL to self-limited or severe forms Awasthi et al.

    Leishmaniasis: a review

    It is known that an exaggerated Th1 response can lead to tissue damage and has been associated with the immunopathogenesis of mucosal lesions Ribeiro-de-Jesus et al. A summary of the main immunological features already described in the tegumentary leishmaniasis is represented in Figure 2.

    Summary of the main immunological features described in mucosal lesions, localized cutaneous leishmaniasis and skin scars of tegumentary leishmaniasis. Predominant cell subtypes were indicated for each clinical form. The blue squares represent the intensity of the parameters indicated in the figure. Concerning the tissue microenvironment, it has also been shown that ATL lesions are characterized by a chronic granulomatous inflammatory reaction, with intense lymphoplasmacytic infiltration Quintella et al.

    Lymphocytes, macrophages and neutrophils predominate in the lesions of typical LCL, defined as those with the presence of ulcers with infiltrated borders and granular bottoms Schubach et al. Morgado et al. These changes could be linked to decreased parasite load Morgado et al. On the other hand, the imbalanced response can both decrease and exacerbate type 1 response that can elicit tissue damage making difficult to control TL. In this context, Maspi et al.

    This uncontrolled response could be responsible for the significant tissue damage, explaining the appearance of extensive, destructive, and difficult-to-treat lesions.

    The detailing of the immune response involved in the formation of TL lesions has been the subject of numerous revisions, but some details are important for understanding the mechanism of cure or therapeutic failure. In this context, other cells participate in the inflammatory process and may influence the progression of TL lesions and some have been implicated as involved in both, the control and the pathogenesis of the infection.

    Neutrophils have also been involved in the decrease in parasite load or in the amplification of macrophage infection Tacchini-Cottier et al.

    In this context, our group identified the presence of neutrophils in lesions with different time of evolution Morgado et al. It was also verified that Leishmania spp. Other studies have shown the influence of different cytokines such as IL and enzymes such as arginase in the pathogenesis of TL Soong et al. Although in part these immunological mechanisms together can reduce the local parasite load, Leishmania is able to escape from immune effectors then persisting in the lesion site Makala et al.

    For example, Leishmania spp. Skin inflammation also plays an important role during the healing of ATL and parasite antigens in ATL scars have already been reported Schubach et al. In situ evaluation of LCL scars demonstrated that after 1 year from healing, the scars presented inflammatory nests surrounded by scar tissue as well as close to vessels and cutaneous glands.

    Inflammatory areas presented similar organization than that observed in active lesions from the same patient, including number and distribution of lymphocytes and macrophages, despite a reduction in the inflammatory areas.

    When scars were examined after 3 year evolution, it was still possible to verify that the inflammatory foci were still present and showing signs of inflammatory activity, including the detection of parasites, but presenting lower cellularity as compared with 1 year scars Morgado et al.

    These results pointed out that the cellular composition of the skin inflammatory reaction changes steadily even after wound healing and, along with the presence of parasites suggests a dynamic balance between parasite multiplication and immune response that could be disrupted in some situations.

    Thus, individuals with persistent parasites may present disease recurrences Saravia et al. In addition, the parasitic persistence may contribute to the continuous immune system stimulation, maintaining a pool of Leishmania -specific effector cells which can be detected in peripheral blood of healed patients Gaafar et al.

    The implications of parasite persistence on TL scars become important for the explanation of cases of reactivation of infection, years after clinical cure and will be discussed later in this review. In the LCL, the cure criterion is clinical and can be defined as healing with complete re-epithelialization, disappearance of crusts, flattening of the borders of the lesions and absence of new lesions Lindoso et al. The healing of the mucosal lesion must be confirmed by otorhinolaryngological examination, until 6 months after the end of the treatment Gontijo and Carvalho, In both situations, it is important to monitor the patient at least up to 12 months after clinical cure for early detection of signs of lesion reactivation.

    In these cases, the Brazilian Health Ministry recommends a second treatment regimen Brazil, It is important to emphasize that, during monitoring, recurrence, therapeutic failure and disease reactivation can be observed. Thus, some authors believe that confirmation of clinical cure is not always satisfactory, due to the occurrence of numerous reports of recurrence even after therapy and total wound healing.

    It would be interesting to be able to standardize healing criteria not only in relation to clinical parameters, but also parasitological and therapeutic. All over the years, an impressive amount of information has been collected. Different factors such as Leishmania species Handler et al.

    In this sense, we would like to highlight some of the findings that may alter the course of Leishmania infection and modify the therapeutic response in leishmaniasis, with an emphasis on TL.

    Parasite Variability The Leishmania sp. For example, in the New World the infection by Leishmania braziliensis produces localized ulcers whereas the infection by L. Mucosal manifestations occur in patients infected by L. Co-infections with different Leishmania species have been described in patients from Manaus, Brazil Camara-Coelho et al. However, the impact of co-infections by different Leishmania species still needs to be elucidated.

    Molecular characterization of Leishmania isolates has been vastly carried out by four classical markers: the rRNA internal transcribed spacer 1 ITS-1 , kDNA minicircles, the heat shock protein 70 HSP70 and the mitochondrial cytochrome b Cyt-b through techniques based on the digestion by restriction endonuclease enzymes and sequencing of amplified gene followed by phylogenetic analysis Buitrago et al.

    These studies have shown the existence of different genotypes and their relation with clinical manifestations and susceptibility to leishmanicidal drugs. As consequence, disease control could be severely compromised by the intrinsic variability of the circulating species that may limit the efficacy of the treatment while favoring the emergence of resistance.

    For example, in a study of patients from Bolivia, L.