Vacuolização neuronal e degeneração espinocerebelar em filhote de Rottweiler / Neuronal vacuolation and spinocerebellar degeneration in a Rottweiller puppy

Background: Spinocerebellar degenerations and neuronal vacuolations are alterations characterized by the formation of vacuoles in the nervous tissue, commonly called status spongiosus. This condition occurs in young Rottweiler dogs causing a disease called Neuronal Vacuolation and Spinocerebellar Degeneration. Clinically, it presents with ataxia of the pelvic limbs, which evolves to generalized ataxia, tetraparesis, and laryngeal paralysis. Histologically, spongiform and vacuolar alterations of the neuropil and neurons are highlighted. This reports a case of neuronal vacuolation and spinocerebellar degeneration in a Rottweiler puppy. Case: Necropsy was performed on the cadaver of a 5-month-old Rottweiler bitch that had been presenting with ataxia for approximately 1 month, in addition to dyspnea, pulmonary crepitations, and microphthalmia. Macroscopic evaluation revealed pale ocular and oral mucosae; marked gastric dilatation and abdominal distension; pulmonary hemorrhage and edema; hepatosplenomegaly; fatty degeneration of the liver; and congestion of meningeal blood vessels. Microscopically, histological evaluation of the spinal cord showed an increase in gray matter cellularity with marked presence of oligodendrocytes and microglia cells; moderate to severe multifocal intracytoplasmic micro- and macrovacuoles with displacement of the neurons' nuclei to the periphery of the cell; central chromatolysis of the neurons adjacent to neurons affected by vacuolation; and mild multifocal necrosis associated with mild multifocal neuronophagia. The white matter exhibited discrete digestion chambers, in addition to marked diffuse congestion of the leptomeninges. In the cerebellum, neurons in the nerve nuclei (emboliform, globose, and fastigial) showed moderate multifocal vacuoles in the cytoplasm, whereas adjacent neurons showed central chromatolysis, necrosis, and mild neuronophagia. Additional histological findings included lymphoid hyperplasia, fatty degeneration of the liver, pulmonary edema, and pulmonary hemorrhage. Discussion: Spongiform and degenerative encephalopathies are diseases recognized worldwide, mainly in cattle and sheep. However, the identification of these changes in new species has led to the need for further investigations. In dogs, the first reports occurred in 1995 and 1997 in Rottweiler animals. This disease affects young dogs, and although its pathogenesis is not completely known, it is believed to be associated with a genetic mutation in the RAB3GAP1 gene. Clinically, it is associated with clinical neurological manifestations, including progressive ataxia of the pelvic limbs, changes in spinal reflex, disordered proprioceptive reactions, laryngeal paralysis, as well as behavioral and gait alterations. In the clinical evaluation, leukoencephalomyelopathy and neuroaxonal dystrophy should be diseases considered as possible differential diagnoses, as they present with similar alterations. However, in histological evaluation, the exclusion of both is basically due to the absence of neuronal vacuolization. Unfortunately, the definitive diagnosis is only made post mortem, through a histopathological evaluation of the nervous tissue. Because it is a disease whose pathogenesis is little known and which shows signs of having a genetic character, histopathological examination for diagnostic purposes in young animals with neurological signs is of great importance.

Er-Bai-Tang decoction improved the movement disorders and neuronal injury in the Parkinson's disease model rats via decreasing p38 MAPK pathway and improving the composition of intestinal flora

Purpose: Our previous study showed that Er-Bai-Tang decoction (EBT) could effectively improve Parkinson's disease (PD) patients' quality of life, sleep, mood, and cognitive disorders, but the mechanism of EBT to treat PD was unclear. So, our study aimed to explore the mechanism of EBT to treat PD via p38 mitogen-activated protein kinases (MAPK) pathway and intestinal flora. Methods: In our study, the PD rat model was established by subcutaneously injecting 2 mg/kg/d rotenone solution, and 23.43 g/kgEBT was used to treat PD model rats. Results: Behavioral test showed that EBT could reverse the motor impairment in the PD model rats. Hematoxylin and eosin result showed that EBT could reduce the cell necrosis in the SNpc area of the PD model rats. Western blotting and real time-polymerase chain reaction showed that EBT could decrease the p38 MAPK expression in the SNpc area of the PD model rats. 16s rRNA sequencing analysis showed that EBT could improve the composition of intestinal flora in the PD model rats. Rikenellaceae at family level and Alistipes and Allobaculum at the genus level were the key species in the PD development and EBT treatment to PD. KEGG showed that EBT might change the iron uptake in PD rats. Conclusions: EBT could improve the motor symptoms and neuronal injury in the PD model rat, and its mechanism may be related to decreasing p38 MAPK pathway and improving the composition of intestinal flora.

Copper deficiency in dairy goats and kids / Deficiência de cobre em cabras leiteiras e cabritos

The clinical, pathological and reproductive aspects of an outbreak of copper deficiency in dairy goats and kids from the semiarid region of Pernambuco, Brazil are described. Ten adult dairy goats with clinical signs of deficiency and four kids presenting enzootic ataxia born from copper deficient does were separated from the herd, and examined. In the dairy goats, the average serum concentration of copper was 6.1±2.8mmol/L and iron was 39.5±8.2mmol/L. In kids, the average serum concentration of copper was 3.8±0.9mmol/L and iron was 38.5±4.1mmol/L. Clinical signs in dairy goats consisted of pale mucous membranes, anemia, emaciation, diarrhea, achromotrichia, brittle hair and alopecia. The main reproductive alterations consisted of prolonged anestrus, embryonic resorption and high indices of retained placenta. The kids born from copper deficient dairy goats were weak, and presented neonatal or late ataxia until 70 days of life. Six dairy goats and four kids were necropsied. Most ovaries examined were small, firm and did not present viable follicles on their surface. Microscopically, there was reduction of viable follicles in addition to disorganization of follicular and stromal structures, with marked follicular atresia. Microscopically, changes in kids with enzootic ataxia consisted of neuronal chromatolysis and axonal degeneration, mainly in neurons of the spinal cord. In this study, the source of high iron was not identified, but it is known that outbreaks of copper deficiency can occur due to excess iron intake, mainly when adequate mineral supplementation is not provided for the goat herds.

Descrevem-se os aspectos clínicos, patológicos e reprodutivos de um surto de deficiência de cobre em cabras leiteiras e em cabritos da região semiárida de Pernambuco, Brasil. Dez cabras leiteiras adultas com sinais clínicos de deficiência de cobre e quatro cabritos com ataxia enzoótica nascidos dessas cabras foram separados do rebanho e examinados. Nas cabras leiteiras, a concentração média de cobre sérico foi de 6,1±2,8mmol/L e a concentração média de ferro sérico foi de 39,5±8,2mmol/L. Nos cabritos, a concentração média de cobre sérico foi de 3,8±0,9mmol/L e a concentração média de ferro sérico foi de 38,5±4,1mmol/L. Os sinais clínicos nas cabras consistiram em mucosas pálidas, anemia, diarreia, acromotriquia, pelos opacos e quebradiços e alopecia. As principais alterações reprodutivas consistiram em anestro prolongado, reabsorção embrionária e aumento da taxa de retenção de placenta. Os cabritos nascidos vivos dessas cabras nasceram fracos, com ataxia neonatal ou desenvolveram ataxia tardia em até 70 dias de vida. Seis cabras leiteiras e quatro cabritos foram necropsiados. Nas cabras, a maioria dos ovários examinados macroscopicamente eram pequenos, firmes e não apresentavam folículos viáveis em sua superfície. Microscopicamente, houve redução de folículos viáveis, além de desorganização das estruturas foliculares, com marcada atresia folicular. Macroscopicamente não foram observadas alterações nos cabritos com ataxia enzoótica. As lesões histológicas observadas nesses cabritos consistiram em cromatólise neuronal e degeneração axonal, principalmente em neurônios da medula espinhal. Neste estudo a fonte dos altos teores de ferro no soro não foi identificada, mas sabe-se que surtos de deficiência de cobre podem ocorrer devido ao excesso de ingestão de ferro, principalmente quando não é fornecida suplementação mineral adequada para os rebanhos caprinos.

Intravitreal injection of peptides PnPa11 and PnPa13, derivatives of Phoneutria nigriventer spider venom, prevents retinal damage

PnPa11 and PnPa13 are synthetic peptides derived from Phoneutria nigriventer spider venom, which display antinociceptive and neuroprotective properties. In this work, we evaluated the safety of intravitreal use and the neuroprotective effect of these peptides. Methods: The cytotoxicity and the antiangiogenic activity of these peptides were evaluated by the sulforhodamine-B method and chicken chorioallantoic membrane (CAM) assay, respectively. The in vivo safety was analyzed in Wistar rats that were intravitreally injected with different doses (0.50; 1.25; 2.50; 3.75 and 5.00 µg/mL) of these peptides (right eye, n = 6). The retinal function was assessed by electroretinography exams (ERG), intraocular pressure (IOP), and histological analyzes. In order to investigate the neuroprotective effect, Wistar rats received intravitreal injections (right eye, n = 6) of peptides at 1.25 µg/mL and then were exposed to blue LED light. In addition, the visual function and the retinal microstructure were verified. Results: Cytotoxicity analyses demonstrated that the peptides did not present any toxicity over ARPE-19 (adult retinal pigmented epithelial) cell line and the antiangiogenic study highlighted that the peptides promoted the reduction of blood vessels. The intravitreal injection did not cause major changes, neither induced any irreversible damage. In the retinal degeneration assay, the ERG records demonstrated that the prior treatment with PnPa11 and PnPa13 protected the retina from damage. Morphological analyses confirmed the ERG findings. Immunoblotting analyses revealed that PnPa11 increased Erk1/2, NR2A, and NR2B retinal expression after the light stress model, but did not cause Akt1 activation, while PnPa13 prevented Erk1/2 and Akt1 dephosphorylation. Conclusions: The intraocular administration of these peptides was well tolerated and presented protective activity against retinal degeneration, suggesting the potential use of these peptides as neuroprotectors in the ophthalmological field.(AU)

Viral distribution of Newcastle disease virus genotype VII in different organs of broiler chickens

The poultry industry in Egypt is still threatened by Newcastle disease despite intensive vaccination programs. Bothvaccinated and unvaccinated poultry flocks have experienced Newcastle disease virus (NDV) genotype VII outbreakswithin the last few years. This study was performed to investigate the pathogenesis of NDV genotype VII in differentorgans of broiler chickens. Fifty, 1-day-old chicks were divided into 2 equal groups with 25 animals in each group. Group 1served as the non-infected (negative control) group, while group 2 was infected by intranasal inoculation of 0.1 mlcontaining 106 EID50 of NDV genotype VII. Three chicks were sacrificed from each group at 2, 5, and 10 days postinfection (dpi). Tissue sections from the nasal conchae, larynx, trachea, lungs, heart, kidneys, and brain were collected forhistopathology and immunohistochemistry. Quantitative RT-PCR (qRT-PCR) was also performed on the tracheal samples.The infected group showed severe respiratory signs and had greenish-colored diarrhea. Mortalities were 6, 4, 6, and 2 chicksat 5, 6, 7, and 9 dpi, respectively. Grossly, congestion of the mucosa of the trachea and larynx was recorded at 5 dpi.Histopathological examination of different organs revealed tracheitis, pneumonia, laryngitis, nephritis, brain perivascularcuffing, and neuronal degeneration. NDV antigen was detected by IHC in all examined organs except the brain. Strong viralantigen expression by IHC was observed at 5 and 7 dpi in most of the studied organs. Viral antigen expression was alsodetected in the endothelial cells of blood vessels, cilia, surface epithelium, and goblet cells of the nasal conchae, larynx, andtrachea in addition to the cytoplasm of cardiomyocytes and in the epithelium lining the renal tubules.

Viral distribution of Newcastle disease virus genotype VII in different organs of broiler chickens

The poultry industry in Egypt is still threatened by Newcastle disease despite intensive vaccination programs. Bothvaccinated and unvaccinated poultry flocks have experienced Newcastle disease virus (NDV) genotype VII outbreakswithin the last few years. This study was performed to investigate the pathogenesis of NDV genotype VII in differentorgans of broiler chickens. Fifty, 1-day-old chicks were divided into 2 equal groups with 25 animals in each group. Group 1served as the non-infected (negative control) group, while group 2 was infected by intranasal inoculation of 0.1 mlcontaining 106 EID50 of NDV genotype VII. Three chicks were sacrificed from each group at 2, 5, and 10 days postinfection (dpi). Tissue sections from the nasal conchae, larynx, trachea, lungs, heart, kidneys, and brain were collected forhistopathology and immunohistochemistry. Quantitative RT-PCR (qRT-PCR) was also performed on the tracheal samples.The infected group showed severe respiratory signs and had greenish-colored diarrhea. Mortalities were 6, 4, 6, and 2 chicksat 5, 6, 7, and 9 dpi, respectively. Grossly, congestion of the mucosa of the trachea and larynx was recorded at 5 dpi.Histopathological examination of different organs revealed tracheitis, pneumonia, laryngitis, nephritis, brain perivascularcuffing, and neuronal degeneration. NDV antigen was detected by IHC in all examined organs except the brain. Strong viralantigen expression by IHC was observed at 5 and 7 dpi in most of the studied organs. Viral antigen expression was alsodetected in the endothelial cells of blood vessels, cilia, surface epithelium, and goblet cells of the nasal conchae, larynx, andtrachea in addition to the cytoplasm of cardiomyocytes and in the epithelium lining the renal tubules.(AU)

Epidemiological aspects of natural poisoning by Prosopis juliflora in ruminants in semiarid areas of the state of Bahia, Brazil, invaded by the plant

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.

Epidemiological aspects of natural poisoning by Prosopis juliflora in ruminants in semiarid areas of the state of Bahia, Brazil, invaded by the plant / Aspectos epidemiológicos da intoxicação natural por Prosopis juliflora em ruminantes em áreas do semiárido baiano invadidas pela planta

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)

Wobbly syndrome in an Africa pygmy hedgehog (Atelerix albiventris): neuropathological and immunohistochemical studies / Síndrome de Wobbly em um ouriço pigmeu africano (Atelerix albiventris): estudo neuropatológico e imuno-histoquímico

A three-year-old female African pygmy hedgehog (Atelerix albiventris), born and domiciled in Brazil, presented apathy, prostration, and difficulty to stay standing. Its parents were siblings but did not present clinical signs related to this condition. As its clinical condition worsened, the animal was euthanized and referred for necropsy. No gross lesions were found in the central nervous system (CNS). Histologically, there was vacuolation with axonal degeneration in the white matter of the CNS and in peripheral nervous tissue. The Kluver-Barrera (KB) stain confirmed demyelination in vacuolated areas. Immunohistochemistry using several neural markers confirmed astrocytosis and microgliosis associated with vacuolated areas. In addition, there was a mild decrease in the immuno intensity of myelin proteolipid protein (PLP) in these areas. These results suggest a genetic origin of the present demyelination, which resulted in the wobbly syndrome described in this report.(AU)

Um ouriço pigmeu africano de três anos de idade, nascido e domiciliado no Brasil, apresentou apatia, prostração e dificuldade em permanecer em estação. Os pais deste ouriço eram irmãos, mas não apresentaram sinais clínicos relacionados a esta condição. Com a piora dos sinais clínicos, o animal foi eutanasiado e encaminhado para necropsia. Não foram encontradas lesões macroscópicas no sistema nervoso central (SNC). Histologicamente, havia vacuolização com degeneração axonal na substância branca do SNC e no tecido nervoso periférico. A coloração de Kluver-Barrera (KB) confirmou desmielinização nas áreas vacuolizadas e a imuno-histoquímica utilizando vários marcadores, confirmou astrocitose e microgliose associadas com as áreas de vacuolização. Além disso, houve discreta diminuição da imunointensidade da proteína proteolipídica da mielina (PLP) nessas áreas. Estes resultados sugerem origem genética da desmielinização que resultou na síndrome de wobbly descrita neste relato.(AU)

Intoxicação por chumbo em bovinos mantidos em área de treinamento militar / Lead poisoning in cattle held in a military training area

Background: Lead poisoning is one of the major toxic diseases of cattle. Contamination occurs with ingestion of products containing lead, especially batteries, or through contaminated pastures and water sources. Clinical signs are neurological and necropsy findings and histopathological changes may vary depending on the clinical presentation. Although the disease is widely reported in the literature, there are rare descriptions of intoxication in cattle raised in military training areas. This work describes the epidemiological, clinical and anatomopathological features of an outbreak of lead poisoning in cattle kept in a military artillery training camp.Case: Fifteen cattle out of a herd of sixty 4-6 year-old, mixed breed castrated males were affected. The cattle were held in a 100 ha of native pasture used for military artillery training. After three weeks in this area, the affected cattle had predominantly neurological clinical manifestations, characterized by somnolence, ambulatory incoordination, muscle tremors, bruxism, aimless walking, blindness and decubitus. The clinical course was 24-72 h. Eight of the 15 affected cattle died and two were necropsied. Necropsy finds were non-specific and the histological lesions of both necropsied cattle were restricted to the brain and kidneys. Laminar neuronal necrosis, neuropil vacuolization (spongiosis) and vascular endothelial hypertrophy were observed in the telencephalic cortex. Additionally there was astrocytic degeneration and neuronophagia. There was degeneration and necrosis of renal tubular epithelium and in one bovine there were intranuclear inclusion bodies in the renal epithelial cells; these inclusion bodies were highlighted using both modified Ziehl-Neelsen and periodic acid Schiff (PAS) stains. The levels of lead found in the kidneys and livers of the two necropsied cattle were respectively 51.7 μg/g and 41.00 μg/g for one of the necropsied cattle; and 431μg/g and 39.0 μg/g for the other.[...]

Intoxicação por chumbo em bovinos mantidos em área de treinamento militar / Lead poisoning in cattle held in a military training area

Background: Lead poisoning is one of the major toxic diseases of cattle. Contamination occurs with ingestion of products containing lead, especially batteries, or through contaminated pastures and water sources. Clinical signs are neurological and necropsy findings and histopathological changes may vary depending on the clinical presentation. Although the disease is widely reported in the literature, there are rare descriptions of intoxication in cattle raised in military training areas. This work describes the epidemiological, clinical and anatomopathological features of an outbreak of lead poisoning in cattle kept in a military artillery training camp.Case: Fifteen cattle out of a herd of sixty 4-6 year-old, mixed breed castrated males were affected. The cattle were held in a 100 ha of native pasture used for military artillery training. After three weeks in this area, the affected cattle had predominantly neurological clinical manifestations, characterized by somnolence, ambulatory incoordination, muscle tremors, bruxism, aimless walking, blindness and decubitus. The clinical course was 24-72 h. Eight of the 15 affected cattle died and two were necropsied. Necropsy finds were non-specific and the histological lesions of both necropsied cattle were restricted to the brain and kidneys. Laminar neuronal necrosis, neuropil vacuolization (spongiosis) and vascular endothelial hypertrophy were observed in the telencephalic cortex. Additionally there was astrocytic degeneration and neuronophagia. There was degeneration and necrosis of renal tubular epithelium and in one bovine there were intranuclear inclusion bodies in the renal epithelial cells; these inclusion bodies were highlighted using both modified Ziehl-Neelsen and periodic acid Schiff (PAS) stains. The levels of lead found in the kidneys and livers of the two necropsied cattle were respectively 51.7 μg/g and 41.00 μg/g for one of the necropsied cattle; and 431μg/g and 39.0 μg/g for the other.[...](AU)

Abiotrofia cerebelar em um gato: relato de caso / Cerebellar abiotrophy in a feline: case report

Um caso de abiotrofia cerebelar em um gato com 45 dias de idade foi diagnosticado no Laboratório de Patologia Animal, Hospital Veterinário da Universidade Federal de Campina Grande. O animal apresentava, havia 15 dias, apatia, anorexia, desidratação, ataxia, hipermetria, espasticidade dos membros torácicos e pélvicos, tremores de intenção, nistagmo, opistótono, déficit proprioceptivo e ausência de resposta de ameaça. Clinicamente, havia a suspeita de hipoplasia cerebelar, e, devido ao prognóstico desfavorável, o animal foi eutanasiado. Na necropsia, não foram observadas alterações macroscópicas. Microscopicamente, as lesões estavam restritas ao cerebelo e caracterizavam-se por alterações neurodegenerativas e necróticas, com desaparecimento segmentar dos neurônios de Purkinje. Nessas áreas, também se verificaram espaços em branco, denominado aspecto de cesto vazio, resultantes da perda dos neurônios de Purkinje, além de raros esferoides axonais e proliferação dos astrócitos de Bergmann. Em algumas áreas, a camada granular estava hipocelular e havia moderada gliose multifocal na camada molecular. O diagnóstico de abiotrofia cerebelar foi realizado com base nos dados epidemiológicos, clínicos e, principalmente, pelas alterações histopatológicas dos neurônios de Purkinje características da doença.(AU)

The aim of this report was to describe a case of cerebellar abiotrophy in cat with 45-year-old diagnosed at the Animal Pathology Laboratory, Veterinary Hospital of the Federal University of Campina Grande. The animal had presented 15-day apathy, anorexia, dehydration and neurological signs, characterized by ataxia, hypermetria, spasticity of fore and hindlimbs, intention tremor, nystagmus, opisthotonos, proprioceptive deficits, and absence of threat response. Clinically, cerebellar hypoplasia was suspected and the animal was euthanized due to poor prognosis. During necropsy, gross lesions were not observed. Microscopically the lesions were restricted to the cerebellum and were characterized by neurodegenerative and necrotic damage with segmental disappearance of the Purkinje cells. In these areas, there were also empty spaces, called the empty basket aspect, resulting from the loss of Purkinje cells, as well as rare axonal spheroids and proliferation of Bergmann's astrocytes. In some areas, the granular layer was hypocellular and there was moderate multifocal gliosis in the molecular layer. The diagnosis of cerebellar abiotrophy was based on epidemiological, clinical and mainly on histopathological changes in neurons of Purkinje disease characteristics.(AU)

Abiotrofia cerebelar em um gato: relato de caso / Cerebellar abiotrophy in a feline: case report

Um caso de abiotrofia cerebelar em um gato com 45 dias de idade foi diagnosticado no Laboratório de Patologia Animal, Hospital Veterinário da Universidade Federal de Campina Grande. O animal apresentava, havia 15 dias, apatia, anorexia, desidratação, ataxia, hipermetria, espasticidade dos membros torácicos e pélvicos, tremores de intenção, nistagmo, opistótono, déficit proprioceptivo e ausência de resposta de ameaça. Clinicamente, havia a suspeita de hipoplasia cerebelar, e, devido ao prognóstico desfavorável, o animal foi eutanasiado. Na necropsia, não foram observadas alterações macroscópicas. Microscopicamente, as lesões estavam restritas ao cerebelo e caracterizavam-se por alterações neurodegenerativas e necróticas, com desaparecimento segmentar dos neurônios de Purkinje. Nessas áreas, também se verificaram espaços em branco, denominado aspecto de cesto vazio, resultantes da perda dos neurônios de Purkinje, além de raros esferoides axonais e proliferação dos astrócitos de Bergmann. Em algumas áreas, a camada granular estava hipocelular e havia moderada gliose multifocal na camada molecular. O diagnóstico de abiotrofia cerebelar foi realizado com base nos dados epidemiológicos, clínicos e, principalmente, pelas alterações histopatológicas dos neurônios de Purkinje características da doença.(AU)

The aim of this report was to describe a case of cerebellar abiotrophy in cat with 45-year-old diagnosed at the Animal Pathology Laboratory, Veterinary Hospital of the Federal University of Campina Grande. The animal had presented 15-day apathy, anorexia, dehydration and neurological signs, characterized by ataxia, hypermetria, spasticity of fore and hindlimbs, intention tremor, nystagmus, opisthotonos, proprioceptive deficits, and absence of threat response. Clinically, cerebellar hypoplasia was suspected and the animal was euthanized due to poor prognosis. During necropsy, gross lesions were not observed. Microscopically the lesions were restricted to the cerebellum and were characterized by neurodegenerative and necrotic damage with segmental disappearance of the Purkinje cells. In these areas, there were also empty spaces, called the empty basket aspect, resulting from the loss of Purkinje cells, as well as rare axonal spheroids and proliferation of Bergmann's astrocytes. In some areas, the granular layer was hypocellular and there was moderate multifocal gliosis in the molecular layer. The diagnosis of cerebellar abiotrophy was based on epidemiological, clinical and mainly on histopathological changes in neurons of Purkinje disease characteristics.(AU)

ASPECTOS PATOLÓGICOS DAS DOENÇAS NUTRICIONAIS EM SUÍNOS

O diagnóstico das deficiências nutricionais na suinocultura deve ser realizado após estudo detalhado da alimentação fornecida aos suínos, envolvendo a mensuração quantitativa e qualitativa dos nutrientes das dietas, além de considerar alterações no manejo nutricional. As causas mais frequentes de deficiências nutricionais estão relacionadas a erros de formulação e preparo de premixes e/ou rações com excesso ou deficiência de algum nutriente. Nessa tese estão incluídos três manuscritos abordando casos clínicos de desequilíbrios nutricionais. O primeiro manuscrito teve o objetivo de descrever os achados epidemiológicos e clínico-patológicos de 22 surtos de urolitíase em suínos em crescimento e terminação. Os suínos afetados eram machos e a letalidade foi de 100%. Os urólitos foram submetidos ao método de determinação qualitativa dos componentes minerais, os quais foram compatíveis com carbonato de cálcio e fosfato de amônio magnesiano. A análise da ração de crescimento revelou baixos níveis de cálcio, em relação ao fósforo, perfazendo uma relação Ca:P de aproximadamente 0,35:1. A principal causa da morte dos suínos foi relacionada à desidratação e ao uroperitônio. O segundo manuscrito teve o objetivo de descrever dois eventos de mielopatia degenerativa em leitões de quatro a 27 dias de idade. A taxa de mortalidade atingiu 40%. A cromatografia líquida de alta eficiência indicou baixos níveis de ácido pantotênico nas amostras de premix e nas rações das fases de gestação e lactação fornecidas às porcas. Os leitões apresentavam depressão severa, fraqueza, anorexia, diarreia, ataxia sensorial e déficits posturais e paresia, sendo mais pronunciada nos membros pélvicos. A necropsia de vinte e dois leitões não demonstrou lesões macroscópicas significativas. Histologicamente, houve degeneração e necrose de neurônios da medula espinhal, principalmente no núcleo torácico e neurônios motores alfa no corno ventral na intumescência lombar e neurônios motores alfa no corno ventral na intumescência cervical. Degeneração axonal e de mielina mínima a moderada foi observada no funículo dorsal da medula espinhal e nas raízes nervosas dorsal e ventral. O terceiro manuscrito teve o objetivo de descrever os achados patológicos e toxicológicos de um quadro de fragilidade óssea generalizada compatíveis com osteoporose de origem nutricional. Quarenta e seis porcos apresentaram fraqueza muscular, paresia e paralisia de membros posteriores, emagrecimento, decúbito lateral e óbito, com evolução clínica de sete a 10 dias. Dois suínos foram submetidos à necropsia, na qual foram observadas formação de calo ósseo e múltiplas fraturas em membros, costelas e vértebras. A histologia revelou uma diminuição difusa e acentuada da espessura e do número de trabéculas. Sobrecarga significativa de zinco e consequente deficiência de cobre foram determinadas por espectrometria de absorção atômica.

The diagnosis of nutritional deficiencies in pig farming must be carried out after a detailed study of the feed provided to pigs, involving quantitative and qualitative nutrient measurement in the diets, in addition to considering changes in nutritional management. The most frequent causes of nutritional deficiencies are due to errors in the formulation and preparation of premixes and/or rations with excess or deficiency of some nutrient. This thesis includes three manuscripts with clinical cases of nutritional imbalances. The first manuscript aimed to describe the epidemiological and clinical-pathological findings of 22 outbreaks of urolithiasis in growing and finishing pigs. The affected pigs were male, and the lethality was 100%. The uroliths were submitted for qualitative determination of the mineral components, which were compatible with calcium carbonate and magnesium ammonium phosphate. The analysis of the grower ration showed low levels of calcium when compared with phosphorus levels, making a Ca: P ratio of approximately 0.35:1. The main cause of death was related to dehydration and uroperitoneum. The second manuscript aimed to describe two events of degenerative myelopathy in piglets from four to 27 days old. The mortality rate reached 40%. High-performance liquid chromatography indicated low levels of pantothenic acid in the premix samples and the rations of gestation and lactation phases provided to the sows. Piglets presented with severe depression, weakness, anorexia, diarrhea, sensory ataxia, and postural deficits and paresis, which were more pronounced in the pelvic limbs. Necropsy of 22 piglets demonstrated no significant gross lesions. Histologically, there was neuronal degeneration and necrosis in the spinal cord, primarily in the thoracic nucleus and alpha-motor neurons in the ventral horn in the lumbar intumescence, as well as in the alpha-motor neurons in the ventral horn in the cervical intumescence. Minimal to moderate axonal and myelin degeneration were observed in the dorsal funiculus of the spinal cord, as well as in the dorsal and ventral nerve roots. The third manuscript aimed to describe the pathological and toxicological findings of an outbreak of osteoporosis of nutritional origin. Forty-six pigs presented with muscle weakness, hind limb paresis and paralysis, weight loss, lateral recumbency, and death, with a clinical course of seven to 10 days. Two pigs were submitted to necropsy, in which bone callus formation and multiple fractures in the limbs, ribs, and vertebrae were observed. Histology revealed a diffuse and marked decrease in thickness and the number of bone trabeculae. Significant zinc overload and consequent copper deficiency were determined by atomic absorption spectrometry.

Déficit de memória em ratos submetidos à indução a doença de alzheimer por infusão intracerebral de beta-amiloide1-42 / Memory deficit in rats submitted to induction alzheimer's disease in infusion of intracerebral beta-amiloide1-42

Alzheimer's disease (AD) was established as the neurodegenerative dementia, which leads to progressive and irreversible cognitive decline, memory loss, attention and judgment. It is characterized by molecular injuries resulting from the accumulation of charged neuritic plaques of β-amyloid and neurofibrillary tangles causing oxidative damage and inflammatory. Thus, the aim of this study was to evaluate the learning and memory of rats seven days after infusion of β-amiloide1-42. The β-amiloide1-42 was prepared in saline protein (1ug / uL) and incubated at 37 ° C for three days to form the aggregate. The animals were anesthetized with the combination of ketamine (100 mg / kg) and xylazine (10 mg / kg) intraperitoneally, and fixed in a stereotaxic route. The aggregate was infused directly in the hippocampus (5UL bilaterally) in the coordinates, AP: -3.5 mm; LL: ± 2.0 mm; DV: -3.5. The learning and memory was assessed using the Morris water maze. The apparatus consists of a circular water tank (120 cm diameter and 60 cm high) with an escape platform (12.5 cm in diameter and 38 cm high) positioned invisible to the mice 2 cm below the water level. The tank was divided by imaginary lines (N, S, L, and O) in four quadrants (1, 2, 3 and 4) and identified by the same geometrical symbols, which remained the same throughout the study. The animals were placed facing the geometric shapes and the exhaust time measured during four consecutive days (training). In the fifth and final day it was taken to the escape platform and computed the total residence time in the target quadrant (test). The maximum time for each step was 60s. This study was approved by Ethics Committee for Animal Use (CEUA) of the State University of Ceará (UECE) by the number 2542310/2015. To analyze the learning we used the ANOVA two way with Bonferroni post-test. To verify differences in memory between the groups we used the Student t test. P <0.05 significance level was adopted[...]

Déficit de memória em ratos submetidos à indução a doença de alzheimer por infusão intracerebral de beta-amiloide1-42 / Memory deficit in rats submitted to induction alzheimer's disease in infusion of intracerebral beta-amiloide1-42

Alzheimer's disease (AD) was established as the neurodegenerative dementia, which leads to progressive and irreversible cognitive decline, memory loss, attention and judgment. It is characterized by molecular injuries resulting from the accumulation of charged neuritic plaques of β-amyloid and neurofibrillary tangles causing oxidative damage and inflammatory. Thus, the aim of this study was to evaluate the learning and memory of rats seven days after infusion of β-amiloide1-42. The β-amiloide1-42 was prepared in saline protein (1ug / uL) and incubated at 37 ° C for three days to form the aggregate. The animals were anesthetized with the combination of ketamine (100 mg / kg) and xylazine (10 mg / kg) intraperitoneally, and fixed in a stereotaxic route. The aggregate was infused directly in the hippocampus (5UL bilaterally) in the coordinates, AP: -3.5 mm; LL: ± 2.0 mm; DV: -3.5. The learning and memory was assessed using the Morris water maze. The apparatus consists of a circular water tank (120 cm diameter and 60 cm high) with an escape platform (12.5 cm in diameter and 38 cm high) positioned invisible to the mice 2 cm below the water level. The tank was divided by imaginary lines (N, S, L, and O) in four quadrants (1, 2, 3 and 4) and identified by the same geometrical symbols, which remained the same throughout the study. The animals were placed facing the geometric shapes and the exhaust time measured during four consecutive days (training). In the fifth and final day it was taken to the escape platform and computed the total residence time in the target quadrant (test). The maximum time for each step was 60s. This study was approved by Ethics Committee for Animal Use (CEUA) of the State University of Ceará (UECE) by the number 2542310/2015. To analyze the learning we used the ANOVA two way with Bonferroni post-test. To verify differences in memory between the groups we used the Student t test. P <0.05 significance level was adopted[...](AU)

DETECÇÃO MOLECULAR, HISTOLÓGICA E IMUNOHISTOQUÍMICA DE Pestivirus H EM UM BEZERRO NATURALMENTE INFECTADO COM SINAIS NEUROLÓGICOS

Os Pestivírus são membros do gênero Pestivirus, família Flaviviridae e classificados em 11 espécies pelo ICTV (Pestivirus A ao K). Os Pestivirus são vírus com envelope esférico, com polaridade positiva de RNA de fita simples, genoma completo de 12,5 kb, sua ORF codifica uma poliproteína de 3.998 aminoácidos, com dois produtos genéticos únicos (Npro e Erns). Infecções causadas por Pestivirus A, B e H são similares. Pestivirus H já foi detectado por RT-PCR codificando os genes 5´UTR, Npro e E2 em sangue, soro e órgãos de bovinos, contudo, não há associação com sinais neurológicos. O presente trabalho descreve a primeira detecção de Pestivirus H em tecidos do sistema nervoso central de um bezerro com sinais clínicos neurológicos e suas características molecular, histológica e imunohistoquímica. O bezerro apresentava síndrome cerebelar e morreu 20 dias após a internação e foi necropsiado. Fragmentos de SNC, coração, fígado, rim, pulmão, intestino e baço foram submetidos a RT-PCR. Amostras de tecido do SNC e linfonodo mesentérico foram processadas para avaliação histopatológica e imunohistoquímica. Os fragmentos de rim, SNC e intestino foram positivos para a região 5'UTR, SNC e intestino foram positivos para a região Npro. Os melhores amplicons nos ensaios de RT-PCR, 5UTR (SNC) e Npro (SNC e intestino) foram sequenciados e a sequência de nucleotídeos e a análise filogenética para a cepa 5'UTR exibiram 93,6 a 99,4%, 85%, 89,4 a 89,9% e 85,7% de identidade nt com as cepas de Pestivirus H subgrupo a, b, c e d, respectivamente, e 71,5 % e 75,6% de identidade nt com a cepa de Pestivirus A (NADL) e Pestivirus B (890), respectivamente. As cepas Npro mostraram 99,7% de identidade nt entre si e 90,2 a 96,5% de identidade nt com outras cepas de Pestivirus H e 67,3 a 67,5% e 66,3 a 66,5% de identidade nt com cepa de Pestivirus A (NADL) e Pestivirus B (890), respectivamente. As alterações histopatológicas incluíram necrose neuronal no cérebro, e necrose e degeneração de células Purkinje do cerebelo. Houve imunorreatividade para antígenos do BVDV no córtex cerebral, cérebro e medula espinhal. Este estudo fornece informações sobre o Pestivirus H em tecidos do SNC em bezerro com sinais neurológicos, sugerindo a inclusão do Pestivirus H na investigação etiológica de síndromes neurológicas.

Pestiviruses are members of the genus Pestivirus, family Flaviviridae and classified into 11 species recognized by ICTV (Pestivirus A to K). Pestiviruses are spherical enveloped viruses, single-stranded RNA positive-polarity, its complete genome is 12.5 kb and their ORF encodes a 3,998 amino acid polyprotein with two unique genetic products (Npro and Erns). Infections caused by Pestivirus A, B and H are similar. Pestivirus H has already been detected by RT-PCR encoding the 5´UTR, Npro and E2 genes in blood, serum and several bovine organs, however, there are no association with neurological signs. The present study describes the first detection of Pestivirus H in tissues of the central nervous system of a calf with neurological clinical signs, and its molecular, histological and immunohistochemical characteristics. The calf presented cerebellar syndrome and died 20 days after hospitalization, being necropsied. Fragments of CNS, heart, liver, kidney, lung, intestine and spleen were submitted to RT-PCR. Samples of CNS and mesenteric lymph node were processed for histopathological and immunohistochemistry evaluation. The kidney, CNS, and intestine fragments were positive to 5UTR region, CNS and intestine fragments were positive to Npro region. The better amplicons in the 5UTR (CNS) and Npro (CNS and intestine) RT-PCR assays were sequenced and the nucleotide sequence and phylogenetic analysis to the 5UTR strain exhibited 93.6 to 99.4%, 85%, 89.4 to 89.9%, and 85.7% of nt identity with Pestivirus H strains subgroup a, b, c, and d, respectively, and 71.5% and 75.6% of nt identity with Pestivirus A strain (NADL) and Pestivirus B (890), respectively. The Npro strains showed 99.7% of nt identity to each other and 90.2 to 96.5% of nt identity with other Pestivirus H strains and 67.3 to 67.5% and 66.3 to 66.5% of nt identity with Pestivirus A (NADL) and Pestivirus B (890), respectively. The histopathologic alterations included neuronal necrosis at the cerebrum and moderate necrosis and degeneration of Purkinje cells of the cerebellum. There was positive immunoreactivity for antigens of BVDV in cerebral cortex, cerebrum and spinal cord. This study provides information about the Pestivirus H in CNS tissues of a calf with neurological signs, suggesting the inclusion of Pestivirus H in the etiological investigation of neurological syndromes.

utilizando modelagem neuronal""Correlação entre Transtorno do Espectro do Autismo (TEA) e Distúrbio Muscular de Duchenne (DMD):estudo de casos

O Transtorno do Espectro do Autismo (TEA) compreende um quadro complexo do neurodesenvolvimento acompanhado por prejuízos na interação social e na comunicação, com padrões restritos e estereotipados de comportamento, interesses ou atividades.A prevalência mundial é de cerca de 1-2%.A Distrofia Muscular de Duchenne (DMD) é uma doença recessiva causada por uma mutação no gene da distrofina, responsável pela síntese da proteína que leva o mesmo nome e que fica localizado na região p21 do cromossomo X. Ao nascimento os pacientes portadores da DMD são aparentemente normais, com os primeiros sintomas aparecendo geralmente entre os 3 e 5 anos de idade, quando se observa fraqueza muscular e degeneração progressiva da musculatura esquelética. Há também relatos de que um terço dos pacientes apresenta algum déficit cognitivo. A prevalência é de 1em cada 3300 meninos, e por isso é considerada uma das doenças genéticas pediátricas de maior ocorrência.Nosso grupo tem modelado o TEA e a DMD in vitro, através da produção de células pluripotentes induzidas de pacientes diagnosticados com essas patologias, e a posterior diferenciação destas células em células do SNC. Assim como nos autistas, identificamos que os neurônios dos pacientes com DMD apresentavam conexões neurais alteradas. Além disso, existe na literatura descrição de que 3,1% dos pacientes com DMD também apresentam sinais clínicos de autismo. Neste trabalho buscamos investigar o perfil celular de pacientes comprometidos com as duas patologias, autismo e DMD. Para tanto, produzimos iPSC de meninos de uma mesma família, para modelar os fenótipos de células do SNC, comparando com um grupo neurotípico (controle). Foi possível observar que a reprogramação para produção das iPSC a partir da coleta de células-tronco de dente decíduo foi eficiente, vantajosa e pouco estressante aos pacientes, permitindo a diferenciação em NPC e neurônio. Não foi possível verificar diferenças morfológicas entre os portadores de TEA e DMD e os controles, entretanto, temos agora disponível materiais que nos permitirão realizar outras análises para verificar essas possíveis variações. Além disso, tivemos acesso a análises genéticas prévias realizadas pela família onde se observaram alterações em genes como SETD2 E AUTS2, porém não foi possível relacionar tais mutações genéticas ao quadro do TEA apresentado pelos trigêmeos, mas através do DNA coletado da família e essas análises genéticas prévias, poderemos realizar mais estudos acerca dessas mutações.

Autism Spectrum Disorder (ASD) comprises a complex neurodevelopmental disorder, with impairment in social interaction and communication, with restricted and stereotyped patterns of behavior, interests, or activities. The worldwide prevalence is about 1-2%. Duchenne Muscular Dystrophy (DMD) is a recessive disease caused by a mutation in the dystrophin gene located in the Xp21, responsible for the synthesis of the protein that bears the same name. The prevalence of DMD is 1: 3300 boys, which is why it is considered one of the most common pediatric genetic diseases. At birth, patients with DMD are apparently healthy, with the first symptoms generally appearing between 3 and 5 years of age, when muscle weakness and progressive skeletal muscle degeneration are observed. There are also reports that one-third of patients have some cognitive impairment. Besides, there is a description in the literature that 3.1% of DMD patients also have clinical signs of autism. Our group has modeled TEA and DMD in vitro, through the production of induced pluripotent stem cells (iPSC) from patients diagnosed with these pathologies, and the subsequent differentiation of these cells into CNS cells. As with ASD, we found that the neurons of patients with DMD had altered neural connections. In this work, we seek to investigate the cell profile of patients compromised with both pathologies, ASD, and DMD, concomitantly. For this purpose, we produced iPSC from a family of triplet boys from stem cells from deciduous teeth, which were later efficiently differentiated into NPC and neuron. It was not possible to verify morphological differences in the cells of patients with ASD and DMD and the controls with the preliminary experiments presented in this thesis. However, the production of these cells allows other analyses to be carried out to verify these possible variations. Also, we had access to previous genetic analyzes carried out by the family, where changes in genes such as SETD2 and AUTS2, reported as related to ASD, were observed. However, using just these data, it was not possible to correlate these mutations with the ASD in the triplet. Still, through the collected DNA of the family and these previous genetic analyzes, we will be able to carry out more studies.

Key-Gaskell syndrome in Brazil: first case report / Síndrome de Key-Gaskell: primeiro relato de caso no Brasil

Feline dysautonomia is a devastating disease characterized by neuronal degeneration in autonomic ganglia that results in clinical signs related to dysfunction of the sympathetic and parasympathetic nervous systems. The cause is unknown and this disease has a poor prognosis and no definitive treatment. Most reports have been described in few countries around the world, but the prevalence may be underestimated in countries like Brazil. This study describes the progression and clinicopathological changes of dysautonomia in a 17-month-old female Brazilian shorthair cat.(AU)

Disautonomia felina é uma doença devastadora, caracterizada por degeneração neuronal em gânglios autonômicos, a qual resulta em sinais clínicos relacionados à disfunção dos sistemas simpático e parassimpático. Sua causa é desconhecida, o prognóstico desfavorável e não há tratamento definitivo disponível. A maioria dos relatos foi descrita em países ao redor do mundo, mas sua prevalência pode estar subestimada em países como o Brasil. Este estudo descreve a progressão e as alterações clínico-patológicas da disautonomia em um gato de pelo curto brasileiro, do sexo feminino, de 17 meses de idade.(AU)

Intoxicação e uso racional da Prosopis juliflora casos espontâneos em bovinos e caprinos no estado da Bahia

Objetivou-se com este estudo descrever a ocorrência de surtos de intoxicação espontânea pelo consumo de vagens de Prosopis juliflora (algaroba), em bovinos e caprinos no Estado da Bahia. Os dados referentes à epidemiologia, histórico e sinais clínicos dos surtos foram obtidos com os proprietários ou pelo médico veterinário responsável. O primeiro surto (PS) ocorreu em maio de 2011 em uma propriedade localizada no município de Juazeiro e acometeu um rebanho composto por 150 caprinos. O segundo surto (SS) ocorreu em fevereiro de 2015 no município de Iaçu e atingiu um rebanho composto por 20 caprinos. O terceiro surto (TS) ocorreu em julho e setembro de 2014, em uma propriedade rural localizada no município de Tucano e afetou um rebanho formado por 30 bovinos. O quarto surto (QS) aconteceu em agosto de 2016, em uma propriedade composta por um rebanho de 110 bovinos. Dos sete animais que apresentavam quadro clínico grave e prognóstico ruim, seis tiveram eutanásia e foram necropsiados para confirmação diagnóstica, sendo quatro caprinos (C1-PS, C2-PS, C3-SS e C4-SS) e dois bovinos (B1-TS e B2-TS). Nos surtos estudados, os achados clínicos (PS, SS, TS e QS) e histopatológicos (PS, SS e TS) foram compatíveis com intoxicaçãos por algaroba. Clinicamente observou-se principalmente progressiva perda de peso, atrofia dos músculos da mastigação, mandíbula pendulosa, protrusão de língua, dificuldade de apreensão e mastigação dos alimentos, inclinação da cabeça (cara torta) durante a mastigação ou ruminação e salivação excessiva. À necropsia observaram-se caquexia, atrofia e palidez do músculo masseter, além de fragmentos reconhecíveis de vagens de algaroba no rúmen e/ou retículo. A avaliação histopatológica revelou degeneração do núcleo motor do nervo trigêmeo e atrofia por desnervação do músculo masseter com substituição por tecido fibroso. Medidas de controle e profilaxia da intoxicação, bem com orientações sobre possível comercialização das vagens e a exploração da madeira da algaroba informadas aos produtores. Comprovou-se que surtos de intoxicação natural por algaroba ocorrem em bovinos e caprinos no estado da Bahia em áreas ainda não mapeadas, sendo essa intoxicação comprovada, pela primeira vez, com base em exames necroscópicos e histopatológicos.

The objective of this study was to describe the occurrence of outbreaks of spontaneous intoxication due to the consumption of Prosopis juliflora pods in cattle and goats in the State of Bahia. The history of ingestion of "mesquite beans" pods along with classic clinical signs of the "jaw and tonque trouble" and epidemiological data of the four outbreaks were obtained from technical visits, with the assistance of Veterinary Doctors of the CDP / UFBA and UFRB responsible for the visits and by rural staff. The first outbreak (PS) occurred in May 2011 at a property located in the municipality of Juazeiro and affected a herd of 150 goats. The Second Surge (SS) occurred in February 2015 in the municipality of Iaçu and reached a herd composed of 20 goats. The third outbreak (TS) occurred in July and September 2014, in a rural property located in the municipality of Tucano and affected a herd of 30 cattle. The Outbreak Room (QS) happened in August of 2016, in a property consisting of a herd of 110 cattle. Of the seven animals that presented a severe clinical condition and poor prognosis, six were euthanized and necropsied for diagnostic confirmation, four goats (C1-PS, C2-PS, C3-SS and C4-SS) and two bovines (B1-TS and B2 -TS), a bovine (B3-QS) was not allowed its euthanasia. During necropsy samples of the CNS and masseter muscle fixed in 10% formalin were collected. The clinical findings (PS, SS, TS and QS) and histopathological findings (PS, SS and TS) verified in the outbreaks reported here were compatible with algaroba intoxications. Clinically we observed mainly progressive weight loss, atrophy of chewing muscles, pendulous mandible, tongue protrusion, difficulty in seizing and chewing food, tilting of the "jaw and tonque trouble" head during chewing or rumination and excessive salivation. In the laboratory tests of the animals evaluated (C3-SS, C4-SS and B3-QS) anemia and hypoproteinemia were observed. At necropsy he observed cachexia, atrophy, paleness of the masseter muscle and recognizable fragments of "mesquite beans" pods. Histologically, it observed degeneration of the motor nucleus of the trigeminal nerve and atrophy by denervation of the masseter muscle with replacement by fibrous tissue. Control measures and prophylaxis of intoxication and management with "algaroba", it is discussed the need to develop research to determine the economic viability and sustainability of the algaroba exploiting its forage potential (animal feeding and commercialization of pods) and timber (production of firewood, coal, cuttings and mourners). P. juliflora intoxication with necroscopic and histopathological record in cattle and goats was reported for the first time in BA. Showing to be an important disease for both species in the State.