Astragaloside IV alleviates stroke-triggered early brain injury by modulating neuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway

Purpose: Stroke is an acute cerebrovascular disease. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with an established therapeutic effect on central nervous system diseases. This study examined the neuroprotective properties and possible mechanisms of AS-IV in stroke-triggered early brain injury (EBI) in a rat transient middle cerebral artery occlusion (MCAO) model. Methods: The neurological scores and brain water content were analyzed. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was utilized to determine the infarct volume, neuroinflammatory cytokine levels, and ferroptosis-related genes and proteins, and neuronal damage and molecular mechanisms were evaluated by terminal deoxynucleotidyl transferase dutp nickend labeling (TUNEL) staining, western blotting, and real-time polymerase chain reaction. Results: AS-IV administration decreased the infarct volume, brain edema, neurological deficits, and inflammatory cytokines TNF-α, interleukin-1ß (IL-1ß), IL-6, and NF-κB, increased the levels of SLC7A11 and glutathione peroxidase 4 (GPX4), decreased lipid reactive oxygen species (ROS) levels, and prevented neuronal ferroptosis. Meanwhile, AS-IV triggered the Nrf2/HO-1 signaling pathway and alleviated ferroptosis due to the induction of stroke. Conclusion: Hence, the findings of this research illustrate that AS-IV administration can improve delayed ischemic neurological deficits and decrease neuronal death by modulating nuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway.

Cerebral infarction and thrombotic meningoencephalitis in a calf due to candidiasis / Infarto cerebral e meningoencefalite trombótica em um bezerro devido a candidíase

We described a case of cerebral infarction and thrombotic meningoencephalitis due to candidiasis in a seven-month-old calf. The death occurred three days after the onset of apathy, fever, and the head's lateral deviation to the left. Macroscopic changes in the brain consisted of asymmetry of telencephalic hemispheres; the right hemisphere was enlarged, causing cerebellar herniation. A focally extensive red area was observed on the surface of the right occipital lobe. At cross-sections of the fixed brain, the lesions revealed to be extensive, red-brown, soft or cavitated areas affecting the white and grey matter from the level of the thalamus to the cerebellum and compressing subjacent structures. Histologically, there was acute, coalescent, multifocal necrosupurative meningoencephalitis, associated with vasculitis, congestion, thrombosis, edema, infarction, and intralesional fungal hyphae. The diagnosis of cerebral infarction and thrombotic meningoencephalitis due to candidiasis was made by the pathological changes, the staining and morphological characteristics of the agent, and immunohistochemistry. The cerebral infarction and thrombotic meningoencephalitis in cattle can result from vascular lesions due to infection by Candida sp.; although uncommon, this case demonstrated that candidiasis should be part of a list of differential diagnoses of severe brain injuries in cattle.

Descreve-se um caso de infarto cerebral e meningoencefalite trombótica devido a candidíase em um bezerro de sete meses de idade. A morte ocorreu três dias após o início de apatia, febre e desvio lateral da cabeça para a esquerda. As alterações macroscópicas no cérebro consistiam em assimetria dos hemisférios telencefálicos; o hemisfério direito estava aumentado, causando herniação cerebelar. Uma extensa área vermelha focal foi observada na superfície do lobo occipital direito. Nos cortes transversais do encéfalo fixado, as lesões revelaram áreas extensas, marrom-avermelhadas, moles ou cavitadas, afetando a substância branca e cinzenta desde o nível do tálamo até o cerebelo e comprimindo as estruturas subjacentes. Histologicamente, havia meningoencefalite necrossupurativa multifocal aguda, coalescente, associada a vasculite, congestão, trombose, edema, infarto e hifas fúngicas intralesionais. O diagnóstico de infarto cerebral e meningoencefalite trombótica devido a candidíase foi feito pelas alterações patológicas, coloração e características morfológicas do agente e imuno-histoquímica. O infarto cerebral e meningoencefalite trombótica em bovinos pode resultar de lesões vasculares devido à infecção por Candida sp.; embora incomum, este caso demonstra que a candidíase deve fazer parte de uma lista de diagnósticos diferenciais de lesões cerebrais graves em bovinos.

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.

Ulinastatin alleviates early brain injury after intracerebral hemorrhage by inhibiting necroptosis and neuroinflammation via MAPK/NF-κB signaling pathway

Purpose: Spontaneous intracerebral hemorrhage (ICH) is a major public health problem with a huge economic burden worldwide. Ulinastatin (UTI), a serine protease inhibitor, has been reported to be anti-inflammatory, immune regulation, and organ protection by reducing reactive oxygen species production, and inflammation. Necroptosis is a programmed cell death mechanism that plays a vital role in neuronal cell death after ICH. However, the neuroprotection of UTI in ICH has not been confirmed, and the potential mechanism is unclear. The present study aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in ICH-induced EBI in a C57BL/6 mouse model. Methods: The neurological score, brain water content, neuroinflammatory cytokine levels, and neuronal damage were evaluated. The anti-inflammation effectiveness of UTI in ICH patients also was evaluated. Results: UTI treatment markedly increased the neurological score, alleviate the brain edema, decreased the inflammatory cytokine TNF-α, interleukin­1ß (IL­1ß), IL­6, NF­κB levels, and RIP1/RIP3, which indicated that UTI-mediated inhibition of neuroinflammation, and necroptosis alleviated neuronal damage after ICH. UTI also can decrease the inflammatory cytokine of ICH patients. The neuroprotective capacity of UTI is partly dependent on the MAPK/NF-κB signaling pathway. Conclusions: UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation, and necroptosis.

Ulinastatin alleviates early brain injury after intracerebral hemorrhage by inhibiting oxidative stress and neuroinflammation via ROS/MAPK/Nrf2 signaling pathway

Purpose: Spontaneous intracerebral hemorrhage (ICH) is still a major public health problem, with high mortality and disability. Ulinastatin (UTI) was purified from human urine and has been reported to be anti-inflammatory, organ protective, and antioxidative stress. However, the neuroprotection of UTI in ICH has not been confirmed, and the potential mechanism is unclear. In the present study, we aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in ICH-induced early brain injury in a C57BL/6 mouse model. Methods: The neurological score, brain water content, neuroinflammatory cytokine levels, oxidative stress levels, and neuronal damage were evaluated. Results: UTI treatment markedly increased the neurological score, alleviated brain edema, decreased the levels of the inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), IL-6, and NF-κB, decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and upregulated the levels of glutathione (GSH), superoxide dismutase (SOD), and Nrf2. This finding indicated that UTI-mediated inhibition of neuroinflammation and oxidative stress alleviated neuronal damage after ICH. The neuroprotective capacity of UTI is partly dependent on the ROS/MAPK/Nrf2 signaling pathway. Conclusions: UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation and oxidative stress.

Cerebrolysin alleviates early brain injury after traumatic brain injury by inhibiting neuroinflammation and apoptosis via TLR signaling pathway

Purpose: Traumatic brain injury (TBI) is a major cause of death and disability. Cerebrolysin (CBL) has been reported to be anti-inflammatory by reducing reactive oxygen species (ROS) production. However, the neuroprotection of CBL in TBI and the potential mechanism are unclear. We aimed to investigate the neuroprotection and mechanisms of CBL in TBI. Methods: The TBI model was established in strict accordance with the Feeney weight-drop model of focal injury. The neurological score, brain water content, neuroinflammatory cytokine levels, and neuronal damage were evaluated. The involvement of the early brain injury modulatory pathway was also investigated. Results: Following TBI, the results showed that CBL administration increased neurological scores and decreased brain edema by alleviating blood­brain barrier (BBB) permeability, upregulating tight junction protein (ZO­1) levels, and decreasing the levels of the inflammatory cytokines tumor necrosis factor­α (TNF­α), interleukin­1ß (IL­1ß), IL­6, and NF­κB. The TUNEL assay showed that CBL decreased hippocampal neuronal apoptosis after TBI and decreased the protein expression levels of caspase­3 and Bax, increasing the levels of Bcl­2. The levels of Toll­like receptor 2 (TLR2) and TLR4 were significantly decreased after CBL treatment. In TBI patients, CBL can also decrease TNF­α, IL­1ß, IL­6, and NF­κB levels. This result indicates that CBL­mediated inhibition of neuroinflammation and apoptosis ameliorated neuronal death after TBI. The neuroprotective capacity of CBL is partly dependent on the TLR signaling pathway. Conclusions: Taken together, the results of this study indicate that CBL can improve neurological outcomes and reduce neuronal death against neuroinflammation and apoptosis via the TLR signaling pathway in mice.

Atypical chronic copper poisoning in a sheep secondary to copper wire ingestion: case report / Intoxicação crônica por cobre atípica em ovino pelo consumo de fios de cobre: relato de caso

A 14-month-old female Texel sheep that came from a herd made up of 19 animals showed haemoglobinuria, apathy, and anorexia, and died two days after the start of the clinical signals. The sheep remained in a natural grassland, where trailers were repaired, and multiple copper wires were deposited on the pasture. The animal had tachycardia, tachypnoea, pale mucous membranes, groaning pain on abdominal palpation, circling, head pressing, intensely hemolyzed plasma, and intense azotaemia. The necropsy showed focally extensive oedema in the inguinal and medial region of pelvic limbs, kidneys dark brown, and liver diffusely yellow with an evident moderate diffuse lobular pattern. The abomasum had a considerable amount of enameled material of thickness, firm to the cut, with 1-5 mm (copper wires). Histopathological examination showed marked diffuse tubular and glomerular coagulative necrosis in the kidneys, in addition to neutrophils, macrophages, lymphocytes, and plasma cells with moderate multifocal nephritis. The liver showed centrilobular necrosis, moderate hepatocellular edema, multifocal cholestasis, and in the lungs and brain mild to moderate diffuse edema. Copper content in the frozen liver (in natura) reached 1,598 mg/kg. Copper mesh ingestion led to sheep poisoning, which in this case was considered an atypical form of chronic primary copper poisoning.

Um ovino Texel de 14 meses de idade, que fazia parte de um rebanho de 19 animais, apresentou hemoglobinúria, apatia, anorexia e morreu dois dias após o início dos sinais clínicos. Os ovinos permaneciam em campo nativo, onde eram realizados consertos de trailers, e múltiplos fios de cobre ficavam depositados na pastagem. O animal apresentou taquicardia, taquipneia, mucosas pálidas, gemido de dor à palpação abdominal, além de andar em círculo, e pressão da cabeça contra obstáculos, plasma intensamente hemolisado e azotemia intensa. Na necropsia, havia edema na região inguinal e medial de membros pélvicos focalmente extenso, rins enegrecidos, e o fígado estava difusamente amarelado, com padrão lobular evidente difuso moderado. No abomaso, havia grande quantidade de material esmaltado, com 1-5mm de espessura, firme, que rangia ao ser cortado (fios de cobre). No exame histopatológico nos rins, havia necrose tubular e glomerular hemoglobinúrica difusa acentuada, além de nefrite de neutrófilios, macrófagos, linfócitos e plasmócitos multifocal moderada. No fígado, havia necrose centrolobular, tumefação hepatocelular e colestase multifocais moderadas; nos pulmões e no cérebro, edema difuso discreto a moderado. A dosagem de Cu no fígado revelou a presença de 1598mg/kg. A ingestão de malhas de cobre levou à intoxicação do ovino que, nesse caso, foi considerada uma forma atípica de intoxicação primária crônica por cobre.

Penile fractures in young bulls raised in feedlots in Southern Brazil

Background: Penile fracture is a pathology of young cattle that perform precocious and disordered breeding. The incompatibility of height between males and females and sodomy between males cause a great pressure on the sigmoid flexure and retractor muscle of the penis, which are the main causes and sites of organ injury. This study aimed to describe the epidemiological and pathological aspects of penile fractures observed in young bulls raised in pre-export feedlots (PEFs) in southern Brazil. Cases: In 2 PEFs located in the municipalities of Pelotas (property 1) and Capão do Leão (property 2), 3 male cattle [1 from property 1 and 2 from property 2] presented subcutaneous edema in the foreskin and perineum, associated with dysuria. The evolution of the clinical picture was approximately 20 days in all cases, with evolution to death. The bovine necropsied on property 1 had an increased volume and inguinal edema, involving the penis and scrotal sac. Necrosis of the subcutaneous tissue and local musculature was also observed. The testicles were surrounded by the necrotic tissue, and the right testis was swollen, with flaccid parenchyma adhering to the tunica albuginea. In the necropsy of 1 bull from property 2, an increase in the inguinal volume was observed, with an extensive area of necrosis and edema extending from the prepuce to the caudal musculature of the scrotal sac. There were also marked varicosis in the sigmoid flexure and necrosis of the adjacent region, without the involvement of the corpus cavernosum. During the necropsy of the 2 young bulls, fragments of organs from the abdominal, thoracic, and brain cavities were collected and fixed in 10% buffered formalin. From the bull of the property 2, an anatomical piece consisting of the penis, prepuce, and testicles was also collected and fixed in 10% buffered formalin. After 48 h, the tissue samples were cleaved, embedded in paraffin, cut into 3-µm-thick sections, and stained using hematoxylin and eosin (HE). A histological evaluation of the penile lesions in both cattle revealed intense hemorrhage, congestion, and necrosis of the muscles and tissues adjacent to the corpus cavernosum. In addition to areas of dystrophic calcification, neutrophil and macrophage infiltration was also observed. In the bull from the property 1, an intense edema and proliferation of fibrous tissue surrounding the urethra were noted. There were also marked tubular degeneration and intense infiltration of neutrophils, lymphocytes, and macrophages in the inner portion of the tunica albuginea. Discussion: In the present cases, the diagnosis was based on epidemiological data associated with clinical signs and pathology. The macroscopic lesions observed were probably due to the involvement of blood vessels adjacent to the penis, which suffered trauma during sodomy mating among cattle. These lesions have been described in other reports of this pathology and in diseases, such as acropostitis-phimosis, fibropapilloma of the glans, preputial abscess, and urolithiasis, and the differential diagnosis of these diseases must be carried out, as they have different etiologies. In the bulls of the present study, no lesions were observed in the corpus cavernosum, and this condition was attributed to the presence of varicosis and accumulation of urine in the prepuce, due to the difficulty in exposing the penis. Histologically, there were intense hemorrhage, congestion, and necrosis of the muscles and tissues adjacent to the corpus cavernosum, with the infiltration of neutrophils and macrophages, and areas of dystrophic calcification. The presence of necrotic lesions in tissues adjacent to the penis may be related to hypoxia, vascular lesions, or the action of chemical elements present in the urine. In both cases, vascular lesions were present, which were attributed to the main triggering factor for the disease.

Meningioma intracraniano em cão - tratamento com radioterapia / Intracranial meningioma in a dog - treatment with radiotherapy

Background: The most common primary brain neoplasm is meningioma. Dolichocephalic breeds are predisposed and there is no sexual predilection. Clinical signs depend on the location and size of the tumor and have a progressive course. Primary treatement includes surgery, radiotherapy or both. This study aimed to describe the treatment of a dog with suspected intracranial meningioma with definitive radiotherapy, which resulted in significant clinical improvement and prolonged survival. Case: A 9-year-old Shetland Shepherd bitch was diagnosed with a head tilt to the left side that progressed over a few weeks. She previously received corticosteroid therapy, which resulted a clinical improvement that worsened after treatment was discontinued. Computed tomography revealed an extra-axial brain mass in the caudal fossa, lateralized to the right, welldelimited, and measuring approximately 1.5 × 1.4 × 1.7 cm, suggestive of intracranial meningioma. The patient was treated with radiotherapy using Cobalt-60 equipment, with 18 daily fractions of 2.5 Gy at a total dose of 45 Gy using parallel and opposite technique fields. A new tomography performed 30 days after treatment showed a remission of 85% of the initial brain mass measuring approximately 0.9 × 1.0 × 0.5 cm, as well as complete resolution of the clinical signs initially presented. After 14 months, the patient presented with signs of lethargy and ataxia and was medicated with hydroxyurea at a dose of 50 mg/kg 3 times a week and corticosteroid therapy. However, the patient's neurological condition deteriorated, and she was subjected to reirradiation using the same protocol used previously, which resulted in clinical improvement and a 54% reduction in tumor volume on magnetic resonance. As a late side effect, only permanent alopecia in the irradiated region was observed. The patient died of disease 330 days after the second course of radiotherapy, with a total survival time of 1087 days. Discussion: Meningiomas are extra-axial neoplasms of the central nervous system that grow inside the dura mater. The literature shows that meningiomas are more common in dolichocephalic races with a mean age of 9 years, which supports our findings. Meningiomas most commonly affect the cortical thalamus and cerebellopontine region in dogs, which are normally associated with vestibular symptoms, as seen in this case. Diencephalic damage can result in vestibular signals since the thalamus functions as a relay station for vestibular afferent stimuli that are relayed to the cerebral cortex. In addition to the vestibular syndrome, common clinical signs associated with meningiomas in dogs include seizures, behavioral changes, and walking in circles, which are frequently misinterpreted due to tumor-induced side effects, such as cerebral edema, obstructive hydrocephalus, and cerebral hernia. Advanced imaging techniques should be used to diagnose intracranial neoplasms. In this case, computed tomography was critical for diagnosis and treatment planning. Meningioma treatment may comprise palliative measures, surgery, and radiotherapy. Radiotherapy as a single treatment can improve the quality of life with a decrease in clinical signs and a median survival time of approximately 250-536 days, as reported in the literature. Hydroxyurea can be a therapeutic option in inoperable cases and for patients with clinical limitations to undergo successive anesthesia during radiotherapy. Its most serious side effect is progressive myelosuppression. It can cause temporary partial tumor remission and improvement in clinical signs. As previously stated, radiotherapy can be an effective primary treatment option for treating intracranial meningiomas in dogs, with significant improvement in neurological clinical signs and mild side effects.

Crotalaria spectabilis poisoning in a horse

Plant poisoning is an important cause of death in horses and cattle in Brazil. Crotalaria spp. has stood out in this scenario due to its toxic potential caused by monocrotaline, a pyrrolizidine alkaloid found throughout the plant, mainly in seeds. Here is reported a case of Crotalaria spectabilis poisoning a horse. A horse consumed oats contaminated with Crotalaria spectabilis seed and presented clinical signs of toxicosis characterized by jaundice, progressive weight loss, hemoglobinuria, subcutaneous edema in the pectoral region and neurological symptoms typical of hepatic encephalopathy. In the serum evaluation, there was an increase in the activity of the enzymes alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) and aspartate transaminase (AST), urea, creatinine and creatine phosphokinase (CPK). At necropsy, the main macroscopic findings were opaque and congested liver with capsular irregularity and accentuated the lobular pattern, trachea with foamy and pinkish fluid and congested and edematous pulmonary lobes. The main histopathological findings were hepatic fibrosis, periportal ductal hyperplasia, centrilobular necrosis, megalocytosis and binucleated hepatocytes. The brain parenchyma showed perivascular edema and Alzheimer type II astrocytes. Crotalaria spp. is among the main plants that cause acute or chronic mortality after exposure to the toxic compound in horses and farm animals.(AU)

Crotalaria spectabilis poisoning in a horse

Plant poisoning is an important cause of death in horses and cattle in Brazil. Crotalaria spp. has stood out in this scenario due to its toxic potential caused by monocrotaline, a pyrrolizidine alkaloid found throughout the plant, mainly in seeds. Here is reported a case of Crotalaria spectabilis poisoning a horse. A horse consumed oats contaminated with Crotalaria spectabilis seed and presented clinical signs of toxicosis characterized by jaundice, progressive weight loss, hemoglobinuria, subcutaneous edema in the pectoral region and neurological symptoms typical of hepatic encephalopathy. In the serum evaluation, there was an increase in the activity of the enzymes alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) and aspartate transaminase (AST), urea, creatinine and creatine phosphokinase (CPK). At necropsy, the main macroscopic findings were opaque and congested liver with capsular irregularity and accentuated the lobular pattern, trachea with foamy and pinkish fluid and congested and edematous pulmonary lobes. The main histopathological findings were hepatic fibrosis, periportal ductal hyperplasia, centrilobular necrosis, megalocytosis and binucleated hepatocytes. The brain parenchyma showed perivascular edema and Alzheimer type II astrocytes. Crotalaria spp. is among the main plants that cause acute or chronic mortality after exposure to the toxic compound in horses and farm animals.

Hepatic encephalopathy in adult dog secondary to cirrhosis due to congenital biliary agenesis: a case report / Encefalopatia hepática em cão adulto secundária a cirrose causada por agenesia biliar congênita: relato de caso

Gallbladder agenesis is a congenital malformation that is considered extremely rare in dogs. The disease can course asymptomatically or with clinical signs, usually non-specific and including vomiting, anorexia, diarrhea, ascites, and lethargy. The objective of this report was to describe the clinical and anatomopathological aspects of a dog with hepatic encephalopathy secondary to gallbladder agenesis. This condition can be diagnosed during surgery or imaging examinations; however, it is often an incidental finding. In the biochemical examinations, a decrease in alanine aminotransferase and an increase in alkaline phosphatase and hypoalbuminemia were observed. During the necropsy, hepatomegaly was observed with absence of the gallbladder, congestion, cerebral edema, lipiduria, and pulmonary edema. Microscopically, there was intense fibrosis and inflammation in the liver due to chronic cholangiohepatitis (cirrhosis of the liver). The consequence of this lesion secondary to gallbladder agenesis was hepatic encephalopathy. Chronic liver failure exposes the cerebral cortex to toxins that are not metabolized by the liver, such as ammonia, mercaptans, short-chain fatty acids, scatols, indols, and aromatic amino acids. These toxins cause reversible damage to the brain, which results in neurological disorders. In this report, the dog had no clinical neurological signs, and the diagnosis of this condition was observed histologically. Dogs with gallbladder agenesis usually have clinical and pathological findings of hepatobiliary lesions such as cholestasis, cholangiohepatitis, and, in severe cases, hepatic encephalopathy, which are necessary to differentiate from other diseases that affect the hepatobiliary system, such as cholelithiasis, neoplasms, and chronic hepatitis.

A agenesia de vesícula biliar é uma má formação congênita, considerada extremamente rara em cães. A doença pode cursar de forma assintomática ou com sinais clínicos, geralmente, inespecíficos que incluem vômitos, anorexia, diarreia, ascite e letargia. O objetivo deste relato foi descrever os aspectos clínicos e anatomopatológicos de um cão com encefalopatia hepá-tica secundária a agenesia da vesícula biliar, esta condição pode ser diagnosticada durante uma cirurgia ou exames de imagem, entretanto frequentemente é um achado incidental. Como resultados, nos exames bioquímicos observou-se a diminuição da alanina aminotransferase, aumento da fosfatase alcalina e hipoalbuminemia. Durante a necropsia foi observado hepatomegalia com ausência da vesícula biliar, congestão e edema cerebral, lipidúria e edema pulmonar. Microscopicamente, no fígado havia intensa fibrose e inflamação pela colangiohepatite crônica (cirrose hepática). A consequência desta lesão secundária a agenesia da vesícula biliar, foi a encefalopatia hepática. A insuficiência hepática crônica expõe o córtex cerebral às toxinas não metabo-lizadas pelo fígado, tais como a amônia, mercaptanos, ácidos graxos de cadeia curta, escatóis, indóis e aminoácidos aromáti-cos. Essas toxinas causam danos reversíveis ao encéfalo, o que resulta em distúrbios neurológicos. No presente caso, o cão não apresentou sinais clínicos neurológicos e o diagnóstico desta condição foi observado histologicamente. Cães com agenesia de vesícula biliar, geralmente exibem achados clínicos e patológicos de lesões hepatobiliares, como colestase, conlangiohepatite e, em casos graves, encefalopatia hepática, sendo necessário diferenciar de outras doenças que acometem o sistema hepatobiliar, como colelitíase, neoplasias e hepatites crônicas.

Hepatic encephalopathy in adult dog secondary to cirrhosis due to congenital biliary agenesis: a case report / Encefalopatia hepática em cão adulto secundária a cirrose causada por agenesia biliar congênita: relato de caso

Gallbladder agenesis is a congenital malformation that is considered extremely rare in dogs. The disease can course asymptomatically or with clinical signs, usually non-specific and including vomiting, anorexia, diarrhea, ascites, and lethargy. The objective of this report was to describe the clinical and anatomopathological aspects of a dog with hepatic encephalopathy secondary to gallbladder agenesis. This condition can be diagnosed during surgery or imaging examinations; however, it is often an incidental finding. In the biochemical examinations, a decrease in alanine aminotransferase and an increase in alkaline phosphatase and hypoalbuminemia were observed. During the necropsy, hepatomegaly was observed with absence of the gallbladder, congestion, cerebral edema, lipiduria, and pulmonary edema. Microscopically, there was intense fibrosis and inflammation in the liver due to chronic cholangiohepatitis (cirrhosis of the liver). The consequence of this lesion secondary to gallbladder agenesis was hepatic encephalopathy. Chronic liver failure exposes the cerebral cortex to toxins that are not metabolized by the liver, such as ammonia, mercaptans, short-chain fatty acids, scatols, indols, and aromatic amino acids. These toxins cause reversible damage to the brain, which results in neurological disorders. In this report, the dog had no clinical neurological signs, and the diagnosis of this condition was observed histologically. Dogs with gallbladder agenesis usually have clinical and pathological findings of hepatobiliary lesions such as cholestasis, cholangiohepatitis, and, in severe cases, hepatic encephalopathy, which are necessary to differentiate from other diseases that affect the hepatobiliary system, such as cholelithiasis, neoplasms, and chronic hepatitis.(AU)

A agenesia de vesícula biliar é uma má formação congênita, considerada extremamente rara em cães. A doença pode cursar de forma assintomática ou com sinais clínicos, geralmente, inespecíficos que incluem vômitos, anorexia, diarreia, ascite e letargia. O objetivo deste relato foi descrever os aspectos clínicos e anatomopatológicos de um cão com encefalopatia hepá-tica secundária a agenesia da vesícula biliar, esta condição pode ser diagnosticada durante uma cirurgia ou exames de imagem, entretanto frequentemente é um achado incidental. Como resultados, nos exames bioquímicos observou-se a diminuição da alanina aminotransferase, aumento da fosfatase alcalina e hipoalbuminemia. Durante a necropsia foi observado hepatomegalia com ausência da vesícula biliar, congestão e edema cerebral, lipidúria e edema pulmonar. Microscopicamente, no fígado havia intensa fibrose e inflamação pela colangiohepatite crônica (cirrose hepática). A consequência desta lesão secundária a agenesia da vesícula biliar, foi a encefalopatia hepática. A insuficiência hepática crônica expõe o córtex cerebral às toxinas não metabo-lizadas pelo fígado, tais como a amônia, mercaptanos, ácidos graxos de cadeia curta, escatóis, indóis e aminoácidos aromáti-cos. Essas toxinas causam danos reversíveis ao encéfalo, o que resulta em distúrbios neurológicos. No presente caso, o cão não apresentou sinais clínicos neurológicos e o diagnóstico desta condição foi observado histologicamente. Cães com agenesia de vesícula biliar, geralmente exibem achados clínicos e patológicos de lesões hepatobiliares, como colestase, conlangiohepatite e, em casos graves, encefalopatia hepática, sendo necessário diferenciar de outras doenças que acometem o sistema hepatobiliar, como colelitíase, neoplasias e hepatites crônicas.(AU)

Frontal cystic meningioma removed by a partial transfrontal craniotomy in a cat

Background: Meningiomas are the most frequently reported intracranial tumors in cats. It is known to arise at the point of arachnoid cells project into the dural venous sinuses. Cats with intracranial meningiomas are treated by surgical management as the tumors are commonly delineated from normal brain tissue and are not likely to adhere to the cerebral parenchyma. Although meningioma is the most common intracranial tumor in cats, the incidence of cystic meningioma is low. The objective of the current study is to report a case of frontal meningioma with peritumoral cystic structure removed by a partial transfrontal craniotomy. Case: A 10-year-old castrated British shorthair cat was referred to the Baeksan Feline Medical Center with a recent onset of seizures. On the physical examination, the patient was bright and alert. Neurological examinations were unremarkable at the time of presentation. Hematologic examinations were within normal limits. Thoracic and abdominal radiography, and abdominal ultrasonography revealed unremarkable findings. Magnetic resonance imaging revealed an extra-axial mass cranial to the frontal lobe. On the sagittal plane, a cystic structure was identified in the frontal area on post-contrast T1W images. No contrast enhancement of the cystic wall was identified after intravenous injection of contrast medium on T1W. On the transverse plane of T2W images, midline shift to the left due to peritumoral edema was observed. The mass was removed via partial transfrontal craniotomy. Postoperative radiography was performed to ensure appropriate placement of the mesh. The patient recovered uneventfully after anesthesia. After the surgery, the patient was closely monitored in an intensive care unit between 24 and 48 h. Based on the histologic findings, the final diagnosis was a fibroblastic meningioma. Nineteen months after the surgery, there was no seizure activity identified by the owner. Discussion: Depending on the location of the cyst, meningiomas can be classified into 4 types according to the human literature. In types 1 and 2, the whole cyst is located within the tumor, resulting in contrast enhancement of the cystic wall. In types 3 and 4, the cysts are located outside the tumor, and no contrast enhancement of the cystic wall is observed. In type 3, the cyst lies adjacent to the brain parenchyma rather than adjacent to the tumor and the meningioma is related to a cerebrospinal fluid cyst bordered by the arachnoid. It is important to classify the type of cystic meningioma prior to surgery in order to decide whether to remove the cystic wall. In type 2, the cystic wall is infiltrated by tumor cells, while the cystic wall of type 3 meningioma is composed of gliotic tissue without any tumor cells. Therefore, in type 2, the meningiomas with cystic walls should be removed for the prevention of recurrence, while in type 3 meningioma, the tumor can be managed by cyst decompression and excision of the solid component. Based on the Nauta classification, the cystic meningioma reported here was considered to be type 3. Therefore, the surgical procedure aimed to remove the solid component of the mass, leaving the cystic wall attached to the normal brain. As the solid part of the meningioma was located beneath the internal plate of the left frontal bone, the partial transfrontal craniotomy was sufficient to expose and remove the entire mass. To the author's knowledge, this is first case report describing a patient with frontal meningioma with a peritumoral cyst removed by a partial transfrontal craniotomy based on the Nauta classification.(AU)

Intoxicação espontânea por brotos de Xanthium spp. em bovinos no sul do Rio Grande do Sul / Spontaneous poisoning by sprouts of Xanthium spp. in cattle in southern Rio Grande do Sul

Background: Xanthium spp., the cockleburs, are invasive plants found on riverbanks, lakeshores, and floodplains. Ingestion of Xanthium sprouts or fruit causes cocklebur toxicosis, which is characterized clinically and pathologically by acuteliver failure. The main lesion observed is an accentuation of the lobular pattern of the liver (nutmeg appearance), whichis microscopically characterized by coagulation necrosis in the centrilobular region, hepatocyte degeneration in otherregions of the hepatic parenchyma, and sinusoidal congestion. The objective of this study was to describe an outbreak ofspontaneous cattle poisoning by ingestion of Xanthium spp. sprouts in the southern region of Rio Grande do Sul, Brazil.Case: In September 2018, a beef cattle farm located in Rio Grande county, Rio Grande do Sul, Brazil, reported significantmortality of cattle in a short period of time. There were 700 cattle on the property, divided by class into three differentherds, all kept under extensive conditions in native wetlands. All fields were heavily infested by cocklebur, with mostplants in the budding stage. Twenty animals developed muscle tremors, salivation, aggression, and recumbency. Theclinical course lasted 24 to 48 h, with a lethal outcome in all cases. An 18-month-old male crossbreed bovine was sent tothe Regional Diagnostic Laboratory of the Universidade Federal de Pelotas (UFPel) School of Veterinary Medicine fornecropsy. Gross examination revealed ascites and accentuation of the lobular pattern of the liver. Organ fragments wereharvested and fixed in 10% buffered formalin. Microscopically, the liver exhibited marked coagulation necrosis in thecentrilobular region and vacuolization of the hepatocyte cytoplasm in the midzonal and periportal regions. In the brain,there was perineuronal edema, cytoplasmic shrinkage and basophilia, gliosis, and satellitosis...

Intoxicação espontânea por brotos de Xanthium spp. em bovinos no sul do Rio Grande do Sul / Spontaneous poisoning by sprouts of Xanthium spp. in cattle in southern Rio Grande do Sul

Background: Xanthium spp., the cockleburs, are invasive plants found on riverbanks, lakeshores, and floodplains. Ingestion of Xanthium sprouts or fruit causes cocklebur toxicosis, which is characterized clinically and pathologically by acuteliver failure. The main lesion observed is an accentuation of the lobular pattern of the liver (nutmeg appearance), whichis microscopically characterized by coagulation necrosis in the centrilobular region, hepatocyte degeneration in otherregions of the hepatic parenchyma, and sinusoidal congestion. The objective of this study was to describe an outbreak ofspontaneous cattle poisoning by ingestion of Xanthium spp. sprouts in the southern region of Rio Grande do Sul, Brazil.Case: In September 2018, a beef cattle farm located in Rio Grande county, Rio Grande do Sul, Brazil, reported significantmortality of cattle in a short period of time. There were 700 cattle on the property, divided by class into three differentherds, all kept under extensive conditions in native wetlands. All fields were heavily infested by cocklebur, with mostplants in the budding stage. Twenty animals developed muscle tremors, salivation, aggression, and recumbency. Theclinical course lasted 24 to 48 h, with a lethal outcome in all cases. An 18-month-old male crossbreed bovine was sent tothe Regional Diagnostic Laboratory of the Universidade Federal de Pelotas (UFPel) School of Veterinary Medicine fornecropsy. Gross examination revealed ascites and accentuation of the lobular pattern of the liver. Organ fragments wereharvested and fixed in 10% buffered formalin. Microscopically, the liver exhibited marked coagulation necrosis in thecentrilobular region and vacuolization of the hepatocyte cytoplasm in the midzonal and periportal regions. In the brain,there was perineuronal edema, cytoplasmic shrinkage and basophilia, gliosis, and satellitosis...(AU)

Polioencephalomalacia (PEM) in calves associated with excess sulfur intake / Polioencefalomalacia em bezerros associada à ingestão de alimento com excesso de enxofre

Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to-3-month-old calves. Occurrence of PEM is rare in calves at such a young age.(AU)

A polioencefalomalacia (PEM) é a caracterização morfológica para o amolecimento da substância cinzenta encefálica, e uma de suas principais etiologias é a ingestão excessiva de enxofre. Este trabalho descreve um surto desta enfermidade em bezerros de um a três meses de idade em uma propriedade de Santa Catarina. O lote era composto por 27 bezerros machos da raça Jersey, com alimentação composta por ração inicial, milho inteiro triturado e sal mineral. Deste lote, 10 animais adoeceram, apresentando sinais de apatia, anorexia e cegueira, com evolução para fraqueza generalizada. Nove bezerros morreram e três foram submetidos a necropsia, que demonstraram achatamento das circunvoluções cerebrais além de áreas de amolecimento e coloração amarelada no córtex cerebral. Realizou-se exame histopatológico que evidenciou necrose laminar profunda associada a edema perineuronal e perivascular, além de neurônios com citoplasma enrugado, eosinofílico ou vacuolizado. A dosagem de enxofre resultou em 8010mg/Kg no milho, 6385mg/Kg na ração, 1060mg/Kg no sal mineral e 2,3mg/L na água, atingindo valores muito acima do tolerado, totalizando a ingestão diária de cerca de 6533,5mg de enxofre/animal/dia. Como diagnóstico diferencial realizou-se dosagem de chumbo de amostras de rim e fígado dos três bezerros com resultado negativo. Ainda, o último bovino a adoecer foi tratado com 20mg/Kg de tiamina e 0,2mg/Kg de dexametasona IM, QID, durante três dias e recuperou-se. De acordo com os achados anatomopatológicos e o excesso de enxofre na dieta, sugere-se que a intoxicação por enxofre seja a causa de PEM nestes bezerros de um a três meses de idade, sendo essa enfermidade rara em bovinos tão jovens.(AU)

Polioencephalomalacia (PEM) in calves associated with excess sulfur intake / Polioencefalomalacia em bezerros associada à ingestão de alimento com excesso de enxofre

Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to-3-month-old calves. Occurrence of PEM is rare in calves at such a young age.(AU)

A polioencefalomalacia (PEM) é a caracterização morfológica para o amolecimento da substância cinzenta encefálica, e uma de suas principais etiologias é a ingestão excessiva de enxofre. Este trabalho descreve um surto desta enfermidade em bezerros de um a três meses de idade em uma propriedade de Santa Catarina. O lote era composto por 27 bezerros machos da raça Jersey, com alimentação composta por ração inicial, milho inteiro triturado e sal mineral. Deste lote, 10 animais adoeceram, apresentando sinais de apatia, anorexia e cegueira, com evolução para fraqueza generalizada. Nove bezerros morreram e três foram submetidos a necropsia, que demonstraram achatamento das circunvoluções cerebrais além de áreas de amolecimento e coloração amarelada no córtex cerebral. Realizou-se exame histopatológico que evidenciou necrose laminar profunda associada a edema perineuronal e perivascular, além de neurônios com citoplasma enrugado, eosinofílico ou vacuolizado. A dosagem de enxofre resultou em 8010mg/Kg no milho, 6385mg/Kg na ração, 1060mg/Kg no sal mineral e 2,3mg/L na água, atingindo valores muito acima do tolerado, totalizando a ingestão diária de cerca de 6533,5mg de enxofre/animal/dia. Como diagnóstico diferencial realizou-se dosagem de chumbo de amostras de rim e fígado dos três bezerros com resultado negativo. Ainda, o último bovino a adoecer foi tratado com 20mg/Kg de tiamina e 0,2mg/Kg de dexametasona IM, QID, durante três dias e recuperou-se. De acordo com os achados anatomopatológicos e o excesso de enxofre na dieta, sugere-se que a intoxicação por enxofre seja a causa de PEM nestes bezerros de um a três meses de idade, sendo essa enfermidade rara em bovinos tão jovens.(AU)

Outbreak of Clostridium perfringens type D enterotoxemia in sheep / Surto de enterotoxemia por Clostridium perfringens tipo D em ovinos

This work describes the first Brazilian laboratory-confirmed outbreak of enterotoxemia caused by Clostridium perfringens type D in sheep, which occurred in the state of Paraná. We address the epidemiological aspects involved, the diagnostic modalities employed, and the clinical signs and pathological findings observed. Eight healthy pregnant female sheep with no history of vaccination for clostridiosis presented with a history of abrupt feeding changes and neurological manifestations that quickly evolved to illness, coma and death. Four other females with clinical neurological signs were referred to the Veterinary Hospital of the Universidade Federal do Paraná, Palotina Sector. These animals presented with lethargy, motor incoordination, opisthotonus, pedal movements, muscle tremors, spastic paralysis, bruxism, mandibular trismus, sialorrhea, hyperexcitability and the inability to stand. They were examined and euthanized due to the seriousness of the clinical picture with an unfavorable prognosis. We performed gross anatomical and microscopic analyses of the organs and intestinal contents. We also performed bacterial isolation with molecular typing. From the intestinal contents, we detected toxins by means of the seroneutralization technique in mice. At necropsy, we noted pulmonary edema (2/4), necrotizing enteritis (4/4) and hyperemia of the leptomeninges (1/4). Microscopically, we observed lymphohistiocytic interstitial pneumonia, necrotic enteritis associated with the presence of rods, and nephrosis with interstitial lymphohistiocytic nephritis. No significant brain lesions were observed. Using serum neutralization, we identified epsilon toxin in the intestinal contents of all four animals. C. perfringens type D was identified. Based on the history, clinical signs, postmortem findings, and laboratory confirmation of the presence of epsilon toxin, we concluded that C. perfringens type D enterotoxemia caused this outbreak of sheep deaths.

Este trabalho descreve o primeiro surto brasileiro com confirmação laboratorial de enterotoxemia em ovinos por Clostridium perfringens tipo D, ocorrido no estado do Paraná, abordando os aspectos epidemiológicos envolvidos, sinais clínicos observados, achados patológicos e diagnóstico empregado. Oito fêmeas ovina, gestantes, em bom estado corporal e com histórico de mudanças bruscas na alimentação, sem histórico de vacinação para clostridioses, apresentaram manifestações clínicas neurológicas que logo evoluíram para decúbito, coma e morte. Outras quatro fêmeas apresentaram os sinais clínicos neurológicos e foram encaminhadas ao Hospital Veterinário da Universidade Federal do Paraná, setor Palotina. Os animais foram examinados e submetidos à eutanásia devido à gravidade do quadro clínico e prognóstico desfavorável. Destes quatro animais foram coletados fragmentos de órgãos e do conteúdo intestinal. Foi realizada análise macroscópica e microscópica dos órgãos, bem como isolamento bacteriano, tipificação molecular do agente e a detecção das toxinas por meio da técnica de soroneutralização em camundongos a partir do conteúdo intestinal. Os quatro ovinos examinados apresentaram letargia, incoordenação motora, opistótono, movimentos de pedalagem, tremores musculares, paralisia espástica, bruxismo, trismo mandibular, sialorréia, hiperexcitabilidade e decúbito. Na necropsia, constatou-se edema pulmonar (2/4), enterite necrohemorrágica (4/4) e hiperemia de leptomeninges (1/4). Microscopicamente havia pneumonia intersticial linfohistiocitária, enterite necrótica associada com a presença de bastonetes e nefrose com nefrite intersticial linfohistiocitária. Não foram observadas lesões encefálicas dignas de nota em função do quadro agudo da doença. Por meio da soroneutralização foi possível identificar a presença da toxina épsilon no conteúdo intestinal dos quatro...

Outbreak of Clostridium perfringens type D enterotoxemia in sheep / Surto de enterotoxemia por Clostridium perfringens tipo D em ovinos

This work describes the first Brazilian laboratory-confirmed outbreak of enterotoxemia caused by Clostridium perfringens type D in sheep, which occurred in the state of Paraná. We address the epidemiological aspects involved, the diagnostic modalities employed, and the clinical signs and pathological findings observed. Eight healthy pregnant female sheep with no history of vaccination for clostridiosis presented with a history of abrupt feeding changes and neurological manifestations that quickly evolved to illness, coma and death. Four other females with clinical neurological signs were referred to the Veterinary Hospital of the Universidade Federal do Paraná, Palotina Sector. These animals presented with lethargy, motor incoordination, opisthotonus, pedal movements, muscle tremors, spastic paralysis, bruxism, mandibular trismus, sialorrhea, hyperexcitability and the inability to stand. They were examined and euthanized due to the seriousness of the clinical picture with an unfavorable prognosis. We performed gross anatomical and microscopic analyses of the organs and intestinal contents. We also performed bacterial isolation with molecular typing. From the intestinal contents, we detected toxins by means of the seroneutralization technique in mice. At necropsy, we noted pulmonary edema (2/4), necrotizing enteritis (4/4) and hyperemia of the leptomeninges (1/4). Microscopically, we observed lymphohistiocytic interstitial pneumonia, necrotic enteritis associated with the presence of rods, and nephrosis with interstitial lymphohistiocytic nephritis. No significant brain lesions were observed. Using serum neutralization, we identified epsilon toxin in the intestinal contents of all four animals. C. perfringens type D was identified. Based on the history, clinical signs, postmortem findings, and laboratory confirmation of the presence of epsilon toxin, we concluded that C. perfringens type D enterotoxemia caused this outbreak of sheep deaths.(AU)

Este trabalho descreve o primeiro surto brasileiro com confirmação laboratorial de enterotoxemia em ovinos por Clostridium perfringens tipo D, ocorrido no estado do Paraná, abordando os aspectos epidemiológicos envolvidos, sinais clínicos observados, achados patológicos e diagnóstico empregado. Oito fêmeas ovina, gestantes, em bom estado corporal e com histórico de mudanças bruscas na alimentação, sem histórico de vacinação para clostridioses, apresentaram manifestações clínicas neurológicas que logo evoluíram para decúbito, coma e morte. Outras quatro fêmeas apresentaram os sinais clínicos neurológicos e foram encaminhadas ao Hospital Veterinário da Universidade Federal do Paraná, setor Palotina. Os animais foram examinados e submetidos à eutanásia devido à gravidade do quadro clínico e prognóstico desfavorável. Destes quatro animais foram coletados fragmentos de órgãos e do conteúdo intestinal. Foi realizada análise macroscópica e microscópica dos órgãos, bem como isolamento bacteriano, tipificação molecular do agente e a detecção das toxinas por meio da técnica de soroneutralização em camundongos a partir do conteúdo intestinal. Os quatro ovinos examinados apresentaram letargia, incoordenação motora, opistótono, movimentos de pedalagem, tremores musculares, paralisia espástica, bruxismo, trismo mandibular, sialorréia, hiperexcitabilidade e decúbito. Na necropsia, constatou-se edema pulmonar (2/4), enterite necrohemorrágica (4/4) e hiperemia de leptomeninges (1/4). Microscopicamente havia pneumonia intersticial linfohistiocitária, enterite necrótica associada com a presença de bastonetes e nefrose com nefrite intersticial linfohistiocitária. Não foram observadas lesões encefálicas dignas de nota em função do quadro agudo da doença. Por meio da soroneutralização foi possível identificar a presença da toxina épsilon no conteúdo intestinal dos quatro...(AU)