Comparison of lidocaine, levobupivacaine or ropivacaine for distal paravertebral thoracolumbar anesthesia in ewes.

OBJECTIVE: To compare the effects of lidocaine, levobupivacaine, or ropivacaine on the onset time and duration of anesthesia of the flank of ewes, using the distal paravertebral thoracolumbar approach. STUDY DESIGN: Randomized experimental study. ANIMALS: Twenty-six healthy mixed-breed ewes (46 ± 3.1 kg). METHODS: Thoracolumbar paravertebral nerve blocks were performed using the distal approach in sheep for ruminal fistulation. The 13th thoracic (T13), first lumbar (L1) and second lumbar (L2) nerves were infiltrated with 2% lidocaine (group GLI, n = 9), 0.5% levobupivacaine (group GLE, n = 8) or 0.5% ropivacaine (group GRO, n = 9); 1.5 mL on the dorsal branch and 2.5 mL on the ventral branch, total volume of 12 mL per ewe. Anesthesia onset time and duration were assessed by application of superficial and deep pin pricks, and skin clamping with a hemostat. Heart rate, respiratory rate, rectal temperature and systemic arterial pressures were recorded prior to nerve block (T0), after the anesthetic agent injection and onset time (T1) and predetermined time points during the surgical procedure (T2-T6). RESULTS: Incomplete nerve blocks were present in five of the 26 ewes enrolled in the study and they were not included in the statistical analyzes. Onset times in GLI, GLE and GRO were 1.5 ± 0.5, 3.1 ± 1.5 and 2.1 ± 0.8 minutes, respectively, with GLE significantly longer than GLI. The durations of anesthesia for GLI, GLE and GRO were 80 ± 27, 649 ± 68 and 590 ± 40 minutes, respectively, with the duration of GLI significantly shorter than GLE and GRO. There were no clinically important changes in cardiopulmonary variables. CONCLUSION AND CLINICAL RELEVANCE: Administration of levobupivacaine and ropivacaine at the distal paravertebral site to block nerves T13, L1 and L2 produced a longer duration of anesthesia of the ewe's flanks compared with lidocaine.

Primary Photosensitization by Chamaecrista serpens in Santa Inês Sheep.

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.

Hepatogenous photosensitization in ruminants and horses caused by the ingestion of Chamaecrista serpens in Brazil.

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.

Toxicity of the different vegetative stages of Amorimia pubiflora to sheep.

Toxic plants containing monofluoroacetate (MFA) cause sudden death in livestock in Australia, South Africa and Brazil, causing economic losses to producers. The objective of this study was to determine the amount of MFA present in young leaves, mature leaves, senescent leaves, and seeds of Amorimia pubiflora harvested at different times of the year and to determine their toxic effect on sheep. Samples of Amorimia pubiflora were collected during April, August and December of 2015 and March of 2016, separated according to the vegetative stage (young leaves, seeds, mature leaves, and senescent leaves), dried in an oven, and administered in daily doses of 5 g/kg/body weight (bw) of fresh leaves to sheep through ruminal cannulae. The experiment was divided into four stages according to the time of collection of the plant so that each sheep received a different vegetative stage of the plant (young leaves, mature leaves, and senescent leaves). Only in the second stage of the experiment was it possible to collect A. pubiflora seeds, which were administered using the same method used for the administration of the leaves. The sheep were dosed with the plant until they showed clinical signs of toxicosis or until the plant was no longer available. Aliquots of leaves and seeds of A. pubiflora were analyzed for MFA concentration. The seeds and young leaves had higher concentrations of MFA than did the mature (harvested in August and December) and senescent (harvested in December) leaves. However, all vegetative stages of the plant were toxic and caused fatal poisoning. The results of our study showed that A. pubiflora is toxic to sheep even when MFA concentrations are low, demonstrating that the presence of this substance is a risk factor for the occurrence of poisoning. Knowing the toxic principle and its variations allow us to determine the conditions for the occurrence of plant toxicosis as well as possible treatment, control, and prophylaxis methods, contributing significantly to the reduction of economic losses on farms due to plant poisoning.

Experimental poisoning by Vernonia rubricaulis in sheep.

In order to evaluate the susceptibility of sheep to V. rubricaulis and to establish the clinical signs, serum biochemistry, and pathological findings, eight sheep were fed varying doses of V. rubricaulis. The onset of clinical signs occurred 6-48 h after the ingestion of V. rubricaulis. Clinical courses lasted 6-56 h after the ingestion of the plant. Serum activities of aspartate aminotransferase, gamma-glutamyl transferase, and alkaline phosphatase were highly elevated and glucose blood levels were low in affected sheep. Clinical signs consisted of apathy, anorexia, dry muzzle, respiratory distress, abdominal pain, and mushy feces with streaks of blood and mucus. Two sheep had neurological signs including muscle fasciculation, nystagmus, paddling movements, and blindness. Liver necrosis could be detected antemortem through liver biopsy. Five sheep died and three recovered. The liver was affected in all necropsied sheep; it increased in volume and had marked accentuation of the lobular pattern with red, depressed areas intercalated with a pale yellow network. Ascites and hydropericardium were consistent findings. Microscopically, centrilobular to massive coagulative necrosis was observed. Coagulative necrosis was also observed in a few proximal renal tubules. Microscopic lesions were not found in any other organs. The severity of liver lesions was proportional to the dose. Chemical analysis to detect carboxyatractyloside in V. rubricaulis plant material was negative. It is concluded that V. rubricaulis poisoning in sheep is clinically, biochemically, and pathologically characteristic of an acute hepatoxicosis.

Enterolobium contortisiliquum is a cause of acute ruminal acidosis in sheep.

The ingestion of pods of Enterolobium contortisiliquum is associated with digestive disturbances, photosensitivity and abortion in domestic ruminants. This experiment was designed to test the hypothesis that digestive disturbances in this toxicosis are really caused by acute ruminal acidosis. Three sheep fed large doses (10-15 g/kg/body weight [bw]) of E. contortisiliquum pods developed ruminal acidosis and were treated with sodium bicarbonate to try to control this metabolic disturbance, thus providing additional evidence of the involvement of ruminal acidosis in the pathogenesis of toxicosis. Two of the sheep died, and one recovered after treatment. In the two sheep that developed severe signs of ruminal acidosis, the values of blood lactate were 18 mg/dL and 196.88 mg/dL, indicating metabolic acidosis as the cause of death. Additionally, four sheep developed elevated serum levels of aspartate aminotransferase and gamma glutamyl transferase, indicating that the pods had hepatotoxic effects. Necropsy findings included the accentuation of the hepatic lobular pattern and multiple focally extensive red areas in the rumen mucosa and on the surface of the liver. Repeated ingestion of small doses induced tolerance but did not induce cumulative effects. Histopathologically, the epithelial mucosa of the rumen and reticulum exhibited swollen and vacuolated epithelia with intraepithelial pustules. Focal ulceration of the mucosa was also observed. Multifocal vacuolar degeneration of hepatocytes and scattered individual hepatocellular necrosis were evident in the liver. We concluded that the main clinical manifestation of intoxication by E. contortisiliquum pods in sheep was acute ruminal lactic acidosis and metabolic acidosis. Ingestion of repeated sublethal doses could stimulate proliferation of the ruminal fauna that degrades the sugar present in the pods, and thereby prevent the occurrence of ruminal acidosis. The plant is also hepatotoxic, and no abortions were observed.

Ingestion of the pods of Enterolobium contortisiliquum causes hepatogenous photosensitization in cattle.

Enterolobium contortisiliquum (Leg. Mimosoidae) is reported as a poisonous plant related to photosensitization and photodermatitis, digestive disturbs and abortion. To date, the clinical and pathological features of photosensitization has not been reproduced or only reproduced associated with very mild presentations. The objective of this study was to reproduce in cattle the clinicopathological features of photosensitization associated with the ingestion of the pods of E. contortisiliquum. The pods were harvested from a property with a history of an ongoing outbreak of photosensitization and abortion in cattle. Six 24-month-old steers were cannulated and used in the experiment, two of them served as negative controls. E. contortisiliquum pods were administered to four steers through ruminal cannula. In the first phase of the experiment, daily doses of 30 g/kg/body weight (bw) and 20 g/kg/bw were administered to Bovines 1 and 2 respectively, for three consecutive days. In the second phase, starting four days after the last daily feeding of the pods, these two bovines were challenged with the same doses of the pods for three consecutive days and another two steers (Bovines 3 and 4) were fed 15 g/kg/bw each for three consecutive days. In the two phases, the steers developed signs compatible with ruminal acidosis which were more severe during the second phase. Three and five days after the administration of the pods, two steers presented photodermatitis characterized by hyperemia and edema on the skin of the dorsum of the neck, of the shaved skin around the cannula, of muzzle and ear. Lesions evolved to dermal necrosis with sloughing and subsequent scar retraction and dermal thickening. Ulceration of mucosae exposed to sunlight was also observed. All the steers which received the pods had significant elevations in the serum activities of gamma-glutamyl transferase (GGT) and aspartate aminotransferase (AST). The levels of GGT and AST remained elevated for up to 12 days after the administration of the pods was discontinued. Histopathological hepatic changes detected by liver biopsies were hepatocellular swelling and randomly scattered individual hepatocellular necrosis. The current study presents solid experimental evidence that the ingestion of E. contortisiliquum definitely induces the classical lesions of hepatogenous photosensitization in cattle.

Accidental monensin poisoning in buffaloes in Bahia, Brazil / Intoxicação acidental por monensina em búfalos na Bahia, Brasil

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)

Accidental monensin poisoning in buffaloes in Bahia, Brazil / Intoxicação acidental por monensina em búfalos na Bahia, Brasil

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.

Accidental monensin poisoning in buffaloes in Bahia, Brazil

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.

Cattle diseases in Mato Grosso do Sul, Brazil: a 24-year survey (1995-2018) / Doenças de bovinos em Mato Grosso do Sul, Brasil: uma pesquisa de 24 anos (1995-2018)

We reviewed the records of 5,083 cattle necropsies performed from January 1995 to December 2018 and filed at the Laboratory of Anatomic Pathology (LAP) of the "Universidade Federal de Mato Grosso do Sul" (UFMS). These necropsies were performed either by LAP-UFMS faculty (22.33%) or by field veterinary practitioners (77.67%) who subsequently submitted material for histological evaluation at the LAP-UFMS. Conclusive diagnoses were reached in 46.21% of the protocols (2,349 cases), and approximately 65% of the cases were classified as inflammatory or parasitic diseases, with rabies being the most diagnosed disease (20.82% of total conclusive diagnosis). There were a large number of protocols in which the diagnosis was of nonsuppurative meningoencephalitis of unknown cause (NSMUC). Those were the main differentials for rabies and bovine herpesvirus-5 necrotizing meningoencephalitis (NME); that is, the number of rabies cases may be even higher if one considers that many cases of NSMUC might be undiagnosed rabies cases. Toxic and toxic-infectious diseases were the second most prevalent category, and botulism cases represented 41% of this category. The other categories corresponded to less than 20% of the total diagnoses and were distributed in decreasing order of frequency as degenerative diseases (9.79%), diseases caused by physical agents (3.87%), other diseases (2.13%), neoplasms and tumor-like lesions (1.79%), metabolic or nutritional disorders (1.75%) and congenital malformations (0.64%). The large number of inconclusive diagnoses was mainly due to improper conditions of mailed-in material for histopathological evaluation, namely, nonrepresentative samples of all organs, autolysis, and the absence of epidemiological and clinical-pathological information.(AU)

Em um levantamento sobre doenças de bovinos, revisamos os protocolos de 5.083 necropsias de bovinos realizadas no período de janeiro de 1995 a dezembro de 2018 e arquivados no Laboratório de Anatomia Patológica (LAP) da Universidade Federal de Mato Grosso do Sul (UFMS). Essas necropsias foram realizadas pelos veterinários e professores do LAP-UFMS (22,33%) ou por médicos veterinários de campo (77,67%) que, posteriormente, submeteram ao LAP-UFMS material para avaliação histológica. Diagnósticos foram conclusivos em 46,21% dos casos protocolados (2349), e aproximadamente 65% deles foram classificados como doenças inflamatórias ou parasitárias, sendo a raiva a doença mais diagnosticada (20,82% dos diagnósticos conclusivos). Havia um grande número de protocolos nos quais o diagnóstico era de encefalite/meningoencefalite não supurativa de causa indeterminada, para o qual os dois principais diferenciais são raiva e meningoencefalite necrosante por herpesvírus bovino; isso sugere que o número de casos de raiva pode ser ainda maior, se considerarmos que muitos destes podem ser casos de raiva não diagnosticados adequadamente. As doenças tóxicas e toxi-infecciosas foram a segunda categoria mais prevalente; dentre elas, os casos de botulismo compuseram 41%. As demais categorias corresponderam a menos de 20% do total de diagnósticos e foram distribuídas em ordem decrescente de frequência, em doenças degenerativas (9,79%), doenças causadas por agentes físicos (3,87%), outras doenças (2,13%), neoplasmas e lesões tumoriformes (1,79%), distúrbios metabólicos ou nutricionais (1,75%) e malformações congênitas (0,64%). O grande número de diagnósticos inconclusivos deveu-se principalmente às condições inadequadas do material enviado ao LAP-FAMEZ para avaliação histopatológica, ou seja, amostras não representativas de todos os órgãos, autolisadas ou acompanhadas de poucas de informações epidemiológicas e clínico-patológicas.(AU)

Healing of brain lesions in sheep recovered from amprolium-induced polioencephalomalacia / Cicatrização das lesões cerebrais em ovinos recuperados de polioencefalomalacia induzida por amprólio

To evaluate the outcome of acute lesions in the brains of sheep that completely clinically recover from acute polioencephalomalacia (PEM), ten sheep were used in this experiment. Eight of those sheep received varying doses of amprolium to induce PEM. Four sheep were treated intramuscularly with 40mg/kg/body weight with thiamine to allow recovery and four sheep were left untreated. Two control sheep did not receive either amprolium or thiamine and were kept along with the other eight sheep for the duration of the experiment. Except for the two drugs, the diet and water source were the same for the ten sheep. Two sheep receiving high daily doses of amprolium and one sheep receiving a lower dose had acute deaths and developed acute brain lesions consisting of neuronal laminar cortical necrosis (red neurons), edema, reactive astrocytes, swollen endothelial cells and gitter cells infiltration. Four sheep that recovered from lower doses of amprolium-induced PEM after being treated with thiamine and another one that recovered spontaneously were euthanatized six months after clinical recovery and had gross changes consisting of segmental absence of cortical tissue. Histologically these segmental cortex-deprived areas corresponded to quasi-empty spaces where only vessels and gitter cells existed. No changes were seen in the brains of the two control sheep.(AU)

Para avaliar a evolução das lesões agudas no cérebro de ovinos que se recuperam clinicamente de polioencefalomalacia aguda (PEM), dez ovinos foram usados neste experimento. Oito desses ovinos receberam doses variáveis de amprólio para induzir PEM. Quatro ovinos foram tratados intramuscularmente com 40mg/kg/peso corporal de tiamina para permitir a recuperação, e outros quatro ficaram sem tratamento. Dois ovinos controles não receberam amprólio nem tiamina e foram mantidos com os outros oito ovinos durante a duração do experimento. Exceto pelas duas drogas, a dieta e a fonte de água eram as mesmas para os dez ovinos. Dois ovinos que receberam doses diárias altas de amprólio, e um que recebeu doses menores, tiveram mortes agudas e desenvolveram lesões cerebrais constituídas por necrose neuronal laminar cortical (neurônios vermelhos), edema, tumefação de células endoteliais, astrócitos reativos, tumefação de células endoteliais e infiltração por células gitter. Quatro ovinos que se recuperam da PEM induzida por amprólio, após tratamento com tiamina, e outro que se recuperou espontaneamente, permaneceram clinicamente normais e foram submetidos a eutanásia seis meses após a recuperação clínica. Na necropsia, apresentavam alterações macroscópicas caracterizadas por ausência segmentar de tecido corticocerebral. Histologicamente, essas áreas privadas de tecido cortical consistiam de espaços praticamente vazios onde apenas vasos e células gitter eram vistos. Não foram encontradas alterações no encéfalo das duas ovelhas controle.(AU)

Economic impact of an outbreak of botulism in a cattle feedlot / Impacto econômico de um surto de botulismo em confinamento de bovinos

Botulism is a febrile disease, fatal in most cases, which affects the muscles of locomotion, chewing, and swallowing, as well as the diaphragm and intercostal muscles, causing flaccid paralysis and respiratory arrest. In bovines, the etiology is due to the ingestion of neurotoxins types C and D formed by the bacterium Clostridium botulinum in an animal or vegetal substance, during decomposition. Vaccination is one of the most effective prophylactic means to prevent this disease. In this study, an outbreak of botulism was evaluated in a feedlot with 6,300 finishing cattle, wherein 25 died as a consequence of contracting this disease. The economic losses resulting from the deaths were analyzed, and economic analysis was conducted, involving the estimated cost of vaccination for the whole herd under risk, with the objective of evaluating whether this prophylactic practice is a viable action plan. The financial loss due to the deaths resulting from botulism in the case studied was found to be R$55,560.00, equivalent to 0.39% of the total monetary value of the herd. The cost of immunizing the entire herd under risk was 14.06% (for toxins exclusive to toxins C and D) and 22.22% (for polyvalent vaccines against clostridiosis) of the financial loss incurred as a consequence of the recorded deaths. It was concluded that botulism is a disease that can cause a significant economic impact on intensive livestock production systems, and that vaccination is an economically viable prophylactic action if performed with adequate sanitary planning.(AU)

O botulismo é uma doença afebril, fatal na maioria dos casos, que afeta os músculos da locomoção, mastigação, deglutição e também o diafragma e os músculos intercostais, causando paralisia flácida e parada respiratória. Nos bovinos a etiologia é devido à ingestão de neurotoxinas tipos C e D previamente formadas pela bactéria Clostridium botulinum em matéria animal ou vegetal em decomposição. A vacinação é um dos meios profiláticos mais eficazes para prevenir esta doença. Neste trabalho, estudou-se um surto de botulismo em um confinamento com 6300 bovinos em terminação, no qual 25 morreram devido a esta doença. Foram analisadas as perdas econômicas em consequência das mortes, e por meio do percentual do prejuízo contabilizado, foi realizada uma análise econômica referente ao custo estimado da vacinação para todo do rebanho sob-risco com o objetivo de avaliar se esta prática profilática é um plano de ação viável. Como resultado, o prejuízo financeiro devido às mortes resultantes do botulismo no caso estudado foi de R$ 55.560,00 o equivalente a 0,39% do valor monetário total do rebanho. O custo da vacinação para imunizar todo o rebanho sob-risco foi equivalente a 14,06% (para vacinas exclusivas para toxinas C e D) e 22,22% (para vacinas polivalentes contra clostridioses) relativo ao prejuízo financeiro em consequência dos óbitos registrados. Concluiu-se que o botulismo é uma doença que pode provocar impacto econômico significativo em sistemas de corte intensivos em bovinos, e que, a vacinação é um meio profilático economicamente viável se for realizada por meio de um planejamento sanitário adequado.(AU)

Estimativas de perdas econômicas causadas por reação granulomatosa local após uso de vacina oleosa contra febre aftosa em bovinos de Mato Grosso do Sul / Estimates of economic losses caused by local granulomatous reaction after use of an oily vaccine against FMD in cattle of Mato Grosso do Sul

Lesões exacerbadas à vacina contra a febre aftosa foram observadas em 1.815 de um total de 5.000 bovinos abatidos em frigorífico com inspeção federal. Essas lesões resultaram na condenação de parte das carcaças de acordo com o Regulamento da Inspeção Industrial e Sanitária de Produtos de Origem Animal. Os bovinos haviam sido vacinados em maio de 2012 e abatidos em setembro do mesmo ano e divididos em Lotes 1 e 2 constituídos respectivamente por 1.500 e 315 bovinos. As lesões de reação vacinal eram caracterizadas por nódulos protuberantes, circunscritos, bem delimitados, firmes e de tamanhos variáveis, distribuídos multifocalmente na musculatura do aspecto lateral do pescoço; ao corte apresentavam exsudato purulento. Amostras da lesão de 28 bovinos foram avaliadas histologicamente e os principais achados foram piogranulomas com espaços claros circulares de tamanhos variados no centro, circundados por intenso infiltrado de neutrófilos íntegros e necróticos, circundados por macrófagos epitelioides com citoplasma vacuolizado, ocasionais células gigantes multinucleadas e, mais externamente, por abundante tecido conjuntivo em meio observavam-se linfócitos e plasmócitos. Culturas bacterianas realizadas em amostras do exsudato da lesão de seis bovinos resultaram negativas. Quando as carcaças afetadas foram submetidas ao toalete foi retirado em média 1,8 e 2,0 kg de músculo da área afetada, respectivamente dos Lotes 1 e 2. O prejuízo econômico da propriedade de origem dos bovinos afetados foi de R$ 20.424,00, considerando o preço pago pela arroba do boi no mês e ano da ocorrência. Esses valores à época seriam suficientes para adquirir 29,17 bezerros desmamados para engorda. Se considerarmos 5.000 bovinos vacinados forem considerados como população sob risco o coeficiente de morbidade seria de 0,36%. Os resultados deste estudo demonstram que perdas por reação vacinal, mesmo quando não provocam sinais clínicos marcantes, podem ocasionar importantes prejuízos econômicos...

Lesions caused by excessive reaction to foot and mouth vaccine were observed in 1,815 out of 5,000 cattle slaughtered in a slaughterhouse under federal meat inspection. Such lesions resulted in condemnation of the affect parts of the carcasses in accordance with the Brazilian Federal Meat Inspection Regulations. The affected cattle had been vaccinated on May 2012 and then slaughtered in September of the same year. They were allotted to two groups with 1,500 (Groups 1) and 315 cattle (Group 2). Post vaccination lesions were characterized as salient, firm variable sized nodules multifocally distributed in the musculature of the lateral neck. Pus oozed at the cut surface of these nodules. Samples of 28 cattle were submitted for histopathological examination; main findings were pyogranulomas with central variable-sized clear spaces surrounded by marked infiltrate of viable and dead neutrophils, which were surrounded by epithelioid macrophages with vacuolated cytoplasm and occasional multinucleated giant cell. This inflammatory reaction was walled by abundant connective tissue infiltrated by lymphocytes and plasma cells. Samples of the lesion of six cattle were submitted to bacteriological culture with negative results. When affected carcasses went through dressing, there was an average of 1.8 and 2.0 kg of muscle tissue cut off from the carcasses respectively of Group 1 and 2. Economic losses in the farm of origin of the affected cattle was R$ 20,424.00, considering the price paid by kg of cattle for slaughter at the time of the occurrence. This amount at that time was enough to buy 29.17 weaned calves for fattening. If one considers theses 5,000 cattle vaccinated on the farm as the population at risk, the morbidity rate would be 0.36%. These results indicate that the losses due to vaccine reaction, even with no overt clinical signs, may cause important economic losses...

Intoxicação experimental por Simarouba versicolor (Simaroubaceae) em ovinos e indução de resistência ao consumo da planta / Experimental poisoning by Simarouba versicolor (Simaroubaceae) in sheep and induced resistance to consumption of the plant

Simarouba versicolor é uma árvore semidecídua pertencente à família Simaroubaceae. Um surto de intoxicação por S. versicolor em bovinos por brotos da planta presente no pasto em Mato Grosso do Sul e sua reprodução experimental foram descritos. Esse estudo teve por objetivos verificar experimentalmente se os ovinos podem ser utilizados como modelo clínico-patológico no estudo da intoxicação por Simarouba versicolor St. Hil. (fam. Simaroubaceae), determinar se há indução de resistência pela ingestão de pequenas e repetidas doses e, se a planta mantém sua toxicidade quando dessecada. Foram realizados dois experimentos, sendo o primeiro com folhas verdes ou folhas dessecadas e trituradas de S. versicolor em doses únicas de 5g/kg, 5g/kg e 3g/kg a três ovinos (Ovino 1, 2 e 3 respectivamente). O experimento 2, foi realizado com diferentes doses diárias de folhas dessecadas e trituradas de S. versicolor em quatro ovinos que receberam 1,5g/kg, 0,75g/kg, 0,6g/kg e 0,3g/kg e, com um ovino que recebeu 3g/kg como controle positivo (Ovino 4). A administração foi suspensa quando os ovinos apresentaram sinais clínicos da intoxicação. Após doze dias de recuperação, os animais sobreviventes foram desafiados com a mesma dose diária da planta ingerida anteriormente para avaliar o desenvolvimento de resistência. Os sinais clínicos observados nos dois experimentos caracterizaram-se por anorexia, mucosas oculares congestas, polidipsia, sialorreia, fezes pastosas que evoluíram para diarreia líquida fétida esverdeada, decúbito lateral e morte para os Ovinos 1 a 7. As principais lesões histológicas observadas foram necrose do tecido linfoide (linfonodos, baço, placas de Peyer) e enterite necrosante. Com os resultados obtidos, pode-se concluir que os ovinos podem ser utilizados como modelo experimental clínico-patológico na intoxicação por S. versicolor. Com o método utilizado, não houve resistência ao consumo diário de folhas da planta pelos ovinos e, as folhas mantiveram sua toxicidade quando dessecadas.(AU)

Simarouba versicolor St. Hil. is a semideciduous tree belonging to the Simaroubaceae family. An outbreak of poisoning in cattle by shoots of S. versicolor present in the pasture in Mato Grosso do Sul and experimental reproduction of the poisoning was described. This study aimed to verify experimentally whether sheep could be used as a clinical-pathological model in the study of the poisoning caused by S. versicolor, to determine if there develops resistance induced by ingestion of small and repeated doses of the leaves, and if the plant keeps its toxicity when dried. Two experiments were conducted: Experiment 1 with green leaves or dried and powdered leave of S. versicolor, given in single doses of 5g/kg, 5g/kg and 3g/kg to three sheep (Sheep 1, 2 and 3 respectively). Experiment 2 was made with different daily doses of dried and powdered leaves of S. versicolor; to four sheep was given 1.5g/kg, 0.75g/kg, 0.6g/kg and 0.3g/kg, and the positive control (Sheep 4) received 3g/kg. The administration was suspended when the animals showed clinical signs of poisoning. After twelve days of recovery, the surviving sheep were challenged with the same daily dose given previously, to assess the development of resistance. Clinical signs observed in both experiments were characterized by anorexia, congested ocular mucosa, polydipsia, drooling, loose stools which evolved into fetid greenish watery diarrhea, lateral decumbency and death of Sheep 1 to 7. The main histological lesions observed were necrosis of lymphoid tissue (lymph nodes, spleen, Peyer's patches) and necrotizing enteritis. With the results it can be concluded that sheep can be used as experimental model for the clinic-pathological aspects of poisoning by S. versicolor. The method used has not shown resistance to the daily consumption of the plant by the sheep, and the leaves kept their toxicity when dried.(AU)