Studies in regard to the classification and putative toxicity of Fridericia japurensis (Arrabidaea japurensis) in Brazil.

Numerous plant species worldwide including Palicourea marcgravii (Rubiaceae) and Tanaecium bilabiatum (Bignoniaceae) in Brazil cause acute cardiac failure (sudden death) and are known to contain monofluoroacetate (MFA). Other Bignoniaceae species including Fridericia japurensis (Arrabidaea japurensis) are reported to cause sudden death in livestock in the Brazilian state of Roraima and are suspected to contain MFA due to the similarity of clinical signs. In this study herbarium specimens of Fridericia japurensis and field collections suspected to be F. japurensis were analyzed for MFA, and plant material from the field collections was dosed to rabbits. No MFA was detected in the herbarium specimens authoritatively identified as F. japurensis; however, MFA was detected in the field collections, which were identified as T. bilabiatum. Rabbits dosed orally with T. bilabiatum died acutely. Voucher toxic specimens initially described as F. japurensis were incorrectly identified, and the correct botanical name for this plant is T. bilabiatum (Arrabidaea bilabiata). Based on this study we conclude that there are no data to support the toxicity of F. japurensis and that the plant previously reported under this name as causing acute cardiac failure in cattle in Roraima is T. bilabiatum. This research highlights the importance of voucher specimens as part of any toxic plant investigation and corrects the literature regarding these toxic plants.

Effects of Passiflora nitida Kunth leaf extract on digestive enzymes and high caloric diet in rats.

The present study investigated inhibition of pancreatic lipase and metabolic effects of high caloric diet in rats. The Passiflora nitida hydroethanol leaf extract (PNE) was used in in vitro assays or administered to rats to study dyslipidemia. Inhibition of lipase in vitro was studied by a spectrophotometric assay using orlistat as the positive control. The effects of PNE on reduction of postprandial triglyceride were studied by oral fat-overloading in rats. Metabolic alterations were induced using the cafeteria diet and 4 weeks post-treatment with PNE or orlistat and blood samples were collected and biochemical analyses were performed. Liver and retroperitoneal fat tissues were obtained to analyze weight and steatosis. IC50 (lg/mL) values for pancreatic lipase inhibition were 21.2 ± 0.8 and 0.1 ± 0.01 for PNE and orlistat, respectively. Oral administration of lipid emulsion resulted in postprandial hypertriglyceridemia at 3 h postadministration and when rats were then administered PNE and orlistat there was decreased of triglyceride levels by 15 % compared to control. Although the energy consumption by the cafeteria diet had been higher, there was no significant weight gain observed in the study groups. The cafeteria diet resulted in a significant increase of weight in the retroperitoneal fat and hypertriglyceridemia levels that could be significantly reduced by PNE and orlistat treatment. We hypothesized that PNE administration prevented the hypertriglyceridemia in rats with a high caloric diet, possibly owing to reduction of lipid absorption and pancreatic lipase inhibition.

Surto de salmonelose pelo sorovar Dublin em bezerros no Maranhão / Outbreak of salmonellosis by serovar Dublin in calves in the State of Maranhão, Brazil

Um surto de salmonelose em bezerros causado pela Salmonella enterica subsp. enterica sorovar Dublin é relatado em uma fazenda no município de Timon, Maranhão. De um total de 62 bezerros, 22 (35,5%) adoeceram e destes nove (40,9%) morreram. Os sinais clínicos incluíram febre, depressão, anorexia e, em alguns casos, sinais respiratórios, neurológicos, entéricos ou artrites, com curso clínico hiperagudo ou subagudo. As principais lesões macroscópicas foram hepatomegalia com áreas pálidas multifocais a coalescentes, esplenomegalia e líquido nas cavidades torácica e abdominal. Histologicamente foram observados granulomas paratifoides no fígado, rim e baço, além de trombos e agregados bacterianos em vasos sanguíneos de diversos órgãos. O surto foi controlado com a adoção de antibioticoterapia adequada aliada a correção de algumas medidas sanitárias na propriedade.

An outbreak of salmonellosis due to Salmonella enterica subsp. enterica sorovar Dublin is reported in calves in a farm in the municipality of Timon, state of Maranhão. From a total of 62 calves, 22 (35.5%) were affected and 9 (40.9%) died. Clinical signs were fever, depression, anorexia, and, in some cases, respiratory, neurological or enteric signs, or arthritis. The clinical manifestation period was hyperacute to subacute. Main gross lesions were enlarged liver and spleen, and presence of exudate in the cavities. Histologically, paratyphoid granuloma were seen in the liver, kidney, and spleen. Thrombosis and bacterial aggregates in blood vessels were observed in various organs. After the realization of the antibiogram the outbreak was controlled by adoption of appropriate antibiotic therapy combined with the correction of sanitary measures.

Poisoning by Indigofera lespedezioides in horses.

Poisoning by Indigofera lespedezioides is reported in horses in the state of Roraima, northern Brazil. The main clinical signs are anorexia, sleepiness, unsteady gait, severe ataxia, weakness, stumbling, and progressive weight loss. To induce the disease experimentally, a 7-year-old horse was introduced in a small paddock invaded by the plant. The first nervous signs were observed 44 days from the start of grazing. The animal was euthanized on day 59. No significant gross lesions were observed upon necropsies of the experimental horse as well as one spontaneously affected horse. Upon histologic examination neuronal lipofuscinosis was observed in the brain, cerebellum, and spinal cord. Wallerian-type degeneration was observed on some mesencephalic tracts. Neuronal and axonal degeneration and lipofuscinosis were observed on electron microscopy examination. Indospicine was detected in four samples of I. lespedezioides with concentrations ranging from 63 to 1178 µg/g whereas nitro toxins could be detected in only one of the samples at a concentration of 2.5 mg/g. In conclusion, poisoning by I. lespedezioides is very similar to those poisonings by Indigofera linnaei and Indigofera hendecaphylla. Based on the preponderance of indospince and lack of nitro toxins in the samples it is proposed that indospicine is the toxic compound responsible for the poisoning.

Experimental swainsonine poisoning in goats ingesting Ipomoea sericophylla and Ipomoea riedelii (Convolvulaceae)

Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05 percent and 0.01 percent swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004 percent of the dry matter in goats ingesting 1.5 percent bw of the dry matter. For goats ingesting 2 percent-2.5 percent bw of dry matter this dose would be 0.00024 percent-0.0003 percent of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean...

Ipomoea sericophylla e Ipomoea riedelii causam uma doença de armazenamento de glicoproteínas em caprinos. Este trabalho relata a intoxicação experimental em caprinos por I. sericophylla e I. riedelii contendo 0,05 por cento e 0,01 por cento de swainsonina, respectivamente. Foram utilizados três grupos de quatro animais. O Grupo 1 recebeu doses diárias de 2g/kg peso vivo (pv) de I. sericophylla dessecada (150mg de swainsonina/kg). Os caprinos deste grupo apresentaram sinais clínicos 36-38 dias após o início da ingestão. O Grupo 2 ingeriu diariamente 2g/kg de I. riedelii dessecada (30mg de swainsonina/kg) por 70 dias. Como não foram observados sinais clínicos a dose de suainsonina foi aumentada para 60mg/kg por outros 70 dias. Os caprinos do Grupo 2 apresentaram sinais clínicos 26-65 dias após o aumento da dose de swainsonina para 60mg/kg. O Grupo 3 foi utilizado como controle. Neste experimento, a menor dose tóxica de swainsonina foi de 60mg/kg, que representa 0,0004 por cento da matéria seca, em caprinos ingerindo 1,5 por cento pv de matéria seca. Para caprinos ingerindo 2 por cento-2,5 por cento pv de matéria seca essa dose corresponderia a 0,00024 por cento-0,0003 por cento da matéria seca. Após o final do experimento dois caprinos foram eutanasiados e outros seis foram observados para conferir a recuperação dos sinais clínicos. Quatro caprinos que continuaram ingerindo as plantas contendo suainsonina por 39-89 dias após os primeiros sinais clínicos permaneceram com sinais clínicos irreversíveis, enquanto que dois caprinos que ingeriram as plantas por 15 e 20 dias após os primeiros sinais clínicos se recuperaram totalmente. Estes resultados e os de trabalhos anteriores sugerem que as lesões irreversíveis, devidas à perda neuronal, ocorrem quando os caprinos continuam ingerindo a planta por aproximadamente 30 dias após o início dos sinais clínicos. Os sinais clínicos e as lesões histológicas foram similares às descritas anteriormente...

Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil / Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil

Descrevem-se 7 surtos de polioencefalomalacia em caprinos e 3 surtos em ovinos no semi-árido nordestino. Foram afetados animais de diversas idades em diferentes épocas do ano. Em 5 surtos os animais eram suplementados com concentrados e em 5 consumiam somente pastagem. Em um dos surtos os ovinos estavam recebendo à vontade uma mistura múltipla contendo 1,3 por cento de flor de enxofre. Os sinais clínicos caracterizaram-se por cegueira, depressão, pressão da cabeça contra objetos, andar em círculos, ranger de dentes, incoordenação, paralisia espástica, ataxia, diminuição dos reflexos palpebral e pupilar, estrabismo lateral, nistagmo e pupilas dilatadas. De 9 animais tratados com tiamina e dexametasona, 7 se recuperaram e 2 morreram. O diagnóstico foi feito com base na recuperação após o tratamento e/ou a presença de alterações histológicas características. O curso clínico variou de 2 a 15 dias. Três animais foram necropsiados. Um animal apresentou herniação do cerebelo em direção ao Forame magno e amolecimento das circunvoluções cerebrais e, ao corte, coloração amarelada e cavitação da substância cinzenta do córtex. Outro animal apresentou somente herniação do cerebelo. No terceiro animal não foram observadas lesões macroscópicas. As alterações histológicas caracterizaram-se por necrose laminar do córtex cerebral e, em dois animais, por lesões de malácia no tálamo e colículo rostral. Desconhece-se a etiologia em 9 dos surtos estudados. Em outro se sugere que tenha sido causado por intoxicação por enxofre, contido principalmente na mistura múltipla constituída por com 1,3 por cento de flor de enxofre (96 por cento de enxofre) e 30 por cento de cama de galinha (0,39 por cento de enxofre).

Sudden bovine death from Mascagnia rigida in northeastern Brazil.

One outbreak of sudden death occurred in the Agreste region of Paraiba, Brazil in a herd of 129 cattle. When the herd was driven from the area, 40 cattle had clinical signs characterized by instability, staggering and lying down or falling. Twenty cattle died and the other 20 recovered. Dry Mascagnia rigida collected in the paddockwas administrated to 3 groups of 2 rabbits each at doses of 1.25, 2.5 or 5 g/kg bw. All rabbits ingesting 2.5 and 5 g/kg bw died acutely between 3 h 25 min and 16h 15 min after dosing. M rigida collected in another farm where the disease was not observed was given to 3 groups of 2 rabbits each at doses of 5, 10 or 20 g/kg bw. Only I rabbit died suddenly 3 h and 25 min after ingestion of 20 g/kg bw. These results tend to support M rigida as a cause of sudden death in cattle and rabbits They also demonstrate variations in the toxicity of the plant, which seems reflective of the variation in disease occurrence in different areas where it occurs.