Clinical Outcomes of the Deleterious Effects of Aluminum on Neuro-Cognition, Inflammation, and Health: A Review.

Introduction: In the scenario of metal toxicity, aluminum (Al) stands out as a ubiquitous type of metal that can be combined with other elements and form different compounds. Al is widely used daily as an adjuvant in vaccines, antacids, food additives (as components of AI-containing food additives), skin care products, cosmetics, and kitchenware, and can be an element or contaminant present in our daily life. Objective: To present a review of the main deleterious effects of Al on human health. Methods: The search was carried out from September 2022 to February 2023 in the Scopus, PubMed, Science Direct, Scielo, and Google Scholar databases, using scientific articles from 2012 to 2023. The quality of the studies was based on the GRADE instrument, and the risk of bias was analyzed according to the Cochrane instrument. Results and Conclusions: A total of 115 files were search returned. Further, 95 articles were evaluated, and 44 were included in this review. Based on the results, measuring Al's relevance to health is essential in medicine. Several studies have demonstrated clinical outcomes and metabolic alterations with Al exposure. The tolerable weekly intake established by the European Food Safety Authority (EFSA) of 1 mg Al/kg body weight can be achieved through dietary exposure alone. Proven neurotoxicity in humans is the critical adverse effect of Al. A carcinogenic effect of Al has not been proven so far. Preventive medicine advocates that exposure to Al should be kept as low as possible. Chelating agents, such as calcium disodium ethylene diamine tetraacetic acid and deferoxamine, are options for acute poisoning, and monomethysilanetriol supplementation may be a long-term strategy with chelation potential. Further studies are needed to assess the impacts of Al on human health.

Chronic lead intoxication in a jaguar (Panthera onca) shot with round lead pellets: case report / Intoxicação crônica por chumbo em uma onça pintada (Panthera onca) alvejada com projéteis de chumbo: relato de caso

Lead is a heavy metal and an important cause of acute or chronic toxicosis in humans, domestic, and wild animals. This report aims to describe a case of chronic lead poisoning in a jaguar (Panthera onca) kept under human care that was rescued from the wild environment. The animal was rescued in poor condition in 2004 and kept under human care at the Belo Horizonte Zoological Garden (Minas Gerais, Brazil) until 2020, when it presented with anorexia, vomiting and ataxia. Over the past years the animal had episodes of anemia and increased serum urea and creatinine. Radiography demonstrated 21 radiopaque projectiles on the right side of the face. At necropsy there were multiple projectiles surrounded by fibrous tissue in the subcutaneous of the right side of the face, fibrinous peritonitis, multiple gastric ulcers, and melena. The lead dosage was performed using the atomic absorption spectrometry technique using renal tissue collected at necropsy, with a result of 908 ppb (µg/kg). The findings of projectiles associated with the dosage of lead above the reference limits allow the diagnosis of chronic intoxication in this case.

Chumbo é um metal pesado e uma causa importante de toxicose crônica no homem e em animais domésticos e selvagens. Este relato teve como objetivo descrever um caso de intoxicação crônica por chumbo em uma onça-pintada (Panthera onca), mantida sob cuidados humanos, que foi resgatada de seu ambiente natural em 2004, em pobre condição corporal. O animal foi encaminhado ao zoológico de Belo Horizonte (MG, Brasil), onde permaneceu até 2020, quando desenvolveu anorexia, vômitos e ataxia. Durante os últimos anos, o animal teve episódios de anemia e aumento da concentração sérica de ureia e creatinina. O exame radiográfico demonstrou 21 projéteis radiodensos na face direita. À necropsia, foram observados vários projéteis envoltos por tecido conjuntivo no subcutâneo da face esquerda, peritonite fibrinosa, múltiplas úlceras gástricas e melena. A concentração de chumbo foi determinada por espectrometria de absorção atômica em amostras de tecido renal, indicando 908 ppb (µg/kg). O achado de projéteis de chumbo associado à elevada concentração de chumbo é compatível com intoxicação crônica por chumbo neste caso.

Systemic oxalosis in a free-ranging green turtle (Chelonia mydas).

A female juvenile green turtle (Chelonia mydas), found alive in Guanabara Bay, Rio de Janeiro, Brazil, was weak, dehydrated and cachectic, with a healed fracture in the caudal portion of the carapace. Despite supportive treatment, the animal died after 9 days. At necropsy the main lesions were pallor of visceral organs, arthritis and deposits of whitish granular material in the wall of large arteries and the trachea. Histopathological analysis revealed mild to severe deposition of crystals, consistent with calcium oxalate, in both kidneys and the spleen, heart, small intestine, pancreas, thymus and salt gland, as well as bacterial meningitis, septic arthritis, spirorchidiasis and a fibropapilloma on the nictitating membrane. The main pathological findings were suggestive of septic shock, mainly due to the bacterial meningitis and septic arthritis, with systemic oxalosis and spirorchidiasis as contributing lesions. Although renal oxalosis has been described in green turtles as an incidental finding, presumably due to ingestion of oxalate-containing plants, this turtle had an unusual systemic deposition of oxalate crystals.

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.

Intoxicação de cães por maconha: sinais clínicos e tratamento / Marijuana poisoning in dogs: clinical signs and treatment

Intoxicações por drogas recreativas como Cannabissativa, comumente conhecida como maconha, estão cada vez mais presentes nas clínicas de atendimento veterinário. A Cannabis contém mais de 500 compostos diferentes e mais de 80 canabinoides conhecidos; destes, o delta-9 tetrahidrocanabinol (THC) é o mais psicoativo e responsável pela maioria dos sintomas de intoxicação. Os canabinoides são substâncias exógenas extraídas da Cannabis e se ligam aos receptores CB1 e CB2 do sistema endocanabinoide. Em cães, dentre os sinais clínicos de intoxicação mais presentes destacam-se: agitação, ataxia, midríase, aumento da sensibilidade ao som, hiperestesia, sialorreia, distúrbios neurológicos, espasmos musculares e início agudo de incontinência urinária. Muitas vezes o diagnóstico de intoxicação por maconha é difícil, principalmente porque os tutores resistem em admitir a exposição a drogas ilícitas com receio das implicações legais. O médico-veterinário deve ganhar a confiança do tutor do animal para que o diagnóstico possa ser realizado precocemente e iniciado o tratamento mais adequado para a situação. O tratamento inclui monitoramento clínico, cuidados de suporte, administração de fluidos intravenosos, administração de carvão ativado, indução de vômitos, administração de antieméticos, suporte térmico (aquecimento/resfriamento) e monitoramento da pressão arterial. Os médicos-veterinários são os principais responsáveis pela educação dos tutores nessas circunstâncias, sendo de grande importância enfatizar para os tutores manterem agentes tóxicos fora do acesso dos animais.(AU)

Intoxications by recreational drugs such as Cannabissativa, commonly known as marijuana, are increasingly present in veterinary care clinics. Cannabis contains over 500 different compounds and over 80 known cannabinoids; of these, delta-9 tetrahydrocannabinol (THC) is the most psychoactive and responsible for most symptoms of intoxication. Cannabinoids are exogenous substances extracted from Cannabis and bind to the CB1 and CB2 receptors of the endocannabinoid system. Among the most common clinical signs of intoxication in dogs are: agitation, ataxia, mydriasis, increased sensitivity to sound, hyperesthesia, drooling, neurological disorders, muscle spasms and acute onset of urinary incontinence. The diagnosis of marijuana intoxication is often difficult, mainly because tutors resist in admitting exposure to illicit drugs for fear of the legal implications. The Veterinarian must gain the trust of the animal's tutor so that the diagnosis can be carried out early and the most appropriate treatment for the situation can be initiated. Treatment includes: clinical monitoring, supportive care, administration of intravenous fluids, administration of activated charcoal, induction of vomiting, administration of antiemetics, thermal support (warming/cooling), and blood pressure monitoring. Veterinarians are primarily responsible for the education of tutors in these circumstances, and it is of great importance to emphasize that tutors must keep toxic agents away from animal's acess.(AU)

Intoxicação em gatos atendidos em um hospital veterinário universitário da cidade de São Paulo: análise retrospectiva de 2010 a 2021 / Intoxication in cats attended in a veterinary teaching hospital of São Paulo city: a retrospective analysis from 2010 to 2021

O aumento da população pet no Brasil causou maior proximidade da convivência de gatos com o ser humano e a falta de conhecimento do proprietário quanto às particulares felinas pode favorecer a ocorrência de toxicoses. Assim, o presente estudo apresenta as principais causas de intoxicações em gatos registrados no Hospital Veterinário (Hovet) da Faculdade de Medicina Veterinária e Zootecnia da Universidade de São Paulo (FMVZ-USP), no período de janeiro de 2010 a dezembro de 2021. Os resultados mostraram que a frequência de ocorrência anual de casos de intoxicações em gatos variou de 0,71% (5/704) a 2,68% (9/336), e os principais agentes responsáveis por intoxicações foram os praguicidas anticolinesterásicos, como carbamatos e organofosforados (50% - 48/96), e os medicamentos, em particular, os anti-inflamatórios não esteroidais (31,25% - 30/96). Houve casos em que não foi identificada a substância envolvida (7,29% - 7/96), o que dificulta a abordagem terapêutica. Em casos de urgência, devem ser inicialmente instituídas as medidas destinadas à manutenção das funções vitais do animal, e, posteriormente, de suporte ao animal. Nestes casos, é importante a realização do diagnóstico diferencial das possíveis causas de intoxicação de acordo com os sinais e histórico clínico, bem como a colheita de amostras para análise toxicológica.(AU)

The increase in the pet population in Brazil with the greater proximity of the coexistence of cats with humans and the owner's lack of knowledge about feline particulars can favor the occurrence of toxicosis. Thus, the present study performs a retrospective survey of poisoning in cats registered by the Daily Care Records of cats received at the Veterinary Hospital (Hovet) of the School of Veterinary Medicine and Animal Science at the University of São Paulo (FMVZ-USP), from January 2010 to December 2021. The results showed that the annual occurrence of cases of poisoning in cats ranged from 0.71% (5/704) to 2.68% (9/336), and the main agents responsible for poisoning were anticholinesterase pesticides, such as carbamates and organophosphates ( 50% - 48/96), and medications, in particular, non-steroidal anti-inflammatory drugs (31,25% - 30/96). There were also cases in which it was not possible to identify the substance involved (7.29% - 7/96), which makes the therapeutic approach difficult. In these cases, it is important to make a differential diagnosis to potential cases of intoxication according to clinic signs and clinic history, in addition to collecting samples for toxicologic analysis. In urgent cases, measures must be used to maintain the animal's vital functions and, later, supportive measures for the animal.(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...(AU)

Clinical Findings Associated with Ornithodoros brasiliensis Tick Parasitism in Travelers, Southern Brazil.

We report a series of clinical cases associated with parasitism by the Ornithodoros brasiliensis tick in a group of travelers in the Caxias do Sul municipality, Southern Brazil. These cases draw attention to underdiagnosed noninfectious syndromes caused by ticks with restricted local distributions.

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...

Human parasitism and toxicosis by Ornithodoros rietcorreai (Acari: Argasidae) in an urban area of Northeastern Brazil.

The soft tick, Ornithodoros rietcorreai, is a parasite of the rodent, Kerodon rupestris, and, to a lesser extent, of bats living in rock cavities in Northeastern Brazil. This report describes the first recorded episodes of human parasitism by this argasid tick, reported to the Brazilian Ministry of Health in September 2017. We assessed outdoor environments, roofs, animal nests and chicken coops in five houses located in an urban area of Russas City, Ceará State, Brazil. Our results confirmed the presence of the tick in two of the assessed houses. The collected specimens were molecularly identified as O. rietcorreai. Of the ten individuals living in the investigated properties, three reported being parasitized by ticks. Although O. rietcorreai ticks were recovered from the evaluated houses, the primary hosts for the ticks were not identified. The retrospective medical records of parasitized individuals reported the following: local pruritus 3/3, malaise 3/3, local edema and erythema 3/3, local rash 3/3, local pain 3/3, slow lesion healing 3/3 and paresthesia 1/3. One of the individuals reported four parasitism episodes (March, June, July and August 2017) and required medical attention and the administration of anti-allergy and anti-inflammatory drugs. The aforementioned reports were the first to address human parasitism, with subsequent toxicosis, by this tick species in Brazilian urban areas. Attention was drawn to the potential consequences of such episodes to the health of previously exposed individuals.

Comportamiento de la intoxicación moderada y severa por Ofidiotoxicosis Bothrópica en Córdoba- Colombia / Behavior of moderate and severe poisoning by ofidiotoxicosis bothropica in Cordoba. Colombia

Objetivo. Analizar la distribución de ofidiotoxicosis por mordedura de serpientes del género Bothrops entre la población que labora en la actividad agrícola en Córdoba, Colombia. Materiales y métodos. Descriptivo, retrospectivo. La población fue la información de 272 víctimas de accidentes ofídicos entre 2013-2015. Resultados. La prevalencia de accidente ofídico en el departamento de Córdoba se estima por año entre 12 a 13 casos por/100.000h. Los principales sistemas afectados por ofidiotoxicosis fueron digestivo (68%), neuromuscular (39,5%) y hematológico (27,6%); la sintomatología de ofidiotoxicosis incluyó nefrotoxicidad secundaria (27,6%), vómito (23.1%) y falla ventilatoria (16,7%%). Conclusiones. La ofidiotoxicosis que predomina en Córdoba es Bothropica por las especies atrox y asper.

Objective. To identify the factors associated with the non-reporting of adverse events in diagnostic support services in a primary level of care, in order to make decisions aimed at providing a safe care to its users. Materials and methods. This research corresponds to a retrospective descriptive, exploratory study. Based on the analysis of the records of the management and follow-up records of adverse events not reported in the institution's patient safety program, during the period from January 1, 2010 to December 31, 2015. Results. 46.5% of adverse events in the clinical laboratory service and 45% of adverse events in the diagnostic imaging service during the study period were not reported by default; situation that affects the safety of the patient indicating a poor culture on the report of adverse events. Conclusions. The highest percentage of unreported adverse events in diagnostic support services during the study period was not carried out of fear, this situation was attributed to the staff involved fearing that punitive actions were taken as a consequence of the presentation of these events.

Vascular injury in spontaneous subacute toxicosis caused by organic arsenic in cattle / Injúria vascular na toxicose subaguda espontânea causada por arsênio orgânico em bovinos

Monosodium methanearsonate (MSMA) is an organic form of arsenic present in the formulations of some herbicides. Accidental ingestion of pasture contaminated with arsenic may lead to toxicosis in cattle. Almost 200 head of cattle maintained in an area sprayed with MSMA presented with intense diarrhea and dehydration after grazing. Subsequently, 16 of these animals died. Toxic levels of arsenic (>1.5µg/g) were detected in the kidney, liver, urine, and skeletal muscle of 6 animals. At gross inspection were observed multifocal to coalescent ulcers in the mucosa from on the forestomachs associated with hemorrhagic areas and marked wall edema. Microscopic examination mainly showed fibrinoid necrosis of vessels with multifocal thrombosis associated with ischemic infarction that were characterized by large transmural necrotic areas in the forestomachs. The clinical and pathological changes interestingly showed that this form of arsenic although considered less toxic, has caused severe vascular injury in forestomachs of cattle.(AU)

Metano-arseniato ácido monossódico (MSMA) é uma forma orgânica de arsênio, presente nas formulações de alguns herbicidas. A ingestão acidental de pasto contaminado por arsênio pode levar a toxicose em bovinos. Aproximadamente 200 bovinos que estavam em uma pastagem pulverizada com MSMA manifestaram intensa diarreia e desidratação após o pastejo. Subsequentemente, 16 animais morreram. Níveis tóxicos de arsênio (>1.5µg/g) foram detectados no rim, fígado, urina e músculo esquelético de 6 animais. A inspeção macroscópica revelou úlceras multifocais a coalescentes na mucosa de pré-estômagos, adjacentes a focos de hemorragia e intenso edema de parede. A avaliação microscópica revelou, predominantemente, necrose fibrinoide de vasos com trombose multifocal associada a infarto, caracterizado por grandes áreas de necrose transmural em pré-estômagos. As alterações clínicas e patológicas, interessantemente, demonstraram que esta forma de arsênio, apesar de ser considerada menos tóxica, causou severa injúria vascular em pré-estômagos de bovinos.(AU)

Vascular injury in spontaneous subacute toxicosis caused by organic arsenic in cattle / Injúria vascular na toxicose subaguda espontânea causada por arsênio orgânico em bovinos

Monosodium methanearsonate (MSMA) is an organic form of arsenic present in the formulations of some herbicides. Accidental ingestion of pasture contaminated with arsenic may lead to toxicosis in cattle. Almost 200 head of cattle maintained in an area sprayed with MSMA presented with intense diarrhea and dehydration after grazing. Subsequently, 16 of these animals died. Toxic levels of arsenic (>1.5µg/g) were detected in the kidney, liver, urine, and skeletal muscle of 6 animals. At gross inspection were observed multifocal to coalescent ulcers in the mucosa from on the forestomachs associated with hemorrhagic areas and marked wall edema. Microscopic examination mainly showed fibrinoid necrosis of vessels with multifocal thrombosis associated with ischemic infarction that were characterized by large transmural necrotic areas in the forestomachs. The clinical and pathological changes interestingly showed that this form of arsenic although considered less toxic, has caused severe vascular injury in forestomachs of cattle.(AU)

Metano-arseniato ácido monossódico (MSMA) é uma forma orgânica de arsênio, presente nas formulações de alguns herbicidas. A ingestão acidental de pasto contaminado por arsênio pode levar a toxicose em bovinos. Aproximadamente 200 bovinos que estavam em uma pastagem pulverizada com MSMA manifestaram intensa diarreia e desidratação após o pastejo. Subsequentemente, 16 animais morreram. Níveis tóxicos de arsênio (>1.5µg/g) foram detectados no rim, fígado, urina e músculo esquelético de 6 animais. A inspeção macroscópica revelou úlceras multifocais a coalescentes na mucosa de pré-estômagos, adjacentes a focos de hemorragia e intenso edema de parede. A avaliação microscópica revelou, predominantemente, necrose fibrinoide de vasos com trombose multifocal associada a infarto, caracterizado por grandes áreas de necrose transmural em pré-estômagos. As alterações clínicas e patológicas, interessantemente, demonstraram que esta forma de arsênio, apesar de ser considerada menos tóxica, causou severa injúria vascular em pré-estômagos de bovinos.(AU)

Vascular injury in spontaneous subacute toxicosis caused by organic arsenic in cattle

ABSTRACT: Monosodium methanearsonate (MSMA) is an organic form of arsenic present in the formulations of some herbicides. Accidental ingestion of pasture contaminated with arsenic may lead to toxicosis in cattle. Almost 200 head of cattle maintained in an area sprayed with MSMA presented with intense diarrhea and dehydration after grazing. Subsequently, 16 of these animals died. Toxic levels of arsenic (>1.5g/g) were detected in the kidney, liver, urine, and skeletal muscle of 6 animals. At gross inspection were observed multifocal to coalescent ulcers in the mucosa from on the forestomachs associated with hemorrhagic areas and marked wall edema. Microscopic examination mainly showed fibrinoid necrosis of vessels with multifocal thrombosis associated with ischemic infarction that were characterized by large transmural necrotic areas in the forestomachs. The clinical and pathological changes interestingly showed that this form of arsenic although considered less toxic, has caused severe vascular injury in forestomachs of cattle.

RESUMO: Metano-arseniato ácido monossódico (MSMA) é uma forma orgânica de arsênio, presente nas formulações de alguns herbicidas. A ingestão acidental de pasto contaminado por arsênio pode levar a toxicose em bovinos. Aproximadamente 200 bovinos que estavam em uma pastagem pulverizada com MSMA manifestaram intensa diarreia e desidratação após o pastejo. Subsequentemente, 16 animais morreram. Níveis tóxicos de arsênio (>1.5g/g) foram detectados no rim, fígado, urina e músculo esquelético de 6 animais. A inspeção macroscópica revelou úlceras multifocais a coalescentes na mucosa de pré-estômagos, adjacentes a focos de hemorragia e intenso edema de parede. A avaliação microscópica revelou, predominantemente, necrose fibrinoide de vasos com trombose multifocal associada a infarto, caracterizado por grandes áreas de necrose transmural em pré-estômagos. As alterações clínicas e patológicas, interessantemente, demonstraram que esta forma de arsênio, apesar de ser considerada menos tóxica, causou severa injúria vascular em pré-estômagos de bovinos.

Hepatogenous chronic copper toxicosis associated with grazing Brachiaria decumbens in a goat

A case of hepatogenous chronic copper toxicosis associated with ingestion of Brachiaria decumbens in a 4-year-old female is reported in a goat from a herd of approximately 1,000 goats of different categories, all grazing in a pasture consisting exclusively of B. decumbens. The goat had chronic weight loss, dehydration, and apathy. Just prior to death it developed anemia, icterus and hemoglobinuria. Necropsy findings included marked icterus, enhanced lobular pattern and orange discoloration of the liver, pulmonary edema, distention of the gall bladder and hemoblobinuric nephrosis. Histopathological examination of the liver revealed marked random degeneration and necrosis of individual hepatocytes, marked bilestasis, intracytoplasmic hemosiderin in hepatocytes and Kupffer cells, birefringent crystals with bile staining in the lumen of bile ducts, and sparse, randomly distributed foamy macrophages. Severe multifocal tubular degeneration and necrosis associated with multiple hyaline and coarsely granular hemoglobin casts were observed in the kidneys. Copper levels determined in liver and kidney samples by atomic absorption spectrophotometry were 410 ppm of liver dry matter and 34.4 ppm (kidney, dry matter). The gross, histopathological findings and copper analysis in the tissues of this goat led to a final diagnosis of hepatogenous chronic copper toxicosis associated with grazing of B. decumbens.

Hepatogenous chronic copper toxicosis associated with grazing Brachiaria decumbens in a goat

A case of hepatogenous chronic copper toxicosis associated with ingestion of Brachiaria decumbens in a 4-year-old female is reported in a goat from a herd of approximately 1,000 goats of different categories, all grazing in a pasture consisting exclusively of B. decumbens. The goat had chronic weight loss, dehydration, and apathy. Just prior to death it developed anemia, icterus and hemoglobinuria. Necropsy findings included marked icterus, enhanced lobular pattern and orange discoloration of the liver, pulmonary edema, distention of the gall bladder and hemoblobinuric nephrosis. Histopathological examination of the liver revealed marked random degeneration and necrosis of individual hepatocytes, marked bilestasis, intracytoplasmic hemosiderin in hepatocytes and Kupffer cells, birefringent crystals with bile staining in the lumen of bile ducts, and sparse, randomly distributed foamy macrophages. Severe multifocal tubular degeneration and necrosis associated with multiple hyaline and coarsely granular hemoglobin casts were observed in the kidneys. Copper levels determined in liver and kidney samples by atomic absorption spectrophotometry were 410 ppm of liver dry matter and 34.4 ppm (kidney, dry matter). The gross, histopathological findings and copper analysis in the tissues of this goat led to a final diagnosis of hepatogenous chronic copper toxicosis associated with grazing of B. decumbens.(AU)

Metronidazole-induced central vestibular syndrome in a horse case report / Síndrome vestibular central em equino após tratamento com metronidazol relato de caso

Metronidazole-induced central vestibular syndrome (CVS) is uncommon in horses. A case of CVS following treatment with metronidazole at therapeutic doses is reported. An adult male mixed breed horse was submitted to antimicrobial therapy with metronidazole (15 mg.kg-1 IV), penicillin-streptomycin (22.000UI.kg-1 IM) and gentamicin (6.6 mg.kg-1 IV) following small intestinal resection. Clinical signs consistent with CVS (ataxia, horizontal gaze nystagmus, strabismus and head tilt) developed on the 12th post-operative day. Metronidazole administration was immediately discontinued. Initial disease progression followed by progressive improvement of clinical signs from day 10 after recognition of CVS manifestations was observed. Metronidazole-induced CVS diagnosis was based on typical CVS manifestations, medical history and remission of clinical signs following discontinuation of treatment

Síndrome vestibular central (SVC) em equinos decorrente de intoxicação por metronidazol é um distúrbio raro. Este relato descreve um caso de SVC após uso de metronidazol em dose terapêutica em equino macho adulto sem raça definida. O animal foi submetido à enterectomia de intestino delgado e a terapia antimicrobiana pós-cirúrgica constava de metronidazol 15 mg.kg-1, por via intravenosa (IV), associado a penicilina com estreptomicina 22.000UI.kg-1, por via intramuscular (IM) e gentamicina 6,6 mg.kg-1, IV. A partir do 12º dia de pós-operatório com administração do metronidazol, o animal iniciou com sinais clínicos que caracterizavam SVC. Ao exame físico, o animal apresentava-se atáxico, com nistagmo horizontal, estrabismo e inclinação lateral da cabeça. Foi suspensa a administração do metronidazol. Nos dias seguintes o quadro agravou-se sendo que a partir do 10º dia após o início das manifestações clínicas os sinais passaram a regredir gradativamente. Diante do quadro apresentado e sua regressão após a suspensão da administração do metronidazol, foi diagnosticada SVC em decorrência de intoxicação por metronidazol baseado no histórico e nas manifestações clínicas do animal

Metronidazole-induced central vestibular syndrome in a horse case report / Síndrome vestibular central em equino após tratamento com metronidazol relato de caso

Metronidazole-induced central vestibular syndrome (CVS) is uncommon in horses. A case of CVS following treatment with metronidazole at therapeutic doses is reported. An adult male mixed breed horse was submitted to antimicrobial therapy with metronidazole (15 mg.kg-1 IV), penicillin-streptomycin (22.000UI.kg-1 IM) and gentamicin (6.6 mg.kg-1 IV) following small intestinal resection. Clinical signs consistent with CVS (ataxia, horizontal gaze nystagmus, strabismus and head tilt) developed on the 12th post-operative day. Metronidazole administration was immediately discontinued. Initial disease progression followed by progressive improvement of clinical signs from day 10 after recognition of CVS manifestations was observed. Metronidazole-induced CVS diagnosis was based on typical CVS manifestations, medical history and remission of clinical signs following discontinuation of treatment(AU)

Síndrome vestibular central (SVC) em equinos decorrente de intoxicação por metronidazol é um distúrbio raro. Este relato descreve um caso de SVC após uso de metronidazol em dose terapêutica em equino macho adulto sem raça definida. O animal foi submetido à enterectomia de intestino delgado e a terapia antimicrobiana pós-cirúrgica constava de metronidazol 15 mg.kg-1, por via intravenosa (IV), associado a penicilina com estreptomicina 22.000UI.kg-1, por via intramuscular (IM) e gentamicina 6,6 mg.kg-1, IV. A partir do 12º dia de pós-operatório com administração do metronidazol, o animal iniciou com sinais clínicos que caracterizavam SVC. Ao exame físico, o animal apresentava-se atáxico, com nistagmo horizontal, estrabismo e inclinação lateral da cabeça. Foi suspensa a administração do metronidazol. Nos dias seguintes o quadro agravou-se sendo que a partir do 10º dia após o início das manifestações clínicas os sinais passaram a regredir gradativamente. Diante do quadro apresentado e sua regressão após a suspensão da administração do metronidazol, foi diagnosticada SVC em decorrência de intoxicação por metronidazol baseado no histórico e nas manifestações clínicas do animal(AU)

Surto de intoxicação por sal em ovinos no estado do Pará / Salt poisoning outbreak in sheep in the state of Pará

O presente trabalho relata um surto de intoxicação por sal em ovinos no Brasil, em uma propriedade no estado do Pará. De um total de 545 ovinos, oito animais adoeceram (1,46%) e quatro destes morreram (50%). A avaliação das instalações e do manejo indicaram como fatores predisponentes a ingestão excessiva de mistura mineral e a restrição hídrica. Os principais sinais clínicos foram decúbito, diminuição ou ausência da sensibilidade cutânea, ausência dos reflexos de ameaça, palpebral e auricular, midríase, nistagmo, opistótono, espasticidade de membros, sonolência e estupor. Havia ainda, timpanismo, diarreia, taquipneia, taquicardia, desidratação e poliúria. A evolução do quadro clínico nos animais que morreram variou de duas horas e meia a 48 horas. As médias das concentrações séricas de sódio e de potássio de 31 ovinos do mesmo lote afetado pela intoxicação, em amostras colhidas durante o surto, revelaram hipernatremia (190mEq/l) e hipercalemia (8,2mEq/l). À necropsia, observou-se em um animal, achatamento das circunvoluções cerebrais. Microscopicamente, neste animal, evidenciou-se vacuolização moderada do neurópilo, particularmente nas lâminas intermediárias do córtex cerebral, com aumento dos espaços perineural e perivascular. Nessas áreas foram observados ainda, acentuada tumefação e edema dos astrócitos e necrose neuronal aguda. A dosagem de sódio no encéfalo de um ovino, revelou-se elevada com valor de 3.513ppm. O diagnóstico foi realizado com base na epidemiologia, nos sinais clínicos, nas lesões macro e microscópicas e nas dosagens de sódio no soro e no encéfalo dos ovinos.(AU)

This paper reports an outbreak of salt poisoning in sheep on a farm in the state of Pará, northern Brazil. Eight (1.46%) animals were affected from a total of 545 sheep and four (50%) of them died. The evaluation of the facilities and the handling indicated as predisposing factors excessive intake of the mineral supplement and water restriction. The main clinical signs were recumbency, decrease or absence of cutaneous sensibility, absence of auricular, palpebral and menace reflex, mydriasis, nystagmus, opisthotonus, spasticity of limbs, somnolence and stupor. Beside these signs bloat, diarrhea, tachypnea, tachycardia, dehydration and polyuria were observed. The course of the disease in animals that died ranged from two hours and a half to 48 hours. The medium of serum concentration of sodium and potassium of 31 sheep from the same group affected on samples collected during the outbreak revealed hypernatremia (190mEq/l) and hyperkalemia (8.2mEq/l). At necropsy, there was flattening of the cerebral gyri in one sheep; in this animal was found vacuolization of the neuropil in the cerebral cortex with moderate intensity in the intermediary and mild on the superficial layers, with increased perineural and perivascular spaces. In these areas there were markedly swollen nucleus of astrocytes with acute neuronal necrosis. The dosage of sodium in the brain of a sheep revealed a high value of 3.513ppm. The diagnosis was made based on the epidemiology, clinical signs, macro and microscopic lesions and in the dosages of sodium in serum and brain.(AU)

Surto de intoxicação por sal em ovinos no estado do Pará / Salt poisoning outbreak in sheep in the state of Pará

O presente trabalho relata um surto de intoxicação por sal em ovinos no Brasil, em uma propriedade no estado do Pará. De um total de 545 ovinos, oito animais adoeceram (1,46%) e quatro destes morreram (50%). A avaliação das instalações e do manejo indicaram como fatores predisponentes a ingestão excessiva de mistura mineral e a restrição hídrica. Os principais sinais clínicos foram decúbito, diminuição ou ausência da sensibilidade cutânea, ausência dos reflexos de ameaça, palpebral e auricular, midríase, nistagmo, opistótono, espasticidade de membros, sonolência e estupor. Havia ainda, timpanismo, diarreia, taquipneia, taquicardia, desidratação e poliúria. A evolução do quadro clínico nos animais que morreram variou de duas horas e meia a 48 horas. As médias das concentrações séricas de sódio e de potássio de 31 ovinos do mesmo lote afetado pela intoxicação, em amostras colhidas durante o surto, revelaram hipernatremia (190mEq/l) e hipercalemia (8,2mEq/l). À necropsia, observou-se em um animal, achatamento das circunvoluções cerebrais. Microscopicamente, neste animal, evidenciou-se vacuolização moderada do neurópilo, particularmente nas lâminas intermediárias do córtex cerebral, com aumento dos espaços perineural e perivascular. Nessas áreas foram observados ainda, acentuada tumefação e edema dos astrócitos e necrose neuronal aguda. A dosagem de sódio no encéfalo de um ovino, revelou-se elevada com valor de 3.513ppm. O diagnóstico foi realizado com base na epidemiologia, nos sinais clínicos, nas lesões macro e microscópicas e nas dosagens de sódio no soro e no encéfalo dos ovinos.(AU)

This paper reports an outbreak of salt poisoning in sheep on a farm in the state of Pará, northern Brazil. Eight (1.46%) animals were affected from a total of 545 sheep and four (50%) of them died. The evaluation of the facilities and the handling indicated as predisposing factors excessive intake of the mineral supplement and water restriction. The main clinical signs were recumbency, decrease or absence of cutaneous sensibility, absence of auricular, palpebral and menace reflex, mydriasis, nystagmus, opisthotonus, spasticity of limbs, somnolence and stupor. Beside these signs bloat, diarrhea, tachypnea, tachycardia, dehydration and polyuria were observed. The course of the disease in animals that died ranged from two hours and a half to 48 hours. The medium of serum concentration of sodium and potassium of 31 sheep from the same group affected on samples collected during the outbreak revealed hypernatremia (190mEq/l) and hyperkalemia (8.2mEq/l). At necropsy, there was flattening of the cerebral gyri in one sheep, in this animal was found vacuolization of the neuropil in the cerebral cortex with moderate intensity in the intermediary and mild on the superficial layers, with increased perineural and perivascular spaces. In these areas there were markedly swollen nucleus of astrocytes with acute neuronal necrosis. The dosage of sodium in the brain of a sheep revealed a high value of 3.513ppm. The diagnosis was made based on the epidemiology, clinical signs, macro and microscopic lesions and in the dosages of sodium in serum and brain.(AU)