Leishmania panamensis transmission in the domestic environment: the results of a prospective epidemiological survey in Santander, Colombia.
ABSTRACT Domestic transmission now appears to be the principal route of Leishmania panamensis infection in deforested regions characterized by the replacement of primary forest by permanent plantations, i,e coffee or cacao crops. This paper presents the results of the disease patterns in a representative population of the Opón focus, in Santander, Colombia.
The principal aims were: 1) to measure the incidence rate in a representative population of the Opón focus; 2) to identify demographic risk factors for infection; 3) to estimate the proportion of infections which cause disease; 4) to estimate the protection against disease from acquired immunity; 5) to estimate the frequency of reactivations, and 6) to estimate the risk of mucosal leishmaniasis.
A 19 month prospective survey of leishmaniasis caused by Leishmania panamensis was carried out amongst 1380 people in a cacao growing region of Santander Department, Colombia. The population was diagnosed clinically and by the Montenegro skin test (at two time points).
The incidence rate was 0.19 infections/person-year, with 31% of infections apparently subclinical. The risk of acquiring cutaneous leishmaniasis decreased with age even in the absence of apparent previous infections. Protective immunity followed both clinical and subclinical infections, persisting for at least 10 years after a primary lesion. Mucocutaneous leishmaniasis was detected in 12% of the population with cutaneous lesions, of which 77% had mild symptoms, and 23% perforated nasal septa. The risk of mucosal leishmaniasis was greatest for males, and for people whose primary cutaneous lesion was on the head.
The average age of infection in Opón, 7.7 years (1/lambda), and the absence of gender as a risk factor is highly indicative of intradomiciliary or peridomiciliary transmission.
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ABSTRACT: This review addresses the question of whether the risk of developing mucosal leishmaniasis (ML) warrants systemic treatment in all patients with New World cutaneous leishmaniasis (CL) or whether local treatment might be an acceptable alternative. The risk of patients with New World CL developing ML after the initial infection has been the main argument for systemic treatment. However, this statement needs re-evaluation and consideration of all the available data. The putative benefit of preventing ML should outweigh the toxicity of systemic antileishmanial therapy. To assess the need for and risk of systemic treatment the following factors were reviewed: the incidence and prevalence of ML in endemic populations and in travellers; the severity of mucosal lesions; the efficacy of current options to treat ML; the toxicity and, to a lesser extent, the costs of systemic treatment; the risk of developing ML after local treatment; and the strengths and limitations of current estimates of the risk of developing ML in different situations. Local treatment might be considered as a valuable treatment option for travellers suffering from New World CL, provided that there are no risk factors for developing ML such as multiple lesions, big lesions (>4 cm(2)), localisation of the lesion on the head or neck, immunosuppression or acquisition of infection in the high Andean countries, notably Bolivia.International Health 09/2012; 4(3):153-63. DOI:10.1016/j.inhe.2012.06.004 · 1.13 Impact Factor
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ABSTRACT: We present a review of current knowledge about mucosal leishmaniasis (ML). Although involvement of mucous membranes is classically admitted in New World leishmaniasis, particularly occurring in infection by Leishmania (L.) braziliensis species complex, ML is also a possible presentation of Old World leishmaniasis, in either L. donovani or L. major species complex infections. Thus, ML has to be considered not only as a Latin American disease but as an Old and New World disease. We describe ML epidemiology, pathogenesis, clinics, diagnosis, and therapy. Considering both its highly disfiguring lesions and its possible lethal outcome, ML should not be underestimated by physicians. Moreover, leishmaniasis is expected to increase its burden in many countries as sandfly vector distribution is widespreading towards non-endemic areas. Finally, the lack of clear understanding of ML pathogenesis and the absence of effective human vaccines strongly claim for more research.06/2013; 2013:805108. DOI:10.1155/2013/805108
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ABSTRACT: Infectious disease incidence is often male-biased. Two main hypotheses have been proposed to explain this observation. The physiological hypothesis (PH) emphasizes differences in sex hormones and genetic architecture, while the behavioral hypothesis (BH) stresses gender-related differences in exposure. Surprisingly, the population-level predictions of these hypotheses are yet to be thoroughly tested in humans. For ten major pathogens, we tested PH and BH predictions about incidence and exposure-prevalence patterns. Compulsory-notification records (Brazil, 2006-2009) were used to estimate age-stratified ♂:♀ incidence rate ratios for the general population and across selected sociological contrasts. Exposure-prevalence odds ratios were derived from 82 published surveys. We estimated summary effect-size measures using random-effects models; our analyses encompass ∼0.5 million cases of disease or exposure. We found that, after puberty, disease incidence is male-biased in cutaneous and visceral leishmaniasis, schistosomiasis, pulmonary tuberculosis, leptospirosis, meningococcal meningitis, and hepatitis A. Severe dengue is female-biased, and no clear pattern is evident for typhoid fever. In leprosy, milder tuberculoid forms are female-biased, whereas more severe lepromatous forms are male-biased. For most diseases, male bias emerges also during infancy, when behavior is unbiased but sex steroid levels transiently rise. Behavioral factors likely modulate male-female differences in some diseases (the leishmaniases, tuberculosis, leptospirosis, or schistosomiasis) and age classes; however, average exposure-prevalence is significantly sex-biased only for Schistosoma and Leptospira. Our results closely match some key PH predictions and contradict some crucial BH predictions, suggesting that gender-specific behavior plays an overall secondary role in generating sex bias. Physiological differences, including the crosstalk between sex hormones and immune effectors, thus emerge as the main candidate drivers of gender differences in infectious disease susceptibility.PLoS ONE 04/2013; 8(4):e62390. DOI:10.1371/journal.pone.0062390 · 3.53 Impact Factor