Polioencefalomalacia experimental em bovinos induzida por toxicose por enxofre

Cunha, Paulo Henrique Jorge da; Badial, Peres Ramos; Cagnini, Didier Quevedo; Oliveira-Filho, José Paes de; Moares, Lívia Fagundes; Takahira, Regina Kiomi; Amorim, Renée Laufer; Borges, Alexandre Secorun

doi:10.1590/s0100-736x2011000100007

Cited by 9 publications

(19 citation statements)

References 41 publications

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“…The presence of increased density is an unusual finding in ruminants with PEM, since only the presence of normal protein concentrations and mild lymphocytic pleocytosis are the described changes (SCOTT, 2004(SCOTT, , 2010. Just as the cases reported here, Stokol et al (2009) demonstrated that 75% of the bovines with PEM showed no pleocytosis; this finding was also described for calves with PEM experimentally induced by sulfur administration (CUNHA et al, 2011). The alteration of reddish coloration of CSF observed in a sample (Case 3) can be attributed to blood contamination due to an accidental trauma of the leptomeningeal vessels during collection.…”

Section: Discussionsupporting

confidence: 75%

“…However, nowadays, not all cases of PEM are associated with thiamine deficiency, and several other etiologies are involved in the pathogenesis of this lesion (SANT'ANA et al, 2009b). Among these causes, we may highlight manifestations of excess sulfur intake (LONERAGAN et al, 1998;CUNHA et al, 2010CUNHA et al, , 2011DELFIOL et al, 2013), salt (OSWEILER et al, 1995;DUARTE et al, 2014), lead intoxication (CEBRA; CEBRA, 2004;LEMOS et al, 2004), and thiamine deficiency SANT'ANA et al, 2009b;GRAÇA et al, 2010) or analogues, such as amprolium (SANT'ANA et al, 2009a;NOGUEIRA et al, 2010), besides ingestion of plants rich in thiaminase, and acute poisoning by Phalaris spp. and by bovine herpesvirus type-5 SANT'ANA et al, 2009b).…”

Section: Polioencephalomalaciamentioning

confidence: 99%

“…In Brazil, PEM is predominant in cattle (NAKAZATO et al, 2000;LEMOS et al, 2004;VIEIRA et al, 2007;CUNHA et al, 2010CUNHA et al, , 2011RIBAS et al, 2013), although there are also reports in sheep (LIMA et al, 2005;VIEIRA et al, 2007;DUARTE et al, 2014), goats (LIMA et al, 2005), and in buffaloes (GUIMARÃES et al, 2008).…”

Section: Polioencephalomalaciamentioning

confidence: 99%

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Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil

Câmara¹,

Batista²,

Soto-Blanco³

2018

SCA

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The present study aimed to describe epidemiological, clinical, laboratorial, and pathological findings of polioencephalomalacia (PEM) in ruminants from the semi-arid region of Rio Grande do Norte, Brazil. A total of seven ruminants (five sheep, one cattle, and one goat) with pathological diagnosis of PEM were included. Four cases were associated with thiamine deficiency, on account of chronic ruminal acidosis caused by diets rich in carbohydrate, with mainly concentrates, ground soybean hulls, and melon. Three ruminants from an outbreak of petroleum poisoning presented macro and microscopic lesions consistent with changes of malacia and edema in deep structures of the brain, as described in ruminants with PEM associated with sulfur intoxication. Major macroscopic changes included congestion of cerebral vessels, edema, and herniation of the cerebellum. The most observed microscopic lesions, among all assessed cases, were laminar and segmental neuronal necrosis at different regions of the brain, spongiosis, nuclear pyknosis, and red nucleus neurons. Cerebrospinal fluid analysis revealed nonspecific alterations, requiring its association with epidemiological, clinical, and pathological findings, as the results described here are similar to those reported in toxic diseases with neurological manifestations, such as botulism. Key words: Livestock. Nutritional diseases. Cerebrospinal fluid. Cerebrocortical necrosis. ResumoO presente trabalho objetiva descrever os achados epidemiológicos, clínicos, laboratoriais e patológicos de casos de polioencefalomalácia (PEM) em ruminantes na região semiárida do Rio Grande do Norte. Sete ruminantes (cinco ovinos, um bovino e um caprino) com diagnóstico patológico de PEM foram incluídos. Quatro casos foram associados à deficiência de tiamina devido acidose láctica ruminal crônica por oferta de alimentação rica em carboidratos, destacando-se os concentrados, casca de soja triturada e melão. Três ruminantes de um surto de intoxicação por petróleo apresentaram lesões macro e microscópicas condizentes com alterações de malácia e edema em estruturas profundas do encéfalo, descritas em ruminantes com PEM associada à intoxicação por enxofre. As principais alterações macroscópicas incluíram congestão dos vasos cerebrais, edema e conificação do cerebelo. Em todos os casos avaliados, as lesões microscópicas mais observadas foram a necrose neuronal laminar e segmentar em diferentes regiões do encéfalo, espongiose, picnose nuclear e a presença de neurônios vermelhos. A análise do líquido cefalorraquidiano revelou alterações inespecíficas, sendo necessário sua associação aos achados epidemiológicos, clínicos e patológicos, pois os resultados aqui descritos são semelhantes aos relatados em doenças tóxicas com manifestações neurológicas, como o botulismo. Palavras-chave: Animais de produção. Doenças nutricionais. Líquido cefalorraquidiano. Necrose cerebrocortical.

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Section: Discussionsupporting

confidence: 75%

Section: Polioencephalomalaciamentioning

confidence: 99%

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Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil

Câmara¹,

Batista²,

Soto-Blanco³

2018

SCA

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“…A doença em ovinos tem ocorrido em forma de surtos (Jeffrey et al 1994, Bulgin et al 1996, Low et al 1996 ou tem sido induzida experimentalmente (Gooneratne et al 1989, Rousseaux et al 1991, McAllister et al 1992, Alves de Oliveira et al 1996, Krasicka et al 1999, Salem et al, 2010. No Brasil, a PEM ocasionada pelo consumo excessivo de enxofre foi descrita em bovinos na forma de surtos (Traverso et al 2001, Cunha et al 2010) e em indução experimental (Cunha et al 2011). Existe apenas um surto de PEM em ovinos relatado no Brasil, em que os autores estimaram que os animais estivessem consumindo quantidades excessivas de enxofre na dieta (Lima et al 2005).…”

Section: Introductionunclassified

“…A técnica de determinação da concentração do sulfeto de hidrogênio ruminal (H 2 S) com utilização de tubos colorimétricos tem sido empregada com sucesso em bovinos para identificar rebanhos que estejam ingerindo alto teor de enxofre na dieta (Gould et al 1997, Cunha et al 2010, 2011. Em ovinos, a técnica foi utilizada somente por Neville et al (2010), que identificaram altos níveis de H 2 S ruminal em animais em dieta com alto teor de enxofre, apesar dos ovinos não terem desenvolvido PEM.…”

Section: Introductionunclassified

Aspectos clínicos e laboratoriais em ovinos submetidos a dietas com níveis elevados de enxofre com objetivo de indução de polioencefalomalácia

et al. 2013

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Pesq. Vet. Bras. 33(4): 435-442, abril 2013 435 RESUMO.-A polioencefalomalacia (PEM) é uma doença neurológica que acomete ruminantes e pode ser desencadeada por diversos fatores, dentre eles o consumo excessivo de enxofre. Este trabalho teve como objetivo verificar a relação entre dietas ricas em enxofre, altos níveis de gás sulfídrico ruminal e a ocorrência de polioencefalomalácia em ovinos. Foram utilizados 18 ovinos, divididos em três grupos (G1, G2 e G3) que receberam diferentes níveis de enxofre na dieta; 0,2%, 0,9% e 1,2%, respectivamente. Exames físicos (frequência cardíaca, frequência respiratória, temperatura retal e motricidade ruminal) e complementares (concentração de sulfeto de hidrogênio ruminal, hemogasometria venosa, pH do fluído ruminal, concentração de cobre sérico e hepático, tomografia computadorizada, ne- is a neuropathologic condition of ruminants that can be induced by a variety of factors including excessive sulfur intake. This study aimed to investigate the relationship between diets rich in sulfur, high levels of ruminal hydrogen sulfide and the occurrence of polioencephalomalacia in sheep. Eighteen sheep were divided into three groups (G1, G2, and G3) and supplemented with 0.2%, 0.9% and 1.2% sulfur in the diet respectively. Clinical evaluation (i.e. heart rate, respiratory rate, rectal temperature and rumen motility) and laboratory exams (i.e. ruminal hydrogen sulfide concentration, venous gas analysis, ruminal pH, serum and liver copper concentration, computed axial tomography, necropsy, and histopathological examination) were performed. Rectal temperature, venous gas and ruminal pH were within normal limits. Tachycardia and tachypnea were observed in sheep of the three groups. Rumen motility was decreased in animals of group G2 and G3 when compared with G1. The higher the sulfur intake, the lower was the serum and liver levels of copper. Increased ruminal hydrogen sulfide concentration was detected in G2 and G3 sheep. None of the animals had clinical signs of PEM. Computed axial tomography, macroscopic and histopathological examination of the central nervous system showed no evidence of PEM. It is suggested that other factors are associated with excessive sulfur consumption for a PEM outbreak to occur in sheep.INDEX TERMS: Cerebrocortical necrosis, polioencephalomalacia, sulfur, ruminal hydrogen sulfide, sheep.

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Amprolium exposure alters mice behavior and metabolism in vivo

Moraes

Rodrigues

Pereira

et al. 2018

Anim Models and Exp Med

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Background Thiamine deficiency ( TD ) models have been developed, mainly using the thiamine analog pyrithiamine. Other analogs have not been used in rodents. We aimed to evaluate the effects and mechanisms of intraperitoneal (ip) amprolium‐induced TD in mice. We also evaluated the associated pathogenesis using antioxidant and anti‐inflammatory compounds (Trolox, dimethyl sulfoxide). Methods Male mice were separated into two groups, one receiving a standard diet (control animals), and the other a TD diet (deficient groups) for 20 days. Control mice were further subdivided into three groups receiving daily ip injections of saline (NaCl 0.9%; Cont group), Tolox (Tr group) or dimethyl sulfoxide ( DMSO ; Dmso group). The three TD groups received amprolium (Amp group), amprolium and Trolox (Amp+Tr group), or amprolium and DMSO (Amp+Dmso group). The animals were subjected to behavioral tests and then euthanized. The brain and viscera were analyzed. Results Amprolium exposure induced weight loss with hyporexia, reduced the behavioral parameters (locomotion, exploratory activity, and motor coordination), and induced changes in the brain (lower cortical cell viability) and liver (steatosis). Trolox co‐treatment partially improved these conditions, but to a lesser extent than DMSO . Conclusions Amprolium‐induced TD may be an interesting model, allowing the deficiency to develop more slowly and to a lesser extent. Amprolium exposure also seems to involve oxidative stress and inflammation, suggested as the main mechanisms of cell dysfunction in TD .

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Polioencefalomalacia experimental em bovinos induzida por toxicose por enxofre

Cited by 9 publications

References 41 publications

Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil

Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil

Aspectos clínicos e laboratoriais em ovinos submetidos a dietas com níveis elevados de enxofre com objetivo de indução de polioencefalomalácia

Amprolium exposure alters mice behavior and metabolism in vivo

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