RESUMO

We report two outbreaks of nitrate and nitrite poisoning in Paraíba, Northeast Brazil. The first, due to Pennisetum purpureum (elephant grass), and the second, due to P. purpureum and Brachiaria spp. (brachiaria grass), both occurred during a prolonged drought. In the first outbreak, the irrigation of the pastures with wastewater and sewage contributed to nitrate accumulation. The second outbreak occurred in pastures cultivated in the border of a dam, that had been submerged for long time accumulating large amounts of organic matter in the soil. Other probably risk factors for nitrate accumulation included the use of chemical fertilizers and herbicides and burning of the vegetation. In the first outbreak, four calves out of a total of 42 cattle died, and in the second outbreak 49 out of 243 cattle, including adults, yearlings, and a 2-day-old calf died. The clinical signs included dyspnea, cyanosis, ataxia, and falls, leading to death. The presence of nitrates was detected in both outbreaks using the diphenylamine test. Quantitative tests were performed in the second outbreak using a portable nitrate meter, and high nitrate concentrations were found. The characteristic macroscopic findings and absence of microscopic lesions and response to treatment with methylene blue were key to the diagnosis of poisoning by nitrates and nitrites. We conclude that poisoning by nitrates and nitrites in ruminants in the semiarid region of Northeastern Brazil is frequent due to the cultivation of grasses in the border of dams that had been covered by water for long periods or in areas irrigated by wastewater and/or sewage. In addition, the use of a portable measuring device is an effective alternative for the quantification of nitrates in pastures.

Relatamos dois surtos de intoxicação por nitrato e nitrito na Paraíba, Nordeste do Brasil. O primeiro por Pennisetum purpureum (capim-elefante), e o segundo por P. purpureum e Brachiaria spp. (capim braquiária); ambos ocorreram durante uma estiagem prolongada. No primeiro surto, a irrigação das pastagens com água poluída e esgoto contribuiu para o acúmulo de nitrato. O segundo surto ocorreu em pastagens cultivadas na borda de uma barragem, que há muito tempo ficavam submersas, acumulando grande quantidade de matéria orgânica no solo. Outros prováveis fatores de risco para o acúmulo de nitrato incluíram o uso de fertilizantes químicos e herbicidas e a queima da vegetação. No primeiro surto, quatro bezerros de um total de 42 bovinos morreram, e no segundo surto 49 de 243 bovinos, incluindo adultos, jovens de um ano e um bezerro de 2 dias de idade morreram. Os sinais clínicos incluíram dispneia, cianose, ataxia e quedas, levando à morte. A presença de nitratos foi detectada em ambos os surtos pelo teste de difenilamina. Testes quantitativos foram realizados no segundo surto usando um medidor portátil de nitrato, e altas concentrações de nitrato foram encontradas. Os achados macroscópicos característicos e a ausência de lesões microscópicas e a resposta ao tratamento com azul de metileno foram fundamentais para o diagnóstico de intoxicação por nitratos e nitritos. Concluímos que a intoxicação por nitratos e nitritos em ruminantes na região semiárida do Nordeste do Brasil é frequente devido ao cultivo de gramíneas nas bordas de barragens que estiveram cobertas por água por longos períodos ou em áreas irrigadas por água poluída e/ou esgoto. Além disso, o uso de medidor portátil é uma alternativa eficaz para a quantificação de nitratos em pastagens.

Assuntos

RESUMO

We report two outbreaks of nitrate and nitrite poisoning in Paraíba, Northeast Brazil. The first, due to Pennisetum purpureum (elephant grass), and the second, due to P. purpureum and Brachiaria spp. (brachiaria grass), both occurred during a prolonged drought. In the first outbreak, the irrigation of the pastures with wastewater and sewage contributed to nitrate accumulation. The second outbreak occurred in pastures cultivated in the border of a dam, that had been submerged for long time accumulating large amounts of organic matter in the soil. Other probably risk factors for nitrate accumulation included the use of chemical fertilizers and herbicides and burning of the vegetation. In the first outbreak, four calves out of a total of 42 cattle died, and in the second outbreak 49 out of 243 cattle, including adults, yearlings, and a 2-day-old calf died. The clinical signs included dyspnea, cyanosis, ataxia, and falls, leading to death. The presence of nitrates was detected in both outbreaks using the diphenylamine test. Quantitative tests were performed in the second outbreak using a portable nitrate meter, and high nitrate concentrations were found. The characteristic macroscopic findings and absence of microscopic lesions and response to treatment with methylene blue were key to the diagnosis of poisoning by nitrates and nitrites. We conclude that poisoning by nitrates and nitrites in ruminants in the semiarid region of Northeastern Brazil is frequent due to the cultivation of grasses in the border of dams that had been covered by water for long periods or in areas irrigated by wastewater and/or sewage. In addition, the use of a portable measuring device is an effective alternative for the quantification of nitrates in pastures.(AU)

Relatamos dois surtos de intoxicação por nitrato e nitrito na Paraíba, Nordeste do Brasil. O primeiro por Pennisetum purpureum (capim-elefante), e o segundo por P. purpureum e Brachiaria spp. (capim braquiária); ambos ocorreram durante uma estiagem prolongada. No primeiro surto, a irrigação das pastagens com água poluída e esgoto contribuiu para o acúmulo de nitrato. O segundo surto ocorreu em pastagens cultivadas na borda de uma barragem, que há muito tempo ficavam submersas, acumulando grande quantidade de matéria orgânica no solo. Outros prováveis fatores de risco para o acúmulo de nitrato incluíram o uso de fertilizantes químicos e herbicidas e a queima da vegetação. No primeiro surto, quatro bezerros de um total de 42 bovinos morreram, e no segundo surto 49 de 243 bovinos, incluindo adultos, jovens de um ano e um bezerro de 2 dias de idade morreram. Os sinais clínicos incluíram dispneia, cianose, ataxia e quedas, levando à morte. A presença de nitratos foi detectada em ambos os surtos pelo teste de difenilamina. Testes quantitativos foram realizados no segundo surto usando um medidor portátil de nitrato, e altas concentrações de nitrato foram encontradas. Os achados macroscópicos característicos e a ausência de lesões microscópicas e a resposta ao tratamento com azul de metileno foram fundamentais para o diagnóstico de intoxicação por nitratos e nitritos. Concluímos que a intoxicação por nitratos e nitritos em ruminantes na região semiárida do Nordeste do Brasil é frequente devido ao cultivo de gramíneas nas bordas de barragens que estiveram cobertas por água por longos períodos ou em áreas irrigadas por água poluída e/ou esgoto. Além disso, o uso de medidor portátil é uma alternativa eficaz para a quantificação de nitratos em pastagens.(AU)

Assuntos

RESUMO

Background: Nitrate and nitrite poisoning is associated with pasture intake that has high nitrate levels and leads to acute methemoglobinemia. Pasture may accumulate nitrate under certain conditions, such as excessively fertilized soil or environmental conditions that enhance the N absorption (rain preceded by a period of drought). After ingestion of plants, this substrate reaches the rumen and, in physiological conditions, is reduced to nitrite and afterward to ammonia. The aim of this study was to evaluate changes in cholinesterase activities and oxidative stress caused by subclinical poisoning for nitrate and nitrite in cattle fed with Pennisetum glaucum in three different fertilization schemes.Materials, Methods & Results: In order to perform the experimental poisoning, the pasture was cultivated in three different paddocks: with nitrogen topdressing (urea; group 1), organic fertilizer (group 2) or without fertilizer (group 3; control). Nitrate accumulation in forage was evaluated by the diphenylamine test. After food fasting of 12 h, nine bovine were randomly allocated to one of the experimental groups and fed with fresh forage (ad libitum) from respective paddock. In different time points from beginning of pasture intake (0, 2, 4, 6 and 9 h) heart rate and respiratory frequency were assessed, as well as mucous membrane color and behavioral changes. Blood samples from jugular vein into vials with and without anticoagulant were collected. From blood samples, serum nitrite levels, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzyme activity were evaluated, as well as oxidative stress through the following parameters: levels of nitrate/nitrite (NOx ), thiobarbituric acid reactive substances (TBARS) and reactive oxygen species (ROS), beyond the antioxidant system by enzyme activity measurement of catalase (CAT) and superoxide dismutase (SOD).[...]

Assuntos

RESUMO

Background: Nitrate and nitrite poisoning is associated with pasture intake that has high nitrate levels and leads to acute methemoglobinemia. Pasture may accumulate nitrate under certain conditions, such as excessively fertilized soil or environmental conditions that enhance the N absorption (rain preceded by a period of drought). After ingestion of plants, this substrate reaches the rumen and, in physiological conditions, is reduced to nitrite and afterward to ammonia. The aim of this study was to evaluate changes in cholinesterase activities and oxidative stress caused by subclinical poisoning for nitrate and nitrite in cattle fed with Pennisetum glaucum in three different fertilization schemes.Materials, Methods & Results: In order to perform the experimental poisoning, the pasture was cultivated in three different paddocks: with nitrogen topdressing (urea; group 1), organic fertilizer (group 2) or without fertilizer (group 3; control). Nitrate accumulation in forage was evaluated by the diphenylamine test. After food fasting of 12 h, nine bovine were randomly allocated to one of the experimental groups and fed with fresh forage (ad libitum) from respective paddock. In different time points from beginning of pasture intake (0, 2, 4, 6 and 9 h) heart rate and respiratory frequency were assessed, as well as mucous membrane color and behavioral changes. Blood samples from jugular vein into vials with and without anticoagulant were collected. From blood samples, serum nitrite levels, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzyme activity were evaluated, as well as oxidative stress through the following parameters: levels of nitrate/nitrite (NOx ), thiobarbituric acid reactive substances (TBARS) and reactive oxygen species (ROS), beyond the antioxidant system by enzyme activity measurement of catalase (CAT) and superoxide dismutase (SOD).[...](AU)

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RESUMO

La metahemoglobinemia es un síndrome clínico dado por la presencia de una forma aberrante de hemoglobina, ocasionada por diversos agentes oxidantes. Se describe un caso clínico de metahemoglobinemia severa asociada a la ingesta de puré de acelgas con alto contenido en nitratos y nitritos. Paciente de un año, con antecedentes de comunicación interauricular (CIA), que presentó un cambio en coloración de la piel 7 h antes, en forma progresiva, acompañado de vómitos. Ingresó al Departamento de Emergencia con cianosis generalizada que no mejoró con oxigenoterapia, taquicardia y tendencia a hipotensión arterial. En cuidados intensivos se realizó ecocardiograma que evidenció CIA sin repercusión hemodinámica. Metahemoglobinemia 37%. Se realizó dosis de azul de metileno al 1% por vía intravenosa, con franca mejoría clínica a la hora de la administración del antídoto y descenso de niveles de metahemoglobina. Alta médica a las 36 horas del ingreso. Existía una relación cronológica entre la exposición a nitratos por ingesta de un puré de acelgas y la aparición del cuadro. Los niveles de nitratos hallados en dicho alimento fueron muy elevados considerando estándares internacionales, lo que sumado a una inadecuada conservación del alimento cocido los días previos, permitió confirmar el planteo etiológico realizado. Resulta importante sospechar esta entidad patológica poco frecuente frente a cianosis que no mejora con oxígeno, y prevenir cuadros similares al descrito mediante una adecuada manipulación y conservación de las verduras con alto contenido en nitratos.

Methemoglobinemia is a clinical syndrome due to the presence of an aberrant form of hemoglobin, caused by various oxidizing agents. The study reports a case of severe methemoglobinemia associated with the ingestion of chard puree with high levels of nitrates and nitrites. A 1-year-old patient with a history of atrial septal defect (ASD), who progressively showed change of skin color 7 hours earlier, accompanied by vomiting. She was admitted to the Emergency Department with generalized cyanosis not improving with oxygen therapy, tachycardia and tendency to hypotension. In the intensive care unit, an echocardiogram showed ASD without hemodynamic complications. Methemoglobinemia 37%. A 1% methylene blue dose was administered intravenously, with clinical improvement one hour after antidote administration and decrease in methemoglobin levels. Medical discharge at 36 hours of admission. There was a chronological relationship between nitrates exposure by ingestion of chard puree and the clinical onset of methemoglobinemia. The toxic cause was confirmed after high nitrates levels were found in this vegetable considering international standards, and an inadequate preservation of the cooked chard on previous days. It is important to suspect this rare pathological entity when cyanosis fails to improve with oxygen, and to prevent poisonings similar to those described by an adequate manipulation and preservation of vegetables with high nitrate levels.

Assuntos

RESUMO

La metahemoglobinemia es un síndrome clínico dado por la presencia de una forma aberrante de hemoglobina, ocasionada por diversos agentes oxidantes. Se describe un caso clínico de metahemoglobinemia severa asociada a la ingesta de puré de acelgas con alto contenido en nitratos y nitritos. Paciente de un año, con antecedentes de comunicación interauricular (CIA), que presentó un cambio en coloración de la piel 7 h antes, en forma progresiva, acompañado de vómitos. Ingresó al Departamento de Emergencia con cianosis generalizada que no mejoró con oxigenoterapia, taquicardia y tendencia a hipotensión arterial. En cuidados intensivos se realizó ecocardiograma que evidenció CIA sin repercusión hemodinámica. Metahemoglobinemia 37%. Se realizó dosis de azul de metileno al 1% por vía intravenosa, con franca mejoría clínica a la hora de la administración del antídoto y descenso de niveles de metahemoglobina. Alta médica a las 36 horas del ingreso. Existía una relación cronológica entre la exposición a nitratos por ingesta de un puré de acelgas y la aparición del cuadro. Los niveles de nitratos hallados en dicho alimento fueron muy elevados considerando estándares internacionales, lo que sumado a una inadecuada conservación del alimento cocido los días previos, permitió confirmar el planteo etiológico realizado. Resulta importante sospechar esta entidad patológica poco frecuente frente a cianosis que no mejora con oxígeno, y prevenir cuadros similares al descrito mediante una adecuada manipulación y conservación de las verduras con alto contenido en nitratos.

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RESUMO

Se presenta el caso de una paciente femenina de 41 años de edad, quien ingirió erróneamente sal de nitratos por bicarbonato de sodio, ingresada a la emergencia del Hospital Universitario de Caracas por pérdida del conocimiento, cianosis y acidosis metabólica. Se demostraron niveles de metahemoglobinemia en un 26,47%. Los síntomas desaparecieron progresivamente con disminución paralela del porcentaje de metahemoglobinemia

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RESUMO

Se analizaron 40 casos consecutivos asistidos durante los dos últimos años, en el Hospital de Niños "Sor María Ludovica" de La Plata, que presentaron metahemoglobinemia (MHb). El 75% de los casos eran menores de 3 meses de vida. El motivo de consulta fueron manifestaciones gastrointestinales (diarrea, vómitos) en el 80% de los casos, cianosis en 17%, enfermedad respiratoria en el 12% y signos neurológicos en el 10%. Analizando los datos se vio que el 70% de los niños no tenían en sus hogares ningún servicio sanitario. El valor medio de MHb fue de 2,1 g/dl (rango 0,4-5,5 g/dl). Todos los niños, con excepción de uno, habían sido destetados. El 100% de los casos fue tratado exitosamente con vitamina C, como única medicación para su MHb

Assuntos

RESUMO

Se analizaron 40 casos consecutivos asistidos durante los dos últimos años, en el Hospital de Niños "Sor María Ludovica" de La Plata, que presentaron metahemoglobinemia (MHb). El 75% de los casos eran menores de 3 meses de vida. El motivo de consulta fueron manifestaciones gastrointestinales (diarrea, vómitos) en el 80% de los casos, cianosis en 17%, enfermedad respiratoria en el 12% y signos neurológicos en el 10%. Analizando los datos se vio que el 70% de los niños no tenían en sus hogares ningún servicio sanitario. El valor medio de MHb fue de 2,1 g/dl (rango 0,4-5,5 g/dl). Todos los niños, con excepción de uno, habían sido destetados. El 100% de los casos fue tratado exitosamente con vitamina C, como única medicación para su MHb (AU)

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