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Simple Summary: In Texas beef markets, the expansion of ethanol production has increased the demand for and utilization of biofuel co-products, like dried distiller grains with solubles, introducing highly variable concentrations of nutrients, such as sulfur, known to impact cattle health. The risk of sulfur toxicity for Texas cattle was estimated using two mathematical nutrition models at two production stages across twelve geographic districts. The assessment identified cattle raised in the South Plains region of northwest Texas as the most susceptible to sulfur toxicity, with those in the finishing production stage being more sensitive. Results also highlighted feed ingredients and water wells by district that significantly contributed to the risk of sulfur toxicity. This research further helps better manage the risk of sulfur toxicity by providing tools translatable nationwide that properly balance beef diets and calculate anticipated sulfur exposure. The purpose of this probabilistic assessment was to estimate the risk of sulfur-induced polioencephalomalacia (S-PEM) for beef raised across Texas, from a dietary perspective. Ruminant nutritionists in Amarillo, TX, formulated two typical nutritional regimens based on cattle production stages, each containing six feed ingredients and well water. The Office of the Texas State Chemist (OTSC), National Research Council (NRC), and the published literature provided S data for feed ingredients. The Texas Water Development Board provided data for S content in Texas well water, categorized into twelve districts established by the Texas A&M AgriLife Research Extension Service. The S-PEM risk was estimated at five different eNDF levels ranging from 0% to 8% in 2% increments, using rumen degradable S (RDS) as an input value. Findings identified cattle raised in the South Plains district as the most susceptible population to S toxicity, with beef in the finishing production stage experiencing increased sensitivity. The most potential (MP) risk scenario suggested that the S-PEM risk could reach 28.5% for growers and 100% for finishers. Results further revealed that when S concentrations in well water exceeded 14.5 mg/L, water became the greatest contributor to RDS content for Texas beef, suggesting that high S content in well water is the most prominent concern for Texas beef. [ABSTRACT FROM AUTHOR]

The purpose of this probabilistic assessment was to estimate the risk of sulfur-induced polioencephalomalacia (S-PEM) for beef raised across Texas, from a dietary perspective. Ruminant nutritionists in Amarillo, TX, formulated two typical nutritional regimens based on cattle production stages, each containing six feed ingredients and well water. The Office of the Texas State Chemist (OTSC), National Research Council (NRC), and the published literature provided S data for feed ingredients. The Texas Water Development Board provided data for S content in Texas well water, categorized into twelve districts established by the Texas A&M AgriLife Research Extension Service. The S-PEM risk was estimated at five different eNDF levels ranging from 0% to 8% in 2% increments, using rumen degradable S (RDS) as an input value. Findings identified cattle raised in the South Plains district as the most susceptible population to S toxicity, with beef in the finishing production stage experiencing increased sensitivity. The most potential (MP) risk scenario suggested that the S-PEM risk could reach 28.5% for growers and 100% for finishers. Results further revealed that when S concentrations in well water exceeded 14.5 mg/L, water became the greatest contributor to RDS content for Texas beef, suggesting that high S content in well water is the most prominent concern for Texas beef.

The signature pathological feature of the pseudolaminar cerebrocortical necrosis found in polioencephalomalacia (PEM) of ruminants is the development of red (eosinophilic) neurons. These neurons are generally considered to be irredeemably injured but we have shown, for the first time, in ovine PEM cases, that most strongly express amyloid precursor protein (APP), which has a neuroprotective role in the brain. By contrast, neurons in unaffected cerebral cortices from control sheep were APP immunonegative. This finding suggests that, rather than being inevitably destined to die, some of these APP immunoreactive cortical neurons may survive and regain structural and functional integrity. [ABSTRACT FROM AUTHOR]

Abstract Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1‐weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3‐year‐old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three‐Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2‐weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W‐hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion‐weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia‐related brain hypoxia. Three‐Tesla MRI enabled identification of the laminar pattern of the cortical lesions.

In Veterinary Clinic, Division of Animal Health, CIRG, Makhdoom, Mathura, eighteen weaned goat kids Barbari breed (from a herd of 45 kids maintained together) were presented with the history of neurological signs. The clinical examination revealed signs including staggering gait, incoordination, muscle tremors, grinding of teeth, nystagmus and apparent blindness opisthotonus followed by collapse and recumbency. The animals were found anorectic. These goats were diagnosed as affected with Polioencephalomalacia. The affected 18 kids were treated initially with injection thiamine hydrochloride (@ 10 mg/kg 10mg/kg intravenous) diluted in 5% dextrose-normal saline (@10ml/kg intravenous) and injection dexamethasone sodium phosphate (@ 1 mg/kg intravenous). Subsequently, five doses of thiamine hydrochloride (@ 10 mg/kg body weight) were given intramuscularly every 12 hours. Out of eighteen affected weaned kids, fifteen kids responded within six hours of initial treatment and recovered completely in 3-4 days of treatment. Thus fifteen cases with neurological signs were recovered with the above protocol of treatment. Three goat kids did not respond well to the treatment and they had to be culled. [ABSTRACT FROM AUTHOR]

Cerebral cortical laminar necrosis (CLN) is a consequence of severe hypoxic, ischemic, or hypoglycemic events. In humans, these cortical lesions show characteristic linear T1‐weighted (T1W) hyperintensity in the late subacute stage. Limited information reporting magnetic resonance imaging (MRI) findings in dogs affected by CLN is available. A 3‐year‐old Belgian Shepherd dog was referred 8 days after sudden onset of blindness after general anesthesia. Neurological examination showed central blindness and mild ataxia. Three‐Tesla MRI examination of the brain revealed bilateral asymmetrical areas of T2‐weighted hyperintensity within the occipital, parietal, temporal, and frontal cortex, involving gray and white matter. Furthermore, linear T1W‐hyperintense lesions were found in the cerebral cortex of the same areas and showed heterogeneous contrast enhancement. Perfusion‐weighted images revealed hyperperfusion in the affected regions. Lesions were compatible with subacute CLN with corresponding edema suspected to be secondary to anesthesia‐related brain hypoxia. Three‐Tesla MRI enabled identification of the laminar pattern of the cortical lesions. [ABSTRACT FROM AUTHOR]

Objective: To assess the clinical efficacy and plasma concentrations of levetiracetam in a goat with seizures., Animal: A 5-month-old doeling., Clinical Presentation, Progression, and Procedures: The goat was referred because of progressive anorexia and lethargy over 3 days. Clinical signs consisted of weakness, obtundation, opisthotonos, anisocoria, and cortical blindness. Initial evaluation was most consistent with polioencephalomalacia., Treatment and Outcome: Neurologic improvement occurred within 4 hours of thiamine administration, with appetite returning over 12 hours. On day 3 of hospitalization, the goat suffered acute onset repetitive seizures that were incompletely responsive to standard interventions over 3 hours. Administration of IV levetiracetam (60 mg/kg) produced resolution of seizure activity within 20 minutes. Levetiracetam was continued twice daily IV, then PO after day 6. Plasma concentrations were above or within therapeutic ranges (5 to 45 μg/mL) as previously established for other species, following both IV and PO levetiracetam. Oral administration (60 mg/kg, PO, q 12 h) resulted in plasma levetiracetam concentrations of 48.1 μg/mL 2 hours after a dose and 23.4 μg/mL 2 hours prior to the next dose., Clinical Relevance: Levetiracetam is a newer anticonvulsant commonly used in humans and small animals due to its efficacy, cost, and wide safety margin. Its use has not previously been reported in domestic small ruminants. In this case, levetiracetam showed excellent clinical efficacy in the face of refractory seizures, with no apparent side effects. Plasma concentrations during oral administration were at the high end of the therapeutic range, indicating absorption in a nonmonogastric species. Further studies are warranted to determine optimal dosing in small ruminants.

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Copyright of Pesquisa Veterinaria Brasileira is the property of Colegio Brasileiro de Patologia Animal - CBPA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Lead poisoning is one of the major toxic diseases of cattle. Contamination occurs with ingestion of products containing lead, especially batteries, or through contaminated pastures and water sources. Clinical signs are neurological and necropsy findings and histopathological changes may vary depending on the clinical presentation. Although the disease is widely reported in the literature, there are rare descriptions of intoxication in cattle raised in military training areas. This work describes the epidemiological, clinical and anatomopathological features of an outbreak of lead poisoning in cattle kept in a military artillery training camp. Case: Fifteen cattle out of a herd of sixty 4-6 year-old, mixed breed castrated males were affected. The cattle were held in a 100 ha of native pasture used for military artillery training. After three weeks in this area, the affected cattle had predominantly neurological clinical manifestations, characterized by somnolence, ambulatory incoordination, muscle tremors, bruxism, aimless walking, blindness and decubitus. The clinical course was 24-72 h. Eight of the 15 affected cattle died and two were necropsied. Necropsy finds were non-specific and the histological lesions of both necropsied cattle were restricted to the brain and kidneys. Laminar neuronal necrosis, neuropil vacuolization (spongiosis) and vascular endothelial hypertrophy were observed in the telencephalic cortex. Additionally there was astrocytic degeneration and neuronophagia. There was degeneration and necrosis of renal tubular epithelium and in one bovine there were intranuclear inclusion bodies in the renal epithelial cells; these inclusion bodies were highlighted using both modified Ziehl-Neelsen and periodic acid Schiff (PAS) stains. The levels of lead found in the kidneys and livers of the two necropsied cattle were respectively 51.7 μg/g and 41.00 μg/g for one of the necropsied cattle; and 431μg/g and 39.0 μg/g for the other. After the diagnosis of intoxication, cattle were removed from the area and the remaining seven affected bovines recovered. Discussion: The diagnosis of lead poisoning in cattle in the current study was based on epidemiological, clinical, anatomopathological data and in the determination of lead levels in the kidney and liver. The association of these data provides an invaluable aid in confirming a presumptive diagnosis of lead poisoning. Pasturing on military artillery training fields is a rarely described form source of lead for the intoxication in bovine species. In such cases, cattle may ingest the lead directly from the soil or through contaminated pastures containing lead dust on the surface of the leaves. Histologically, laminar neuronal necrosis in the telencephalic cortex, associated with tubular necrosis and intranuclear inclusion bodies in tubular epithelial cells, are characteristic features of the intoxication. These changes are usually associated with ischemic anoxia in the nervous system and alteration in nuclear function which interferes in gene expression in the kidney. Lead poisoning in cattle should be differentiated from other neurological conditions, especially rabies, hepatic encephalopathy and several causes of polioencephalomalacia. Areas of military artillery training are unfit for the development of agricultural exploitation activities, as they represent potential sources of contamination for livestock. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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, necropsia e histopatologia) foram realizados. A temperatura retal, a hemogasometria venosa e o pH do fluido ruminal permaneceram dentro dos valores de referência para a espécie. A motricidade ruminal estava diminuída nos grupos G2 e G3 em comparação com o G1 (controle). Quanto maior a ingestão de enxofre, menores foram os níveis de cobre sérico e hepático. Valores elevados de sulfeto de hidrogênio ruminal foram detectados nos grupos G2 e G3. Nenhum animal apresentou sinais clínicos de PEM. Nos exames de tomografia computadorizada, necropsia e exame histopatológico do sistema nervoso central (SNC), não foram observadas alterações compatíveis com PEM. É provável que algum outro fator esteja associado ao excesso de enxofre na dieta para o desenvolvimento de PEM em ovinos.Polioencephalomalacia (PEM) 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.

Fifteen cases of viral meningoencephalitis in Colombian cattle were tested by nested PCR analysis for the detection of bovine herpesvirus 5 (BoHV-5). All fatal cases had shown severe neurological signs and had occurred following natural outbreaks of the disease. The neurological infection was histologically characterized by mild to moderate inflammatory changes in the brain and cerebellum, including meningitis, mononuclear perivascular cuffing, gliosis, haemorrhage, and the presence of Gitter cells (macrophages) accompanying large areas of malacia. No intranuclear inclusion bodies were seen in any of the cases. Results from BoHV-5 molecular extraction analyses showed there were five positive cases thus confirming the presence of the virus in Colombia.Quince casos de meningoencefalitis viral en ganado Colombiano fueron analizados por reacción en cadena de la polimerasa (PCR anidada) para la detección del herpesvirus bovino 5 (BoHV-5). Todos los casos mostraron severos signos neurológicos antes de morir y ocurrieron como brotes naturales de la enfermedad. La infección neurológica fue caracterizada histológicamente por leves a moderados cambios inflamatorios en el cerebro y cerebelo, incluyendo meningitis, manguitos perivasculares, gliosis, hemorragia y la presencia de células Gitter (macrófagos) acompañando grandes áreas de malacia. No se encontraron cuerpos de inclusión intranucleares en ninguno de los casos. Los resultados del análisis de la extracción molecular de BoHV-5 revelaron la existencia de cinco casos positivos, lo cual confirma la presencia del virus en Colombia.Quinze casos de meningoencefalite viral em gado bovino Colombiano foi analisado pela reação em cadeia da polimerasa (PCR) para a detecção do herpesvírus bovino 5 (BoHV-5). Todos os casos mostraram graves sinais neurológicos antes de morrer y aconteceram como surtos naturais da doença. A infecção neurológica foi caracterizada histologicamente por leves a moderados câmbios inflamatórios no cérebro e cerebelo, incluindo meningite, manguitos perivasculares, gliose, hemorragia e a presencia de células gitter (macrófagos) acompanhando grandes áreas de malacia. Não se encontraram corpos de inclusão intranucleares em nenhum dos casos. Os resultados da análise da extração molecular do BoHV-5 por PCR revelaram a existência de cinco casos positivos, os quais confirmam a presença do vírus na Colômbia.

Para estabelecer um modelo experimental para o estudo da etiologia, patologia e patogênese da polioencefalomalacia (PEM) em bovinos, a condição foi induzida em quatro novilhos pela administração oral de amprólio nas doses diárias de 500 e 350mg/kg de peso vivo, respectivamente por 22 e 26-28 dias. Todos os bovinos morreram espontaneamente ou foram eutanasiados in extremis após um curso clínico de 4-7 dias. Três bovinos que receberam 1.000mg/kg de amprólio e dois que receberam 500mg/kg morreram espontaneamente com quadro clínico agudo a subagudo sem desenvolverem sinais e lesões de PEM. Nos novilhos que PEM foi reproduzida, os sinais neurológicos incluíram marcada apatia, incoordenação, posição de cavalete, quedas ocasionais, hiperexcitabilidade, tremores musculares, cegueira, bruxismo, estrabismo, nistagmo, midríase, opistótono, decúbito lateral e movimentos de pedalagem. Os principais achados de necropsia eram restritos ao encéfalo e consistiam de tumefação, achatamento, amolecimento e amarelamento das circunvoluções cerebrais. Histologicamente, havia necrose neuronal segmentar e laminar (neurônios vermelhos) associada a edema, tumefação endotelial, separação das lâminas de neurônios do córtex telencefálico ou entre as substâncias cinzenta e branca e infiltração moderada a acentuada de macrófagos espumosos. Essas alterações eram mais acentuadas nos lobos telencefálicos frontal, parietal e occipital. Adicionalmente, lesões similares e moderadas foram detectadas no mesencéfalo e hipocampo. A necrose neuronal e o edema afetaram uniformemente as camadas de neurônios da substância cinzenta dos lobos telencefálicos frontal, parietal e occipital. Esse modelo experimental de PEM com administração oral de amprólio parece ser útil para o estudo da doença em bovinos, conforme observado anteriormente em ovinos.In order to establish an experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia (PEM) in cattle, the condition was induced into four steers by oral administration of amprolium at daily doses of 500 and 350mg per kg of body weight respectively for 22 and 26-28 days. All steers died spontaneously or were euthanized in extremis after being sick for 4-7 days. Three steers that received the drug at 1,000mg/kg and two that received 500mg/kg died spontaneously with acute or subacute clinical signs and without lesions and signs of PEM. In those steers in which PEM was reproduced, the neurological signs included marked apathy, incoordination, sawhorse stance, occasional falls, hyperexcitability, muscle tremors, blindness, grinding of teeth, strabismus, nystagmus, mydriasis, opisthotonus, and lateral recumbency with paddling movements. Main gross lesions were restricted to the brain and included swelling, flattening, softening and yellow discoloration of the cerebral circumvolutions. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, cleavage of laminar neuronal layers or between gray and white matter and moderate to severe infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telencephalic lobes. Additionally, similar and moderate lesions were detected in the midbrain and hippocampus. Neuronal necrosis and edema affected uniformly the neurons layers of the grey matter of the frontal, parietal and occipital lobes. This experimental model of PEM with oral administration of amprolium may be useful for the study in cattle, as previously observed in sheep.

Para determinar as doenças que ocorrem no sistema nervoso de bovinos no semiárido nordestino, foi realizado um estudo retrospectivo em 411 necropsias de bovinos realizadas no Hospital Veterinário da Universidade Federal de Campina Grande, Patos, Paraíba, entre janeiro de 2000 a dezembro de 2008. Dos 411 casos analisados 139 (33,81%) apresentaram alterações clínicas do sistema nervoso e as fichas foram revisadas para determinar os principais achados referentes à epidemiologia, aos sinais clínicos e às alterações macroscópicas e microscópicas. Em 28 (20,14%) casos o diagnóstico foi inconclusivo. As principais enfermidades foram raiva (48,7% dos casos com sinais nervosos), abscessos cerebrais (7,2%) incluindo três casos de abscesso da pituitária, febre catarral maligna (6,3%), botulismo (6,3%), alterações congênitas (4,5%), traumatismo (4,5%), tuberculose (2,7%), tétano (2,7%), infecção por herpesvírus bovino-5 (2,7%), encefalomielite não supurativa (2,7%), intoxicação por Prosopis juliflora (2,7%), status spongiosus congênito de causa desconhecida (1,8%) e polioencefalomalacia (1,8%). Outras doenças diagnosticadas numa única oportunidade (0,9%) foram criptococose, listeriose, encefalite tromboembólica, linfossarcoma, tripanossomíase e babesiose por Babesia bovis.Diseases of the nervous system of cattle in the semiarid region of northeastern Brazil were evaluated by a retrospective study of 411 cattle necropsies performed in the Veterinary Hospital of the Federal University of Campina Grande, Patos, Paraíba, from January 2000 to December 2008. Of the 411 cases analyzed, 139 (33.81%) were from cattle that presented nervous signs and the records were reviewed to determine the epidemiological, clinical, and macroscopic and histologic main features. Diagnosis was inconclusive in 28 cases (20.14%). In cases with diagnosis the main diseases were rabies (48.7% of the cases with nervous signs), brain abscesses (7.2%) including three cases of pituitary abscesses, malignant catarrhal fever (6.3%), botulism (6.3%), congenital malformations (4.5%), trauma (4.5%), tuberculosis (2.7%), tetanus (2.7%), infection by bovine hervesvirus-5 (2.7%), non-suppurative encephalomyelitis (2.7%), intoxication by Prosopis juliflora (2.7%), congenital status spongiosus of unknown etiology (1.8%), and polioencephalomalacia (1.8%). Other diseases diagnosed only once (0.9%) were cryptococcosis, listeriosis, thromboembolic encephalitis, lymphosarcoma, trypanosso-miasis, and babesiosis by Babesia bovis.

Para estabelecer um modelo experimental para o estudo da etiologia, patologia e patogênese da polioencefalomalacia em ruminantes, a condição foi induzida em cinco ovinos pela administração oral de amprólio nas doses diárias de 500 e 1.000mg/kg de peso animal, respectivamente por 28-59 dias e 13-39 dias. Todos os ovinos morreram ou foram eutanasiados in extremis após um curso clínico de 3-7 dias. Os sinais clínicos incluíam depressão, incoordenação, midríase, bruxismo, cegueira e decúbito com opistótono e movimentos de pedalagem. Salivação excessiva e posição de cavalete foi observada em um ovino e mioclonias em um outro. Os principais achados de necropsia restringiam-se ao sistema nervoso central e incluíam tumefação do encéfalo com achatamento dos giros telencefálicos e hemorragias nos lobos parietal e occipital do telencéfalo; as hemorragias ocorriam também nas áreas submeníngeas da medula espinhal e do mesencéfalo. Histologicamente, havia necrose segmentar laminar de neurônios (neurônios vermelhos) associada a edema, tumefação de células endoteliais, hemorragias e infiltração por macrófagos espumosos (células gitter). Essas alterações eram mais marcadas nos lobos frontal, parietal e occipital do telencéfalo e havia uma demarcação abrupta entre as lesões e o neurópilo normal adjacente. Adicionalmente, lesões semelhantes, mas menos acentuadas, eram observadas no mesencéfalo, tálamo e hipocampo. Levando em consideração a reproducibilidade regular dos aspectos da polioencefalomalacia em ovinos pela administração de amprólio, esse modelo pode ser útil para o estudo da doença.In order to establish an experimental model for the study of the etiology, pathology, and pathogenesis of polioencephalomalacia in ruminants, the condition was induced in five sheep by oral administration of amprolium at daily doses of 500 and 1,000mg per kg of body weight respectively for 28-59 days and for 13-39 days. All sheep died or were euthanized in extremis after illness of 3-7 days. Clinical signs included depression, incoordination, midriasis, grinding of the teeth, blindness, and laying down with opisthotonus and paddling movements. Drooling and a sawhorse stance were observed in one sheep and myoclonus in another one. Main gross lesions were restricted to the central nervous system and included swelling of the brain with flattening of telencephalic gyri, and hemorrhages in the parietal and occipital lobes of the telencephalon, in the submeningeal areas of the spinal cord and in the mesencephalon. Histologically, there was segmental laminar neuronal necrosis (red neurons) associated with edema, swelling of endothelial cells, hemorrhages and infiltration by foamy macrophages (gitter cells). These changes were more marked in the frontal, parietal and occipital telecephalic lobes and there was sharp demarcation between the lesions and the adjacent normal neuropile. Additionally, similar, but less marked lesions were seen in the mesencephalon, thalamus and hippocampus. Considering the consistent reproducible aspects of polioencephalomalacia in sheep using amprolium, this may be an useful model for the study of the disease.

Polioencefalomalacia (PEM) de ruminantes é uma doença complexa. O termo indica um diagnóstico morfológico em que necrose neuronal grave resulta em amolecimento da substância cinzenta do cérebro. Interpretada no início como uma doença única, causada por deficiência de tiamina, acredita-se hoje que várias causas e diferentes mecanismos patogênicos, ou um único mecanismo patogênico disparado por diferentes agentes, sejam responsáveis pelo aparecimento da doença. Neste artigo, as possíveis causas e a patogênese de PEM em ruminantes são criticamente revisadas e discutidas. Também são revisadas a epidemiologia, os sinais clínicos, os achados macro e microscópicos e os métodos de diagnóstico, tratamento e controle.Polioencephalomalacia (PEM) of ruminants is a complex disease. The term indicates a morphological diagnosis where severe neuronal necrosis results in softening of cerebral grey matter. Initially though as a single disease caused by thiamine deficiency, PEM is currently believe to have several causes and different pathogenic mechanisms or a single pathogenic organism triggered by different agents are responsible for the disease. In this paper the possible causes and pathogenesis of PEM in ruminants are critically reviewed and discussed. Also are reviewed the epidemiology, clinical signs, gross and histological findings, methods of diagnosis, treatment and control.

Trinta e um casos de polioencefalomalacia (PEM) diagnosticados de 1999-2008 em bovinos do Sul (13 casos) e Centro-Oeste (18 casos) brasileiros foram estudados. As taxas de morbidade (0,04%-6,66 %), mortalidade (0,04%-6,66 %) e letalidade (50%-100%) foram semelhantes em ambas as regiões estudadas. Não houve uma associação clara entre os casos de PEM e a idade, sexo dos bovinos e sazonalidade. Os casos ocorreram principalmente em bovinos criados de forma extensiva em pastagem. Na Região Sul a doença afetou principalmente bovinos jovens (um ano de idade ou menos), enquanto que principalmente bovinos mais velhos (3 anos de idade ou mais) foram afetados no Centro-Oeste. Os sinais clínicos mais frequentemente observados incluíram cegueira, incoordenação, andar em círculos, opistótono, decúbito e movimentos de pedalagem. A evolução do quadro clínico variou de 12 horas a 8 dias (media 3 dias e meio). Em 11 encéfalos não foram observadas alterações macroscópicas; as principais alterações macroscópicas nos outros casos incluíam congestão com tumefação e achatamento das circunvoluções, amolecimento e amarelamento do córtex telencefálico, focos de hemorragia no tronco encefálico, cerebelo e telencéfalo e herniação cerebelar. As principais alterações histológicas ocorreram no córtex dos lobos telencefálicos occipital, parietal e frontal; no entanto, lesões menos acentuadas e menos frequentemente observadas ocorreram no hipocampo, núcleos da base, tálamo, mesencéfalo e cerebelo. O tipo de lesão microscópica cortical era consistente em todos os casos e incluía necrose neuronal (neurônio vermelho) laminar segmentar, espongiose, tumefação do núcleo das células endoteliais, astrócitos Alzheimer tipo II e infiltração por células gitter. Em 20% dos casos havia um leve infiltrado celular linfo-histiocitário e em 13% dos casos havia leve infiltrado de neutrófilos e eosinófilos. Adicionalmente, lesões necro-hemorrágicas leves ou moderadas foram observadas em 49% dos casos nos núcleos da base, em 39% dos casos no tronco encefálico e em 26% dos casos no tálamo. Lesões telencefálicas foram consistentemente observadas nas lâminas dos córtices dos lobos occipital, parietal e frontal. Nessas regiões as camadas granular externa e interna foram as mais afetadas tanto por neurônios necróticos quanto por edema em todas as regiões avaliadas. Tanto os giros quanto os sulcos foram afetados igualmente.Thirty one cases of polioencephalomalacia (PEM) diagnosed from 1999-2008 in cattle from the Southern (13 cases) and Midwestern (18 cases) Brazil were studied. Morbidity (0.04%-6.66 %), mortality (0.04%-6.66 %), and lethality (50%-100%) rates were similar in both regions studied. There was no clear association between PEM cases and age, sex or seasonality. Cases occurred mainly in cattle raised at pasture; in the Southern the disease affected mainly young cattle (one-year old or less) while mainly older cattle (three-year-old or older) were affected in the Midwest. Clinical signs more frequently observed included blindness, incoordination, circling, opisthotonus, recumbence and peddling movements. Clinical course varied from 12 hours to 8 days (average three days and a half). In 11 cases no gross changes were observed in the brain. Main gross findings in the brain of remaining cases included congestion with swelling and flattening of gyri, softening and yellow discoloration of cerebral cortex, hemorrhagic foci in the brain stem, cerebellum and telencephalon, and cerebellar herniation. The main histopathological changes were in the cortex of occipital, parietal and frontal telencephalic lobes; however less prominent and less frequently found lesions occurred in the hippocampus, basal nuclei, thalamus, midbrain, and cerebellum. The type of microscopic cortical lesions was consistent in all cases and included segmentar laminar neuronal necrosis (red neurons), spongiosis, swollen of vascular endothelial nuclei, Alzheimer type II astrocytes and infiltration of gitter cells. In 20% of the cases there was mild lymphohistiocytic cellular infiltrate and in 13% of the cases there was mild infiltrate by neutrophils and eosinophils. Additionally, mild to moderate necro-hemorrhagic lesions were observed in 49% of the cases in the basal nuclei, in 39% of the cases in brain stem and in 26% of the cases in the thalamus. Brain lesions were consistently found in the cortical laminae of the occipital, parietal and frontal telencephalic lobes. In such locations, most frequently affected cortical layers both by neuronal necrosis and edema were external and internal granular layers. Both gyri and sulci were equally affected.

In the state Mato Grosso do Sul, Brazil, outbreaks of meningoencephalitis by BoHV-5 and polioencephalomalacia (PEM) display similar epidemiological features, suggesting that meningoencephalitis may be associated with reactivation of a latent BoHV-5 infection, during the development of PEM. To test this hypothesis, four 7-8 months old steers negative for BoHV-5 antibodies were inoculated intranasally with BoHV-5 and received amprolium from day 35 to day 105 after inoculation. Because PEM was not produced during this period, ammonium sulphate was given from day 114 to day 180 after inoculation. Two uninfected control steers received amprolium and ammonium sulphate for the same periods. All inoculated cattle developed antibodies against BoHV-5 after inoculation and the virus was isolated from nasal swabs, indicating that they were infected. Two inoculated steers had clinical signs of PEM after 118 and 146 days after virus inoculation. One was euthanized after a clinical manifestation period of seven days and had severe lesions of PEM and meningoencephalitis. BoHV-5 was isolated from the central nervous system of this animal. The other animal recovered but continued to manifest chronic signs of PEM and was euthanatized. On histological examination, the cerebral cortex, caudate nucleus and thalamus had multifocal areas of malacia and mild meningoencephalitis of the cortex. BoHV-5 was not isolated from the brain. One uninfected control steer had signs of neurological disease on day 158 and had lesions of PEM without meningoencephalitis at necropsy. The simultaneous production of PEM and diffuse meningoencephalitis, with isolation of BoHV-5, in one steer treated with ammonium sulphate, 118 days after BoHV-5 inoculation, suggests that latent BoHV-5 was reactivated in this animal submitted to experimental induction of PEM.No Mato Grosso do Sul surtos de meningoencefalite por herpesvírus bovino-5 (BoHV-5) e polioencefalomalacia (PEM) apresentam características epidemiológicas semelhantes, o que sugere que a meningoencefalite pode estar associada com a reativação de uma infecção latente por BoHV-5 em animais com PEM. Para testar esta hipótese, 4 garrotes de 7-8 meses de idade, sem anticorpos séricos para BoHV-5 foram inoculados intranasal com BoHV-5 e receberam amprólio desde o dia 35 até o dia 105 após inoculação. Como não foi reproduzida PEM durante este período, os animais receberam sulfato de amônia desde o dia 114 até o dia 180 após inoculação. Dois bovinos controles, não inoculados, receberam amprólio e sulfato de amônia durante os mesmos períodos. Todos os bovinos inoculados apresentaram anti-corpos contra BoHV-5 após a inoculação e o vírus foi isolado de suabes nasais, indicando que foram infectados. Dois bovinos inoculados tiveram sinais clínicos de PEM após 118 e 146 dias da inoculação de vírus. Um que foi eutanasiado após um curso clínico de 7 dias apresentou lesões severas de PEM e meningoencefalite. BoHV-5 foi isolado do sistema nervoso central. O outro se recuperou, mas continuou a apresentar sinais crônicos de PEM. No exame histológico o córtex cerebral, núcleo caudato e tálamo apresentavam áreas multifocais de malacia e no córtex havia moderada meningoencefalite. BoHV-5 não foi isolado do encéfalo. Um garrote controle, não inoculado, apresentou sinais nervosos aos 158 dias após inoculação e na necropsia apresentava lesões de PEM, mas sem meningoencefalite. A reprodução simultânea de PEM e encefalite difusa em um animal tratado com sulfato de amônia, 118 dias após a inoculação de BoHV-5 e o re-isolamento do vírus do animal infectado sugere que a infecção latente por BoHV-5 foi reativada no animal submetido a indução experimental de PEM.

Two 4-year-old spayed female Siamese cats were seized by the British Columbia Society for the Prevention of Cruelty to Animals after confinement to an abandoned housing unit without food for 9 weeks. One cat was found dead, and the second was euthanized within 24 hours due to neurologic deterioration despite therapy. Polioencephalomalacia of the caudal colliculus, hepatic lipidosis, cachexia, and congestive heart failure with cardiomyocyte atrophy were identified in both cats through postmortem examination and attributed to a prolonged period of starvation. Brain lesions were likely the result of thiamine deficiency (Chastek paralysis), which can be associated with both malnutrition and liver disease. This case highlights the importance of thiamine supplementation during realimentation of cats with hepatic lipidosis. Heart failure resulting from cachexia may have contributed to the death of the first cat and the morbidity of the second cat. [ABSTRACT FROM AUTHOR]

Livestock poisoning by plants is a frequent occurrence which determines severe losses, such as the fall in the milk and meat production, the cost of expensive treatments, the state of immunosuppression, or even the animal's death. Cattle ingest toxic plants only when there is food shortage, when they cannot select what they eat, or when they ingest food for preference, which is the case of Hovenia dulcis fruits, very rich in sucrose. This plant is widely distributed in the southern and southeastern Brazilian regions. In literature, there are some cases of severe human liver injury associated with a long-term of H. dulcis leaf and fruit tea intake, and only one report regarding spontaneous poisoning of goats caused by this plant ingestion. However, its toxic effects associated with spontaneous ingestion by cattle have never been reported. This paper reports the first case of spontaneous poisoning in cattle by H. dulcis, which occurred in a dairy farm in southwest Paraná, Brazil. Three cattle individuals showed anorexia, ruminal atony, severe diarrhea and neurological tournament, head pressing, blindness, ataxia, and circling. The necropsy of the animals was done, and the remaining alterations were restricted to the digestive system and brain. The clinical signs presented by the animals are characteristic of polioencephalomalacia (PEM), caused by changes in the thiamine metabolism. Furthermore, clinical signs, gross, and microscopic lesions as well as the large amount of the plant throughout the digestive segment led to a diagnosis. [ABSTRACT FROM AUTHOR]

Para determinar a distribuição das lesões histológicas que ocorrem no sistema nervoso central (SNC) de bovinos naturalmente infectados por herpesvírus bovino-5 (BHV-5) foram estudados 12 bovinos provenientes de 10 surtos da enfermidade diagnosticados pelo Laboratório Regional de Diagnóstico (LRD) da Faculdade de Veterinária da UFPel, entre 1986 e 2003. A epidemiologia, história clínica e evolução da enfermidade foram obtidas dos arquivos do LRD. Cortes do SNC foram realizados nos materiais conservados em formalina 10%, abrangendo as regiões frontal, parietal, temporal e occipital do córtex telencefálico, cápsula interna e núcleos da base, tálamo, colículo rostral, ponte, pedúnculos cerebelares, cerebelo, bulbo na altura do óbex e medula cervical. As secções foram processadas rotineiramente e coradas por hematoxilina e eosina. Foram avaliadas a distribuição e intensidade das lesões inflamatórias e de malacia, que foram relacionadas com os aspectos epidemiológicos e clínicos da doença. Surtos da enfermidade foram observados em todas as estações ano. Foram afetados bovinos de 2 a 24 meses, de diferentes raças e de ambos os sexos. Macroscopicamente, foram observadas áreas amareladas e deprimidas no córtex telencefálico de cinco bovinos necropsiados. Adicionalmente, essas lesões foram observadas no tálamo, núcleos da base e cápsula interna de dois bovinos. Congestão e hemorragias multifocais foram observadas na maioria dos casos. Em todos os bovinos estudados a lesão histológica caracterizou-se por meningoencefalite não-supurativa observada em todas os cortes, porém mais acentuada no córtex frontal. Áreas de malacia focal ou difusa com presença de células "Gitter" foram observadas em todas as regiões do córtex cerebral e nos núcleos da base, cápsula interna e tálamo. Em alguns casos, lesões discretas de malacia foram observadas no colículo rostral, ponte, bulbo, cerebelo e medula cervical. Corpúsculos de inclusão intranucleares foram encontrados em todos os casos estudados nas diferentes regiões do córtex cerebral, preferentemente em áreas que apresentavam lesões inflamatórias e de malacia discretas a moderadas. Em dois casos estes corpúsculos foram observados, também, nos núcleos da base e tálamo. Foi observado que a intensidade das lesões histológicas não é proporcional ao curso clínico da enfermidade. A presença de lesões de malacia em diferentes regiões do SNC, aspecto não mencionado na maioria dos trabalhos anteriores sobre a doença, pode ser devida a variações na patogenicidade das cepas virais envolvidas. Outra possibilidade é que a encefalite tenha ocorrido em conseqüência da reativação do BHV-5 em animais afetados por polioencefalomalacia. Essa seqüência de eventos já foi demonstrada previamente em experimentos realizados pelo grupo de pesquisa dos autores.The distribution of the histological lesions in the central nervous system (CNS) of cattle naturally infected by bovine herpes virus type-5 (BHV-5) was determined in 12 affected calves from 10 outbreaks of the disease diagnosed by the Regional Diagnostic Laboratory (LRD) at Pelotas University, from 1986 to 2003. The epidemiological data, clinical signs and duration of clinical course were obtained from the files of LRD. Transversal sections were performed at different levels in 10% formalin-fixed CNS. The sections were made in the frontal, parietal, temporal e occipital lobes of the telencephalic hemispheres, basal ganglia and internal capsule, thalamus, anterior colliculus, pons, cerebellar peduncles, cerebellum, medulla oblongata and cervical spinal cord. Paraffin embedded tissues were sectioned and stained with hematoxylin and eosin. The severity and distribution of the inflammatory and malacic lesions were evaluated in all sections. These lesions were related with the epidemiological and clinical aspects of the disease. The outbreaks of the disease were observed in different seasons of the year. Affected animals were 2 to 24-month-old, of different breeds and both sexes. Gross lesions characterized by yellow and depressed areas in the cerebral cortex were observed in five calves. In two of them, similar lesions were additionally observed in thalamus, basal nuclei, and internal capsule. Congestion and multifocal hemorrhages were observed in most cases. The histological lesions were characterized by non-suppurative meningoencephalitis in all sections of CNS, but more severe in the frontal cortex. Focal or widespread malacia with infiltration of Gitter cells were observed in all sections of cerebral cortex, basal ganglia, internal capsule, and thalamus. In some cases mild malacia was also observed in the rostral colliculi, pons, medulla, cerebellum and cervical spinal cord. Intranuclear inclusion bodies were seen in all cases studied; they were frequent in regions of the cerebral cortex near mild to moderate inflammatory or malacic lesions. In two cases the inclusion bodies were also seen in the basal ganglia and thalamus. The severity of the histological lesions was not proportional with the clinical course of the disease. The presence of lesions of malacia in different regions of the CNS, an aspect not mentioned in most reports of BHV-5 infections, could be due to variable pathogenicity of different virus isolates. Alternatively, it is possible that BHV-5 encephalitis occurs due to the reactivation of the virus in cattle previously affected by polioencefalomacia; this last sequence of events was already demonstrated experimentally by our research group.

Nineteen bovines of both sexes aging from 5 month-old to 5 year-old, were referred to a veterinary hospital. Clinical signs were observed from 6 hours to 10 days before. Thirteen animals were found in permanent lateral recumbency, five showed motor incoordination, 15 were exclusively fed on grass pasture, three showed partial loss of visual acuity, 14 were blindness, 16 showed presence of normal pupillary reflex, 16 decreased ruminal motility, 14 decreased sensorium (depression, semicoma or coma) and eight showed opisthotonos. Dehydration and dried feces were directly related to the time of evolution of the process. All the animals were administrated vitamin B1 and showed a marked improvement of the clinical status within 4 to 48 hours after treatment. The longer the time between the onset of the clinical signs and treatment, the greater the delay for the restoration of the vision. The treatment was very effective for a rapid response of the animal.

Twenty-four steers (initial BW = 385 ± 1.1 kg) were blocked by BW and randomly assigned to 3 dietaty treatments (0, 30, or 60% wet distillers grains with solubles [WDGS]; DM basis) and were fed individually to determine the effect of WDGS on live growth and carcass performance, visceral organ mass, trace mineral status, and polioencephalomalacia biomarkers. Steers were slaughtered at 125, 150, 164, and 192 d (2 blocks/ slaughter date) when external fat depth was approximately 1.3 cm based on visual appraisal. Steers fed 30% WDGS had greater DMI than those fed 0 or 60% WDGS (P < 0.05), and steers fed 60% WDGS had the lowest carcass-adjusted ADG (P < 0.09) of the 3 treatments. Nonetheless, WDGS concentration did not alter feed efficiency (P > 0.41) on either live or carcass-adjusted basis. Steers fed 30% WDGS had greater liver S and Mn concentrations (DM basis) and lower liver Fe concentrations than control steers (P <0.10; initial values used as a covariate), and feeding 60% WDGS decreased liver Cu and increased liver Fe (P <0.10) compared with feeding 30% WDGS. Cytochrome c oxidase (COX) activity in brain tissue tended to be decreased with 60 vs. 30% WDGS (P = 0.12), and COX activity decreased linearly (P = 0.06) in lung tissue as dietaty WDGS concentration increased. Likewise, gut fill linearly increased (P = 0.01 ) with increasing WDGS concentration. Feeding 30% WDGS increased fractional mass (g/kg of empty BW) of the small intestine (P < 0.10) compared with controls, whereas 60% WDGS increased fractional kidney mass (P <0.10) compared with 30% WDGS. Overall, results suggest that gut fill, Cu status, and COX activity seem to be compromised by WDGS when fed at 60% of diet DM in diets based on steam-flaked com, which suggests a greater susceptibility to polioencephalomalacia. [ABSTRACT FROM AUTHOR]

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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 B1 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 B1 injections. [ABSTRACT FROM AUTHOR]

The number of large feedlot operations, similar to that of USA and Canada, has notably increased in Mexico in the last three decades. Clinical and laboratory diagnoses of neurological diseases in feedlot cattle are crucial in Mexico and Central America because of the high incidence of bovine paralytic rabies (BPR). Because of its zoonotic potential, BPR must be promptly diagnosed and differentiated from other bovine neurological diseases such as thrombotic meningoencephalitis (TME), polioencephalomalacia (PEM) and botulism. More recently, BPR and botulism have been diagnosed with increasing frequency in Mexican feedlots. Neither BPR nor botulism has relevant gross lesions, thus post-mortem diagnosis without laboratory support is impossible. Herein, we describe five outbreaks of neurological diseases in Mexican feedlots in which BPR, botulism and PEM were diagnosed either independently or in combination. A diagram illustrating the most conspicuous pathologic findings and ancillary laboratory test required to confirm the diagnoses of these neurological diseases in feedlot cattle is proposed. [ABSTRACT FROM AUTHOR]

Squirrel monkeys (Saimirispp) are one of the most consistently used New World primates in biomedical research and are increasingly being used in neuroscience research, including models of drug abuse and addiction. Spontaneous neurologic disease in the squirrel monkey is uncommonly reported but includes various infectious diseases as well as cerebral amyloidosis. Hypernatremia is an extremely serious condition of hyperosmolarity that occurs as a result of water loss, adipsia, or excess sodium intake. Neurologic effects of hypernatremia reflect the cellular dehydration produced by the shift of water from the intracellular fluid space into the hypertonic extracellular fluid space. Severe hypernatremia may result in cerebrocortical laminar necrosis (polioencephalomalacia) in human patients as well as in a number of domestic species, including pigs, poultry, and ruminants. We report the clinical, histopathologic, and immunohistochemical findings of polioencephalomalacia in 13 squirrel monkeys. Polioencephalomalacia in these animals was associated with hypernatremia that was confirmed by serum levels of sodium greater than 180 mmol/L (reference range, 134.0–154.0 mmol/L [mEq/L]). All animals had concurrent diseases or experimental manipulation that predisposed to adipsia. Immunohistochemical investigation using antibodies to neuronal nuclei (NeuN), CNPase, Iba-1, and CD31 revealed necrosis of predominantly cerebral cortical layers 3, 4, and 5 characterized by neuronal degeneration and loss, oligodendrocytic loss, microglial proliferation, and vascular reactivity. The squirrel monkey is exquisitely sensitive to hyperosmolar metabolic disruption and it is associated with laminar cortical necrosis. [ABSTRACT FROM PUBLISHER]

This study examined the role of sulfur (S) in the pathogenesis of S-induced polioencephalomalacia (PEM) in beef cattle in the context of thiamine status and metabolism. Thiamine, thiamine monophosphate (TMP) and thiamine pyrophosphate (TPP) status in rumen fluid, blood and brain tissue were determined in beef heifers fed 2 levels of S [low S (LS) vs. high S (HS)] at 2 forage-to-concentrate ratios (F:C). High S diet did not affect ruminal and blood thiamine status. Interestingly, however, HS diet showed increased brain thiamine levels. No gross or histopathological changes indicative of PEM were detected in the brains of the heifers. Of note, during the course of the present study, we documented an outbreak of S-induced PEM in commercial feedlot steers. Brain thiamine variables in experimental animals fed HS diet were then contrasted with brain thiamine status in PEM affected feedlot steers. Interestingly, in clinically normal animals, exposure to HS diet resulted in increased levels of both TMP and TPP in the brain tissue, in comparison to animals fed LS diet. In contrast, the PEM affected brains showed overall lower levels of thiamine phosphates. It is noteworthy that TPP levels were 36.5% lower, despite 4.9-fold higher free thiamine in PEM brains compared to normal brains. Our results indicate that high dietary S may increase the metabolic demand for TPP, and that animals incapable of maintaining requisite levels of brain TPP are at high risk to develop fulminant cerebrocortical necrosis. [ABSTRACT FROM AUTHOR]

Sulphur-induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is frequently associated with the consumption of high-sulphur (S) water and subsequent poor performance. Currently, there is no economical method for S removal from surface water sources, and alternative water sources are typically neither readily available nor cost-effective. Determination of genes differentially expressed in response to high-S water consumption may provide a better understanding of the physiology corresponding to high dietary S and ultimately lead to the development of treatment and prevention strategies. The objective of this study was to determine changes in gene expression in the liver, an organ important for S metabolism, of fibre-fed steers consuming high-S water. For this study, liver tissues were collected on the final day of a trial from yearling steers randomly assigned to low-S water control (566 mg/kg SO4; n = 24), high-S water (3651 mg/kg SO4; n = 24) or high-S water plus clinoptilolite supplemented at either 2.5% ( n = 24) or 5.0% ( n = 24) of diet dry matter (DM). Microarray analyses on randomly selected healthy low-S control ( n = 4) and high-S ( n = 4; no clinoptilolite) steers using the Affymetrix GeneChip Bovine Genome Array revealed 488 genes upregulated (p < 0.05) and 154 genes downregulated (p < 0.05) in response to the high- vs. low-S water consumption. Real-time RT-PCR confirmed the upregulation (p < 0.10) of seven genes involved in inflammatory response and immune functions. Changes in such genes suggest that ruminant animals administered high-S water may be undergoing an inflammation or immune response, even if signs of sPEM or compromised health are not readily observed. Further study of these, and other affected genes, may deliver new insights into the physiology underlying the response to high dietary S, ultimately leading to the development of treatments for high S-affected ruminant livestock. [ABSTRACT FROM AUTHOR]

Abstract: The incidence of polioencephalomalacia and concentrations of ruminal hydrogen sulfide ([H2S]) in feedlot cattle appear to be greatest during the first 30 days of being fed a high sulfur (S) finishing diet. It was hypothesized that delaying exposure to high-S until cattle are fully adapted to a high-concentrate diet would reduce the peak [H2S], thus reducing potential for S-induced polioencephalomalacia. Sixty Angus crossbred-steers were moved into the feedlot and fed a moderate S (0.3% S) step-up diet for 7 days. Then steers were weighed (443±12.8kg), blocked by weight, and randomly assigned to one of three dietary treatments: (1) two moderate-S (0.3% S) step-up diets fed for 7d each (days 1–14) followed by a moderate S finishing diet (days 15–98; MS), (2) two high-S (0.6% S) step-up diets fed for 7d each (days 1–14) followed by a high S finishing diet (days 15–98; HS), or (3) two moderate-S (0.3% S) step-up diets fed for 7d each (days 1–14) followed by a moderate S finishing (0.3% S) diet for the first 28 days of the finishing period (days 15–42), followed by the high-S diet (0.6% S) for the remainder of the trial (days 43–98; Delayed S; DS). Ruminal [H2S] and pH were measured 6h post-feeding on days 15, 21, 28, 42, 49, 56, 70, 84, and 98. The numerically greatest [H2S] (4948mg/L) occurred in HS-steers on day 42 (28d on the finishing ration) and on day 70 (28d after starting high-S) for DS-steers (3690mg/L). The maximum [H2S] of HS-steers tended to be greater (P=0.09) than DS-steers, despite S intake not differing (P=0.75). The elevated ruminal [H2S] of HS-steers on day 42, was likely not due to a decreased ruminal pH during adaptation to the finishing diet as pH did not differ due to treatment (P=0.40) or day (P=0.16). Overall, HS-steers had a 15% decrease (P=0.02) in average daily gain compared to MS-steers whereas gain of DS-steers was intermediate, not differing from MS (P=0.13) or HS (P=0.26) steers. These findings suggest that there may not be any additional increase in steer gains by delaying S inclusion in the diet until after the first 28 days of finishing, though it may decrease the maximum ruminal H2S concentration. [Copyright &y& Elsevier]

Poor performance and S-induced polioencephalomalacia (sPEM) have been observed in ruminant livestock in high-S drinking water regions. No gainful method of removing S from drinking water is available and therefore a feed supplement that negates the effects of high-S water is needed. Our objective was to determine if supplementing Mo improves health and performance of steers administered a high-fiber diet and high-S drinking water. We hypothesized that if the supplemental Mo adequately bound excess S in the rumen, it would not be available at toxic concentrations. Yearling steers (n = 96; 260.0 ± 1.3 kg BW) were stratified by pretrial BW into 12 feedlot pens (n = 8 steers per pen). One of 3 treatments, low-S water (LS; 375 mg S04/L), high-S water (HS; 2,218 mg S04/L), or high-S water plus Mo (HSMO; 2,218 mg S04/L; 187.5 mg Mo/kg DM), were randomly assigned to pens within 4 blocks for a 56-d trial. Body weights were recorded on d -2, -1, 29, 56, and 57, ruminal H2S concentrations were measured by rumenocentesis on d -1, 29, and 57, and liver biopsies were performed on d -1 and 57. Performance data were analyzed over the 56-d trial period (overall) as well as over 2 periods: Period 1 (d 0 to d 28) and Period 2 (d 29 to d 56). One case of sPEM was confirmed by the presence of cortical lesions in the HS treatment group. Daily DMI and ADG were affected by treatment and period (P < 0.001) main effects. The LS steers had the greatest (P < 0.05) DMI followed by HS and HSMO steers, respectively. Similar results were observed for ADG. Daily water intake was affected (P < 0.001) by period only, with greater daily water intake in Period 2 than Period 1. Change in hepatic concentrations of Cu, Fe, and Mo over the course of the trial were all affected (P < 0.001) by treatment. Hepatic Cu increased from d 1 to 57 in LS and HS steers but was depleted in HSMO steers. Hepatic Fe and Mo increased in HSMO steers only. Ruminal H2S concentrations were affected by treatment (P < 0.021), with greater H2S concentrations in HSMO compared with LS and HS steers. Signs of Mo toxicity such as severe diarrhea, loss of body condition, anorexia, changes in hair color, and stiffness in joints were observed in the Mo supplemented steers. These results indicate that added dietary Mo does not adequately bind excess S in the rumen, causing aggravated toxic effects from potentially both the high dietary S and Mo. [ABSTRACT FROM AUTHOR]

To determine if ruminal hydrogen sulfide, urine thiosulfate, or blood sulfhemoglobin could be used as diagnostic indicators for sulfur-induced polioencephalomalacia, 16 steers (8 cannulated, 368 ± 12 kg; 8 unmodified, 388 ± 10 kg; mean ± standard error) were fed 1 of 2 dietary treatments. Diets consisted of a low sulfate (0.24% S; control) wheat midd–based pellet or the control pellet with sodium sulfate added to achieve a high-sulfate (0.68% S) pellet. As designed, intake did not differ (P = 0.80) between treatments. At 8 hr postfeeding, ruminal hydrogen sulfide was not affected by cannulation (P = 0.35) but was greater (P < 0.01) in high S (6,005 ± 475 mg/l) than control (1,639 ± 472 mg/l) steers. Time of day of sampling affected (P = 0.01) ruminal hydrogen sulfide, with peak concentrations occurring 4–12 hr after feeding. Urine was collected prefeeding (AM) and 7–9 hr postfeeding (PM). Urine thiosulfate concentrations of high S steers sampled in the PM were greater (P > 0.01) than in the AM. However, there was no difference due to time of sampling for control. In both the AM and PM, urine thiosulfate concentrations of high S were greater (P > 0.01) than control. Although hydrogen sulfide and thiosulfate were elevated by increased dietary S intake, a concentration at which polioencephalomalacia is likely to occur could not be determined. Sampling urine for thiosulfate or rumen gas for hydrogen sulfide of nonsymptomatic pen mates 4–8 hr after feeding may be useful to assess sulfur exposure and differentiate between causes of polioencephalomalacia. [ABSTRACT FROM PUBLISHER]

Feeding increased concentrations of distillers dried grains with solubles (DDGS) to ruminants has been avoided due to risks of S toxicity and concerns about animal performance. The objective of this study was to evaluate the influence of feeding an increasing concentration of DDGS and corn processing method on animal performance, incidence of polioencephalomalacia (PEM), and concentration of H2S gas in feedlot steers. Sixty steer calves (336 ± 13.2 kg) were individually fed for an average of 136 d in a completely random design with a 3 x 2 factorial arrangement of treatments. Main effects included concentration of DDGS (20, 40, or 60% DM basis) and corn processing method [highmoisture (HMC; 71.7% DM) vs. dry-rolled corn (DRC; 86.2% DM)] resulting in treatments of 1) 20% DDGS with DRC, 2) 40% DDGS with DRC, 3) 60% DDGS with DRC, 4) 20% DDGS with HMC, 5) 40% DDGS with HMC, and 6) 60% DDGS with HMC. Ruminal H2S gas concentrations were measured on d 0, 7, 14, 21, 28, 35, 49, 63, and 91 via rumen puncture. Animal performance and carcass characteristic data were collected. The day x corn processing x DDGS interaction for H2S gas concentrations was not significant (P = 0.91). Ruminal H2S concentration increased with increasing DDGS concentration (P < 0.001) and day (P < 0.001), but was not influenced by corn processing method (P = 0.94). Carcass-adjusted final BW decreased linearly (P = 0.009), whereas carcass-adjusted ADG decreased quadratically (P = 0.05) with increasing concentration of DDGS in the diet. Carcass-adjusted G:F was not affected (P ≥ 0.28) by increasing concentration of DDGS in the diet. Carcass characteristics reflected the decrease in final BW with decreased HCW (P = 0.009), as well as decreased fat depth (P 0.005) with increasing concentrations of DDGS. The combination of decreased HCW and backfat thickness resulted in decreased (P = 0.02) yield grade with increasing DDGS inclusion. There were no confirmed cases of PEM. In conclusion, corn processing did not influence animal performance, incidence of PEM, or H2S concentrations under the conditions of this study. Feeding 60% DDGS in beef cattle finishing diets is not recommended due to poor animal performance. [ABSTRACT FROM AUTHOR]

Limited data are available regarding the influence of thiamine supplementation on the incidence of polioencephalomalacia (PEM) in lambs fed diets containing increased concentrations of S in the diet (>0.7%). Therefore, our objective was to evaluate the influence of thiamine supplementation on feedlot performance, carcass quality, ruminal hydrogen sulfide gas concentrations, and incidence of PEM in lambs fed a finishing diet containing 60% distillers dried grains with solubles (DDGS; DM basis). Two studies were conducted using completely randomized designs to evaluate the influence of concentration of thiamine supplementation. Study 1 used 240 lambs fed in 16 pens, whereas study 2 used 55 individually fed lambs. Lamb finishing diets contained 60% DDGS, which resulted in a dietary S concentration of 0.73% (DM basis). Treatments diets were based on the amount of supplemental thiamine provided: 1) no supplemental thiamine (CON), 2) 50 mg/animal per day (LO), 3) 100 mg/animal per day (MED), or 4)150 mg/animal per day (HI). Additionally, in study 2, a fifth treatment was included, which contained 0.87% S (DM basis; increased S provided by addition of dilute sulfuric acid) and provided 150 mg of thiamine/animal per day (HI+S). In study 1, ADG decreased quadratically (P = 0.04), with lambs fed the CON, LO, and MED diets gaining BW at a greater rate than lambs fed the HI diet. In study 1, DMI responded quadratically (P < 0.01), whereas G:F tended to differ linearly (P = 0.08) to concentration of thiamine supplementation, with MED lambs having greater DMI and decreased G:F. No differences (P ⩾ 0.17) in lamb performance were observed in study 2. In both studies, most carcass characteristics were unaffected, with the exception of a tendency for decreased carcass conformation (study 1; P = 0.09) and greater flank streaking (study 2; P = 0.03). No differences in ruminal hydrogen sulfide concentration (P> 0.05) among treatments were apparent until d 10, at which point lambs fed the LO diet had less hydrogen sulfide concentrations than all other treatments. Lambs fed HI had the greatest concentrations of hydrogen sulfide on d 31 (1.07 g of hydrogen sulfide /m3 P < 0.009). Ruminal pH did not differ (P = 0.13) and averaged 5.6 ± 0.06. No clinical cases of PEM were observed during the course of either study. The use of thiamine as a dietary additive to aid in the prevention of PEM in finishing lambs does not appear to be necessary under the conditions of this study. [ABSTRACT FROM AUTHOR]

Sulfur-induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is associated with consumption of diets with increased S (high-S). High-S water is commonly found in many western states and is a major source of dietary S for grazing cattle. Consumption of high-S water has been associated with sPEM and decreased performance. Identification of a feed supplement that would counteract the negative effects of high-S water would decrease the incidence of sPEM and prevent performance reductions in regions with problematic water sources. The objectives of this study were to 1) determine the effects of administering high-S drinking water to foragefed feedlot steers on health and performance, and 2) determine the effectiveness of clinoptilolite, a clay mineral with increased cation-exchange capacity, in negating the effects of high-S drinking water. Yearling steers (n = 96; 318.2 ± 2.1 kg of BW) were randomly assigned to 1 of 4 treatments for a 77-d trial period: control with low-S water (566 mg of S04/L), high-S water (3,651 mg of S04/L), or high-S water plus clinoptilolite supplemented at 2.5 or 5.0% of the diet DM. Feed and water consumption were measured daily, .and all steers were weighed on d -2, -1, 29, 53, 76, and 77. Plasma sam-ples were collected on d 0, 58, and 77, and liver samples on d 0 and 77. There was a greater (P ⩾ 0.046) frequency of sPEM in high-S steers than control steers, but no differences among high-S treatment groups. In total, 12 cases of sPEM were confirmed by the presence of cortical lesions in steers consuming high-S water. Daily DM1 (P = 0.002) and daily water intake (P = 0.001) were less in high-S water steers than control steers. No differences (P> 0.546) in ADG or G:F were observed. Plasma Cu decreased (P = 0.029) to a greater magnitude in high-S water steers than the control steers over the 77-d trial period. Mineral analyses of hepatic tissue from randomly selected healthy steers from each treatment group (n = 10 per treatment) showed an interaction (P < 0.034) of sample time and treatment for Cu, Se, and Zn concentrations. These results suggest that clinoptilolite does not negate the effects of high-S water, and administration of high-S water decreases herd health through an increased incidence of sPEM and reduced nutritional status. [ABSTRACT FROM AUTHOR]

Sulfur-induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is associated with consumption of diets with increased S (high-S). High-S water is commonly found in many western states and is a major source of dietary S for grazing cattle. Consumption of high-S water has been associated with sPEM and decreased performance. Identification of a feed supplement that would counteract the negative effects of high-S water would decrease the incidence of sPEM and prevent performance reductions in regions with problematic water sources. The objectives of this study were to 1) determine the effects of administering high-S drinking water to foragefed feedlot steers on health and performance, and 2) determine the effectiveness of clinoptilolite, a clay mineral with increased cation-exchange capacity, in negating the effects of high-S drinking water. Yearling steers (n = 96; 318.2 ± 2.1 kg of BW) were randomly assigned to 1 of 4 treatments for a 77-d trial period: control with low-S water (566 mg of S04/L), high-S water (3,651 mg of S04/L), or high-S water plus clinoptilolite supplemented at 2.5 or 5.0% of the diet DM. Feed and water consumption were measured daily, .and all steers were weighed on d -2, -1, 29, 53, 76, and 77. Plasma sam-ples were collected on d 0, 58, and 77, and liver samples on d 0 and 77. There was a greater (P ⩾ 0.046) frequency of sPEM in high-S steers than control steers, but no differences among high-S treatment groups. In total, 12 cases of sPEM were confirmed by the presence of cortical lesions in steers consuming high-S water. Daily DM1 (P = 0.002) and daily water intake (P = 0.001) were less in high-S water steers than control steers. No differences (P> 0.546) in ADG or G:F were observed. Plasma Cu decreased (P = 0.029) to a greater magnitude in high-S water steers than the control steers over the 77-d trial period. Mineral analyses of hepatic tissue from randomly selected healthy steers from each treatment group (n = 10 per treatment) showed an interaction (P < 0.034) of sample time and treatment for Cu, Se, and Zn concentrations. These results suggest that clinoptilolite does not negate the effects of high-S water, and administration of high-S water decreases herd health through an increased incidence of sPEM and reduced nutritional status. [ABSTRACT FROM AUTHOR]