Sulfur‐associated polioencephalomalacia in cattle grazing plants in the Family Brassicaceae

McKenzie, R. A.; Carmichael, AM; Schibrowski, Meghan; Duigan, SA; Gibson, JA; Taylor, J. A.

doi:10.1111/j.1751-0813.2008.00387.x

Cited by 27 publications

(26 citation statements)

References 18 publications

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“…Porém, pesquisas têm indicado que os achados clínicos e histopatológicos são similares entre as diversas causas de PEM (Gould 2000, Burgess 2008, Sant ' Ana et al 2009a. A associação entre dietas com alto teor de enxofre e a ocorrência de PEM em bovinos foi confirmada por vários autores, tanto na forma de surtos (Coghlin 1944, Dickie et al 1979, Raisbeck 1982, Hibbs & Thilsted 1983, Haris 1987, Beke & Hironata 1991, Hamlen et al 1993, Jeffrey et al 1994, Bulgin et al 1996, Low et al 1996, McAllister et al 1997, Niles et al 2000, Traverso et al 2001, Haydock 2003, Kul et al 2006, McKenzie et al 2009) ou por induções experimentais (Mella et al 1976, Sager et al1990, Gould et al 1991, McAllister et al 1992, Cummings et al 1995Gould et al 1997, Niles et al 2002, Loneragan et al 2005, Cunha et al, 2008.…”

Section: Introductionunclassified

Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul

Cunha

Bandarra²,

Dias³

et al. 2010

Pesq. Vet. Bras.

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613Pesq. Vet. Bras. 30(8):613-617, agosto 2010 RESUMO.-Neste trabalho descreve-se surto de polioencefalomalacia em bovinos decorrente da ingestão de dieta com excessiva concentração de enxofre em uma propriedade no Rio Grande do Sul. O lote era composto por 30 bezerros, mantidos em um piquete com azevém (Lolium multiflorum) e suplementados com ração e sal mineral. Seis bezerros morreram e dois deles foram necropsiados; amostras de tecido hepático para dosagem de chumbo e fragmentos do sistema nervoso central para histopatológico foram colhidos. Um dos bezerros foi examinado antes da morte e sinais neurológicos encefálicos foram constatados. Foi estabelecido o teor de enxofre nos componentes da dieta e água, a produção de sulfeto de hidrogênio ruminal em cinco bovinos do mesmo lote e realizada PCR de um bloco de parafina para detecção de DNA do herpevirus bovino tipo 5. O consumo total de enxofre foi de 0,38% da matéria seca fornecida aos animais e as dosagens de sulfeto de hidrogênio ruminal em animais do mesmo lote variaram de 1.000 a 2.500ppm. Os achados histopatológicos indicaram necrose laminar do córtex cerebral. Não foi detectado chumbo na amostra de tecido hepáti-co e não foi identificado DNA do herpesvirus bovino tipo 5 no encéfalo. O quadro clínico de síndrome cerebrocortical associado aos elevados valores do sulfeto de hidrogênio ruminal, alta ingestão de enxofre na dieta e os achados histopatológi-cos permitem estabelecer o excesso de enxofre como causador da polioencefalomalacia. An outbreak of polioencephalomalacia in cattle caused by ingestion of high sulphur diet, in Rio Grande do Sul, Brazil is described. One group of 30 calves was kept in Italian ryegrass (Lolium multiflorum) pasture and supplemented with concentrate and minerals. Six calves died, necropsy was performed in two of them and liver samples (for lead determination) and fragments of central nervous system were collected. Clinical and neurological examination was performed in one calf and confirmed brain involvement. Sulphur content on dietary components and water, ruminal hydrogen sulfide production in five calves of the same group and PCR from formalin-fixed paraffin-embedded cerebral tissues to detect bovine herpesvirus 5 DNA was perfomed. The total sulphur intake was 0.38% dry matter and the values of ruminal sulfide concentration ranged from 1,000 to 2,500ppm. Lead It was not detected in the liver samples and PCR was negative for bovine herpesvirus 5. The brain lesions were characterized by laminar neuronal necrosis. The clinical signs of cerebrocortical syndrome associated with high ruminal sulfide values, elevated intake of dietary sulphur and histological lesions confirmed that the excess of sulphur caused the polioencephalomacia in these calves.INDEX TERMS: Cerebrocortical necrosis, diagnostic, ruminal hydrogen sulfide.

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Section: Introductionunclassified

Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul

Cunha

Bandarra²,

Dias³

et al. 2010

Pesq. Vet. Bras.

View full text Add to dashboard Cite

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“…Similarly, an acute course of the disease leading to deaths was observed in single-component feeding with cruciferous plants (24), in which sulphur content is 3-5 times higher than in other plants commonly used in cattle feeding. In cruciferous plants it is about 1.5 % of dry matter, but only slightly lower concentrations can be found in fodder plants from industrial areas.…”

Section: Aetiology and Occurrencementioning

confidence: 82%

“…The cause of the disease can be a single component diet fed over a sustained period and containing ingredients with high sulphur content, especially by-products from the mining and food industries. Mining and industrial water, cruciferous plants, some concentrates and milk substitutes, and also molasses and spent grain have high sulphur content (5,13,17,20,21,24,29). The ingestion of sulphur with water can be exceptionally high in situations of drought and high temperature when animals drink heavily (14,23,34).…”

Section: Aetiology and Occurrencementioning

confidence: 99%

Polioencephalomalacia in ruminants caused by excessive amount of sulphur - a review

Lutnicki

Madej

Riha

et al. 2014

Bulletin of the Veterinary Institute in Pulawy

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Polioencephalomalacia as a result of sulphur excess is a growing problem in cattle and sheep, mainly in young, growing animals. It is common in different regions of the world. The disease develops favoured by certain conditions such as sustained provision of feed and water with high sulphur content, use of dietary supplements containing sulphur, and a habitat with high hydrogen sulphide concentration. Pathogenesis of the disease is complex, but very important are oxidative-antioxidative imbalance, dysfunction of vessels, and secondary cerebral cortex ischaemia as a result of direct and/or indirect action of sulphur metabolites, namely hydrogen sulphide, sulphides, and sulphites. Clinical signs and changes in the cerebral cortex in the form of degenerative necrotic lesions are similar to those observed in polioencephalomalacia caused by vitamin B 1 deficiency, and lead and salt intoxication. Highly increased sulphur content (more than 0.3-0.4 of dry matter) in the diet is the basis for differential diagnosis, as well the high concentration of hydrogen sulphide in gas and sulphides in rumen fluid. In prophylaxis and treatment the most important measure is to limit sulphur intake and in acute cases to neutralise low pH in rumen and administer vitamin B 1 injections.

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“…Furthermore, sulfur-containing plants can contribute to a large amount of sulfur. 90 Cattle exposed to manure gas with a high H 2 S content developed PEM, making inhalation of gas a potential source for sulfur intoxication. 91 In beef calves, experimental diets containing more than 4000 ppm sulfur produce neurologic disease due to PEM, and subclinical brain lesions have been observed in a few calves with consumption of sulfur lower than 4000 ppm.…”

Section: Sulfurmentioning

confidence: 99%

“…Histopathology of the brain reveals signs of PEM, such as laminar and cortical spongiosis and neuronal necrosis within the cerebral cortex. 90 Differential diagnoses for neurologic disorders in cattle include lead poisoning, sodium poisoning, thiamine deficiency-induced PEM, hypovitaminosis A, and Histophilus somni meningoencephalitis. Sulfur-induced PEM does not cause a decrease in rumen or blood thiamine concentrations.…”

Section: Varga and Puschnermentioning

confidence: 99%

Retrospective study of cattle poisonings in California: recognition, diagnosis, and treatment

Varga¹,

Puschner²

2012

VMRR

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Abstract:In this retrospective study all suspect bovine intoxications submitted to the California Animal Health and Food Safety Laboratory between January 1, 2000 and December 31, 2011 were reviewed. A total of 1199 cases were submitted, but a diagnosis of intoxication was only established in 13.5% of cases. In these cases, overexposures to minerals, metals, and poisonous plants were determined as the most commonly diagnosed poisonings in cattle in California. Nitrate/nitrite poisoning was the most commonly diagnosed plant-associated intoxication, followed by gossypol and oleander. This study details the diagnostic challenges and treatment options for the most commonly diagnosed intoxications. To ensure proper treatment and prevention of new cases, accurate diagnosis is necessary, and therefore this review provides an essential tool for the food animal practitioner. Available toxicological analyses are offered at select laboratories, which can be time consuming and expensive, yet the potential for residues in consumed animal products and implications for human health necessitate testing and consultation. Any potential exposure to a toxicant in cattle should be reviewed to determine whether a residue hazard exists. Therapy focuses on immediate removal of the toxicant from the environment and from the gastrointestinal tract. With few antidotes available, most are cost prohibitive to treat numerous affected cattle. In addition, most antidotes will require extra-label drug use and establishment of meat and milk withdrawal times.

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Sulfur‐associated polioencephalomalacia in cattle grazing plants in the Family Brassicaceae

Cited by 27 publications

References 18 publications

Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul

Surto de polioencefalomalacia por ingestão excessiva de enxofre na dieta em bezerros no Rio Grande do Sul

Polioencephalomalacia in ruminants caused by excessive amount of sulphur - a review

Retrospective study of cattle poisonings in California: recognition, diagnosis, and treatment

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