Neuropathology of natural canid alphaherpesvirus 1 infection in dogs

The neuropathology of canid alphaherpesvirus 1 (CaHV-1) infection in dogs has been reported, but the importance of the cerebellar lesions in the routine diagnosis remains relatively understated in the veterinary literature. Here we characterize the neuropathology of natural CaHV-1 infection in 25 dogs. The disease affected predominantly male dogs (22 cases). Clinical signs in 15 cases varied and sudden death was reported in 10 cases. All dogs had the typical areas of necrosis and hemorrhage in multiple organs with eosinophilic intranuclear viral inclusions in epithelial and/or inflammatory cells in multiple organs in 21 cases. Cerebral swelling and reddening were reported in 3 cases. Neurohistologic changes consisted of mild lymphoplasmacytic meningoencephalitis with occasional vasculitis and widespread glial nodules. Rare intranuclear viral inclusions (4 cases) were observed in endothelial cells or inflammatory cells in glial nodules. Cerebellum was examined in 11 cases and had extensive segmental necrosis of Purkinje cell layer (8 cases) and granule neurons in the internal (9 cases) or external (2 cases) granular cell layer. Intranuclear viral inclusions were observed in 8 cases and occurred in necrotic granule neurons in the inner granular cell layer (7 cases), outer granular cell layer (2 cases), Purkinje neurons (1 case), or endothelial cells (1 case). Diagnostic confirmation in 23 cases was based on routine histology and fluorescent antibody testing for CaHV-1 on fresh or frozen tissue samples. A routine diagnosis was based solely on the visualization of intranuclear viral inclusions in 2 cases.(AU)

Lysosomal storage disease induced by Sida planicaulis (Sin. Sida carpinifolia) (Malvaceae) in sheep in the state of Rio de Janeiro / Doença do armazenamento lisossomal induzida por Sida planicaulis (Sin. Sida carpinifolia) (Malvaceae) em ovinos no estado do Rio de Janeiro

Ingestion of S. planicaulis (Sin. S. carpinifolia) causes lysosomal storage disease in sheep. The main toxic compound of this plant, swainsonine, inhibits the enzymatic activity of α-mannosidase I and II, resulting in lysosomal storage of glycoproteins. We describe a case of spontaneous poisoning by S. planucaulis in Rio de Janeiro state, Brazil. Physical examination of affected animals revealed proprioceptive deficit, motor incoordination, staggering movement, and head tremors. Histopathological evaluation showed severe swelling/cytoplasmic vacuolization in Purkinje neurons, with a foamy appearance and occasional karyolysis or karyopyknosis, and intense vacuolization of acinar cells of the pancreas and, less markedly, thyroid follicular cells. The positive lectin-histochemistry labeling for Con A, WGA and sWGA lectins characterized the disease as a glycoproteinosis. The ultrastructural evaluation revealed numerous vacuoles up to 2.5µm in diameter bounded by membranes up to 20nm thick in pancreatic acinar cells. The diagnosis of S. planicaulis toxicity was established based on epidemiological data, clinicopathological, lectino-histochemical, and ultrastructural findings. This is the second report of spontaneous poisoning of sheep by S. planicaulis in Brazil, but the first in the Southeastern Brazil.

A ingestão de S. planicaulis (Sin. S. carpinifolia) tem sido responsabilizada por doença do armazenamento lisossomal em ovinos. O principal composto tóxico dessa planta, a swainsonina, inibe atividade enzimática da α-manosidase I e II, que redunda no armazenamento de glicoproteínas no interior de lisossomos. Descreveu-se um caso de intoxicação espontânea por S. planicaulis no estado do Rio de Janeiro, Brasil. O exame físico dos animais afetados revelou déficit proprioceptivo, incoordenação motora, cambaleio à movimentação e tremores de intenção e na cabeça. A avaliação histopatológica evidenciou severa tumefação/vacuolização citoplasmática em neurônios de Purkinje, com aspecto espumoso e eventual cariólise ou cariopicnose e intensa vacuolização de células acinares do pâncreas e, menos marcadamente, foliculares da tireoide. O exame lectino-histoquímico positivo para as lectinas Con A, WGA e sWGA foi capaz de caracterizar a enfermidade como uma glicoproteinose. A avaliação ultraestrutural revelou numerosos vacúolos de até 2,5µm de diâmetro, delimitados por membranas de até 20nm de espessura em células acinares do pâncreas. O diagnóstico da intoxicação por S. planicaulis foi estabelecido com base nos dados epidemiológicos, nos achados clínico-patológicos e confirmado pelas avaliações lectino-histoquímica e ultraestrutural. Esta é segunda descrição da intoxicação natural por S. planicaulis em ovinos no Brasil e a primeira na região Sudeste do país.

Congestive heart failure in a young cat with excessive moderator bands (false tendons) in the left ventricle / Insuficiência cardíaca congestiva em um gato jovem com bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo

ABSTRACT: Left ventricular false tendons are fibrous or fibromuscular bands that transverse the ventricular cavity and have no attachment to the mitral valve in many species. In cats it is considered a congenital defect that is rarely related to clinical disease and death in adult cats. A 45 days-old mixed breed cat had a history of inappetence since birth. At the physical exam the patient was lethargic and presented restrictive dyspnoea. At necropsy, there were marked ascites, hydrothorax, hepatomegaly with enhanced lobular pattern (nutmeg liver), and the lungs were markedly diminished (compressive pulmonary atelectasis). The heart was enlarged due to marked dilation of the cardiac chambers. Moreover, multiple slightly whitish and irregular cord-like structures were connecting the posterior papillary muscle to the interventricular septum (excessive moderator bands /left ventricular false tendons) at the left ventricle. Microscopically, these structures were characterized by a marked proliferation of fibrous connective tissue intermixed with Purkinje cells and well-differentiated cardiomyocytes lined by a single layer of endocardium. This study described a case of excessive moderator bands (left ventricular false tendons) in a young cat associated with congestive heart failure and death.

RESUMO: Falsos tendões são bandas fibrosas ou fibromusculares que atravessam a cavidade do ventrículo esquerdo, sem ligação com a valva mitral, em várias espécies. Nos gatos, a alteração é considerada um defeito congênito que raramente está relacionada com alterações clínicas e morte em gatos adultos. Um gato de 45 dias de idade, sem raça definida e com histórico de inapetência desde o nascimento foi encaminhado para atendimento veterinário. Ao exame físico apresentou letargia e dispneia restritiva. À necropsia, havia acentuada ascite, hidrotórax, hepatomegalia com evidenciação do padrão lobular (fígado noz-moscada) e os pulmões apresentavam-se acentuadamente diminuídos (atelectasia pulmonar compressiva). O coração apresentava acentuada dilatação das câmaras cardíacas. Em ventrículo esquerdo, havia numerosas estruturas brancacentas semelhantes a cordas conectando o músculo papilar ao septo interventricular (bandas moderadoras excessivas/falsos tendões). Microscopicamente, estas estruturas apresentavam acentuada proliferação de tecido conjuntivo fibroso, além de células de Purkinje e cardiomiócitos bem diferenciadas revestidas por uma única camada de endocárdio. O objetivo deste trabalho é descrever um caso de bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo de um gato jovem com insuficiência cardíaca congestiva e morte.

Congestive heart failure in a young cat with excessive moderator bands (false tendons) in the left ventricle / Insuficiência cardíaca congestiva em um gato jovem com bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo

Left ventricular false tendons are fibrous or fibromuscular bands that transverse the ventricular cavity and have no attachment to the mitral valve in many species. In cats it is considered a congenital defect that is rarely related to clinical disease and death in adult cats. A 45 days-old mixed breed cat had a history of inappetence since birth. At the physical exam the patient was lethargic and presented restrictive dyspnoea. At necropsy, there were marked ascites, hydrothorax, hepatomegaly with enhanced lobular pattern (nutmeg liver), and the lungs were markedly diminished (compressive pulmonary atelectasis). The heart was enlarged due to marked dilation of the cardiac chambers. Moreover, multiple slightly whitish and irregular cord-like structures were connecting the posterior papillary muscle to the interventricular septum (excessive moderator bands /left ventricular false tendons) at the left ventricle. Microscopically, these structures were characterized by a marked proliferation of fibrous connective tissue intermixed with Purkinje cells and well-differentiated cardiomyocytes lined by a single layer of endocardium. This study described a case of excessive moderator bands (left ventricular false tendons) in a young cat associated with congestive heart failure and death.

Falsos tendões são bandas fibrosas ou fibromusculares que atravessam a cavidade do ventrículo esquerdo, sem ligação com a valva mitral, em várias espécies. Nos gatos, a alteração é considerada um defeito congênito que raramente está relacionada com alterações clínicas e morte em gatos adultos. Um gato de 45 dias de idade, sem raça definida e com histórico de inapetência desde o nascimento foi encaminhado para atendimento veterinário. Ao exame físico apresentou letargia e dispneia restritiva. À necropsia, havia acentuada ascite, hidrotórax, hepatomegalia com evidenciação do padrão lobular (fígado noz-moscada) e os pulmões apresentavam-se acentuadamente diminuídos (atelectasia pulmonar compressiva). O coração apresentava acentuada dilatação das câmaras cardíacas. Em ventrículo esquerdo, havia numerosas estruturas brancacentas semelhantes a cordas conectando o músculo papilar ao septo interventricular (bandas moderadoras excessivas/falsos tendões). Microscopicamente, estas estruturas apresentavam acentuada proliferação de tecido conjuntivo fibroso, além de células de Purkinje e cardiomiócitos bem diferenciadas revestidas por uma única camada de endocárdio. O objetivo deste trabalho é descrever um caso de bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo de um gato jovem com insuficiência cardíaca congestiva e morte.

Congestive heart failure in a young cat with excessive moderator bands (false tendons) in the left ventricle / Insuficiência cardíaca congestiva em um gato jovem com bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo

Left ventricular false tendons are fibrous or fibromuscular bands that transverse the ventricular cavity and have no attachment to the mitral valve in many species. In cats it is considered a congenital defect that is rarely related to clinical disease and death in adult cats. A 45 days-old mixed breed cat had a history of inappetence since birth. At the physical exam the patient was lethargic and presented restrictive dyspnoea. At necropsy, there were marked ascites, hydrothorax, hepatomegaly with enhanced lobular pattern (nutmeg liver), and the lungs were markedly diminished (compressive pulmonary atelectasis). The heart was enlarged due to marked dilation of the cardiac chambers. Moreover, multiple slightly whitish and irregular cord-like structures were connecting the posterior papillary muscle to the interventricular septum (excessive moderator bands /left ventricular false tendons) at the left ventricle. Microscopically, these structures were characterized by a marked proliferation of fibrous connective tissue intermixed with Purkinje cells and well-differentiated cardiomyocytes lined by a single layer of endocardium. This study described a case of excessive moderator bands (left ventricular false tendons) in a young cat associated with congestive heart failure and death.(AU)

Falsos tendões são bandas fibrosas ou fibromusculares que atravessam a cavidade do ventrículo esquerdo, sem ligação com a valva mitral, em várias espécies. Nos gatos, a alteração é considerada um defeito congênito que raramente está relacionada com alterações clínicas e morte em gatos adultos. Um gato de 45 dias de idade, sem raça definida e com histórico de inapetência desde o nascimento foi encaminhado para atendimento veterinário. Ao exame físico apresentou letargia e dispneia restritiva. À necropsia, havia acentuada ascite, hidrotórax, hepatomegalia com evidenciação do padrão lobular (fígado noz-moscada) e os pulmões apresentavam-se acentuadamente diminuídos (atelectasia pulmonar compressiva). O coração apresentava acentuada dilatação das câmaras cardíacas. Em ventrículo esquerdo, havia numerosas estruturas brancacentas semelhantes a cordas conectando o músculo papilar ao septo interventricular (bandas moderadoras excessivas/falsos tendões). Microscopicamente, estas estruturas apresentavam acentuada proliferação de tecido conjuntivo fibroso, além de células de Purkinje e cardiomiócitos bem diferenciadas revestidas por uma única camada de endocárdio. O objetivo deste trabalho é descrever um caso de bandas moderadoras excessivas (falsos tendões) em ventrículo esquerdo de um gato jovem com insuficiência cardíaca congestiva e morte.(AU)

The microanatomy of the central nervous system and brain of the Indo-Pacific seahorse, Hippocampus barbouri, during development

The central nervous system (CNS) of Teleostei is a complex system of self-governance and its morphology is reflected in the physiological and reproductive behaviors. The Indo-Pacific seahorse, Hippocampus barbouri Jordan & Richard son, 1908, is a new candidate species for aquaculture in Thailand. In this study, we investigated the brain morphology of H. barbouri across various developmental windows. Light microscopic observations of adult brains revealed a large optic tectum in the mesencephalon, whereas the cerebral hemispheres and the cerebellum are of medium size. The detailed brain structures were generally similar to those of other teleosts; however, only five distinct layers were present in the optic tectum, including the stratum marginale, stratum opticum, stratum album central, stratum griseum central, and stratum periventriculae, versus six layers observed in other fish. One day after birth (1 DAB) the brain was a packed structure without any clear sub-structures. The number of capillaries in the optic tectum began to increase at 6 DAB, and at 14 DAB several features, including small blood vessels in the optic tectum and Purkinje cells, became noticeable. By 35 DAB, the optic tectum became highly vascularized and included five layers. Additionally, large Purkinje cells were developed in the cerebellum. Based on the brain development pattern, we speculate that the predatory ability of this fish starts to develop from 6 to 14 days after birth.

The microanatomy of the central nervous system and brain of the Indo-Pacific seahorse, Hippocampus barbouri, during development

The central nervous system (CNS) of Teleostei is a complex system of self-governance and its morphology is reflected in the physiological and reproductive behaviors. The Indo-Pacific seahorse, Hippocampus barbouri Jordan & Richard son, 1908, is a new candidate species for aquaculture in Thailand. In this study, we investigated the brain morphology of H. barbouri across various developmental windows. Light microscopic observations of adult brains revealed a large optic tectum in the mesencephalon, whereas the cerebral hemispheres and the cerebellum are of medium size. The detailed brain structures were generally similar to those of other teleosts; however, only five distinct layers were present in the optic tectum, including the stratum marginale, stratum opticum, stratum album central, stratum griseum central, and stratum periventriculae, versus six layers observed in other fish. One day after birth (1 DAB) the brain was a packed structure without any clear sub-structures. The number of capillaries in the optic tectum began to increase at 6 DAB, and at 14 DAB several features, including small blood vessels in the optic tectum and Purkinje cells, became noticeable. By 35 DAB, the optic tectum became highly vascularized and included five layers. Additionally, large Purkinje cells were developed in the cerebellum. Based on the brain development pattern, we speculate that the predatory ability of this fish starts to develop from 6 to 14 days after birth.(AU)

Tremorgenic syndrome caused by Ipomoea pes caprae in cattle / Síndrome tremorgênica causada pela ingestão de Ipomoea pes caprae em bovinos

Poisonous plants are a significant cause of death among adult cattle in Brazil. Plants that affect the central nervous system are widely spread throughout the Brazilian territory and comprise over 30 toxic species, including the genus Ipomoea, commonly associated with a lysosomal storage disease and a tremorgenic syndrome in livestock. We describe natural and experimental Ipomoea pes caprae poisoning in cattle from a herd in the Northside of Rio de Janeiro, Brazil. Affected cattle presented episodes of severe ataxia, abnormal posture followed by falling, muscular tremor, contraction, and spasticity, more prominent in the limbs, intensified by movement and forthcoming, and recumbence. Grossly, a substantial amount of leaves and petioles were found in the rumen. Histopathological examination showed degenerative neuronal changes, mostly in cerebellar Purkinje cells, which were confirmed with Bielschowsky silver. The characteristic clinical changes and mild histological lesion strongly suggested a tremorgenic syndrome. Lectin- immunohistochemistry evaluation reinforced this hypothesis; all lectins tested failed to react with affect neurons and Purkinje cells, which ruled out an underlying lysosomal storage disease. One calf given I. pes caprae leaves experimentally developed clinical signs similar to natural cases. On the 28th day of the experiment, the plant administration was suspended, and the calf recovered within four days. I. pes caprae's spontaneous tremorgenic syndrome in cattle is conditioned to exclusive feeding for several months. We were able to experimentally reproduce toxic clinical signs 12 days following the ingestion.(AU)

A intoxicação por plantas tóxicas está entre as três causas de morte mais importantes em bovinos adultos no Brasil. O grupo das plantas que causam alterações neurológicas, muito bem representada no país, encerra mais de trinta espécies tóxicas, entre as quais do gênero Ipomoea, amplamente distribuídas no território brasileiro. As plantas tóxicas desse gênero podem causar doenças do armazenamento ou síndrome tremorgênica. Descrevem-se a intoxicação natural e reprodução experimental por Ipomoea pes caprae em bovinos, verificada no norte do Estado do Rio de Janeiro. Foram observados episódios de intensa ataxia locomotora, postura anormal seguida de queda, incapacidade de levantar-se, tremores, contrações, espasticidades musculares nos membros, intensificados após estimulação ou a simples aproximação e decúbito. Nos bovinos afetados há mais de 6 meses, os sinais clínicos tornavam-se permanentes. À necropsia havia apenas significativa quantidade de folhas e pecíolos da planta no rúmen. O estudo histopatológico evidenciou lesões neuronais degenerativas principalmente nos neurônios de Purkinje. A impregnação argêntica pela técnica de Bielschowsky ratificou esses achados microscópicos. As lesões histológicas sutis associadas ao quadro clínico indicam que trata-se de intoxicação tremorgênica. O fato de não haver nenhum armazenamento intracitoplasmático, confirmado pelo resultado do estudo lectino-histoquímico (não houve afinidade das lectinas Con-A, WGA e sWGA e de outras lectinas empregadas aos neurônios de Purkinje e outros neurônios afetados), é suficiente para descartar a possibilidade de tratar-se de doença do armazenamento. No bezerro intoxicado experimentalmente verificaram-se sinais clínicos semelhantes, entretanto, com a interrupção do fornecimento da planta no 28º dia, os sinais clínicos desapareceram após quatro dias. I. pes caprae causa síndrome tremorgênica espontânea em bovinos, quando ingerida como alimentação exclusiva durante períodos prolongados (muitos meses). Experimentalmente, os primeiros sinais clínicos da intoxicação foram reproduzidos após 12 dias de ingestão da planta.(AU)

Tremorgenic syndrome caused by Ipomoea pes caprae in cattle / Síndrome tremorgênica causada pela ingestão de Ipomoea pes caprae em bovinos

Poisonous plants are a significant cause of death among adult cattle in Brazil. Plants that affect the central nervous system are widely spread throughout the Brazilian territory and comprise over 30 toxic species, including the genus Ipomoea, commonly associated with a lysosomal storage disease and a tremorgenic syndrome in livestock. We describe natural and experimental Ipomoea pes caprae poisoning in cattle from a herd in the Northside of Rio de Janeiro, Brazil. Affected cattle presented episodes of severe ataxia, abnormal posture followed by falling, muscular tremor, contraction, and spasticity, more prominent in the limbs, intensified by movement and forthcoming, and recumbence. Grossly, a substantial amount of leaves and petioles were found in the rumen. Histopathological examination showed degenerative neuronal changes, mostly in cerebellar Purkinje cells, which were confirmed with Bielschowsky silver. The characteristic clinical changes and mild histological lesion strongly suggested a tremorgenic syndrome. Lectin- immunohistochemistry evaluation reinforced this hypothesis; all lectins tested failed to react with affect neurons and Purkinje cells, which ruled out an underlying lysosomal storage disease. One calf given I. pes caprae leaves experimentally developed clinical signs similar to natural cases. On the 28th day of the experiment, the plant administration was suspended, and the calf recovered within four days. I. pes caprae's spontaneous tremorgenic syndrome in cattle is conditioned to exclusive feeding for several months. We were able to experimentally reproduce toxic clinical signs 12 days following the ingestion.(AU)

A intoxicação por plantas tóxicas está entre as três causas de morte mais importantes em bovinos adultos no Brasil. O grupo das plantas que causam alterações neurológicas, muito bem representada no país, encerra mais de trinta espécies tóxicas, entre as quais do gênero Ipomoea, amplamente distribuídas no território brasileiro. As plantas tóxicas desse gênero podem causar doenças do armazenamento ou síndrome tremorgênica. Descrevem-se a intoxicação natural e reprodução experimental por Ipomoea pes caprae em bovinos, verificada no norte do Estado do Rio de Janeiro. Foram observados episódios de intensa ataxia locomotora, postura anormal seguida de queda, incapacidade de levantar-se, tremores, contrações, espasticidades musculares nos membros, intensificados após estimulação ou a simples aproximação e decúbito. Nos bovinos afetados há mais de 6 meses, os sinais clínicos tornavam-se permanentes. À necropsia havia apenas significativa quantidade de folhas e pecíolos da planta no rúmen. O estudo histopatológico evidenciou lesões neuronais degenerativas principalmente nos neurônios de Purkinje. A impregnação argêntica pela técnica de Bielschowsky ratificou esses achados microscópicos. As lesões histológicas sutis associadas ao quadro clínico indicam que trata-se de intoxicação tremorgênica. O fato de não haver nenhum armazenamento intracitoplasmático, confirmado pelo resultado do estudo lectino-histoquímico (não houve afinidade das lectinas Con-A, WGA e sWGA e de outras lectinas empregadas aos neurônios de Purkinje e outros neurônios afetados), é suficiente para descartar a possibilidade de tratar-se de doença do armazenamento. No bezerro intoxicado experimentalmente verificaram-se sinais clínicos semelhantes, entretanto, com a interrupção do fornecimento da planta no 28º dia, os sinais clínicos desapareceram após quatro dias. I. pes caprae causa síndrome tremorgênica espontânea em bovinos, quando ingerida como alimentação exclusiva durante períodos prolongados (muitos meses). Experimentalmente, os primeiros sinais clínicos da intoxicação foram reproduzidos após 12 dias de ingestão da planta.(AU)

Meroanencephaly in an English Pointer neonate

Background: Malformations are structural or functional abnormalities in the organs and structures present at birth. Theseconditions are rarely described in the newborns of dogs and can lead to their death. Meroanencephaly is a defect of theneural tube closure malformation, a type of anencephaly and results from a failure of closure of the rostral neuropore(neural crest), and consequently the development of the calvary becomes defective. This study aims to characterize theclinical-pathological aspects of neonatal meroanencephaly since brain malformations are rare in newborn dogs.Case: A 2-day-old English Pointer canine was sent for a necropsy. The newborn belonged to a litter of eight puppies, andonly this one had macroscopic cranial alterations. Another puppy that died as a consequence of being trampled by thebitch was also necropsied. The newborn was alive for 48 h until death and presented apathy, crying, sucking reflex andopisthotonus. Macroscopic examination of the baby revealed flattening of the skull, with a slit at the site of bone symphysis fusion, and a slit in the skin of the parietal region, covered by thin, translucent meningeal tissue. The newborn hadno other macroscopic changes. The heads of the two animals were examined by radiography to identify the features ofanencephaly in one of the animals by visualizing skull bone flattening. Upon removing the skin and exposing the cranialcavity, an irregular reddish mass was revealed, that corresponded microscopically to area cerebrovasculosa, composed ofneurons and rudimentary glial tissue, vascular neoformation and, hemorrhage and congestion. The cranial nerves was notpossible to observe. There was disorganization of the brain areas with no limitation of white and gray matter and scarceneurons and also a region similar to the cerebellum, with a molecular layer but without the Purkinje neurons. In the spinal...

Meroanencephaly in an English Pointer neonate

Background: Malformations are structural or functional abnormalities in the organs and structures present at birth. Theseconditions are rarely described in the newborns of dogs and can lead to their death. Meroanencephaly is a defect of theneural tube closure malformation, a type of anencephaly and results from a failure of closure of the rostral neuropore(neural crest), and consequently the development of the calvary becomes defective. This study aims to characterize theclinical-pathological aspects of neonatal meroanencephaly since brain malformations are rare in newborn dogs.Case: A 2-day-old English Pointer canine was sent for a necropsy. The newborn belonged to a litter of eight puppies, andonly this one had macroscopic cranial alterations. Another puppy that died as a consequence of being trampled by thebitch was also necropsied. The newborn was alive for 48 h until death and presented apathy, crying, sucking reflex andopisthotonus. Macroscopic examination of the baby revealed flattening of the skull, with a slit at the site of bone symphysis fusion, and a slit in the skin of the parietal region, covered by thin, translucent meningeal tissue. The newborn hadno other macroscopic changes. The heads of the two animals were examined by radiography to identify the features ofanencephaly in one of the animals by visualizing skull bone flattening. Upon removing the skin and exposing the cranialcavity, an irregular reddish mass was revealed, that corresponded microscopically to area cerebrovasculosa, composed ofneurons and rudimentary glial tissue, vascular neoformation and, hemorrhage and congestion. The cranial nerves was notpossible to observe. There was disorganization of the brain areas with no limitation of white and gray matter and scarceneurons and also a region similar to the cerebellum, with a molecular layer but without the Purkinje neurons. In the spinal...(AU)

Neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state, Brazil / Enfermidades neurológicas em bovinos causadas por plantas e micotoxinas no estado de Santa Catarina

This study described the epidemiological and clinical-pathological aspects of 25 outbreaks of neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state. Six of them were due to Sida carpinifolia poisoning, five to Solanum fastigiatum, five to Phalaris angusta, three to Claviceps paspali, three to Claviceps purpurea, and three outbreaks were of unknown etiology. The clinical signs observed in the affected cattle were mild to severe and characterized by generalized muscle tremors, incoordination, hypermetria, wide-based stance, intentional head tremors, dull staring eyes, and frequent ear twitching, with convulsions in some cases. At necropsy, lesions were observed only for P. angusta poisoning, characterized by gray-greenish discoloration in thalamus and midbrain. Microscopically, rarefaction and/or disappearance of Purkinje neurons with substitution by Bergmann cells were observed for S. carpinifolia and S. fastigiatum poisoning. For P. angusta poisoning, thin granular brown-yellowish pigment was observed in the cytoplasm of some neurons. Gross and microscopic findings were not observed in three outbreaks of tremorgenic disease of unknown etiology. Experiments conducted with leaves, flowers and seeds of Ipomoea indivisa and Ipomoea triloba, as well as with maize and soybean residues contaminated with Ipomoea spp. did not reproduced clinical signs.(AU)

Descrevem-se os aspectos epidemiológicos e clinico-patológicos de 25 surtos de enfermidade neurológica em bovinos no estado de Santa Catarina causadas por plantas e micotoxinas. Destes, seis corresponderam a intoxicação por Sida carpinifolia, cinco por Solanum fastigiatum, cinco por Phalaris angusta, três por Claviceps paspali, três por Claviceps purpurea e três surtos de etiologia não definida. Os sinais clínicos observados nos bovinos afetados eram de intensidade leve a acentuada e caracterizados por tremores musculares generalizados, incoordenação, hipermetria, aumento da base de sustentação, balanço contínuo de cabeça, olhar atento e movimentos frequentes de orelhas, e em alguns surtos convulsões. Por meio de necropsia foram observadas alterações somente na intoxicação por P. angusta as quais caracterizaram por coloração cinza-esverdeada no tálamo e mesencéfalo. Na histologia, rarefação e/ou desaparecimento de neurônios de Purkinje com substituição por células de Bergmann foram observadas na intoxicação por S. carpinifolia e S. fastigiatum. Na intoxicação por P. angusta foi observado no citoplasma de alguns neurônios do tronco encefálico com pigmentação finamente granular marrom-amarelada. Nos três surtos de enfermidade tremorgênica com etiologia não definida não foram observadas lesões macroscópicas e microscópicas. Experimentos com folhas, flores e sementes de Ipomoea indivisa e Ipomoea triloba e resíduos de milho e soja contaminados com sementes destas duas plantas não produziram alterações clínicas.(AU)

Neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state, Brazil / Enfermidades neurológicas em bovinos causadas por plantas e micotoxinas no estado de Santa Catarina

This study described the epidemiological and clinical-pathological aspects of 25 outbreaks of neurological diseases in cattle caused by plants and mycotoxins in Santa Catarina state. Six of them were due to Sida carpinifolia poisoning, five to Solanum fastigiatum, five to Phalaris angusta, three to Claviceps paspali, three to Claviceps purpurea, and three outbreaks were of unknown etiology. The clinical signs observed in the affected cattle were mild to severe and characterized by generalized muscle tremors, incoordination, hypermetria, wide-based stance, intentional head tremors, dull staring eyes, and frequent ear twitching, with convulsions in some cases. At necropsy, lesions were observed only for P. angusta poisoning, characterized by gray-greenish discoloration in thalamus and midbrain. Microscopically, rarefaction and/or disappearance of Purkinje neurons with substitution by Bergmann cells were observed for S. carpinifolia and S. fastigiatum poisoning. For P. angusta poisoning, thin granular brown-yellowish pigment was observed in the cytoplasm of some neurons. Gross and microscopic findings were not observed in three outbreaks of tremorgenic disease of unknown etiology. Experiments conducted with leaves, flowers and seeds of Ipomoea indivisa and Ipomoea triloba, as well as with maize and soybean residues contaminated with Ipomoea spp. did not reproduced clinical signs.(AU)

Descrevem-se os aspectos epidemiológicos e clinico-patológicos de 25 surtos de enfermidade neurológica em bovinos no estado de Santa Catarina causadas por plantas e micotoxinas. Destes, seis corresponderam a intoxicação por Sida carpinifolia, cinco por Solanum fastigiatum, cinco por Phalaris angusta, três por Claviceps paspali, três por Claviceps purpurea e três surtos de etiologia não definida. Os sinais clínicos observados nos bovinos afetados eram de intensidade leve a acentuada e caracterizados por tremores musculares generalizados, incoordenação, hipermetria, aumento da base de sustentação, balanço contínuo de cabeça, olhar atento e movimentos frequentes de orelhas, e em alguns surtos convulsões. Por meio de necropsia foram observadas alterações somente na intoxicação por P. angusta as quais caracterizaram por coloração cinza-esverdeada no tálamo e mesencéfalo. Na histologia, rarefação e/ou desaparecimento de neurônios de Purkinje com substituição por células de Bergmann foram observadas na intoxicação por S. carpinifolia e S. fastigiatum. Na intoxicação por P. angusta foi observado no citoplasma de alguns neurônios do tronco encefálico com pigmentação finamente granular marrom-amarelada. Nos três surtos de enfermidade tremorgênica com etiologia não definida não foram observadas lesões macroscópicas e microscópicas. Experimentos com folhas, flores e sementes de Ipomoea indivisa e Ipomoea triloba e resíduos de milho e soja contaminados com sementes destas duas plantas não produziram alterações clínicas.(AU)

Cardiac rhabdomyoma in a slaughtered pig / Rabdomioma cardíaco em um suíno de abate

Rhabdomyoma is a rare neoplasm of striated muscle that occurs predominantly in the myocardium. In animals, cardiac rhabdomyoma are observed as incidental lesions in slaughter pigs and have been rarely described in other species, such as cattle, dogs, and deer. This report describes a case of cardiac rhabdomyoma in a male pig at slaughter age that died suddenly in the pre-slaughter period. At necropsy, multiple nodules were observed in the right and left ventricular walls and the interventricular septum. Histopathological examination showed neoplastic proliferation composed of polyhedral cells, with vacuolated cytoplasm that sometimes presented a spider cell appearance. Histochemical staining with Schiffs periodic acid revealed glycogen granules in the cytoplasm of neoplastic cells. The neoplastic cells were positive for desmin, neuron-specific enolase, atrial natriuretic peptide, and vimentin by immunohistochemistry, to varying degrees. The anatomopathological and immunohistochemical findings observed in this case confirmed the diagnosis of cardiac rhabdomyoma, possibly originating from the Purkinje fibers.(AU)

Rabdomioma é um neoplasma raro de músculo estriado que ocorre predominantemente no miocárdio. Em animais rabdomiomas cardíacos são observados como lesões incidentais em suínos de abate, raramente descrito em outras espécies como bovinos, cães e cervos. Neste relato descreve-se um caso de rabdomioma cardíaco em um suíno, macho, em idade de abate que morreu subitamente no período pré-abate. Na necropsia visualizou-se múltiplos nódulos nas paredes ventriculares direita e esquerda, e septo interventricular. O exame histopatológico mostrou proliferação neoplásica composta por células poliédricas, com citoplasma vacuolizado que por vezes apresentavam aspecto de célula de aranha. Na coloração histoquímica de ácido periódico de Schiff evidenciaram-se grânulos de glicogênio no citoplasma das células neoplásicas. As células neoplásicas foram imunorreativas na imuno-histoquímica para desmina, enolase neurônio específica, peptídeo natriurético atrial e vimentina em diferentes graus. Os achados anatomopatológicos e imuno-histoquímicos observados neste caso confirmam o diagnóstico de rabdomioma cardíaco, possivelmente com origem das fibras de Purkinje.(AU)

Kernicterus in an adult dog

Background: Kernicterus or bilirubin encephalopathy is a condition rarely observed in animal characterized by a yellowish discoloration of the central nervous system. It is a potentially fatal condition due to bilirubin neurotoxic effects caused by the increase of non-conjugated bilirubin pigment, which passes blood brain barrier and has been attributed to an imbalance between albumin and bilirubin levels. Intracellular bilirubin is toxic for cells and can cause decrease in protein synthesis, specially albumin, depression of cell respiration and cellular death. This paper describes kernicterus in a 2-year-old Great Dane female dog.Case: Clinically, the animal showed apathy, lethargy, weight loss and jaundice, which progressed to vomiting and neurological signs characterized by loss of consciousness and eventually coma. Blood parameters were within normal range, except for high levels of alanine aminotransferase (523 U/L), suggesting a liver lesion. The animal was submitted to euthanasia due to the poor prognosis, and at post-mortem examination it showed dehydration and severe jaundice, especially oral, vaginal and ocular mucosas, subcutaneous tissue and blood vessels intima surface. The liver had an accentuated lobular pattern, and the stomach mucosa was reddened. Multiple petechiae were observed in the epicardium, as well as icterus in the blood vessels of the heart. Furthermore, the brain and cerebellum cortex, thalamic region and nuclei region of brainstem showed extensive icteric areas. Microscopically, the liver presented a mononuclear portal hepatitis, centrilobular necrosis and presence of yellowish pigments. The brain had neuronal necrosis, mild vacuolization of the white matter, perineuronal edema and Alzheimer type II astrocytes, while cerebellum showed Purkinje cells necrosis. Hepatic cooper measurement was within range values, and direct imunofluorescence for the detection of Leptospira sp. was negative.[...]

Kernicterus in an adult dog

Background: Kernicterus or bilirubin encephalopathy is a condition rarely observed in animal characterized by a yellowish discoloration of the central nervous system. It is a potentially fatal condition due to bilirubin neurotoxic effects caused by the increase of non-conjugated bilirubin pigment, which passes blood brain barrier and has been attributed to an imbalance between albumin and bilirubin levels. Intracellular bilirubin is toxic for cells and can cause decrease in protein synthesis, specially albumin, depression of cell respiration and cellular death. This paper describes kernicterus in a 2-year-old Great Dane female dog.Case: Clinically, the animal showed apathy, lethargy, weight loss and jaundice, which progressed to vomiting and neurological signs characterized by loss of consciousness and eventually coma. Blood parameters were within normal range, except for high levels of alanine aminotransferase (523 U/L), suggesting a liver lesion. The animal was submitted to euthanasia due to the poor prognosis, and at post-mortem examination it showed dehydration and severe jaundice, especially oral, vaginal and ocular mucosas, subcutaneous tissue and blood vessels intima surface. The liver had an accentuated lobular pattern, and the stomach mucosa was reddened. Multiple petechiae were observed in the epicardium, as well as icterus in the blood vessels of the heart. Furthermore, the brain and cerebellum cortex, thalamic region and nuclei region of brainstem showed extensive icteric areas. Microscopically, the liver presented a mononuclear portal hepatitis, centrilobular necrosis and presence of yellowish pigments. The brain had neuronal necrosis, mild vacuolization of the white matter, perineuronal edema and Alzheimer type II astrocytes, while cerebellum showed Purkinje cells necrosis. Hepatic cooper measurement was within range values, and direct imunofluorescence for the detection of Leptospira sp. was negative.[...](AU)

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

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

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

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

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

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

Degenerative axonopathy associated with copper deficiency in pigs

ABSTRACT: The epidemiological, clinic and morphological (pathological and ultrastructural) aspects of four outbreaks of copper deficiency affecting 21- to 90-day-old pigs in the Northeast region of Brazil are reported. Clinical signs began with paraparesis and ataxia and progressed to flaccid or spastic paralysis of the pelvic and thoracic limbs, followed by sternal and/or lateral recumbence. In addition, some animals showed dog-sitting position and intention tremors. The clinical manifestation period was 5-20 days. Significant gross lesions were not observed; however, microscopically, symmetrical degeneration of the white matter with ballooned myelin sheaths containing occasional macrophages was observed, mainly in the spinal cord. Two pigs presented with necrosis ad loss of Purkinje cells and ectopic Purkinje cells in the granular layer and cerebellar white matter. A ultrastructural analysis showed different degrees of damage of myelinated axons in the spinal segments, including an absence of the axoplasm structures with only axonal residues remaining. The myelin sheaths were degenerated and often collapsed into the space previously occupied by the axon. These results suggest that myelin degeneration is secondary to the axonal lesion. Finally, the concentration of copper in the liver was determined using atomic absorption spectrophotometry and was found to be low (ranging from 2.2 to 10.8 ppm). In conclusion, in the Brazilian semiarid region, Cu deficiency occurs in 21 to 90-day-old pigs that ingested different types of waste in their food.

RESUMO: São relatados os achados epidemiológicos, clínicos e morfológicos (patológicos e ultraestruturais) de quatro surtos de deficiência de cobre em suínos afetados entre 21 e 90 dias de idade na região Nordeste do Brasil. Os sinais clínicos iniciaram com paraparesia e ataxia, que progrediu a paralisia flácida ou espástica dos membros pélvicos e torácicos, seguido de decúbito esternal e/ou lateral. Além disso, alguns animais apresentaram posição de cão sentado e tremores de intenção. O período de manifestação clínica variou de 5-20 dias. Não foram observadas lesões macroscópicas significativas; no entanto, microscopicamente, foi observada degeneração simétrica da substância branca com fragmentação das bainhas de mielina, contendo ocasionais macrófagos, principalmente na medula espinal. Dois suínos apresentaram necrose e perda de células de Purkinje e células de Purkinje ectópicos na camada granular da substância branca cerebelar. A análise ultraestrutural mostrou diferentes graus de lesões em axônios mielinizados em segmentos da medula espinhal, incluindo o desaparecimento de estruturas do axoplasma, restando apenas restos axonais. A bainha de mielina encontrava-se degenerada e muitas vezes, colapsada dentro do espaço previamente ocupado pelo axônio. Esses resultados sugerem que a degeneração da mielina é secundária à lesão axonal. Finalmente, a concentração do cobre no fígado foi determinada usando espectrometria de absorção atômica e revelou baixos valores (variando de 2,2-10,8ppm). Conclui-se que na região semiárida do Brasil ocorre deficiência de cobre em suínos de 21 a 90 dias de idade alimentados com diferentes tipos de resíduos.

Degenerative axonopathy associated with copper deficiency in pigs / Axonopatia degenerativa associada com deficiência de cobre em suínos

The epidemiological, clinic and morphological (pathological and ultrastructural) aspects of four outbreaks of copper deficiency affecting 21- to 90-day-old pigs in the Northeast region of Brazil are reported. Clinical signs began with paraparesis and ataxia and progressed to flaccid or spastic paralysis of the pelvic and thoracic limbs, followed by sternal and/or lateral recumbence. In addition, some animals showed dog-sitting position and intention tremors. The clinical manifestation period was 5-20 days. Significant gross lesions were not observed; however, microscopically, symmetrical degeneration of the white matter with ballooned myelin sheaths containing occasional macrophages was observed, mainly in the spinal cord. Two pigs presented with necrosis ad loss of Purkinje cells and ectopic Purkinje cells in the granular layer and cerebellar white matter. A ultrastructural analysis showed different degrees of damage of myelinated axons in the spinal segments, including an absence of the axoplasm structures with only axonal residues remaining. The myelin sheaths were degenerated and often collapsed into the space previously occupied by the axon. These results suggest that myelin degeneration is secondary to the axonal lesion. Finally, the concentration of copper in the liver was determined using atomic absorption spectrophotometry and was found to be low (ranging from 2.2 to 10.8 ppm). In conclusion, in the Brazilian semiarid region, Cu deficiency occurs in 21 to 90-day-old pigs that ingested different types of waste in their food.(AU)

São relatados os achados epidemiológicos, clínicos e morfológicos (patológicos e ultraestruturais) de quatro surtos de deficiência de cobre em suínos afetados entre 21 e 90 dias de idade na região Nordeste do Brasil. Os sinais clínicos iniciaram com paraparesia e ataxia, que progrediu a paralisia flácida ou espástica dos membros pélvicos e torácicos, seguido de decúbito esternal e/ou lateral. Além disso, alguns animais apresentaram posição de cão sentado e tremores de intenção. O período de manifestação clínica variou de 5-20 dias. Não foram observadas lesões macroscópicas significativas; no entanto, microscopicamente, foi observada degeneração simétrica da substância branca com fragmentação das bainhas de mielina, contendo ocasionais macrófagos, principalmente na medula espinal. Dois suínos apresentaram necrose e perda de células de Purkinje e células de Purkinje ectópicos na camada granular da substância branca cerebelar. A análise ultraestrutural mostrou diferentes graus de lesões em axônios mielinizados em segmentos da medula espinhal, incluindo o desaparecimento de estruturas do axoplasma, restando apenas restos axonais. A bainha de mielina encontrava-se degenerada e muitas vezes, colapsada dentro do espaço previamente ocupado pelo axônio. Esses resultados sugerem que a degeneração da mielina é secundária à lesão axonal. Finalmente, a concentração do cobre no fígado foi determinada usando espectrometria de absorção atômica e revelou baixos valores (variando de 2,2-10,8ppm). Conclui-se que na região semiárida do Brasil ocorre deficiência de cobre em suínos de 21 a 90 dias de idade alimentados com diferentes tipos de resíduos.(AU)