Atypical chronic copper poisoning in a sheep secondary to copper wire ingestion: case report / Intoxicação crônica por cobre atípica em ovino pelo consumo de fios de cobre: relato de caso

A 14-month-old female Texel sheep that came from a herd made up of 19 animals showed haemoglobinuria, apathy, and anorexia, and died two days after the start of the clinical signals. The sheep remained in a natural grassland, where trailers were repaired, and multiple copper wires were deposited on the pasture. The animal had tachycardia, tachypnoea, pale mucous membranes, groaning pain on abdominal palpation, circling, head pressing, intensely hemolyzed plasma, and intense azotaemia. The necropsy showed focally extensive oedema in the inguinal and medial region of pelvic limbs, kidneys dark brown, and liver diffusely yellow with an evident moderate diffuse lobular pattern. The abomasum had a considerable amount of enameled material of thickness, firm to the cut, with 1-5 mm (copper wires). Histopathological examination showed marked diffuse tubular and glomerular coagulative necrosis in the kidneys, in addition to neutrophils, macrophages, lymphocytes, and plasma cells with moderate multifocal nephritis. The liver showed centrilobular necrosis, moderate hepatocellular edema, multifocal cholestasis, and in the lungs and brain mild to moderate diffuse edema. Copper content in the frozen liver (in natura) reached 1,598 mg/kg. Copper mesh ingestion led to sheep poisoning, which in this case was considered an atypical form of chronic primary copper poisoning.

Um ovino Texel de 14 meses de idade, que fazia parte de um rebanho de 19 animais, apresentou hemoglobinúria, apatia, anorexia e morreu dois dias após o início dos sinais clínicos. Os ovinos permaneciam em campo nativo, onde eram realizados consertos de trailers, e múltiplos fios de cobre ficavam depositados na pastagem. O animal apresentou taquicardia, taquipneia, mucosas pálidas, gemido de dor à palpação abdominal, além de andar em círculo, e pressão da cabeça contra obstáculos, plasma intensamente hemolisado e azotemia intensa. Na necropsia, havia edema na região inguinal e medial de membros pélvicos focalmente extenso, rins enegrecidos, e o fígado estava difusamente amarelado, com padrão lobular evidente difuso moderado. No abomaso, havia grande quantidade de material esmaltado, com 1-5mm de espessura, firme, que rangia ao ser cortado (fios de cobre). No exame histopatológico nos rins, havia necrose tubular e glomerular hemoglobinúrica difusa acentuada, além de nefrite de neutrófilios, macrófagos, linfócitos e plasmócitos multifocal moderada. No fígado, havia necrose centrolobular, tumefação hepatocelular e colestase multifocais moderadas; nos pulmões e no cérebro, edema difuso discreto a moderado. A dosagem de Cu no fígado revelou a presença de 1598mg/kg. A ingestão de malhas de cobre levou à intoxicação do ovino que, nesse caso, foi considerada uma forma atípica de intoxicação primária crônica por cobre.

Crise hemolítica em um cão com hepatite crônica associada ao cobre / Hemolytic crisis in a dog with copper-associated chronic hepatitis

Background: Copper is an essential micronutrient for the body to function properly. However, although it is a vital element,an excess of copper in the body is extremely toxic. Copper toxicity has been reported mainly in sheep. In dogs, clinicopathological signs of toxicity are characterized by chronic liver failure. This means that the hemolytic crisis so commonin sheep is a condition rarely associated with toxicity in dogs, so there are very few descriptions of this condition in theveterinary literature. The purpose of this report is to describe a case of hemolytic crisis in a dog with copper-associatedchronic hepatitis.Case: A medium-sized 6-year-old bitch was brought to the Veterinary Hospital of the Federal University of Santa Maria,with clinical presentation of apathy, anorexia and red urine. A physical examination revealed mildly jaundiced mucosaand dark brown urine. A urinalysis indicated the presence of protein, bilirubin and occult blood. The blood count revealedhypochromic macrocytic anemia, leukocytosis due to left shift neutrophilia and thrombocytopenia. Serum biochemistryshowed elevated levels of alanine aminotransferase and alkaline phosphatase. The animal was given a blood transfusiondue to the severity of her anemia, but her clinical condition worsened and she died, whereupon her body was sent for necropsy. This necropsy revealed conspicuous signs of jaundice, splenomegaly and altered liver and kidney color. The liverwas brownish, with its natural surface firm and slightly irregular. The kidneys were diffusely blackened. The urine wasdark brown. Fragments of different organs were collected, fixed in 10% buffered formalin solution, routinely processedfor histopathology and stained with hematoxylin and eosin. A histological dissection of the liver showed the hepatic lobesdissected by fibrosis, forming islands of hepatocytes and numerous lymphocytes and...(AU)

Crise hemolítica em um cão com hepatite crônica associada ao cobre / Hemolytic crisis in a dog with copper-associated chronic hepatitis

Background: Copper is an essential micronutrient for the body to function properly. However, although it is a vital element,an excess of copper in the body is extremely toxic. Copper toxicity has been reported mainly in sheep. In dogs, clinicopathological signs of toxicity are characterized by chronic liver failure. This means that the hemolytic crisis so commonin sheep is a condition rarely associated with toxicity in dogs, so there are very few descriptions of this condition in theveterinary literature. The purpose of this report is to describe a case of hemolytic crisis in a dog with copper-associatedchronic hepatitis.Case: A medium-sized 6-year-old bitch was brought to the Veterinary Hospital of the Federal University of Santa Maria,with clinical presentation of apathy, anorexia and red urine. A physical examination revealed mildly jaundiced mucosaand dark brown urine. A urinalysis indicated the presence of protein, bilirubin and occult blood. The blood count revealedhypochromic macrocytic anemia, leukocytosis due to left shift neutrophilia and thrombocytopenia. Serum biochemistryshowed elevated levels of alanine aminotransferase and alkaline phosphatase. The animal was given a blood transfusiondue to the severity of her anemia, but her clinical condition worsened and she died, whereupon her body was sent for necropsy. This necropsy revealed conspicuous signs of jaundice, splenomegaly and altered liver and kidney color. The liverwas brownish, with its natural surface firm and slightly irregular. The kidneys were diffusely blackened. The urine wasdark brown. Fragments of different organs were collected, fixed in 10% buffered formalin solution, routinely processedfor histopathology and stained with hematoxylin and eosin. A histological dissection of the liver showed the hepatic lobesdissected by fibrosis, forming islands of hepatocytes and numerous lymphocytes and...

Young ovine death during hyperimmunization: crotalic envenomation or copper toxicosis?

The unfavorable evolution of a young ovine during hyperimmunization process with Crotalus durissus terrificus venom was investigated in order to differentiate its origin between ophidic envenomation and copper toxicosis. Clinical, laboratory, necroscopic and histological exams as well as evaluation and measurement of heavy metals (copper) in the kidneys and in the liver were carried out. Blood counts revealed anemia and serological tests showed high levels of blood urea nitrogen, creatinine, aspartate aminotransferase, creatine phosphokinase, total bilirubin and indirect bilirubin; which indicates liver, kidney and skeletal muscle damages. At necropsy, the animal presented hepatopathy and nephropathy. Histological examination revealed renal and hepatic features that may imply copper intoxication. Copper levels were 237.8 µg/g in the liver and 51.2 µg/g in the kidneys. Although the amount of metal found in both organs was below the level that can cause death, according to the literature, anatomopathological signs were suggestive of copper intoxication. Therefore, the hypothesis of metal toxicosis during the hyperimmunization process became more consistent than the crotalic envenomation one.

Young ovine death during hyperimmunization: crotalic envenomation or copper toxicosis?

The unfavorable evolution of a young ovine during hyperimmunization process with Crotalus durissus terrificus venom was investigated in order to differentiate its origin between ophidic envenomation and copper toxicosis. Clinical, laboratory, necroscopic and histological exams as well as evaluation and measurement of heavy metals (copper) in the kidneys and in the liver were carried out. Blood counts revealed anemia and serological tests showed high levels of blood urea nitrogen, creatinine, aspartate aminotransferase, creatine phosphokinase, total bilirubin and indirect bilirubin; which indicates liver, kidney and skeletal muscle damages. At necropsy, the animal presented hepatopathy and nephropathy. Histological examination revealed renal and hepatic features that may imply copper intoxication. Copper levels were 237.8 µg/g in the liver and 51.2 µg/g in the kidneys. Although the amount of metal found in both organs was below the level that can cause death, according to the literature, anatomopathological signs were suggestive of copper intoxication. Therefore, the hypothesis of metal toxicosis during the hyperimmunization process became more consistent than the crotalic envenomation one.(AU)

Copper toxicosis in sheep fed dairy cattle ration in São Paulo, Brazil

Intoxicação crônica por cobre foi observada em um rebanho de 20 ovinos no município de Franca, São Paulo. Três meses após o início do arraçoamento com feno e ração concentrada peletizada para bovinos de leite, seis animais apresentaram anorexia, icterícia severa e urina marrom escura, e vieram a óbito. Diagnosticou-se doença hemolítica com base em sinais clínicos, alterações macroscópicas observadas na necropsia e observações histológicas. À necropsia todos os ovinos apresentaram icterícia severa, fígado amarelado com padrão lobular evidente e rins escuros. As principais alterações histológicas incluíram necrose hepática periacinar e nefrose hemoglobinúrica. Acúmulos de cobre foram demonstrados nos hepatócitos e macrófagos pela coloração rodamina e níveis elevados de cobre mediante espectrofotometria de absorção atômica no soro, fígado e rins de dois ovinos afetados e na ração fornecida.(AU)