Clinical and histologic outcome in a dog surviving massive hepatic necrosis.

This report describes the clinical and histologic recovery of a 2-year-old mixed-breed dog presented with hypovolemic shock, markedly increased serum alanine amino transferase activity, and hemoabdomen. Emergency exploratory surgery revealed a friable liver with multiple capsule hemorrhages necessitating removal of the left lateral lobe. Histologic evaluation showed acute massive hepatic necrosis with centrilobular and midzonal distribution. The dog survived, and all monitored laboratory values normalized within 7 weeks. A liver biopsy taken 8 weeks after presentation revealed normal hepatic architecture with a few, randomly distributed neutrophilic foci. Follow-up included intermittent determination of liver variables including liver function tests for a period of 7 years. The dog's health status, and all test results remained normal during this time. Complete recovery and good long-term quality of life after life-threatening acute liver failure secondary to massive hepatic necrosis is possible in dogs.

Hematological and pathological features of massive hepatic necrosis in two radiated tortoises (Astrochelys radiata).

Two radiated tortoises (Astrochelys radiata) exhibited anorexia and hypokinesia. In both cases, hematological and serum biochemical examinations revealed high alkaline phosphatase levels, moderately high aspartate aminotransferase levels and white blood cell counts approximately within the normal range. Despite being treated, the tortoises died 9 and 43 days after the first clinical examination. Gross pathological examinations revealed that the livers of both animals were extremely swollen and contained pale yellow necrotic tissue. Histopathological assessment revealed that the livers contained a massive area of hepatic necrosis surrounded by migration of macrophages and multinucleated giant cells. In one of the cases, severe fibrosis was observed. The present study provides reference information for similar cases in the future.

Toxic myopathy and acute hepatic necrosis in cattle caused by ingestion of Senna obtusifolia (sicklepod; coffee senna) in Brazil.

The epidemiological, clinical and pathological findings of field and experimental Senna obtusifolia (sicklepod; coffee senna) poisoning in cattle are described. The low availability of good quality forage and high rate of infestation of pastures by S. obtusifolia were the factors that led to poisonous plant ingestion. In this study, the morbidity ranged between 2% and 27.9%, and the lethality was 100%. For the experimental study, six cattle were fed with the aerial parts of S. obtusifolia collected in three different seasons at 9%-38% of the animal's body weight. The experimental and field diseases were similar. The main clinical signs were diarrhea, reluctance to move, muscular weakness and recumbency. The gross findings included pale discoloration of the skeletal muscle. Microscopically, the affected cattle showed degeneration and necrosis of the skeletal muscles and occasionally of the cardiac muscles. Additionally, two cattle showed centrilobular hepatic necrosis. In this study, S. obtusifolia collected from the same farm showed seasonal variation in toxicity. Poisoning by S. obtusifolia is an important cause of death of cattle in the Central Western region of Brazil. The toxicosis caused by this plant is similar to S. occidentalis poisoning; however, in S. obtusifolia poisoning, acute hepatic necrosis is sometimes present.

Liver necrosis and photosensitisation in cattle after eating Persicaria lapathifolia (pale knotweed) and Persicaria orientalis (Prince's feather).

Cattle deaths in two contemporaneous incidents were attributed to acute intoxication with Persicaria lapathifolia and P. orientalis when the plants were under heat and moisture stress. To our knowledge this is the first confirmed report of acute, fatal hepatic necrosis associated with ingestion of these plants.

Perreyia flavipes larvae toxicity / Toxicidade das larvas de Perreyia flavipes

Fresh or thawed Perreyia flavipes larvae were ground and mixed with water and orally ad ministered to sheep. At 5mg/kg, neither clinical nor enzymatic changes were observed. Unique do ses of 7.5 and 10mg/kg induced characteristic clinical signs of Perreyia sp. larvae poisoning, increased GGT and AST values, and decreased glycemic curves. However, doses of 5, 10, and 15mg/kg repeated at 30 or 15 days intervals caused no disease and mild disease followed by death, respectively. These fin dings indicate that these animals probably developed some degree of tolerance to the toxins in P. flavipes larvae. Ultrastru ctural examination of liver revealed proliferation of the smooth endoplasmic reticulum in the hepatocytes, which may be associated with an increased ability to metabolize toxins and could consequently lead to the tolerance observed in the present study. Further investigations may elucidate whether such tolerance effects could be applied as a control measure for P. flavipes poioning or other hepatotoxic diseases. In addition, clinicopathological findings were discussed.

Larvas frescas ou descongeladas de Perreyia flavipes foram moídas e misturadas com água e administradas de forma oral a ovinos. Com 5mg/kg, não foram observados achados clínicos ou enzimáticos. Doses únicas de 7,5 e 10mg/kg induziram a sinais clínicos característicos de intoxicação pelas larvas de Perreyia sp., os níveis de GGT e AST estavam aumentados e as curvas glicêmicas estavam diminuídas. Entretanto, doses de 5, 10 e 15mg/kg repetidas em intervalos de 30 ou 15 dias não causou doença ou causou doença discreta seguida de morte, respectivamente. Estes achados indicam que estes animais provavelmente desenvolveram algum grau de tolerância para as toxinas presentes nas lar-Larvas frescas ou descongeladas de Perreyia flavipes foram vas de P. flavipes. O exame ultraestrutural do fígado revelou moídas e misturadas com água e administradas de forma proliferação do retículo endoplasmático liso de hepatócioral a ovinos. Com 5mg/kg, não foram observados acha-tos, o que pode ser associado a um aumento na capacidade dos clínicos ou enzimáticos. Doses únicas de 7,5 e 10mg/ de metabolizar toxinas e conseqüentemente levar à tolekg induziram a sinais clínicos característicos de intoxicação rância observada no presente estudo. Outras investigações pelas larvas de Perreyia sp., os níveis de GGT e AST estavam poderão esclarecer se os efeitos de tal tolerância poderiam aumentados e as curvas glicêmicas estavam diminuídas. ser aplicados como medida de controle da intoxicação por Entretanto, doses de 5, 10 e 15mg/kg repetidas em interva-P. flavipes ou outras doenças hepatotóxicas. Além disso, os los de 30 ou 15 dias não causou doença ou causou doença resultados clínico-patológicos foram discutidos.

Renal cortex copper concentration in acute copper poisoning in calves / Concentração de cobre no córtex renal na intoxicação aguda de cobre em bezerros

The aim of this study was to estimate the diagnostic value of renal cortex copper (Cu) concentration in clinical cases of acute copper poisoning (ACP). A total of 97 calves that died due to subcutaneous copper administration were compiled in eleven farms. At least, one necropsy was conducted on each farm and samples for complementary analysis were taken. The degree of autolysis in each necropsy was evaluated. The cases appeared on extensive grazing calf breeding and intensive feedlot farms, in calves of 60 to 200 kg body weight. Mortality varied from 0.86 to 6.96 percent, on the farms studied. The first succumbed calf was found on the farms between 6 and 72 hours after the susbcutaneous Cu administration. As discrepancies regarding the reference value arose, the local value (19.9 parts per million) was used, confirming the diagnosis of acute copper poisoning in 93 percent of the analyzed kidney samples. These results confirm the value of analysis of the cortical kidney Cu concentration for the diagnosis of acute copper poisoning.

O objetivo deste trabalho foi estimar o valor diagnóstico de concentração de cobre (Cu) no córtex do rim em casos clínicos da intoxicação cobre aguda (ACP). Um total de 97 bezerros foi compilado em onze fazendas. Pelo menos, uma necropsia foi realizada em cada caso e foram colhidas amostras para análise complementar. O grau de autólise em cada necropsia foi avaliado. Os casos aparecem em criação extensiva e também em fazendas de confinamento intensivo. Os pesos dos animais variavam de 60 até 200 kg. Mortalidade variou entre 0,86 e 6,96 por cento, em todas as fazendas estudadas, o primeiro animal morto foi observado entre 6 e 72 horas após à administração parenteral de Cu. Surgirem discrepâncias em relação ao valor de referência a ser usado. O valor local (19. 9 partes por milhão) foi usado, confirmando o diagnóstico de intoxicação aguda de cobre em 93 por cento das amostras analisadas nos rins. Estes resultados confirmam o valor diagnóstico da concentração de Cu no rim córtex para o diagnóstico de ACP.

Intoxicação aguda com sementes de Crotalaria spectabilis (Leg. Papilionoideae) em suínos / Acute poisoning with Crotalaria spectabilis (Leg. Papilionoideae) seeds in pigs

Relata-se necrose hepatocelular em suínos após consumo de ração que continha grãos de sorgo-granífero (Sorghum bicolor) acidentalmente contaminado com sementes de Crotalaria spectabilis. Morreram 76 suínos em quatro propriedades no município de Juscimeira, MT. Os sinais clínicos iniciaram-se 24-48 horas após o consumo da ração contaminada e foram caracterizados por depressão, letargia, apatia, inapetência, vômito, mucosas ictéricas ou pálidas, ascite, decúbito esternal, decúbito lateral com movimentos de pedalagem e convulsões, a evolução clínica foi de 48-60 horas seguida de morte. As Principais alterações macroscópicas foram fígado aumentado de tamanho com evidenciação do padrão lobular, ascite e hidrotórax com líquido de coloração amarelo avermelhado contendo filamentos com aspecto de fibrina, linfonodos aumentados e edema pulmonar interlobular. A doença foi reproduzida utilizando-se 16 suínos divididos em seis grupos que receberam sementes de C. spectabilis em diferentes doses. Necrose hepatocelular ocorreu em sete suínos, sendo dois que receberam doses diárias 2,5g/kg e cinco que receberam doses únicas de 5,0 e 9,5g/kg. Dez doses diárias de 0,5 e 1,25g/kg causaram fibrose hepática.

Hepatocellular necrosis are reported in swine after consumption of diets containing grains of "sorgo-granífero" (Sorghum bicolor) accidentally contaminated with Crotalaria spectabilis seeds in the municipality of Juscimeira, MT. Clinical signs began 24-48 hours after consumption of contaminated ration and were characterized by depression, lethargy, apathy, loss of appetite, vomiting, pale or jaundiced mucous membranes, ascites, lateral recumbency, the lateral position with paddling and convulsions, clinical outcome was 48-60 hours followed by death. 76 pigs died in four properties. The main gross lesions were liver increased in size and lobular illustration with red-brown central areas interspersed with yellowish areas, ascites and hydrothorax with reddish-yellow liquid containing filaments with aspect of fibrin, enlarged lymph nodes and interlobular pulmonary edema. The disease was experimentally reproduced with 16 pigs divided into six groups that received seeds of C. spectabilis in different doses. Hepatocellular necrosis occurred in seven pigs, two of which received daily doses of 2.5g/kg and five who received single doses of 5 and 9.5g/ kg. Ten daily doses of 0.5 and 1.25g/kg caused liver fibrosis.

Intoxicação por Trema micrantha (Ulmaceae) em caprinos no Estado de Santa Catarina / Poisoning by Trema micrantha (Ulmaceae) in goats in the State of Santa Catarina

Vinte e cinco caprinos, criados em piquetes, morreram nos cinco dias subsequentes ao fornecimento de folhas de Trema micrantha (fam.Ulmaceae), uma árvore com nome comum de grandiúva. Quatro caprinos foram necropsiados e amostras de vísceras foram coletadas para exame histológico. As principais alterações clínicas foram: apatia, anorexia, cabeça apoiada contra obstáculos, decúbito e morte. Achados macroscópicos incluíram sufusões no epicárdio e endocárdio; fígado levemente amarelado e com padrão lobular evidente e, em um caso, acompanhado de hemorragias multifocais. Na histologia observou-se necrose hepática, que variava de centrolobular a massiva, compatível com hepatopatia tóxica. No SNC havia satelitose, tumefação neuronal, edema periaxonal, perivascular. O diagnóstico de intoxicação por Trema micrantha foi baseado no quadro clínico e lesional de hepatite tóxica associado ao uso da planta para alimentação de caprinos.

Twenty five goats, maintained in paddocks, had died in five subsequent days after have been offered leaves, mixed in the ration, of Trema micrantha, a tree commonly called grandiúva. Four animals were necropsied and samples were collected for histopathology. Clinical signs included apathy, anorexia, head pressing against obstacles, decubitus and death. Macroscopic findings included suffusions in the epi- and endocardium, a yellowish liver with pronounced lobular pattern, in one goat, the liver presented additionally multiple visible hemorrhages. Histological examination revealed centrilobular to massive hepatic necrosis consistent with acute liver toxicosis. In the brain, satelitosis, neuronal swelling, and perineuronal and perivascular edema was found. The diagnosis of poisoning by Trema micrantha was based in the clinical picture characteristic of toxic hepatitis associated in the feeding of the plant to the goats.

Intestinal volvulus with coagulative hepatic necrosis in a chicken.

A 7-week-old SPF chicken inoculated at 4 weeks of age with chicken anemia virus was puffed up depressed and had ruffled feathers and a good body condition. Intestinal volvulus involving the jejunum and part of the duodenum forming two loops with one knob was observed. Microscopically, venous infarction of the obstructed loops, periportal and sublobular multifocal coagulative hepatic necrosis and granulomatous inflammation of the cecal tonsils were observed. Gram staining revealed no bacteria in hepatic tissue; however, gram-positive bacilli were detected in the necrotic debris in the intestinal lumen. Immunosuppression might have predisposed the chicken to intestinal and cecal tonsil infection that then progressed to volvulus. Loss of the mucosal barrier in infarction might allow bacterial toxins and vasoactive factors to escape into the systemic circulation (toxemia) and be responsible for the hepatic necrosis.