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This study aimed to clarify the type of photosensitization induced by C. serpens and to verify if the plant remains toxic after being collected and stored. Eight crossbred sheep, aged between 6 and 36 months, were divided into three groups (G1 to G3). Over 30 days, daily, G1 received an exclusive diet of C. serpens, and G2 and G3 received 10 g/kg/BW and 20 g/kg/BW, respectively. Two other sheep were used as controls (CG). Before administration, the plant had been harvested every 15 days. Liver biopsies and blood samples were taken from all sheep on day zero and weekly. All sheep that received the plant developed clinical signs of photosensitization, and no changes were observed in the serum activities of AST and GGT. On day 30, all sheep except Ov1 from G1 and Ov7 were euthanized and necropsied. All sheep that received the plant developed clinical signs. Macroscopic or histologic lesions were not observed in the liver. Ov 1 recovered 13 days after the end of ingestion. These results demonstrated that C. serpens causes primary photosensitization. It is advisable to avoid grazing on pastures invaded by the plant or to remove them from the pastures immediately after observing the first signs.

RESUMEN

Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution (<24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.

Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda (<24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.

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RESUMEN

ABSTRACT: Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution ( 24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.

RESUMO: Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda ( 24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.

RESUMEN

Monensin is an ionophore antibiotic (IA) widely used for growth promotion and weight gain in the production of ruminants. However, it has caused intoxication in several species, including buffaloes, mainly because of the ignorance or disrespect of the recommendations for use in each animal species. The objective of this study was to describe, for the first time, clinical-epidemiological and anatomopathological data of an outbreak of accidental poisoning by monensin in buffalos and rediscuss the recommendation of the use of IA in the production of this species. The outbreak affected 21 adult buffaloes after consumption of remains from a feed formulated on the farm and whose constituents were mixed by hand. Clinical and first death signs were observed 24 hours after ingestion of this food. In general, the clinical picture was characterized by muscle weakness, tremors, difficulty in locomotion, and decubitus. Fifteen buffaloes presented clinical signs of poisoning (71.5% morbidity), followed by death (100% lethality), after acute to subacute evolution (<24h to 96h). Laboratory tests indicated elevated serum activity of creatine phosphokinase and aspartate aminotransferase enzymes. Three buffaloes underwent necropsy, and samples from several organs were collected for histopathological examination. The main injuries found were hyaline degeneration and multifocal segmental necrosis in the skeletal and cardiac striated muscles (myopathy and degenerative-necrotic multifocal multifocal-necrotic cardiopathy). The diagnosis was confirmed by the toxicological evaluation of suspected ration remains, which detected 461.67mg/kg of monensin. The death of 71.5% buffaloes in this lot occurred due to a succession of errors, which included faults in the formulation of the ration and, above all, due to the use of monensin in a highly sensitive species. Despite the possible beneficial effects of IA use as a dietary supplement for buffaloes, we are of the opinion that IAs should never be used in bubalinoculture since any increment in production does not compensate for the imminent risk of death due to a small safety margin for this species and the absence of antidotes.(AU)

Monensina é um antibiótico ionóforo (AI) amplamente empregado na produção de ruminantes para promoção de crescimento e ganho de peso, mas que tem causado intoxicação em diversas espécies, incluindo os búfalos, principalmente, pelo desconhecimento ou desrespeito das recomendações de uso e às particularidades de cada espécie animal. Objetivou-se descrever, pela primeira vez na Bahia, dados clínico-epidemiológicos e anatomopatológicos de um surto de intoxicação acidental por monensina em búfalos e rediscutir a recomendação do uso de AI na produção de bubalinos. O surto acometeu um lote de 21 búfalos adultos após consumo de sobras de uma ração para bovinos formulada na fazenda e cujos constituintes eram misturados à mão. Os sinais clínicos e primeiros óbitos foram observados 24 horas após a ingestão dessa ração. O quadro clínico, em geral, se caracterizou por fraqueza muscular, tremores, dificuldade de locomoção e decúbito. Quinze búfalos apresentaram sinais clínicos de intoxicação (morbidade 71,5%), seguido de morte (letalidade 100%), após evolução aguda a subaguda (<24h até 96h). Exames laboratoriais indicaram acentuada elevação na atividade sérica das enzimas CPK e AST. Três búfalos foram necropsiados, sendo coletadas amostras de diversos órgãos para exame histopatológico. A principal lesão encontrada foi degeneração hialina e necrose segmentar multifocal nos músculos estriados esqueléticos e cardíacos (miopatia e cardiopatia degenerativo-necrótica tóxica multifocal polifásica). O diagnóstico foi confirmado pela avaliação toxicológica das sobras da ração suspeita, que detectou 461,67mg/kg de monensina. A morte de 71,5% dos búfalos deste lote ocorreu devido a uma sucessão de erros, que incluíram falhas na formulação da ração e, sobretudo, devido ao uso da monensina em uma espécie altamente sensível. Enfatizamos que, apesar dos possíveis efeitos benéficos do uso AIs como suplemento dietético para bubalinos, somos da opinião que os AIs nunca devem ser empregados na bubalinocultura, uma vez que os eventuais incrementos na produção não compensam o risco iminente de morte, devido a pequena margem de segurança para essa espécie e a inexistência de antídotos.(AU)

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Congenital malformations are morphofunctional abnormalities of tissues and organs that can occur during embryonic or fetal development in all animal species. Among these, dicephalus is characterized by the development of an individual with two heads and two necks, due to the total duplication of facial, cranial, and brain structures. Reports of dicephalus in cattle are scarce and do not normally emphasize radiographic and bone anatomy characteristics. The objective was to describe a case of a stillborn dicephalus calf. The duplication of the head, brain, neck, and two thoracic vertebral columns, isolated from each other, with 13 vertebrae each was verified radiographically. There were 13 pairs of ribs, the ones on the right side articulated with the thoracic spine on the right and the left ones with the spine on the left. Caudally at T13, there was only one lumbar spine, sacral and coccygeal. In the ventrodorsal projection, L1, L2, L3, and L6 had the shape of a butterfly (suggestive of hemivertebrae). At necropsy, in addition to craniocervical and spinal morphological changes, collapsed lungs, duplication of the heart with anastomosis between the aortic arches of the hearts, and duplication of the upper digestive tract were observed. Additionally, there was arthrogryposis of the pelvic limbs. Corpse maceration, followed by the skeletal assembly, showed the bone changes previously observed and confirmed the suspicion of hemivertebrae.

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Congenital malformations are morphofunctional abnormalities of tissues and organs that can occur during embryonic or fetal development in all animal species. Among these, dicephalus is characterized by the development of an individual with two heads and two necks, due to the total duplication of facial, cranial, and brain structures. Reports of dicephalus in cattle are scarce and do not normally emphasize radiographic and bone anatomy characteristics. The objective was to describe a case of a stillborn dicephalus calf. The duplication of the head, brain, neck, and two thoracic vertebral columns, isolated from each other, with 13 vertebrae each was verified radiographically. There were 13 pairs of ribs, the ones on the right side articulated with the thoracic spine on the right and the left ones with the spine on the left. Caudally at T13, there was only one lumbar spine, sacral and coccygeal. In the ventrodorsal projection, L1, L2, L3, and L6 had the shape of a butterfly (suggestive of hemivertebrae). At necropsy, in addition to craniocervical and spinal morphological changes, collapsed lungs, duplication of the heart with anastomosis between the aortic arches of the hearts, and duplication of the upper digestive tract were observed. Additionally, there was arthrogryposis of the pelvic limbs. Corpse maceration, followed by the skeletal assembly, showed the bone changes previously observed and confirmed the suspicion of hemivertebrae.(AU)

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This study aimed to describe the first reports of outbreaks of hepatogenous photosensitization in cattle, sheep, and horses caused by spontaneous ingestion of Chamaecrista serpens, as well as to reproduce poisoning in sheep experimentally. Eleven photodermatitis outbreaks of unknown cause occurred in cattle, sheep and horses on nine farms in the semiarid region of Bahia, northeastern Brazil, between July 2017 and July 2020. Cutaneous lesions of photosensitization initiated until one week after the animals were introduced in paddocks invaded by the plant at the beginning of the rainy season. The photosensitive skin lesions were progressive and consisted of hyperemia, edema, ulcerative-crusted lesions with necrosis, especially in non-pigmented skin areas. The lesions in young animals were more severe. The animals avoided the sun and exhibited hyporexia, weight loss, restlessness, irritability, and severe itching. An experimental study was made using seven sheep, and resulted in photodermatitis, similar to that observed in the natural poisoning, seven days after the beginning of plant ingestion. Two sheep were reserved for the control group. Serum biochemistry changes indicated liver injury caused by the plant. Skin biopsies and liver biopsy guided by ultrasound were performed. The one sheep that had more pronounced skin lesions was euthanized and necropsied. At the necropsy, the liver was enlarged, diffusely pale, and firm, with an evident lobular pattern and an empty gallbladder. Histopathology revealed similar skin and liver lesions in samples from biopsies and the necropsy. There was a marked disorganization of the cords of hepatocytes associated with degenerative necrotic changes on the liver. The cutaneous injuries included orthokeratotic hyperkeratosis, hypergranulosis, acanthosis, and extensive areas of epidermic necrosis and ulceration. Three sheep were protected from sunlight and the lesions regressed within 45 days after the plant's consumption ceased. In conclusion, C. serpens causes hepatogenous photosensitization in ruminants and horses, and should be included in the list of differential diagnoses in cases of photosensitive dermatitis.

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Chondrodysplasia is a congenital or hereditary disorder of the endochondral ossification that results in several degrees of disproportionate dwarfism. Reports of this disease are scarce in the national literature and do not emphasize radiographic characteristics. The goal of this study was to describe the clinicopathological and radiographic aspects of a case of Bulldog type chondrodysplasia in a crossbred bovine fetus in the state of Bahia, Brazil. The fetus exhibited arounded and disproportionate skull, bilateral exophthalmos, inferior brachygnathism, partial tongue protrusion, extremely short limbs, short vertebral column and ventral abdominal hernia. Radiographic evaluation revealed that the diaphysis were the only calcified bone portions of the limbs, that the vertebral column was shortened without vertebral spinal processes and that there was craniofacial disproportion. Microscopic of the femur showed an irregular epiphyseal plaque, formed by denseclusters of chondrocytes with absence of growth plate zones. The metaphysis was markedly short and consisted of thick bony trabeculae, surrounded by cartilaginous islands. It was concluded that fetuses with Bulldog type chondrodysplasia exhibit slight morphological and radiographic variation according to the affected breed and that the gene carrier of chondrodysplasia is present in the miniature Jersey and Punganur population in the state of Bahia.

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Chondrodysplasia is a congenital or hereditary disorder of the endochondral ossification that results in several degrees of disproportionate dwarfism. Reports of this disease are scarce in the national literature and do not emphasize radiographic characteristics. The goal of this study was to describe the clinicopathological and radiographic aspects of a case of Bulldog type chondrodysplasia in a crossbred bovine fetus in the state of Bahia, Brazil. The fetus exhibited arounded and disproportionate skull, bilateral exophthalmos, inferior brachygnathism, partial tongue protrusion, extremely short limbs, short vertebral column and ventral abdominal hernia. Radiographic evaluation revealed that the diaphysis were the only calcified bone portions of the limbs, that the vertebral column was shortened without vertebral spinal processes and that there was craniofacial disproportion. Microscopic of the femur showed an irregular epiphyseal plaque, formed by denseclusters of chondrocytes with absence of growth plate zones. The metaphysis was markedly short and consisted of thick bony trabeculae, surrounded by cartilaginous islands. It was concluded that fetuses with Bulldog type chondrodysplasia exhibit slight morphological and radiographic variation according to the affected breed and that the gene carrier of chondrodysplasia is present in the miniature Jersey and Punganur population in the state of Bahia.(AU)

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Poisoning by Prosopis juliflora (mesquite) leads to neurological signs, cachexia and death, mainly in cattle and goats. Although the uncontrolled spread of mesquite in the Caatinga biome (biological invasion), which alters the epidemiological conditions of intoxication by this plant, has been proved for approximately 20 years, strategies for its control and prophylaxis still remain out of date. These new epidemiological conditions have allowed the uncontrolled consumption of large amounts of in natura mesquite pods by ruminants for long periods in invaded pastures, thus resulting in increased history of poisoning. This study aimed to describe the new epidemiological aspects of P. juliflora poisoning in cattle and goats, 78 years after the introduction of this plant in the country, with emphasis on its degree of invasion, and to update the control and prophylaxis measures of this intoxication and the mapping of areas of outbreak occurrence in the semiarid region of the state of Bahia, Brazil. Seven outbreaks of natural mesquite poisoning, two in goats (OB 1 and OB 2) and five in cattle (OB 3, OB 4, OB 5, OB 6, and OB 7), were studied in loco in the municipalities of Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra and Tabocas do Brejo Velho. In the studied outbreaks, clinical-epidemiological (OB 1 to OB 7) and histopathological (OB 1, OB 2, OB 3, and OB 5) findings were compatible with mesquite poisoning, and this was the first anatomopathological proof of poisoning by this plant in this state. In addition, in the state of Bahia, disease occurs in an area approximately three times larger than previously known. On the farms investigated, mesquite introduction occurred between 1980 and 2005, through the single planting of an average of 33 seedlings. Since then, propagation of this plant has occurred progressively, with gradual invasion of native pastures, which enabled the evaluation of plant spread (biological invasion) on these farms 15 (OB 2), 25 (OB 7), 30 (OB 5 and OB 6), 35 (OB 3) and 40 (OB 1 and OB 4) years after its introduction. Historical information on the introduction and spread of mesquite in the state of Bahia had never been analyzed. In 2020, a degree of mesquite invasion an average 59.57% was verified in the pastures of the seven farms where the outbreaks occurred. The great biological invasion capacity of this plant drew attention, especially in OB 5. The high degree of mesquite invasion observed (new epidemiological conditions) justifies the increased number of cases of poisoning observed in this study. Processing of P. juliflora pods (grinding) was not carried out on any farm (OB 1 to OB 7), and ruminants uncontrollably consumed large amounts of pods in natura for long periods in invaded pastures, which allowed massive dispersal of seeds through feces over decades. The main factors responsible for the gradual invasion of pastures by mesquite over time were absence of crop management plans (silvicultural treatments) and lack of knowledge by producers on disease etiology. Given the new epidemiological conditions, restriction of animal access to in natura pods in pastures and supply of mesquite bran are crucial for the control and prophylaxis of this poisoning, as consumption of in natura pods had a strong correlation with the high degree of invasion in the pastures where the seven outbreaks occurred. Additionally, although the commercialization of pods and exploitation of wood of mesquite trees can provide livestock farmers with extra income - being the correct management for areas invaded by this plant, such practice is either not yet known or not carried out technically or satisfactorily by farmers. In addition to being a threat to the Caatinga's biodiversity, the increasing invasion of semiarid areas by mesquite 78 years after its introduction in the Northeast region of Brazil, is a risk for herds, since the occurrence of poisoning outbreaks may become more frequent. Therefore, it is highly advisable that effective measures be adopted to control P. juliflora propagation.(AU)

A intoxicação por Prosopis juliflora (algaroba) cursa com sinais neurológicos, caquexia e morte, principalmente em bovinos e caprinos. Embora a disseminação descontrolada da algaroba na Caatinga (invasão biológica) tenha sido comprovada há cerca de 20 anos, o que altera as condições epidemiológicas dessa intoxicação, as estratégias de controle e profilaxia permanecem desatualizadas. Essas novas condições epidemiológicas permitem o consumo descontrolado de grande quantidade de vagens in natura de algaroba, por longos períodos, nas pastagens invadidas, o que tem resultado em aumento dos históricos de intoxicação. Objetivou-se com esse estudo descrever os novos aspectos epidemiológicos da intoxicação por P. juliflora em bovinos e caprinos, 78 anos após a introdução da planta no país, com ênfase no grau de invasão da planta, bem como atualizar as medidas de controle e profilaxia dessa intoxicação e das áreas de ocorrência dos surtos no semiárido baiano. Foram estudados in loco sete surtos (S1 a S7) de intoxicação natural por algaroba, sendo dois em caprinos (S1 e S2) e cinco em bovinos (S3, S4, S5, S6 e S7) no semiárido baiano (Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra e Tabocas do Brejo Velho). Nos surtos estudados, os achados clínico-epidemiológicos (S1 a S7) e histopatológicos (S1, S2, S3 e S5) foram compatíveis com intoxicação por algaroba, sendo essa intoxicação comprovada, pela primeira vez, com exames anatomopatológicos na Bahia. Ademais, na Bahia a doença ocorre em uma área cerca de três vezes maior do que a, até então, conhecida. Nas fazendas estudadas a introdução da algaroba ocorreu entre 1980 e 2005, através do plantio único de, em média, 33 mudas. Desde então, a disseminação da planta ocorreu de forma progressiva, invadindo gradativamente as pastagens nativas, o que permitiu avaliar a disseminação da planta (invasão biológica) nessas fazendas cerca de 15 (S2), 25 (S7), 30 (S5 e S6), 35 (S3) e 40 (S1 e S4) anos, após sua introdução. Informações históricas acerca da introdução da algaroba e sua disseminação na Bahia nunca haviam sido estudadas. Em 2020, verificou-se que nas pastagens das sete fazendas onde os surtos ocorreram, o grau de invasão por algaroba alcançou, em média, 59,57%. Chamou a atenção a grande capacidade de invasão biológica da planta, sobretudo, no S5. O alto grau de invasão da algaroba observado (novas condições epidemiológicas) justificou o aumento dos casos de intoxicação verificados nesse estudo. O beneficiamento das vagens (moagem) não era realizado em nenhuma fazenda (S1 a S7) e os ruminantes consumiam de forma descontrolada (livre) grande quantidade de vagens in natura, por longos períodos, nas pastagens invadidas, o que possibilitou a dispersão massiva das sementes da planta pelas fezes ao longo das décadas. O que aliado à inexistência de um plano de manejo do cultivo (tratamentos silviculturais) e ao desconhecimento da etiologia da doença pelos produtores foram os principais fatores responsáveis pela invasão gradativa da planta nas pastagens, ao longo dos anos, o que justifica o aumento dos casos de intoxicação observados na Bahia. Frente às novas condições epidemiológicas, a restrição do acesso dos animais as vagens in natura nas pastagens e o fornecimento do farelo de algaroba são cruciais para o controle e profilaxia dessa intoxicação, pois o consumo das vagens in natura teve forte correlação com o alto grau de invasão das pastagens onde os sete surtos ocorreram. Adicionalmente, embora a comercialização das vagens e a exploração da madeira da algaroba possam proporcionar renda extra aos pecuaristas e serem boas formas de manejo de áreas invadidas por algaroba, tais práticas ainda não são conhecidas ou não são realizadas de forma técnica ou a contento. A crescente invasão da algaroba no semiárido, 78 anos após a sua introdução no Nordeste, além de ser uma ameaça à biodiversidade da Caatinga é um risco para os rebanhos, visto que, a ocorrência de surtos de intoxicação podem se tornar mais frequentes. Desta maneira alerta-se para adoção de medidas efetivas de controle da propagação descontrolada da algaroba.(AU)

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RESUMEN

ABSTRACT: Poisoning by Prosopis juliflora (mesquite) leads to neurological signs, cachexia and death, mainly in cattle and goats. Although the uncontrolled spread of mesquite in the Caatinga biome (biological invasion), which alters the epidemiological conditions of intoxication by this plant, has been proved for approximately 20 years, strategies for its control and prophylaxis still remain out of date. These new epidemiological conditions have allowed the uncontrolled consumption of large amounts of in natura mesquite pods by ruminants for long periods in invaded pastures, thus resulting in increased history of poisoning. This study aimed to describe the new epidemiological aspects of P. juliflora poisoning in cattle and goats, 78 years after the introduction of this plant in the country, with emphasis on its degree of invasion, and to update the control and prophylaxis measures of this intoxication and the mapping of areas of outbreak occurrence in the semiarid region of the state of Bahia, Brazil. Seven outbreaks of natural mesquite poisoning, two in goats (OB 1 and OB 2) and five in cattle (OB 3, OB 4, OB 5, OB 6, and OB 7), were studied in loco in the municipalities of Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra and Tabocas do Brejo Velho. In the studied outbreaks, clinical-epidemiological (OB 1 to OB 7) and histopathological (OB 1, OB 2, OB 3, and OB 5) findings were compatible with mesquite poisoning, and this was the first anatomopathological proof of poisoning by this plant in this state. In addition, in the state of Bahia, disease occurs in an area approximately three times larger than previously known. On the farms investigated, mesquite introduction occurred between 1980 and 2005, through the single planting of an average of 33 seedlings. Since then, propagation of this plant has occurred progressively, with gradual invasion of native pastures, which enabled the evaluation of plant spread (biological invasion) on these farms 15 (OB 2), 25 (OB 7), 30 (OB 5 and OB 6), 35 (OB 3) and 40 (OB 1 and OB 4) years after its introduction. Historical information on the introduction and spread of mesquite in the state of Bahia had never been analyzed. In 2020, a degree of mesquite invasion an average 59.57% was verified in the pastures of the seven farms where the outbreaks occurred. The great biological invasion capacity of this plant drew attention, especially in OB 5. The high degree of mesquite invasion observed (new epidemiological conditions) justifies the increased number of cases of poisoning observed in this study. Processing of P. juliflora pods (grinding) was not carried out on any farm (OB 1 to OB 7), and ruminants uncontrollably consumed large amounts of pods in natura for long periods in invaded pastures, which allowed massive dispersal of seeds through feces over decades. The main factors responsible for the gradual invasion of pastures by mesquite over time were absence of crop management plans (silvicultural treatments) and lack of knowledge by producers on disease etiology. Given the new epidemiological conditions, restriction of animal access to in natura pods in pastures and supply of mesquite bran are crucial for the control and prophylaxis of this poisoning, as consumption of in natura pods had a strong correlation with the high degree of invasion in the pastures where the seven outbreaks occurred. Additionally, although the commercialization of pods and exploitation of wood of mesquite trees can provide livestock farmers with extra income - being the correct management for areas invaded by this plant, such practice is either not yet known or not carried out technically or satisfactorily by farmers. In addition to being a threat to the Caatingas biodiversity, the increasing invasion of semiarid areas by mesquite 78 years after its introduction in the Northeast region of Brazil, is a risk for herds, since the occurrence of poisoning outbreaks may become more frequent. Therefore, it is highly advisable that effective measures be adopted to control P. juliflora propagation.

RESUMO: A intoxicação por Prosopis juliflora (algaroba) cursa com sinais neurológicos, caquexia e morte, principalmente em bovinos e caprinos. Embora a disseminação descontrolada da algaroba na Caatinga (invasão biológica) tenha sido comprovada há cerca de 20 anos, o que altera as condições epidemiológicas dessa intoxicação, as estratégias de controle e profilaxia permanecem desatualizadas. Essas novas condições epidemiológicas permitem o consumo descontrolado de grande quantidade de vagens in natura de algaroba, por longos períodos, nas pastagens invadidas, o que tem resultado em aumento dos históricos de intoxicação. Objetivou-se com esse estudo descrever os novos aspectos epidemiológicos da intoxicação por P. juliflora em bovinos e caprinos, 78 anos após a introdução da planta no país, com ênfase no grau de invasão da planta, bem como atualizar as medidas de controle e profilaxia dessa intoxicação e das áreas de ocorrência dos surtos no semiárido baiano. Foram estudados in loco sete surtos (S1 a S7) de intoxicação natural por algaroba, sendo dois em caprinos (S1 e S2) e cinco em bovinos (S3, S4, S5, S6 e S7) no semiárido baiano (Juazeiro, Iaçu, Tucano, Santa Teresinha, Barra do Mendes, Barra e Tabocas do Brejo Velho). Nos surtos estudados, os achados clínico-epidemiológicos (S1 a S7) e histopatológicos (S1, S2, S3 e S5) foram compatíveis com intoxicação por algaroba, sendo essa intoxicação comprovada, pela primeira vez, com exames anatomopatológicos na Bahia. Ademais, na Bahia a doença ocorre em uma área cerca de três vezes maior do que a, até então, conhecida. Nas fazendas estudadas a introdução da algaroba ocorreu entre 1980 e 2005, através do plantio único de, em média, 33 mudas. Desde então, a disseminação da planta ocorreu de forma progressiva, invadindo gradativamente as pastagens nativas, o que permitiu avaliar a disseminação da planta (invasão biológica) nessas fazendas cerca de 15 (S2), 25 (S7), 30 (S5 e S6), 35 (S3) e 40 (S1 e S4) anos, após sua introdução. Informações históricas acerca da introdução da algaroba e sua disseminação na Bahia nunca haviam sido estudadas. Em 2020, verificou-se que nas pastagens das sete fazendas onde os surtos ocorreram, o grau de invasão por algaroba alcançou, em média, 59,57%. Chamou a atenção a grande capacidade de invasão biológica da planta, sobretudo, no S5. O alto grau de invasão da algaroba observado (novas condições epidemiológicas) justificou o aumento dos casos de intoxicação verificados nesse estudo. O beneficiamento das vagens (moagem) não era realizado em nenhuma fazenda (S1 a S7) e os ruminantes consumiam de forma descontrolada (livre) grande quantidade de vagens in natura, por longos períodos, nas pastagens invadidas, o que possibilitou a dispersão massiva das sementes da planta pelas fezes ao longo das décadas. O que aliado à inexistência de um plano de manejo do cultivo (tratamentos silviculturais) e ao desconhecimento da etiologia da doença pelos produtores foram os principais fatores responsáveis pela invasão gradativa da planta nas pastagens, ao longo dos anos, o que justifica o aumento dos casos de intoxicação observados na Bahia. Frente às novas condições epidemiológicas, a restrição do acesso dos animais as vagens in natura nas pastagens e o fornecimento do farelo de algaroba são cruciais para o controle e profilaxia dessa intoxicação, pois o consumo das vagens in natura teve forte correlação com o alto grau de invasão das pastagens onde os sete surtos ocorreram. Adicionalmente, embora a comercialização das vagens e a exploração da madeira da algaroba possam proporcionar renda extra aos pecuaristas e serem boas formas de manejo de áreas invadidas por algaroba, tais práticas ainda não são conhecidas ou não são realizadas de forma técnica ou a contento. A crescente invasão da algaroba no semiárido, 78 anos após a sua introdução no Nordeste, além de ser uma ameaça à biodiversidade da Caatinga é um risco para os rebanhos, visto que, a ocorrência de surtos de intoxicação podem se tornar mais frequentes. Desta maneira alerta-se para adoção de medidas efetivas de controle da propagação descontrolada da algaroba.

RESUMEN

The objective of this study was to describe for the first time the clinical-epidemiological, laboratory and pathological aspects of different forms of enzootic ataxia in goats and lambs in the state of Bahia, as well as to propose an emergency oral treatment with copper sulfate in an individualized way for neonates. Three outbreaks of enzootic ataxia were studied. The history, clinical signs and epidemiological data were obtained from the owners and checked during the visits. The first outbreak (FO) occurred in 2013 in a property located in the municipality of Itaberaba and affected a herd composed of 90 goats and 130 sheep. The second outbreak (SO) occurred in 2014 in the municipality of Santa Luz and affected a herd of 90 goats and 110 sheep. The third outbreak (TO) occurred in 2018, in a property located in the same municipality of the SO, being the herd constituted by 80 sheep. Samples of blood were collected from all goats and sheep treated for serum copper dosage. Nine animals (five goats and four sheep) that presented a more severe clinical picture and unfavorable prognosis were necropsied for diagnostic confirmation. During the necropsy of the FO, SO and TO animals, liver samples were collected for copper dosage as well as fragments of several organs for histopathology. At the site where the SO occurred, samples of soil and the main forages where the animals were kept were collected to determine copper, iron, molybdenum, sulfur and zinc contents. The clinical and histopathological findings in the three outbreaks studied were characteristic of enzootic ataxia. In the outbreaks studied, the frequency of enzootic ataxia was higher in goats (52) than in lambs (39). In the goats the mean values of serum copper (0.05mg/kg) and hepatic (2.48mg/kg) of the FO and SO were well below their respective reference values, 12 times lower than serum levels and eight times lower in relation to liver contents. On the other hand, TO sheep presented mean values of serum copper (0.015mg/kg) reduced by 40 times. The levels of iron and sulfur were high in the fodder of the property where the SO occurred, already in the soil, iron levels were high and copper levels were reduced. The treatment tested in neonates and lambs with two doses of copper sulphate solution orally at a dose of 20mg/kg for sheep and 35mg/kg for goats during the first and second week of life was effective in prevention of enzootic ataxia in neonates and can be used for emergency control of the disease. The occurrence of enzootic ataxia (congenital and late form) in goats and sheep was first reported in Bahia. It is also worth noting that this disease caused by copper deficiency has caused great damage to the breeders of small ruminants, mainly due to the high mortality of the animals affected.(AU)

Objetivou-se com esse estudo descrever pela primeira vez os aspectos clínico-epidemiológicos, laboratoriais e patológicos de diferentes formas de ataxia enzoótica em cabritos e borregos no estado da Bahia, bem como propor um tratamento oral emergencial com sulfato de cobre de forma individualizada para neonatos. Foram estudados três surtos de ataxia enzoótica. O histórico, sinais clínicos e dados epidemiológicos foram obtidos com os proprietários e verificados durantes as visitas técnicas. O primeiro surto (PS) ocorreu em 2013 em uma propriedade localizada no município de Itaberaba e acometeu um rebanho composto por 90 caprinos e 130 ovinos. O segundo surto (SS) aconteceu em 2014 no município de Santa Luz e afetou um rebanho formado por 90 caprinos e 110 ovinos. O terceiro surto (TS) ocorreu 2018, em uma propriedade localizada no mesmo município do SS, sendo o rebanho constituído por 80 ovinos. Amostras de sangue foram colhidas de todos os caprinos e ovinos atendidos, para dosagem de cobre sérico. Nove animais (cinco caprinos e quatro ovinos) que apresentavam quadro clínico mais grave e prognóstico desfavorável foram necropsiados para confirmação diagnóstica. Durante a necropsia dos animais do PS, SS e TS amostras de fígado foram coletadas para dosagem de cobre, bem como amostras de diversos órgãos para exame histopatológico. Na propriedade onde ocorreu o SS, foram coletadas amostras de solo e das principais forragens onde os animais eram mantidos, a fim de se determinar os teores de cobre, ferro, molibdênio, enxofre e zinco. Os achados clínicos e histopatológicos verificados nos três surtos estudados foram característicos de ataxia enzoótica. Nos surtos estudados, a frequência da ataxia enzoótica foi maior em cabritos (52) do que em cordeiros (39). Nos caprinos os valores médios de cobre sérico (0,05mg/kg) e hepático (2,48mg/kg) do PS e SS encontravam-se muito abaixo dos respectivos valores de referência, sendo 12 vezes menor em relação aos níveis séricos e oito vezes menor em relação aos teores hepáticos. Já os ovinos do TS apresentavam valores médios de cobre sérico (0,015mg/kg) reduzidos cerca de 40 vezes. Os teores de ferro e enxofre encontravam-se elevados nas forragens da propriedade onde ocorreu o SS, já no solo, os níveis de ferro apresentavam-se elevados e os de cobre reduzidos. O tratamento testado nos cabritos e borregos neonatos, com duas administrações individualizadas com solução de sulfato de cobre, por via oral, na dose de 20mg/kg para ovinos e 35mg/kg para caprinos, na primeira e segunda semana de vida, foi eficaz na prevenção da ataxia enzoótica nos neonatos e pode ser utilizado para controle emergencial da doença. Comprovou-se pela primeira vez na Bahia a ocorrência da ataxia enzoótica (forma congênita e tardia) em caprinos e ovinos. Ressalta-se ainda que, esta doença causada por deficiência de cobre, tem cursado com grandes prejuízos aos criadores de pequenos ruminantes, sobretudo, devido à alta mortalidade dos animais acometidos.(AU)

Asunto(s)

RESUMEN

The objective of this study was to describe for the first time the clinical-epidemiological, laboratory and pathological aspects of different forms of enzootic ataxia in goats and lambs in the state of Bahia, as well as to propose an emergency oral treatment with copper sulfate in an individualized way for neonates. Three outbreaks of enzootic ataxia were studied. The history, clinical signs and epidemiological data were obtained from the owners and checked during the visits. The first outbreak (FO) occurred in 2013 in a property located in the municipality of Itaberaba and affected a herd composed of 90 goats and 130 sheep. The second outbreak (SO) occurred in 2014 in the municipality of Santa Luz and affected a herd of 90 goats and 110 sheep. The third outbreak (TO) occurred in 2018, in a property located in the same municipality of the SO, being the herd constituted by 80 sheep. Samples of blood were collected from all goats and sheep treated for serum copper dosage. Nine animals (five goats and four sheep) that presented a more severe clinical picture and unfavorable prognosis were necropsied for diagnostic confirmation. During the necropsy of the FO, SO and TO animals, liver samples were collected for copper dosage as well as fragments of several organs for histopathology. At the site where the SO occurred, samples of soil and the main forages where the animals were kept were collected to determine copper, iron, molybdenum, sulfur and zinc contents. The clinical and histopathological findings in the three outbreaks studied were characteristic of enzootic ataxia. In the outbreaks studied, the frequency of enzootic ataxia was higher in goats (52) than in lambs (39). In the goats the mean values of serum copper (0.05mg/kg) and hepatic (2.48mg/kg) of the FO and SO were well below their respective reference values, 12 times lower than serum levels and eight times lower in relation to liver contents. On the other hand, TO sheep presented mean values of serum copper (0.015mg/kg) reduced by 40 times. The levels of iron and sulfur were high in the fodder of the property where the SO occurred, already in the soil, iron levels were high and copper levels were reduced. The treatment tested in neonates and lambs with two doses of copper sulphate solution orally at a dose of 20mg/kg for sheep and 35mg/kg for goats during the first and second week of life was effective in prevention of enzootic ataxia in neonates and can be used for emergency control of the disease. The occurrence of enzootic ataxia (congenital and late form) in goats and sheep was first reported in Bahia. It is also worth noting that this disease caused by copper deficiency has caused great damage to the breeders of small ruminants, mainly due to the high mortality of the animals affected.(AU)

Objetivou-se com esse estudo descrever pela primeira vez os aspectos clínico-epidemiológicos, laboratoriais e patológicos de diferentes formas de ataxia enzoótica em cabritos e borregos no estado da Bahia, bem como propor um tratamento oral emergencial com sulfato de cobre de forma individualizada para neonatos. Foram estudados três surtos de ataxia enzoótica. O histórico, sinais clínicos e dados epidemiológicos foram obtidos com os proprietários e verificados durantes as visitas técnicas. O primeiro surto (PS) ocorreu em 2013 em uma propriedade localizada no município de Itaberaba e acometeu um rebanho composto por 90 caprinos e 130 ovinos. O segundo surto (SS) aconteceu em 2014 no município de Santa Luz e afetou um rebanho formado por 90 caprinos e 110 ovinos. O terceiro surto (TS) ocorreu 2018, em uma propriedade localizada no mesmo município do SS, sendo o rebanho constituído por 80 ovinos. Amostras de sangue foram colhidas de todos os caprinos e ovinos atendidos, para dosagem de cobre sérico. Nove animais (cinco caprinos e quatro ovinos) que apresentavam quadro clínico mais grave e prognóstico desfavorável foram necropsiados para confirmação diagnóstica. Durante a necropsia dos animais do PS, SS e TS amostras de fígado foram coletadas para dosagem de cobre, bem como amostras de diversos órgãos para exame histopatológico. Na propriedade onde ocorreu o SS, foram coletadas amostras de solo e das principais forragens onde os animais eram mantidos, a fim de se determinar os teores de cobre, ferro, molibdênio, enxofre e zinco. Os achados clínicos e histopatológicos verificados nos três surtos estudados foram característicos de ataxia enzoótica. Nos surtos estudados, a frequência da ataxia enzoótica foi maior em cabritos (52) do que em cordeiros (39). Nos caprinos os valores médios de cobre sérico (0,05mg/kg) e hepático (2,48mg/kg) do PS e SS encontravam-se muito abaixo dos respectivos valores de referência, sendo 12 vezes menor em relação aos níveis séricos e oito vezes menor em relação aos teores hepáticos. Já os ovinos do TS apresentavam valores médios de cobre sérico (0,015mg/kg) reduzidos cerca de 40 vezes. Os teores de ferro e enxofre encontravam-se elevados nas forragens da propriedade onde ocorreu o SS, já no solo, os níveis de ferro apresentavam-se elevados e os de cobre reduzidos. O tratamento testado nos cabritos e borregos neonatos, com duas administrações individualizadas com solução de sulfato de cobre, por via oral, na dose de 20mg/kg para ovinos e 35mg/kg para caprinos, na primeira e segunda semana de vida, foi eficaz na prevenção da ataxia enzoótica nos neonatos e pode ser utilizado para controle emergencial da doença. Comprovou-se pela primeira vez na Bahia a ocorrência da ataxia enzoótica (forma congênita e tardia) em caprinos e ovinos. Ressalta-se ainda que, esta doença causada por deficiência de cobre, tem cursado com grandes prejuízos aos criadores de pequenos ruminantes, sobretudo, devido à alta mortalidade dos animais acometidos.(AU)

Asunto(s)

RESUMEN

ABSTRACT: The objective of this study was to describe for the first time the clinical-epidemiological, laboratory and pathological aspects of different forms of enzootic ataxia in goats and lambs in the state of Bahia, as well as to propose an emergency oral treatment with copper sulfate in an individualized way for neonates. Three outbreaks of enzootic ataxia were studied. The history, clinical signs and epidemiological data were obtained from the owners and checked during the visits. The first outbreak (FO) occurred in 2013 in a property located in the municipality of Itaberaba and affected a herd composed of 90 goats and 130 sheep. The second outbreak (SO) occurred in 2014 in the municipality of Santa Luz and affected a herd of 90 goats and 110 sheep. The third outbreak (TO) occurred in 2018, in a property located in the same municipality of the SO, being the herd constituted by 80 sheep. Samples of blood were collected from all goats and sheep treated for serum copper dosage. Nine animals (five goats and four sheep) that presented a more severe clinical picture and unfavorable prognosis were necropsied for diagnostic confirmation. During the necropsy of the FO, SO and TO animals, liver samples were collected for copper dosage as well as fragments of several organs for histopathology. At the site where the SO occurred, samples of soil and the main forages where the animals were kept were collected to determine copper, iron, molybdenum, sulfur and zinc contents. The clinical and histopathological findings in the three outbreaks studied were characteristic of enzootic ataxia. In the outbreaks studied, the frequency of enzootic ataxia was higher in goats (52) than in lambs (39). In the goats the mean values of serum copper (0.05mg/kg) and hepatic (2.48mg/kg) of the FO and SO were well below their respective reference values, 12 times lower than serum levels and eight times lower in relation to liver contents. On the other hand, TO sheep presented mean values of serum copper (0.015mg/kg) reduced by 40 times. The levels of iron and sulfur were high in the fodder of the property where the SO occurred, already in the soil, iron levels were high and copper levels were reduced. The treatment tested in neonates and lambs with two doses of copper sulphate solution orally at a dose of 20mg/kg for sheep and 35mg/kg for goats during the first and second week of life was effective in prevention of enzootic ataxia in neonates and can be used for emergency control of the disease. The occurrence of enzootic ataxia (congenital and late form) in goats and sheep was first reported in Bahia. It is also worth noting that this disease caused by copper deficiency has caused great damage to the breeders of small ruminants, mainly due to the high mortality of the animals affected.

RESUMO: Objetivou-se com esse estudo descrever pela primeira vez os aspectos clínico-epidemiológicos, laboratoriais e patológicos de diferentes formas de ataxia enzoótica em cabritos e borregos no estado da Bahia, bem como propor um tratamento oral emergencial com sulfato de cobre de forma individualizada para neonatos. Foram estudados três surtos de ataxia enzoótica. O histórico, sinais clínicos e dados epidemiológicos foram obtidos com os proprietários e verificados durantes as visitas técnicas. O primeiro surto (PS) ocorreu em 2013 em uma propriedade localizada no município de Itaberaba e acometeu um rebanho composto por 90 caprinos e 130 ovinos. O segundo surto (SS) aconteceu em 2014 no município de Santa Luz e afetou um rebanho formado por 90 caprinos e 110 ovinos. O terceiro surto (TS) ocorreu 2018, em uma propriedade localizada no mesmo município do SS, sendo o rebanho constituído por 80 ovinos. Amostras de sangue foram colhidas de todos os caprinos e ovinos atendidos, para dosagem de cobre sérico. Nove animais (cinco caprinos e quatro ovinos) que apresentavam quadro clínico mais grave e prognóstico desfavorável foram necropsiados para confirmação diagnóstica. Durante a necropsia dos animais do PS, SS e TS amostras de fígado foram coletadas para dosagem de cobre, bem como amostras de diversos órgãos para exame histopatológico. Na propriedade onde ocorreu o SS, foram coletadas amostras de solo e das principais forragens onde os animais eram mantidos, a fim de se determinar os teores de cobre, ferro, molibdênio, enxofre e zinco. Os achados clínicos e histopatológicos verificados nos três surtos estudados foram característicos de ataxia enzoótica. Nos surtos estudados, a frequência da ataxia enzoótica foi maior em cabritos (52) do que em cordeiros (39). Nos caprinos os valores médios de cobre sérico (0,05mg/kg) e hepático (2,48mg/kg) do PS e SS encontravam-se muito abaixo dos respectivos valores de referência, sendo 12 vezes menor em relação aos níveis séricos e oito vezes menor em relação aos teores hepáticos. Já os ovinos do TS apresentavam valores médios de cobre sérico (0,015mg/kg) reduzidos cerca de 40 vezes. Os teores de ferro e enxofre encontravam-se elevados nas forragens da propriedade onde ocorreu o SS, já no solo, os níveis de ferro apresentavam-se elevados e os de cobre reduzidos. O tratamento testado nos cabritos e borregos neonatos, com duas administrações individualizadas com solução de sulfato de cobre, por via oral, na dose de 20mg/kg para ovinos e 35mg/kg para caprinos, na primeira e segunda semana de vida, foi eficaz na prevenção da ataxia enzoótica nos neonatos e pode ser utilizado para controle emergencial da doença. Comprovou-se pela primeira vez na Bahia a ocorrência da ataxia enzoótica (forma congênita e tardia) em caprinos e ovinos. Ressalta-se ainda que, esta doença causada por deficiência de cobre, tem cursado com grandes prejuízos aos criadores de pequenos ruminantes, sobretudo, devido à alta mortalidade dos animais acometidos.