13 research outputs found

    Eco-epidemiological analysis of rickettsial seropositivity in rural areas of Colombia: A multilevel approach

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    ABSTARCT: Rickettsiosis is a re-emergent infectious disease without epidemiological surveillance in Colombia. This disease is generally undiagnosed and several deadly outbreaks have been reported in the country in the last decade. The aim of this study is to analyze the eco-epidemiological aspects of rickettsial seropositivity in rural areas of Colombia where outbreaks of the disease were previously reported. A cross-sectional study, which included 597 people living in 246 households from nine hamlets in two municipalities of Colombia, was conducted from November 2015 to January 2016. The survey was conducted to collect sociodemographic and household characteristics (exposure) data. Blood samples were collected to determine the rickettsial seropositivity in humans, horses and dogs (IFA, cut-off = 1/128). In addition, infections by rickettsiae were detected in ticks from humans and animals by real-time PCR targeting gltA and ompA genes. Data was analyzed by weighted multilevel clog-log regression model using three levels (person, household and hamlets) and rickettsial seropositivity in humans was the main outcome. Overall prevalence of rickettsial seropositivity in humans was 25.62% (95%CI 22.11-29.12). Age in years (PR = 1.01 95%CI 1.01-1.02) and male sex (PR = 1.65 95%CI 1.43-1.90) were risk markers for rickettsial seropositivity. Working outdoors (PR = 1.20 95%CI 1.02-1.41), deforestation and forest fragmentation for agriculture use (PR = 1.75 95%CI 1.51-2.02), opossum in peridomiciliary area (PR = 1.56 95%CI 1.37-1.79) and a high proportion of seropositive domestic animals in the home (PR20-40% vs 40% vs <20% = 3.14 95%CI 2.43-4.04) were associated with rickettsial seropositivity in humans. This study showed the presence of Rickettsia antibodies in human populations and domestic animals. In addition, different species of rickettsiae were detected in ticks collected from humans and animals. Our results highlighted the role of domestic animals as sentinels of rickettsial infection to identify areas at risk of transmission, and the importance of preventive measures aimed at curtailing deforestation and the fragmentation of forests as a way of reducing the risk of transmission of emergent and re-emergent pathogens

    Domestic dogs in a fragmented landscape in the Brazilian Atlantic Forest: abundance, habitat use and caring by owners

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    This study aimed at estimating the population size and attitudes of residents towards caring for domestic dogs, through questionnaire surveys, as well as the frequency of these animals in different habitats (anthropic and forest patch), using scent stations. The study was conducted in a severely fragmented area of the Brazilian Atlantic Forest. A large number of unrestricted dogs was recorded, averaging 6.2 ind/km². These dogs have owners and are regularly fed. Dog records decreased from the anthropogenic matrix to the forest patch edge, which suggests that dogs act as an edge effect on forest patches. Encounters between domestic dog and wild animals can still be frequent in severely fragmented landscapes, mainly at the forest edges. However the fact that most dogs have an owner and are more frequent in the anthropic habitat suggests that their putative effects are less severe than expected for a carnivore of such abundance, but the reinforcement of responsible ownership is needed to further ameliorate such effects

    Estudo comparativo entre estibogluconato de sódio BP 88® e antimoniato de meglumina no tratamento da leishmaniose cutânea II. Toxicidade bioquímica e cardíaca Comparative study between sodium stibogluconate BP 88®and meglumine antimoniate in cutaneous leishmaniasis treatment. II. Biochemical and cardiac toxicity

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    Foi avaliada a toxicidade de dois antimoniais pentavalentes em 111 pacientes com leishmaniose cutânea. Quarenta e sete pacientes receberam antimoniato de meglumina (Grupo I) e 64 pacientes, estibogluconato de sódio BP 88® (Grupo II), 20mg SbV/kg/dia por 20 dias. Realizou-se a avaliação de aminotransferases, fosfatase alcalina, amilase, creatinina, uréia, exame de urina e eletrocardiograma, antes do tratamento e no décimo e vigésimo dias. Observou-se maior freqüência de valores anormais de aminotransferases no décimo e vigésimo dias de tratamento no grupo II (p < 0,001) e maior proporção de valores anormais de amilase no décimo dia no mesmo grupo (p < 0,001). Houve maior variação dos níveis de aminotransferases, fosfatase alcalina e amilase nos primeiros dez dias no grupo II (p < 0,01). No vigésimo dia observou-se maior variação nos níveis de aminotransferases no grupo II (p = 0,02 e p = 0,03, respectivamente). Quarenta e três porcento dos pacientes do grupo I e 54% dos pacientes do grupo II apresentaram alterações eletrocardiográficas (p = 0,30).<br>Toxicity of two antimonial pentavalents were evaluated in 111 patients with cutaneous leishmaniasis. Forty seven patients received meglumine antimoniate (Group I) and 64 patients, sodium stibogluconate BP 88® (Group II), 20mg SbV/kg/day for 20 days. Evaluation of aminotransferases, alkaline phosphatase, amilase, creatinine, urea, urine analysis and electrocardiogram were performed at baseline, on the tenth and twentieth day of treatment. Greater frequency of aminotransferase abnormal levels were observed on the tenth and twentieth days in group II (p < 0,001) and a greater proportion of amilase abnormal levels at the tenth day in the same group (p < 0,001). There was a greater variation of aminotransferases, alkaline phosphatase and amilase in the first ten days of treatment in group II (p < 0,01). On the twentieth day there was a greater variation of aminotransferase levels in group II (p = 0,02 and p = 0,03, respectively). Forty three percent of group I and 54% of group II showed electrocardiographic abnormalities (p = 0,30)

    Automobilismo: no calor da competição Automovilismo: en el calor de la competición Car racing: in the heat of competition

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    O presente artigo questiona o papel do calor como um fator de risco adicional para o acidente que vitimou Ayrton Senna. O automobilismo de competição constitui um desafio biológico, uma situação estressante do ponto de vista mental e físico. A manutenção da performance depende da disponibilidade de carboidratos e oxigênio, hidratação adequada e temperatura interna constante entre 37 e 38 graus centígrados. A dissipação do calor produzido pelo metabolismo ocorre através do aumento do fluxo de sangue para pele e produção de suor e manter a temperatura cerebral constante se constitui num problema permanente. Verificou-se experimentalmente que a energia necessária para dirigir um automóvel de corrida é comparável a um esporte como o voleibol. Durante uma corrida, o indivíduo está exposto a um microambiente quente na cabina, que pode atingir 50ºC, gerado por fontes de calor mecânicas e ambientais. O bloqueio da evaporação do suor pelo macacão resulta em umidade e desconforto pessoal, o que implica maior esforço mental para dirigir o carro. As medidas contra o calor começam antes da corrida, cuidando-se do estado nutricional, da hidratação e principalmente do condicionamento físico através de exercícios aeróbios regulares e adequados, que permitem aumentar a capacidade de trabalho e a tolerância ao calor, o que resulta em menor fadiga durante a corrida. Outro procedimento importante deveria ser a aclimatação prévia dos pilotos aos ambientes quentes e úmidos. Deve-se fazer o possível para reduzir o aquecimento do veículo e respeitar o sistema de bandeiras de advertência para os riscos de hipertermia. Em conclusão, embora Ayrton Senna fosse um indivíduo com maior risco de desenvolver hipertermia, independentemente de outras causas, não parece ter havido tempo de corrida suficiente para haver produção de calor metabólico capaz de aumentar excessivamente a temperatura interna do piloto nas condições ambientais do autódromo no dia de sua morte.<br>El presente artículo cuestiona el papel del calor como un factor de riesgo adicional para el accidente que sufrió Ayrton Senna. El automovilismo de competición constituye un desafío biológico, una situación estresante desde el punto de vista mental y físico. El mantenimiento de la performance depende de la disponibilidad de los carbohidratos y del oxígeno, hidratación adecuada y temperatura interna constante entre 37 y 38 grados centígrados. La disipación de calor producido por el metabolismo que ocurre a través del aumento del flujo de sangre para mantener la temperatura cerebral constante constituye un problema permanente. Se ha verificado experimentalmente que la energía requerida para conducir un auto de carrera es similar a la requerida para practicar un deporte como el voleibol. Durante una carrera, el individuo está expuesto a un microambiente caliente dentro de la cabina que puede llegar hasta los 50 grados centígrados generado por fuentes de calor como las mecánicas y las ambientales. El bloque del sudor por el mameluco resulta en humedad y disconfor personal, lo que implica un mayor esfuerzo personal para conducir el auto. Las medidas contra el calor comienzan antes de la carrera, cuidando el estado nutricional, la hidratación y principalmente el acondicionamiento físico a través de ejercicios aeróbicos regulares y adecuados, que permitan aumentar la capacidad de trabajo y la tolerancia al calor, lo que resulta en una menor fatiga durante la carrera. Otro procedimiento importante debería ser la aclimatación de los pilotos en ambientes calientes y húmedos. Se debe realizar lo posible en el acondicionamiento del vehículo para respetar el sistema de banderas de advertencia para los riesgos de hipertermia. En conclusión, si ahora Ayrton Senna fuera un individuo con mayor riesgo de desarrollar hipertermia, independientemente de otras causas, no parece haber habido tiempo suficiente en la carrera para la producción del calor metabólico capaz de aumentar excesivamente la temperatura interna del piloto en las condiciones ambientales del autódromo el día de su muerte.<br>The present study discusses the role of heat as an additional risk factor for the accident that killed the pilot Ayrton Senna. The competition car racing is a biological challenge, a stressing situation from the physical and mental point of view. The maintenance of performance depends on the oxygen and carbohydrates availability, adequate hydration and constant internal temperature, between 37 and 38ºC. The dissipation of heat produced by the metabolism occurs through the increase on the cutaneous blood flow and sweat and maintaining brain temperature constant becomes a permanent problem. It was experimentally verified that the energy required to the racecar driving is comparable to a sport such as volleyball. During a car race, the individual is exposed to a hot microenvironment in the cockpit, sometimes reaching 50ºC, generated by mechanical and environmental sources of heat. The obstruction of the sweat evaporation by the racesuit results in humidity and personal discomfort, what leads to higher mental effort to drive the car. The anti-heat measures are adopted before the race, considering the nutritional state, hydration and specially the physical conditioning through adequate and regular aerobic exercises that enable increasing the work capacity and the heat tolerance, resulting in lower fatigue during the car racing. Another important procedure should be the previous acclimation of pilots to hot and humid environments. All efforts should be done to reduce the vehicle heating and to respect the warning flag system for the risks of hyperthermia. Finally, although Ayrton Senna was an individual with higher risk of developing hyperthermia, regardless other causes, it seems not to have elapsed sufficient time of race in order to produce metabolic heat capable to increase excessively the pilot's internal temperature in the environmental conditions of the autodrome in the day of his death

    Óbito durante tratamento da leishmaniose tegumentar americana com stibogluconato de sódio bp 88® (shandong xinhua) Fatal case during treatment of american tegumentary leishmaniasis with sodium stibogluconate bp 88® (shandong xinhua)

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    Os autores relatam a ocorrência de óbito em paciente portador da forma cutânea da LTA no município de Caxias-MA. Trata-se de paciente do sexo masculino, 22 anos, gari, portador de lesão ulcerada no membro inferior (perna esquerda), diagnosticado, após encontro do parasita (Leishmania) na lesão, tratado com stibogluconato de sódio BP88® (Shandong Xinhua) na dose de 10mg/Sb+5/kg/dia/20 dias. Após a 3ª dose apresentou dores articulares, naúseas, mal estar geral. Com a continuação da medicação houve agravamento do quadro com dor epigástrica e no hipocôndrio direito irradiando-se para o hemitórax homolateral. Após a 7ª dose apresentou dispnéia associado à dor torácica de leve intensidade. Na 9ª dose houve piora do quadro, mesmo assim continuou a usar o medicamento até a 11ª dose quando seu estado agravou-se. Foi internado, necessitando de tratamento intensivo. Nos exames realizados apresentou: 4,4 milhões de eritócitos, 10,6% de hemoglobina, 35% de hematócrito, 26.400 de leucócitos, basófilos e mielócitos (0), 59% de segmentados, 30% de linfócitos, 2% de monócitos, plaquetas (normais), glicose 42mg%, uréia 73mg%, creatinina (2,4mg%), eletrocardiograma (bloqueio de ramo direito). Veio a falecer tendo como causa do óbito, insuficiência cárdio respiratória. O relato atual mostra a necessidade de esclarecimento das equipes de saúde quanto ao uso dos Sb+5 e também lembrar o Ministério da Saúde quando da aquisição de novos produtos, preocupar-se com a qualidade e procedência do mesmo.<br>The authors report the occurrence of a fatal case in patient with cutaneous leishmaniasis in the municipality of Caxias, MA. Male patient, 22 years old, road sweeper, presented with an ulcer in left leg, diagnosed as cutaneous leishmaniasis and treated with sodium stibogluconate BP88®(Sb+5) (Shandong Xinhua) at a dose of 10mg/Sb+5/kg/day/20 days. After dose three he presented arthralgia, myalgia, nausea and weakness. During the therapy there was an aggravation of the symptoms with abdominal pain and irradiation into the thorax. After dose seven he presented a picture of associated dyspnea and thoracic pain of mild intensity. At dose nine there was further worsening of the picture, nevertheless the therapy was continued up to dose 11, when the patient's state deteriorated to such an extent that he was hospitalized in the intensive care unit. Exams: erythrocytes, 4.4 million; hemoglobin, 10.6%; hematocrits, 35%; white blood cells 26,400, basophiles and myelocytes (0); segmented leukocytes, 59%; lymphocytes 30%; monocytes 2%; platelets (normal); glucose, 42mg%; urea, 73mg%; creatinine, 2.4mg%; and ECG (blockade of right branch). The patient died from cardiorespiratory insufficiency. The current report underscores the need to clarify health workers regarding the use of Sb+5 and also to remind the Health Ministry to verify the quality and origin when acquiring new products
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