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.

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.

Síndrome do mau ajustamento neonatal em potros: foco em neuroesteróides / Foal mal adjustment syndrome: focus on neurosteroids

O processo de transição do feto para a vida extra-uterina é considerado um período crítico que requer complexas adaptações fisiológicas do potro neonato. Eventos estressores de origem hipóxicoisquêmicas no periparto podem desencadear um quadro de encefalopatia neonatal equina, também conhecida como síndrome do mau ajustamento neonatal. O diagnóstico é feito baseado na avaliação clínica e na anamnese e avaliação do histórico da gestação. Casos leves a moderados tem prognóstico favorável. É imprescindível o entendimento da endocrinologia da gestação, do papel dos neuroesteróides no desenvolvimento do sistema nervoso fetal para que o estabelecimento precoce da terapia adequada seja realizado de maneira bem sucedida. Assim, o objetivo do presente é abordar os principais aspectos clínicos e fisiopatológicos da Síndrome do Mau Ajustamento Neonatal em neonatos equinos, com foco especial no papel dos neuroesteróides durante a maturação cerebral do feto no terço final da gestação e na transição para a vida extra-uterina.

The transition from fetus to extrauterine life is considered a critical period that requires complex physiological adaptations on the part of the newborn foal. Peripartum hypoxic-ischemic stressors can result in equine neonatal encephalopathy, also known to as neonatal maladjustment syndrome. The diagnosis is made based on clinical examination, anamnesis, and a review of the mare’s pregnancy history. Cases that are mild to moderate in severity have a favorable prognosis. It is critical to understand the endocrinology of pregnancy and the role of neurosteroids in the development of the fetal nervous system in order to successfully initiate appropriate therapy early. Thus, the purpose of this article is to discuss the major clinical and pathophysiological aspects of neonatal maladjustment syndrome in equine neonates, with a particular emphasis on the role of neurosteroids during fetal brain maturation in the final third of pregnancy and during the transition to extrauterine life.

Anestesia para correção de shunt portossistêmico com anel de ameróide em cão / Anesthesia for the correction of portosystemic shunt with an ameroid ring in a dog

O shunt ou desvio portossistêmico (DPS) é uma conexão anormal entre a circulação portal e sistêmica, que desvia o fluxo sanguíneo do fígado em variados graus. Nesse contexto, uma anestesia de qualidade e segura faz toda diferença na recuperação do paciente. Com isso, o presente trabalho teve o objetivo de relatar a técnica anestésica utilizada para o tratamento cirúrgico de um caso de shunt portossistêmico congênito em um cão da raça Yorkshire Terrier, fêmea, de quatro anos, pesando aproximadamente quatro quilos, que apresentava sintomas neurológicos decorrentes de encefalopatia hepática, devido à DPS. Para a medicação pré-anestésica (MPA), foi utilizado o cloridrato de remifentanila (2mg), na taxa de 10µg/Kg/h. Propofol (1%) foi utilizado para indução anestésica, na dose de 1mg/Kg/min, e para anestesia periglótica foi usado cloridrato de lidocaína (2%), no volume de 0,1mL/Kg. Quanto à manutenção anestésica, foi utilizado isoflurano (100%), em um vaporizador universal, citrato de maropitant (1%) em infusão contínua, na taxa de 30µg/Kg/h, cloridrato de remifentanila (2%), na mesma taxa utilizada na MPA, cetamina (10%), na taxa de 0,6mg/Kg/h, e brometo de rocurônio (10mg/mL), na dose de 0,15mg/Kg. Antes do início da cirurgia, foi realizado um bloqueio intraperitoneal com cloridrato de ropivacaína (0,4mg/Kg) diluída em 0,4mL/Kg, na dose de 0,1mL/Kg. Durante todo o procedimento cirúrgico, não houveram intercorrências nem alterações nos parâmetros fisiológicos. Dessa forma, pôde-se observar a eficácia da técnica anestésica utilizada para correção de shunt portossistêmico em um cão apresentando sintomatologia neurológica.

Shunt or portosystemic deviation (DPS) is an abnormal connection between portal and systemic circulation that diverts blood flow from the liver to varying degrees. In this context, quality and safe anesthesia makes all the difference in the patient's recovery. Thus, the present study aims to report the anesthetic technique used for the surgical treatment of a case of congenital portosystemic shunt in a four-year-old Yorkshire Terrier dog, weighing approximately four kilograms, which presented neurological symptoms resulting from of hepatic encephalopathy due to DPS. For pre-anesthetic medication (MPA), remifentanil hydrochloride (2mg) was used at a rate of 10µg/Kg/h. Propofol (1%) was used for anesthetic induction at a dose of 1mg/kg/min and for periglotic anesthesia lidocaine hydrochloride (2%) in a volume of 0.1mL/kg was used. As for anesthetic maintenance, isoflurane (100%) in a universal vaporizer, maropitant citrate (1%) in continuous infusion, at the rate of 30µg/Kg/h, remifentanil hydrochloride (2%), at the same rate used in MPA, ketamine (10%) at a rate of 0.6mg/kg/h and rocuronium bromide (10mg/mL), at a dose of 0.15mg/kg. Before the start of surgery, an intraperitoneal block was performed with ropivacaine hydrochloride (0.4mg/kg) diluted in 0.4mL/kg, in the dose of 0.1mL/kg. Throughout the surgical procedure, there were no complications or changes in physiological parameters. Thus, it was possible to observe the effectiveness of the anesthetic technique used to correct portosystemic shunt in a dog presenting neurological symptoms.

Lúpus eritematoso sistêmico associado a manifestações neurológicas em cadela da raça Border Collie / Systemic lupus erythematosus associated with neurological manifestations in a Border Collie bitch

Background: Systemic lupus erythematosus (SLE) is an immune-mediated and multisystemic disorder which etiology is believed to be multifactorial. Its clinical signs vary accordingly to affected organs, cutaneous lesions being the most frequently observed. There are few reports of SLE in dogs with neurological manifestations. Therefore, the aim of this report is to describe a case of SLE in a dog with indicative signs of nervous system involvement. Case: A 6-year-old Border Collie bitch was referred to the Veterinary Hospital (HVU) of the University of Uberaba (UNIUBE) with a history of cluster seizures, inappetence and urinary incontinence. Erythema and flaking of nasal plan were noted on physical examination, and splenomegaly on abdominal palpation. Thrombocytopenia and slightly increased ALT were found on blood tests. Ehrlichiosis was suspected and doxycycline was prescribed along with phenobarbital for the control of seizures. In the follow-up visit, the dog was still presenting urinary incontinence, thrombocytopenia and splenomegaly. Also, an ulcer on the nasal mucocutaneous junction was observed. The patient went through a neurological examination which indicated thalamocortical lesion. Cerebrospinal fluid samples were obtained for cytology, culture and canine distemper test, and serology tests for leishmaniasis, toxoplasmosis and neosporosis were done. No alterations were found in these exams. The histopathology of the nasal lesion was proceeded and showed results consistent with lupus erythematosus. It was prescribed a 15-day course of prednisolone at immunosuppressive dose. The patient showed clinical improvement with this treatment. Azathioprine was started along with gradual removal of prednisolone. After twenty days of discontinuation of this drug, the dog presented epileptic seizures, urinary incontinence, thrombocytopenia, increased ALT and worsened nasal lesion. Prednisolone at immunosuppressive dose was reintroduced and the dose of phenobarbital, increased. One week past this, the patient showed inappetence and an extensive hematoma in the thoracic region. Lab exams confirmed drug-induced acute pancreatitis. All medications were interrupted, the patient was hospitalized, and treatment for pancreatitis was initiated, but the dog passed away. Discussion: For involving multiple body systems and for presenting varied clinical signs, diagnosing SLE can be challenging in clinical routine. The dog from this report was a Border Collie; this breed is considered to be predisposed to this disease. The animal had a history of being exposed to solar radiation for a large part of the day, had dyspigmentation of nasal plan and had no application of sunscreen, predisposing the occurrence of SLE. Neurological signs are uncommon in SLE, but the seizures and the urinary incontinence were the main reasons for the dog's guardian to look for medical assistance. The suspicion for SLE was raised due to cutaneous manifestations and persistent thrombocytopenia along with splenomegaly. Histopathological findings are essential for diagnosing SLE, as well as antinuclear antibody tests. Nonetheless, due to financial limitations, this last test was not performed. Azathioprine is an immunomodulating drug largely used along with glucocorticoids when treating SLE; however, this medication is prone to induce side effects as the ones presented by the dog from this report. Therefore, it is concluded that SLE should be considered as a differential diagnosis in patients showing cutaneous, hematological, systemic and neurological manifestations, considering the variety of signs caused by this disorder.(AU)

Anestesia para correção de shunt portossistêmico com anel de ameróide em cão / Anesthesia for the correction of portosystemic shunt with an ameroid ring in a dog

O shunt ou desvio portossistêmico (DPS) é uma conexão anormal entre a circulação portal e sistêmica, que desvia o fluxo sanguíneo do fígado em variados graus. Nesse contexto, uma anestesia de qualidade e segura faz toda diferença na recuperação do paciente. Com isso, o presente trabalho teve o objetivo de relatar a técnica anestésica utilizada para o tratamento cirúrgico de um caso de shunt portossistêmico congênito em um cão da raça Yorkshire Terrier, fêmea, de quatro anos, pesando aproximadamente quatro quilos, que apresentava sintomas neurológicos decorrentes de encefalopatia hepática, devido à DPS. Para a medicação pré-anestésica (MPA), foi utilizado o cloridrato de remifentanila (2mg), na taxa de 10µg/Kg/h. Propofol (1%) foi utilizado para indução anestésica, na dose de 1mg/Kg/min, e para anestesia periglótica foi usado cloridrato de lidocaína (2%), no volume de 0,1mL/Kg. Quanto à manutenção anestésica, foi utilizado isoflurano (100%), em um vaporizador universal, citrato de maropitant (1%) em infusão contínua, na taxa de 30µg/Kg/h, cloridrato de remifentanila (2%), na mesma taxa utilizada na MPA, cetamina (10%), na taxa de 0,6mg/Kg/h, e brometo de rocurônio (10mg/mL), na dose de 0,15mg/Kg. Antes do início da cirurgia, foi realizado um bloqueio intraperitoneal com cloridrato de ropivacaína (0,4mg/Kg) diluída em 0,4mL/Kg, na dose de 0,1mL/Kg. Durante todo o procedimento cirúrgico, não houveram intercorrências nem alterações nos parâmetros fisiológicos. Dessa forma, pôde-se observar a eficácia da técnica anestésica utilizada para correção de shunt portossistêmico em um cão apresentando sintomatologia neurológica.(AU)

Shunt or portosystemic deviation (DPS) is an abnormal connection between portal and systemic circulation that diverts blood flow from the liver to varying degrees. In this context, quality and safe anesthesia makes all the difference in the patient's recovery. Thus, the present study aims to report the anesthetic technique used for the surgical treatment of a case of congenital portosystemic shunt in a four-year-old Yorkshire Terrier dog, weighing approximately four kilograms, which presented neurological symptoms resulting from of hepatic encephalopathy due to DPS. For pre-anesthetic medication (MPA), remifentanil hydrochloride (2mg) was used at a rate of 10µg/Kg/h. Propofol (1%) was used for anesthetic induction at a dose of 1mg/kg/min and for periglotic anesthesia lidocaine hydrochloride (2%) in a volume of 0.1mL/kg was used. As for anesthetic maintenance, isoflurane (100%) in a universal vaporizer, maropitant citrate (1%) in continuous infusion, at the rate of 30µg/Kg/h, remifentanil hydrochloride (2%), at the same rate used in MPA, ketamine (10%) at a rate of 0.6mg/kg/h and rocuronium bromide (10mg/mL), at a dose of 0.15mg/kg. Before the start of surgery, an intraperitoneal block was performed with ropivacaine hydrochloride (0.4mg/kg) diluted in 0.4mL/kg, in the dose of 0.1mL/kg. Throughout the surgical procedure, there were no complications or changes in physiological parameters. Thus, it was possible to observe the effectiveness of the anesthetic technique used to correct portosystemic shunt in a dog presenting neurological symptoms.(AU)

Intravascular lymphoma in a dog: case report

Intravascular lymphoma is characterized by being a malignant neoplasm of extranodal T or B lymphocytes with exclusive proliferation within the vascular lumen, particularly of small vessels. The clinical signs vary due to the involvement of several organs, mainly the central nervous system. The diagnosis is difficult because many of the tests performed are not conclusive and, therefore, necropsy is the most efficient way to identify this tumor. This case report aims to describe the anatomopathological findings of a case of intravascular lymphoma in a mixed breed, 8 years old dog who presented neurological signs and was submitted to a necroscopic examination with clinical suspicion of granulomatous meningoencephalitis. The necropsy findings were not specific, but the presence of intravascular neoplastic lymphocytes int he brain, spleen, adrenal gland and stomach was verified by microscopy. These cells were positive for the CD3 antibody by immunohistochemistry, confirming the T lymphocyte phenotype. This neoplasm should be considered in the diagnosis of encephalopathies in dogs.(AU)

Intravascular lymphoma in a dog: case report

Intravascular lymphoma is characterized by being a malignant neoplasm of extranodal T or B lymphocytes with exclusive proliferation within the vascular lumen, particularly of small vessels. The clinical signs vary due to the involvement of several organs, mainly the central nervous system. The diagnosis is difficult because many of the tests performed are not conclusive and, therefore, necropsy is the most efficient way to identify this tumor. This case report aims to describe the anatomopathological findings of a case of intravascular lymphoma in a mixed breed, 8 years old dog who presented neurological signs and was submitted to a necroscopic examination with clinical suspicion of granulomatous meningoencephalitis. The necropsy findings were not specific, but the presence of intravascular neoplastic lymphocytes int he brain, spleen, adrenal gland and stomach was verified by microscopy. These cells were positive for the CD3 antibody by immunohistochemistry, confirming the T lymphocyte phenotype. This neoplasm should be considered in the diagnosis of encephalopathies in dogs.

Abordagem clínico-cirúrgica de desvio portossistêmico congênito em pequenos animais: quais as novidades? / Clinical and surgical approach of congenital portosystemic shunt in small animals: are there new informations?

Foi realizada uma revisão sobre a fisiopatogenia, sinais clínicos, diagnóstico e principais tratamentos e técnicas para o desvio portossistêmico em pequenos animais. As fontes pesquisadas foram: CAB, MEDILINE por um período retrospectivo de 20 anos e acervos da Biblioteca da Faculdade de Medicina Veterinária e Zootecnia (FMVZ) da Universidade de São Paulo (USP). O desvio portossistêmico congênito (DPSC) é uma das anormalidades vasculares mais comuns em cães, as raças de pequeno porte apresentam maior incidência. Os DPSCs em cães e gatos são comunicações vasculares que ocorrem do sistema venoso portal para o sistema venoso sistêmico, ou seja, fazem uma via secundária. Há dois tipos de DPSCs, intra-hepático e extra-hepático, observados com frequência em raças de grande porte e miniaturas, respectivamente. O diagnóstico é baseado no histórico de animais jovens com retardo de crescimento, letargia, convulsão ou distúrbio de comportamento principalmente após alimentação, retorno demorado de anestesia ou sedação, crise de encefalopatia hepática, em raças predispostas. A confirmação do vaso anômalo é realizada pela ultrassonografia com doppler, angiografia por tomografia computadorizada ou por ressonância magnética.(AU)

It was performed a review of pathophysiology, clinical signs, diagnostic and main treatments and techniques for portosystemic shunts in small animals. The researched Sources were: a 20 years retrospective research of CAB, MEDILINE and collection of Faculty of MedicineVeterinary and Animal Science (FMVZ) of the Universidade de São Paulo (USP). Congenital portossystemic shunts (CPSS) are one of the vascular abnormalities more common in dogs. Small breeds are the most affected. The CPSS in dogs and cats, are vascular communications between portal venous system and systemic venous system, in other words, a secondary via. There are two types of CPSS, the intrahepatic and extrahepatic shunts, observed in large and small breeds, respectively. The diagnosis is based on clinical findings of young dogs referring delayed development, lethargy, convulsions, behavior disturbances mainly after food ingestion, poor recovery after anesthesia or sedation, hepatic encephalopathy crisis observed breeds with predisposition. Definitive diagnosis of CPSS is done by abdominal doppler ultrasonography, computed tomography angiography or magnetic resonance. Medical management can alleviate signs of hepatic encephalopathy. However, long term treatment is questionable because blood circulation is still bypassing liver to systemic circulation, leading to disturbance of hepatotropic factors distribution to the liver, resulting in liver atrophy. The only definitive treatment is the surgical one. The ideal technique is the progressive attenuation of anomalous vessel and avoid acute portal hypertension. Within the described techniques for surgical treatment, the use of ameroid constrictor represents the safest way of vessel closure. On the other way, some CPS patients can suffer severe perioperative complications. So they need specific clinical and surgical approaches associated to precise image diagnostic to correct localization of the anomalous vessel and surgical success.(AU)

Abordagem clínico-cirúrgica de desvio portossistêmico congênito em pequenos animais: quais as novidades? / Clinical and surgical approach of congenital portosystemic shunt in small animals: are there new informations?

Foi realizada uma revisão sobre a fisiopatogenia, sinais clínicos, diagnóstico e principais tratamentos e técnicas para o desvio portossistêmico em pequenos animais. As fontes pesquisadas foram: CAB, MEDILINE por um período retrospectivo de 20 anos e acervos da Biblioteca da Faculdade de Medicina Veterinária e Zootecnia (FMVZ) da Universidade de São Paulo (USP). O desvio portossistêmico congênito (DPSC) é uma das anormalidades vasculares mais comuns em cães, as raças de pequeno porte apresentam maior incidência. Os DPSCs em cães e gatos são comunicações vasculares que ocorrem do sistema venoso portal para o sistema venoso sistêmico, ou seja, fazem uma via secundária. Há dois tipos de DPSCs, intra-hepático e extra-hepático, observados com frequência em raças de grande porte e miniaturas, respectivamente. O diagnóstico é baseado no histórico de animais jovens com retardo de crescimento, letargia, convulsão ou distúrbio de comportamento principalmente após alimentação, retorno demorado de anestesia ou sedação, crise de encefalopatia hepática, em raças predispostas. A confirmação do vaso anômalo é realizada pela ultrassonografia com doppler, angiografia por tomografia computadorizada ou por ressonância magnética.

It was performed a review of pathophysiology, clinical signs, diagnostic and main treatments and techniques for portosystemic shunts in small animals. The researched Sources were: a 20 years retrospective research of CAB, MEDILINE and collection of Faculty of MedicineVeterinary and Animal Science (FMVZ) of the Universidade de São Paulo (USP). Congenital portossystemic shunts (CPSS) are one of the vascular abnormalities more common in dogs. Small breeds are the most affected. The CPSS in dogs and cats, are vascular communications between portal venous system and systemic venous system, in other words, a secondary via. There are two types of CPSS, the intrahepatic and extrahepatic shunts, observed in large and small breeds, respectively. The diagnosis is based on clinical findings of young dogs referring delayed development, lethargy, convulsions, behavior disturbances mainly after food ingestion, poor recovery after anesthesia or sedation, hepatic encephalopathy crisis observed breeds with predisposition. Definitive diagnosis of CPSS is done by abdominal doppler ultrasonography, computed tomography angiography or magnetic resonance. Medical management can alleviate signs of hepatic encephalopathy. However, long term treatment is questionable because blood circulation is still bypassing liver to systemic circulation, leading to disturbance of hepatotropic factors distribution to the liver, resulting in liver atrophy. The only definitive treatment is the surgical one. The ideal technique is the progressive attenuation of anomalous vessel and avoid acute portal hypertension. Within the described techniques for surgical treatment, the use of ameroid constrictor represents the safest way of vessel closure. On the other way, some CPS patients can suffer severe perioperative complications. So they need specific clinical and surgical approaches associated to precise image diagnostic to correct localization of the anomalous vessel and surgical success.

Traceability of animal protein byproducts in ruminants by multivariate analysis of isotope ratio mass spectrometry to prevent transmission of prion diseases

Ruminant feed containing animal byproduct proteins (ABPs) is prohibited in many countries due to its risk of transmitting prion diseases (PD). In most cases the entire herd is sacrificed, which causes great harm to the producer countries by preventing their exportation of ruminant derived-products. Methods: We used stable isotope ratio mass spectrometry (IRMS) of carbon (13C/12C) and nitrogen (15N/14N) to trace the animal protein in the blood of 15 buffaloes (Bubalus bubalis) divided into three experimental groups: 1 - received only vegetable protein (VP) during 117 days; 2 - received animal and vegetable protein (AVP); and 3 - received animal and vegetable protein with animal protein subsequently removed (AVPR). Groups 2 and 3 received diets containing 13.7% bovine meat and bone meal (MBM) added to a vegetable diet (from days 21-117 in the AVP group and until day 47 in the AVPR group, when MBM was removed). Results: On the 36th day, differences were detectable in the feeding profile (p <0.01) among the three experimental groups, which remained for a further 49 days (85th day). The AVPR group showed isotopic rate reversibility on the 110th day by presenting values similar to those in the control group (VP) (p> 0.05), indicating that it took 63 days to eliminate MBM in this group. Total atoms exchange (> 95%) of 13C and 15N was observed through incorporation of the diet into the AVP and AVPR groups. Conclusions: IRMS is an accurate and sensitive technique for tracing the feeding profile of ruminants through blood analysis, thus enabling investigation of ABP use. enabling investigation of ABP use.(AU)

Traceability of animal protein byproducts in ruminants by multivariate analysis of isotope ratio mass spectrometry to prevent transmission of prion diseases

Background: Ruminant feed containing animal byproduct proteins (ABPs) is prohibited in many countries due to its risk of transmitting prion diseases (PD). In most cases the entire herd is sacrificed, which causes great harm to the producer countries by preventing their exportation of ruminant derived-products. Methods: We used stable isotope ratio mass spectrometry (IRMS) of carbon (13C/12C) and nitrogen (15N/14N) to trace the animal protein in the blood of 15 buffaloes (Bubalus bubalis) divided into three experimental groups: 1 - received only vegetable protein (VP) during 117 days; 2 - received animal and vegetable protein (AVP); and 3 - received animal and vegetable protein with animal protein subsequently removed (AVPR). Groups 2 and 3 received diets containing 13.7% bovine meat and bone meal (MBM) added to a vegetable diet (from days 21-117 in the AVP group and until day 47 in the AVPR group, when MBM was removed). Results: On the 36th day, differences were detectable in the feeding profile (p 0.01) among the three experimental groups, which remained for a further 49 days (85th day). The AVPR group showed isotopic rate reversibility on the 110th day by presenting values similar to those in the control group (VP) (p> 0.05), indicating that it took 63 days to eliminate MBM in this group. Total atoms exchange (> 95%) of 13C and 15N was observed through incorporation of the diet into the AVP and AVPR groups. Conclusions: IRMS is an accurate and sensitive technique for tracing the feeding profile of ruminants through blood analysis, thus enabling investigation of ABP use.(AU)

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos / Hepatic encephalopathy secondary to poisoning by Tephrosia cinerea in sheep

A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.(AU)

In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.(AU)

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos / Hepatic encephalopathy secondary to poisoning by Tephrosia cinerea in sheep

A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.(AU)

In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.(AU)

Encefalopatia hepática secundária à intoxicação por Tephrosia cinerea em ovinos

ABSTRACT: In the semiarid region of northeastern Brazil, Tephrosia cinerea causes periacinar hepatic fibrosis in sheep with severe ascites and, occasionally, nervous signs. Sixteen sheep from six outbreaks of T. cinerea poisoning were studied. All sheep had histologic lesion of periacinar fibrosis and six showed, in the brain, vacuolization (spongy degeneration) of the white matter and junction between grey and white matter and presence of Alzheimer type II astrocytes in the grey matter. The disease was produced experimentally in two sheep, that presented porto-sistemic shunts and similar histologic lesions as those observed in the spontaneous cases. Immunohistochemistry revealed weak labelling with anti-GFAP antibodies suggesting a degenerative alteration of astrocytes with accumulation of dense bodies and reduction of the GFAP. There was strong labelling with anti-S100 antibodies suggesting cellular reactivity with proliferation of mitochondria and endoplasmatic reticulum. Such alterations are characteristic of the effects caused by ammonia on the astrocytes. It is concluded that in poisoning by T. cinerea nervous signs due to hepatic encephalopathy occur in some sheep.

RESUMO: A intoxicação por Tephrosia cinerea causa fibrose hepática periacinar em ovinos na região semiárida do Nordeste, com quadro clínico de ascite acentuada, e, ocasionalmente, com sinais neurológicos. Neste trabalho foram estudadas 16 ovinos em 6 surtos de intoxicação por T. cinerea. Todos os ovinos apresentaram lesões histológicas de fibrose periacinar e seis apresentaram, no encéfalo, vacuolização da substância branca e da junção entre a substância branca e a cinzenta com presença de astrócitos de Alzheimer tipo II na substância cinzenta. A doença foi reproduzida experimentalmente em dois ovinos que apresentaram ascite, desvios vasculares (shunts) porto-sistêmicos e sinais nervosos com lesões histológicas semelhantes a dos casos espontâneos. Na técnica de imuno-histoquímica houve marcação fraca ou ausente do citoplasma astrocitário para o anticorpo anti-GFAP em seis ovinos evidenciando uma alteração degenerativa, em que os astrócitos acumulam corpos densos e reduzem o volume de GFAP. Houve marcação positiva para o anticorpo anti-S100 em oito ovinos, incluindo os dois ovinos experimentais o que sugere reatividade celular, com proliferação mitocondrial e de retículo endoplasmático liso. Estas alterações são caraterísticas dos efeitos da amônia nos astrócitos. Conclui-se que na intoxicação por T. cinerea em alguns ovinos ocorrem sinais nervosos em consequência da encefalopatia hepática.

Polymorphisms in the Prion Protein Gene of cattle breeds from Brazil / Polimorfismos no gene da proteína priônica em bovinos no Brasil

One of the alterations that occur in the PRNP gene in bovines is the insertion/deletion (indel) of base sequences in specific regions, such as indels of 12-base pairs (bp) in intron 1 and of 23- bp in the promoter region. The deletion allele of 23 bp is associated with susceptibility to bovine spongiform encephalopathy (BSE) as well as the presence of the deletion allele of 12 bp. In the present study, the variability of nucleotides in the promoter region and intron 1 of the PRNP gene was genotyped for the Angus, Canchim, Nellore and Simmental bovine breeds to identify the genotype profiles of resistance and/or susceptibility to BSE in each animal. Genomic DNA was extracted for amplification of the target regions of the PRNP gene using polymerase chain reaction (PCR) and specific primers. The PCR products were submitted to electrophoresis in agarose gel 3% and sequencing for genotyping. With the exception of the Angus breed, most breeds exhibited a higher frequency of deletion alleles for 12 bp and 23 bp in comparison to their respective insertion alleles for both regions. These results represent an important contribution to understanding the formation process of the Brazilian herd in relation to bovine PRNP gene polymorphisms.(AU)

Uma das mudanças que ocorrem no gene PRNP em bovinos é a inserção e/ou deleção (indels) de sequências de bases, em determinadas regiões como, por exemplo, as indels de 12 pares de bases (pb) no íntron 1 e 23pb na região promotora. O alelo de deleção de 23pb está relacionado com a suscetibilidade à Encefalopatia Espongiforme Bovina (EEB), assim como a presença do alelo de deleção de 12pb. Neste estudo foi genotipada a variabilidade de nucleotídeos da região promotora e íntron 1 do gene PRNP em bovinos das raças Angus, Canchim, Nelore e Simental, para identificar os perfis genotípicos de resistência e/ou suscetibilidade à EEB de cada animal. Foi realizada a extração de DNA genômico para amplificação das regiões alvo do gene PRNP, por meio da reação em cadeia de polimerase (PCR) utilizando-se primers específicos. Os produtos da PCR foram submetidos à eletroforese em gel de agarose a 3%, e sequenciamento para a realização da genotipagem. Com exceção da raça Angus, a maioria das raças apresentaram maiores frequências do alelo de deleção tanto para 12pb como 23pb, em comparação com seus respectivos alelos de inserção, para as duas regiões. Esses resultados abrem caminhos para o conhecimento de como o rebanho brasileiro está sendo formado com relação aos polimorfismos do gene PRNP bovino.(AU)

Polymorphisms in the Prion Protein Gene of cattle breeds from Brazil / Polimorfismos no gene da proteína priônica em bovinos no Brasil

One of the alterations that occur in the PRNP gene in bovines is the insertion/deletion (indel) of base sequences in specific regions, such as indels of 12-base pairs (bp) in intron 1 and of 23- bp in the promoter region. The deletion allele of 23 bp is associated with susceptibility to bovine spongiform encephalopathy (BSE) as well as the presence of the deletion allele of 12 bp. In the present study, the variability of nucleotides in the promoter region and intron 1 of the PRNP gene was genotyped for the Angus, Canchim, Nellore and Simmental bovine breeds to identify the genotype profiles of resistance and/or susceptibility to BSE in each animal. Genomic DNA was extracted for amplification of the target regions of the PRNP gene using polymerase chain reaction (PCR) and specific primers. The PCR products were submitted to electrophoresis in agarose gel 3% and sequencing for genotyping. With the exception of the Angus breed, most breeds exhibited a higher frequency of deletion alleles for 12 bp and 23 bp in comparison to their respective insertion alleles for both regions. These results represent an important contribution to understanding the formation process of the Brazilian herd in relation to bovine PRNP gene polymorphisms.(AU)

Uma das mudanças que ocorrem no gene PRNP em bovinos é a inserção e/ou deleção (indels) de sequências de bases, em determinadas regiões como, por exemplo, as indels de 12 pares de bases (pb) no íntron 1 e 23pb na região promotora. O alelo de deleção de 23pb está relacionado com a suscetibilidade à Encefalopatia Espongiforme Bovina (EEB), assim como a presença do alelo de deleção de 12pb. Neste estudo foi genotipada a variabilidade de nucleotídeos da região promotora e íntron 1 do gene PRNP em bovinos das raças Angus, Canchim, Nelore e Simental, para identificar os perfis genotípicos de resistência e/ou suscetibilidade à EEB de cada animal. Foi realizada a extração de DNA genômico para amplificação das regiões alvo do gene PRNP, por meio da reação em cadeia de polimerase (PCR) utilizando-se primers específicos. Os produtos da PCR foram submetidos à eletroforese em gel de agarose a 3%, e sequenciamento para a realização da genotipagem. Com exceção da raça Angus, a maioria das raças apresentaram maiores frequências do alelo de deleção tanto para 12pb como 23pb, em comparação com seus respectivos alelos de inserção, para as duas regiões. Esses resultados abrem caminhos para o conhecimento de como o rebanho brasileiro está sendo formado com relação aos polimorfismos do gene PRNP bovino.(AU)

Encefalopatía en gato causada por condicíon simultánea de "shunt" portosistémico y peritonitis infecciosa felina (PIF) no efusiva - reporte de caso / Encefalopathy in cat caused by simultaneous afection of portosystemic "shunt" and non effusive feline infectious peritonitis (FIP) - case report / Encefalopatia em gato causada por afecção simultânea de "shunt" portossistêmico e peritonite infecciosa felina (PIF) não efusiva - relato de caso

Encefalopatías en gatos pueden presentar varias causas, entre ellas, trastornos hepáticos, renales y enfermedades infecciosas. Apesar de diferentes etiologías, es posible que estas encefalopatías ocurran simultáneamente y exacerban los síntomas del animal afectado. La investigación de todas las causas posibles, de acuerdo con la evolución de la situación del animal, es de gran importancia. El objetivo de este trabajo es presentar un caso de encefalopatía en gato de dos fuentes distintas de forma simultánea, encefalopatía hepática por "shunt" portosistémico e causada por la infección del virus de la peritonitis infecciosa felina no efusiva.(AU)

Encefalopthies in felines may be presented by several causes, among them, hepatic affections, renal affections and infectious diseases. Despite the differentiated etiologies, its possible this encefalopathies occurs in simultaneous form and exacerbate the sintomatology of the stricken animal. The investigation of all the possible causes, according to the evolution of the animal situation, is very important. The aim of this paper is to report a case of a cat presenting encefalophaty by two different origins simultaneously, hepatic encefalophaty by portosystemic "shunt" and caused by non-effusive feline infectious peritonitis virus infection.(AU)

Encefalopatias em felinos podem se apresentar por várias causas, dentre elas, distúrbios metabólicos e doenças infecciosas. Apesar de etiologias diferenciadas, é possível que essas encefalopatias ocorram de forma simultânea e exacerbam a sintomatologia do animal acometido. A investigação de todas as possíveis causas, de acordo com a evolução do quadro do animal, é de grande importância. O objetivo deste trabalho é relatar um caso de gato apresentando encefalopatia de duas origens diferentes em simultaneidade, encefalopatia hepática por "shunt" portossistêmico e causada por infecção por vírus da peritonite infecciosa felina não efusiva.

Encefalopatía en gato causada por condicíon simultánea de "shunt" portosistémico y peritonitis infecciosa felina (PIF) no efusiva - reporte de caso / Encefalopathy in cat caused by simultaneous afection of portosystemic "shunt" and non effusive feline infectious peritonitis (FIP) - case report / Encefalopatia em gato causada por afecção simultânea de "shunt" portossistêmico e peritonite infecciosa felina (PIF) não efusiva - relato de caso

Encefalopatías en gatos pueden presentar varias causas, entre ellas, trastornos hepáticos, renales y enfermedades infecciosas. Apesar de diferentes etiologías, es posible que estas encefalopatías ocurran simultáneamente y exacerban los síntomas del animal afectado. La investigación de todas las causas posibles, de acuerdo con la evolución de la situación del animal, es de gran importancia. El objetivo de este trabajo es presentar un caso de encefalopatía en gato de dos fuentes distintas de forma simultánea, encefalopatía hepática por "shunt" portosistémico e causada por la infección del virus de la peritonitis infecciosa felina no efusiva.

Encefalopthies in felines may be presented by several causes, among them, hepatic affections, renal affections and infectious diseases. Despite the differentiated etiologies, its possible this encefalopathies occurs in simultaneous form and exacerbate the sintomatology of the stricken animal. The investigation of all the possible causes, according to the evolution of the animal situation, is very important. The aim of this paper is to report a case of a cat presenting encefalophaty by two different origins simultaneously, hepatic encefalophaty by portosystemic "shunt" and caused by non-effusive feline infectious peritonitis virus infection.

Encefalopatias em felinos podem se apresentar por várias causas, dentre elas, distúrbios metabólicos e doenças infecciosas. Apesar de etiologias diferenciadas, é possível que essas encefalopatias ocorram de forma simultânea e exacerbam a sintomatologia do animal acometido. A investigação de todas as possíveis causas, de acordo com a evolução do quadro do animal, é de grande importância. O objetivo deste trabalho é relatar um caso de gato apresentando encefalopatia de duas origens diferentes em simultaneidade, encefalopatia hepática por "shunt" portossistêmico e causada por infecção por vírus da peritonite infecciosa felina não efusiva.