Outbreak of monensin poisoning in cattle due to supplementation error / Surto de intoxicação por monensina em bovinos devido a erro de suplementação

ABSTRACT: Iatrogenic intoxications occur in domestic animals. Mortality was observed in a group of calves, reaching 20 deaths until the day of the technical visit, with or without sudden clinical signs, on a farm in the city of Pires do Rio, State of Goiás, Brazil. Deaths after the visit were not accounted systematically. Clinical signs included muscle weakness, ataxia, recumbency, bilateral jugular distention, and death. Suspected diagnosis of poisoning by ionophore antibiotics was made based on clinical and laboratory findings from nine animals, which included high plasma CK and LDH levels, as well as on anatomopathological findings of a recently dead calf, which showed myocardial and skeletal muscle degeneration and necrosis. Monensin overdose (25.5 µg/kg in skeletal muscle and 209.4 µg/kg in the liver) was detected by liquid-chromatography and mass-spectrophotometry analysis, contributing to the confirmation of ionophore poisoning diagnosis.

RESUMO: Intoxicações iatrogênicas ocorrem em animais domésticos. Um lote de bezerros apresentou mortalidade, chegando a 20 mortes até o dia da visita técnica, após sinais clínicos súbitos ou ausência destes, em uma propriedade rural do município de Pires do Rio, estado de Goiás, Brasil. As mortes após a visita não foram sistematicamente contabilizadas. Os sinais incluíam fraqueza muscular, ataxia, decúbito, distensão bilateral da veia jugular e morte. Baseado nos achados clínicos e laboratoriais de nove bovinos, que incluíram níveis de CK e LDH elevados no plasma, assim como degeneração e necrose miocárdica e na musculatura esquelética à avaliação anatomopatológica em um dos bezerros mortos, que apresentou degeneração e necrose em miocárdio e músculo esquelético. Uma sobredosagem de monensina (25,5 µg/g no músculo esquelético e 209,4 µg/g no fígado) foi detectada com análise por cromatografia líquida e espectrofotometria de massas, contribuindo para a confirmação do diagnóstico de intoxicação por ionóforos.

Poisoning by Senna obtusifolia in sheep / Intoxicação por Senna obtusifolia em ovinos

In a paddock highly invaded by Senna obtusifolia 10 out of 60 sheep showed muscle weakness and 9 died after a clinical manifestation period of 24-76 hours. Serum activities of creatine kinase were increased in all sheep examined. Multifocal polyphasic muscle segmental degeneration and necrosis was observed in skeletal muscles. Although the plant is a common weed in northeastern Brazil, the poisoning is rare, probably because the animals do not ingest it or due to toxicity variations.(AU)

Em um piquete altamente invadido por Senna obtusifolia, 10 de 60 ovelhas mostraram fraqueza muscular e 9 morreram após um período de manifestação clínica de 24-76 horas. As atividades séricas da creatina quinase foram aumentadas em todos os ovinos examinados. Foi observada degeneração segmentar e necrose polifásica muscular em músculos esqueléticos. Embora a planta seja uma erva daninha comum no Nordeste do Brasil, o envenenamento é raro, provavelmente porque os animais não o ingerem ou devido a variações de toxicidade.(AU)

Placental Lesions in Meconium Aspiration Syndrome

BACKGROUND: Meconium aspiration syndrome (MAS) is defined by respiratory distress requiring supplemental oxygen in a meconium-stained neonate. MAS is clinically subclassified as mild, moderate, and severe according to the oxygen requirement. The aims of this study were to compare the histological findings in the placentas of MAS neonates with those of meconium-stained but non-MAS neonates and to analyze the correlation between the severity of MAS and the grade of its histological parameters. METHODS: We collected 160 singleton term placentas from neonates with meconium staining at birth from a tertiary medical center, Seoul, Republic of Korea. We reviewed hematoxylin and eosin sections of tissue samples (full-thickness placental disc, chorioamniotic membranes, and umbilical cord). RESULTS: Funisitis was present more frequently in MAS than in non-MAS (p < .01), of which the stage was correlated with the severity of MAS (p < .001). The histological findings consistent with maternal underperfusion and chronic deciduitis were more frequent in MAS than in non-MAS (p < .05). There was a correlation between the degree of chorionic vascular muscle necrosis and the severity of MAS (p < .05). CONCLUSIONS: Our results suggest that fetal inflammatory response evidenced by funisitis occurs prenatally in MAS and that the stage of funisitis and of chorionic vascular muscle necrosis may be a predictive marker of the severity of MAS.

Megaesophagus in sheep and goats / Megaesôfago em ovinos e caprinos

ABSTRACT: Megaesophagus is a rare disease in ruminants characterized by regurgitation of rumen contents. In this paper it was described cases of megaesophagus in two sheep and two goats on a farm in the state of Paraíba, Northeastern Brazil. All animals showed regurgitation of rumen contents and weight loss, with a clinical course of several months. At necropsy all animals presented megaesophagus. Histological examination showed segmental muscle necrosis in the esophagus and skeletal muscles. Serum samples from one sheep and one goat were negative for the presence of blue tongue antibodies by ELISA, and whole blood and muscle samples from one goat were negative for this virus by RT PCR. Epidemiological data and pathology suggested that the disease could have been caused by some toxic plant, but known plants causing segmental muscle necrosis were not observed in the areas where the disease occurred.

RESUMO: Megaesôfago é uma enfermidade rara em ruminantes caracterizada por regurgitação do conteúdo ruminal. Neste trabalho, descrevem-se casos de megaesôfago em dois ovinos e dois caprinos no Estado da Paraíba. Todos os animais apresentaram regurgitação do conteúdo ruminal e emagrecimento, com evolução de vários meses. Nas necropsias dos animais, observou-se dilatação esofágica e, em exames histológicos, necrose muscular segmentar no esôfago e músculos esqueléticos. Não foram encontrados anticorpos para o vírus da língua azul nos soros de um ovino e um caprino pela técnica de ELISA. Sangue total e músculo de um caprino resultaram negativos para esse vírus por RT PCR. Sugere-se que a doença seja causada por alguma planta tóxica, mas não foram encontradas plantas conhecidas por causarem necrose segmentar muscular nos piquetes onde ocorreu a doença.

Intoxicação espontânea de bovinos por Senna obtusifolia no Estado do Paraná / Spontaneous Senna obtusifolia poisoning in cattle in the state of Parana, Brazil

Plantas do gênero Senna causam miopatia degenerativa em bovinos e o maior número de relatos envolve Senna occidentalis. O objetivo desse trabalho é relatar, pela segunda vez no Brasil, um surto de intoxicação natural por Senna obtusifolia. É descrito um surto de intoxicação por Senna obtusifolia, na região noroeste do estado do Paraná, que aconteceu em um lote de 200 vacas, com idade entre 45 e 152 meses, introduzidas em um confinamento para melhorar a condição corporal antes do parto. A área do confinamento estava invadida pela planta e as vacas permaneceram no local durante oito dias. Entre quatro e nove dias após a entrada no confinamento 20 vacas adoeceram e somente uma se recuperou. Os sinais consistiram em mioglobinúria, incoordenação e decúbito esternal permanente. As vacas doentes apresentaram aumento das atividades das enzimas creatina quinase, aspartato aminotransferase, gamaglutamiltransferase e fosfatase alcalina. Lesões na musculatura esquelética dos membros posteriores caracterizadas por áreas pálidas representaram as principais alterações observadas à necropsia de quatro bovinos. Necrose segmentar multifocal da musculatura esquelética e necrose paracentral multifocal no fígado foram as alterações histopatológicas mais relevantes. As evidências epidemiológicas, clínicas e patológicas indicam o diagnóstico de intoxicação por Senna obtusifolia. A planta demonstrou ter efeito miotóxico e hepatotóxico nos animais intoxicados e a doença foi quase sempre fatal.

Plants of the genus Senna cause a degenerative myopathy in cattle and most of the reports refer to Senna occidentalis. The aim of this paper is to report, for the second time in Brazil, an outbreak of natural poisoning by Senna obtusifolia. It happened in the northwestern Paraná in a herd of 200 cows, 45 to 152 months of age, which had been placed into a feedlot to improve their nutritional status before the calving period. The cows stayed for eight days in this feedlot infested by the plant. Four to nine days after they got into the feedlot, 20 cows became ill and only one recovered. The clinical signs consisted of myoglobinuria, incoordination and permanent sternal recumbency. The affected cows showed increased activity of creatine phosphokinase, aspartate aminotransferase, gama-glutamyltransferase, and alkaline phosphatase. The main postmortem changes were in skeletal muscles of the hind limbs characterized by pale areas. The histological alterations were multifocal segmental necrosis of skeletal muscles and hepatic multifocal paracentral necrosis. Epidemiological, clinical and pathological data led to the diagnosis of Senna obtusifolia poisoning. The plant showed miotoxic and hepatotoxic effects on the poisoned animals and the disease was almost always lethal.

Surtos de intoxicação por salinomicina em chinchilas (Chinchilla lanigera) / Outbreaks of salinomycin toxicosis in Chinchillas (Chinchilla lanigera)

Quatro surtos de intoxicação por salinomicina são descrito em chinchilas de três municípios do Estado do Rio Grande do Sul. Uma semana após a ingestão de ração contendo 37 ppm de salinomicina, aproximadamente duas mil chinchilas de quatro fazendas expostas diminuíram o consumo da ração. Quatrocentos e vinte sete chinchilas demonstraram apatia. Dessas, duzentos e setenta e sete desenvolveram decúbito esternal e lateral, dispneia e coma, seguidos de morte. As primeiras mortes ocorreram oito dias após a ingestão da ração. A evolução dos sinais clínicos até a morte ou eutanásia foi de 2-5 dias. Os exames bioquímicos do soro sanguíneo em quatro chinchilas revelaram níveis aumentados da alanina aminotransferase, aspartato transaminase, fosfatase alcalina, creatina cinase, glicose, triglicerídeos e colesterol total. Quarenta e cinco chinchilas foram submetidas à necropsia. Os achados macroscópicos consistiam de marcada lipidose hepática em todas as chinchilas necropsiadas; fetos em estado de decomposição em doze chinchilas que estavam prenhes. Microscopicamente, múltiplas fibras musculares esqueléticas estavam hipereosinofílicas, tumefeitas e com perda das estriações. Nas chinchilas que sobreviveram por mais dias era possível observar segmentos fragmentados de miofibras afetadas (necrose flocular) e regeneração de miofibras. No fígado foi observada marcada degeneração gordurosa. Não foram observadas anormalidades microscópicas nos demais órgãos analisados. Análises à procura de aflatoxinas, resíduos de pesticidas e isolamento bacteriano foram negativos. A análise da ração por cromatografia líquida revelou 37ppm de salinomicina na ração. A ração suspeita foi administrada a 12 chinchilas, três das quais (25 por cento) morreram apresentando lesões semelhantes às observadas nas chinchilas com a doença natural. O diagnóstico de intoxicação por salinomicina foi baseado na epidemiologia, lesões histológicas características e na presença de salinomicina na ração administrada nas quatro criações envolvidas.

Four outbreaks of ionophore toxicosis are described in chinchillas from four commercial farms located in three municipalities in the state of Rio Grande do Sul, southern Brazil. Approximately 2,000 chinchillas showed decrease in food intake one week after start ingesting a ration containing 37 ppm of salinomycin. Four hundred and twenty seven chinchillas showed apathy. Of those 277 develop sternal and lateral recumbence, dyspnea and coma followed by death. First deaths occurred eight days after the start on the salinomycin containing ration; clinical course was 2-5 days. Serum chemistry carried out in four chinchillas revealed increased levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, creatinenin kinase, glucose, triglicerids and total cholesterol. Forty five affected chinchillas were necropsied; consistent necropsy findings were marked hepatic lipidosis; additionally twelve pregnant chinchillas had dead decomposing fetuses. Microscopically skeletal muscles had multifocally swollen hypereosinophilic myofibers with loss of cross striations. In those chinchillas that survived longer than a few days, microscopic features in the skeletal muscle included segmental fragmentation of dead fibers (floccular necrosis) and myofiber regeneration. Marked fatty degeneration was observed in the livers of all affected chinchillas. No microscopic changes were observed in other organs. Chemical analysis in the feed consumed by the chinchillas did not detect aflatoxins or pesticides residues; bacterial culture performed in samples of liver and intestinal contents from necropsied chinchillas yielded no significant bacterial growth. Analysis by thin layer chromatography performed in the ration consumed by the chinchillas detected 37 ppm of salinomycin. The suspected ration was fed to 12 chinchillas three of which (25 percent) died with similar lesions to those observed in the natural cases. The diagnosis of salinomycin toxicosis was based in the epidemiology, histology of the lesions, on the detection of significant amounts of salinomycin in the ration used to feed the chinchillas in the four involved farms and on the reproduction of disease by feeding the suspected ration to susceptible chinchillas.

Surto de intoxicação por monensina em avestruzes e equinos no sul do Brasil / Outbreak of monensin poisoning in ostriches and horses in southern Brazil

Descreve-se um surto de intoxicação por monensina em avestruzes e equinos em uma propriedade no Rio Grande do Sul. Oito dias antes do aparecimento dos primeiros sinais clínicos, uma ração comercial formulada para bovinos, cuja composição incluía monensina (177ppm), foi introduzida na dieta dos animais. Três equinos manifestaram dificuldade de movimentação, cólica, sudorese e decúbito permanente; dois morreram em 48 horas após o inicio dos sinais. Três avestruzes adoeceram, dois apresentaram decúbito esternal permanente, o outro estava apático e relutante ao movimento. Dois avestruzes morreram 15 e 30 dias após o início dos sinais. Nas necropsias dos equinos, observou-se miocárdio com palidez multifocal, hemorragia no endocárdio e no epicárdio (principalmente ao redor dos vasos coronarianos) e musculatura esquelética com áreas branco-amareladas bilaterais e focalmente extensas. Essas alterações corresponderam histologicamente, à miopatia e cardiomiopatia necróticas. Nos avestruzes, músculos esqueléticos difusamente pálidos e com múltiplos pequenos pontos brancos corresponderam à necrose segmentar polifásica, com alterações necróticas e regenerativas.

An outbreak of monensin poisoning affected ostriches and horses from a farm in Rio Grande do Sul. Eight days before the onset of clinical signs, a commercial cattle concentrate containing monensin (177ppm) was introduced in the diet of the animals. Three horses showed difficulty moving, cramping, sweating and permanent recumbency, and death within 48 hours. Three ostriches showed sternal permanent recumbency or sluggish and reluctance to move. Two ostriches died 15 and 30 days after the onset of signs. Gross changes in the horses included multifocal myocardial pallor, endocardial and epicardial hemorrhages mainly around the coronary vessels, and bilateral yellowish white foci in skeletal muscles. Histological lesions were necrotic myopathy and cardiomyopathy. At necropsy of ostriches, skeletal muscles were diffusely pale with multiple small white spots, which corresponded to polyphasic segmental necrosis and regenerative changes.

Biologic Wet Dressing with Amnion in Muscle Necrosis of Lower Extremity Caused by Acute Limb Ischemia

Early treatment to facilitate the muscular blood flow can avert myonephropathic metabolic syndrome (MNMS) and major amputation for patients suffering with acute limb ischemia. Delayed reperfusion or microemboli in the small vessels can aggreviate: ischemic changes and lead to irreversible muscle necrosis. Amnion is an excellent biological dressing, and we tried using it to treat anterior compartment muscle necrosis (ACMN). The amnions were aseptically collected from caesarean sections. Additional betadine (1 : 3 solution) and vaseline-soaked gauzes were applied over the amnion as a daily biologic wet dressing. The amnion was replaced every three days. Finally, split skin grafting was performed on the healthy granulation tissue. We treated two patients who happened to have shin muscle necrosis. A 65-year-old man with a femoro-femoral arterial bypass showed graft thrombosis. Thirteen days after performing balloon angioplasty with stent insertion in the right femoral artery, new emboli were found in the stent and in the left popliteal artery. There was an attack of myocardial infarction the next day after embolectomy. The severe MNMS and ACMN at the right shin occurred after cardiopulmonary resuscitation. The dry gangrene was excised 3 months later, and this was followed by a skin graft 4 months later. An 81-year-old woman with atrial fibrillation showed left common femoral arterial obstruction and ACMN on the left shin during the management of congestive heart failure. The dry gangrene was excised 2 months later, and this was followed by a skin graft 3 months later. The amnion dressing shows promises for providing healthy granulation tissue for split skin grafts when treating muscle necrosis of the leg. Biologic dressing with using amnion is an option for limb salvage in the case of muscle necrosis that is caused by acute limb ischemia, although the treatment takes a long time.

Papillary muscle necrosis in neonates and infants: analysis of 209 autopsies

A total of 209 consecutive neonate and infant autopsies were reviewed with special attention to papillary muscle necrosis (PMN) of the heart. Associated major pathological findings were analysed for the evaluation of significant pathological accompaniments of PMN. PMN was found in 52 cases among 171(30.4%) neonates and major pathological accompaniments were bronchopneumonia, hyaline membrane disease, hypoxic neuronal change, sepsis, subarachnoid hemorrhage, disseminated intravascular coagulation (DIC) and acute tubular necrosis, among which hypoxic neuronal change and ATN had a statistically significant higher incidence when compared with the control group. (p < 0.005). PMN was found in 13 cases among 38(34.2%) infants and accompaniments were congenital heart disease, sepsis, bronchopneumonia, DIC and hypoxic neuronal change, all of which showed no difference from the control group in incidence. The results imply that PMN is a kind of organ damage in stressed subjects regardless of age, that it is not a special form of myocardial injury in any specific age group including the newborn period, and is possibly of different pathogenesis and significance.

The Clinical Study of Electrical Burns / 대한정형외과학회잡지

Electrical burns constitude a unique type of thermal injury. Not only may there be a cutaneous burn but frequently hidden local and regional tissue damage exists. Tissue injury and tenden vascular necrosis are complete within eight to ten days follwoing the insult and additional tissue damage can occur because of infection and toxicity of necrotic tissue. Early excision and early graft can prevent this progressiv muscle necrosis because marginally viable tissue at the periphery are saved by the increased vascularity provided by immediate use of flaps or grafting. We have treated 67 cases of electrical burn from 1975 to 1979. The brief summary of the observations were as follows: 1. Good results were obtained in 15 cases after treatment of early excision and early graft. 2. Simultaneous involvements of hand, wrist, elbow, and shoulder were found because of tetanic contraction in alternating current in 21 cases. 3. In one case of spinal atrophic paralysis due to direct injury to spinal cord, paraplegia was permanent.