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Background: Polioencephalomalacia (PEM) is a neurological disease in ruminants, which is characterized by malacia of brain gray matter. Thiamine deficiency and sulfur intoxication are the most common causes of PEM in sheep. Affected animals present signs of cerebrocortical syndrome, including amaurosis, ataxia, head pressing, mental depression, seizures, and opisthotonus. The neurological examination aims to determine the neurolocalization of the lesions and advanced imaging techniques are useful for confirming the affected area(s) in the central nervous system. The aim of this study is to describe clinical features and ante-mortem diagnosis using magnetic resonance imaging (MRI) in a sheep with PEM. Case: A 18-month-old male Dorper sheep from a flock started receiving concentrate 7 days before. According to the owner, no clinical signs of abnormality were observed on the previous morning. However, in the afternoon, the animal became selfisolated and did not follow the flock to the sheepfold. The following day, he was found in recumbency. Physical examination revealed lateral recumbency, rectal temperature 39.5ºC, 52 bpm, 120 bpm, congested mucous membranes, capillary refill time 1 s, ruminal (4/5 min) and intestinal hypomotility. The assessment of the central nervous system revealed a decreased level of consciousness, focal seizures, opisthotonus, and absence of menace response. The following differential diagnoses were listed: PEM, head trauma, focal symmetrical encephalomalacia, bacterial encephalitis, and rabies. Treatment was composed of dexamethasone [0.2 mg/kg - i.v., SID (1st-3rd day), 0.1 mg/kg, i.v., SID (4th-6th day), and 0.05 mg/kg, i.v., SID (7th-9th day)]; mannitol [1 g/kg - i.v. and diazepam 0.4 mg/kg, i.v. single dose at admission]; vitamin B1 [10 mg/kg - i.m., SID], furosemide [1 mg/kg - i.v., SID for 3 days] and sulfadoxine/trimethoprim [30 mg/kg - i.m., SID for 10 days]. After the initial treatment, the patient showed mild clinical improvement; however, the amaurosis was still present. Magnetic resonance imaging of the brain was performed on the 2nd day of hospitalization, showing a symmetrical hypersignal in the parietal and occipital cortices, in the axial and sagittal sequences weighted in T2 and FLAIR. Discussion: This study aimed to describe the clinical signs and MRI findings in a sheep with PEM. In this case, the sudden change to the feed composition probably led to ruminal dysbiosis, inhibition of thiamine-producing microorganisms and proliferation of bacteria that synthesize thiaminase. Thiamine therapy proved to be effective and capable of reverting the clinical signs. The decrease in the level of consciousness, cortical blindness, and opisthotonus are due to alterations in the parietal cortex, in the occipital cortex, and in the cerebellum, respectively, which were demonstrated by hypersignal areas in the MRI. Therefore, the neurolocalization of the lesion based on neurologic examination and the MRI findings were related. The physicochemical and cytological evaluations of the cerebrospinal fluid, and dosage of thiamine and the concentration of hydrogen sulphide in the rumen were not performed. However, the response to thiamine treatment associated with the neurologic examination and MRI findings helped in determining the diagnosis. Additionally, MRI can be used as a useful tool for the ante mortem diagnosis of PEM.

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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.(AU)

O 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.(AU)

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RESUMO

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.

O 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.

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Thiamine is an essential cofactor for several cellular functions. Your deficiency results in important neurological disorders, with mechanisms and lesions not fully understood. The purpose of this work was to evaluate a thiamine deficiency through the model of oral administration of amprolium in mice. The animals, treated for 20 or 80 days, received amprolium in drinking water at doses of 10, 20, and 30 mg/mL (deficient groups A, B, and C, respectively). Deficient groups A and B showed reduction in body weight gain and performance changes in the open field (decreased distance and rearing, and increased grooming) and rotarod (reduced latency to fall) behavioural tests, when treated for 80 days. However, no histological changes were observed in the central nervous system. Moreover, group B animals exposed to amprolium developed proteinuria, with moderate tubular nephrosis, at 80 days. At the highest dose (group C) there was no interest to drink water. The data suggest that the use of oral amprolium in mice may be an interesting and viable model, when using adequate exposure times and doses. The amprolium induces thiamine deficiency progressively and moderately, which may be potentially useful for disturbed pathogenesis studies.(AU)

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Polioencephalomalacia (PEM) of ruminants is a complex disease. The term indicates a morphological diagnosis where severe cortical neuronal necrosis results in softening of cerebral grey matter. Initially though as a single disease caused by thiamine deficiency, it is currently believed that PEM is caused by different etiological agents through different pathogenic mechanisms or trough a single pathogenic mechanism triggered by different agents. In this paper the putative cases and pathogenesis of PEM in ruminants are critically reviewed and discussed. Also reviewed are the epidemiology, clinical signs, gross and histological findings and methods of diagnosis of cases of PEM described in ruminants in Brazil(AU)

Assuntos

RESUMO

Polioencephalomalacia (PEM) of ruminants is a complex disease. The term indicates a morphological diagnosis where severe cortical neuronal necrosis results in softening of cerebral grey matter. Initially though as a single disease caused by thiamine deficiency, it is currently believed that PEM is caused by different etiological agents through different pathogenic mechanisms or trough a single pathogenic mechanism triggered by different agents. In this paper the putative cases and pathogenesis of PEM in ruminants are critically reviewed and discussed. Also reviewed are the epidemiology, clinical signs, gross and histological findings and methods of diagnosis of cases of PEM described in ruminants in Brazil

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The exact causes of the historical recruitment failures of Great Lakes lake trout Salvelinus namaycush are unknown. Thiamine deficiency has been associated with neurological abnormalities in lake trout that lead to early mortality syndrome (EMS) in salmonine swim-up fry, and EMS-related mortality at the swim-up stage is a factor that contributes to the reproductive failure of lake trout populations in the Great Lakes. The potential for adverse effects of thiamine deficiency beyond the swim-up stage is unknown. We investigated the effects of low egg thiamine on behavioral functions in young, post-swim-up lake trout fry. The behavioral endpoints included visual acuity and prey capture rates in the same groups of lake trout fry from each family. Low-thiamine eggs were produced by feeding lake trout broodstock diets entailing thiaminase activity. The thiamine content of the spawned eggs ranged from 0.3 to 26.1 nmol/g. Both visual acuity and prey capture rates were affected by the thiamine content of the eggs. The visual acuity of lake trout was severely affected by low egg thiamine, mainly at thiamine concentrations below the threshold of 0.8 nmol/g but also at higher concentrations in field-collected eggs. Feeding was also reduced with low egg thiamine content. The reduction of prey capture rates was dramatic below 0.8 nmol/g and less dramatic, but still significant, in a portion of the families with egg thiamine concentrations of less than 5.0 nmol/g from both laboratory and field samples. Approximately one-third of the latter families had reduced feeding rates. Deficits in visual acuity may be part of the mechanism leading to decreased feeding rates in these fry. The effects of low egg thiamine on both of the behavioral endpoints studied increase the risk of low recruitment rates in Great Lakes lake trout populations.

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