Age, and non-age-related cytoarchitectural changes in the brain of some Nigerian cattle

Brain is the most vulnerable organ in the body to the ageing processes which operates at variable levels between organs and species. In this study we examine brains histopathologically for architectural changes in four Nigerian cattle breeds. Brains from 246 cattle (Bunaji=80, Muturu=78, Rahaji=62 and Sokoto Gudali=26), aged 1­≥12years were examined at 8 different neuroanatomical locations. All the cattle used were obtained from Abattoir in Ibadan, Nigeria. They were examined at ante-mortem and those without clinical signs suggestive of neurological disease were sampled. Major changes observed were intracellular accumulation of substances (61.4%), neuronal and or axonal degenerations and loss (51.6%), perivascular cuffing (50.0%), extracellular accumulation of substances (29.7%), hypercellularity (19.1%) and spongy state (0.4%), malacia (0.0%), demyelination (0.0%) in 233 cattle. Intraneuronal vacuolations (35%), lipofuscin accumulation (42%), axonal spheroids (50%), inflammatory changes (50%), and brain sand (22%). Although perivascular cuffing was high, there was low incidence of lymphocytic infiltration in the pineal gland in both sexes. Intracellular accumulation of substances, neuronal and or axonal degenerations and loss, and extracellular accumulation of substances display levels of significant changes with age (p<0.0001). Changes starts at the age of 2 years in life in these breeds of cattle due probably to the adverse stress exerted by the tropical climate. The description of histological findings in the brain of symptomless cattle in the present study provides a useful background for diagnostic bovine neuropathology in the tropics.(AU)

Polioencephalomalacia in sheep - clinical and magnetic resonance imaging findings

Background: Polioencephalomalacia (PEM) is a neurological disease in ruminants, which is characterized by malacia of brain gray matter. Thiamine deficiency and sulfur intoxication are the most common causes of PEM in sheep. Affected animals present signs of cerebrocortical syndrome, including amaurosis, ataxia, head pressing, mental depression, seizures, and opisthotonus. The neurological examination aims to determine the neurolocalization of the lesions and advanced imaging techniques are useful for confirming the affected area(s) in the central nervous system. The aim of this study is to describe clinical features and ante-mortem diagnosis using magnetic resonance imaging (MRI) in a sheep with PEM. Case: A 18-month-old male Dorper sheep from a flock started receiving concentrate 7 days before. According to the owner, no clinical signs of abnormality were observed on the previous morning. However, in the afternoon, the animal became selfisolated and did not follow the flock to the sheepfold. The following day, he was found in recumbency. Physical examination revealed lateral recumbency, rectal temperature 39.5ºC, 52 bpm, 120 bpm, congested mucous membranes, capillary refill time 1 s, ruminal (4/5 min) and intestinal hypomotility. The assessment of the central nervous system revealed a decreased level of consciousness, focal seizures, opisthotonus, and absence of menace response. The following differential diagnoses were listed: PEM, head trauma, focal symmetrical encephalomalacia, bacterial encephalitis, and rabies. Treatment was composed of dexamethasone [0.2 mg/kg - i.v., SID (1st-3rd day), 0.1 mg/kg, i.v., SID (4th-6th day), and 0.05 mg/kg, i.v., SID (7th-9th day)]; mannitol [1 g/kg - i.v. and diazepam 0.4 mg/kg, i.v. single dose at admission]; vitamin B1 [10 mg/kg - i.m., SID], furosemide [1 mg/kg - i.v., SID for 3 days] and sulfadoxine/trimethoprim [30 mg/kg - i.m., SID for 10 days]. After the initial treatment, the patient showed mild clinical improvement; however, the amaurosis was still present. Magnetic resonance imaging of the brain was performed on the 2nd day of hospitalization, showing a symmetrical hypersignal in the parietal and occipital cortices, in the axial and sagittal sequences weighted in T2 and FLAIR. Discussion: This study aimed to describe the clinical signs and MRI findings in a sheep with PEM. In this case, the sudden change to the feed composition probably led to ruminal dysbiosis, inhibition of thiamine-producing microorganisms and proliferation of bacteria that synthesize thiaminase. Thiamine therapy proved to be effective and capable of reverting the clinical signs. The decrease in the level of consciousness, cortical blindness, and opisthotonus are due to alterations in the parietal cortex, in the occipital cortex, and in the cerebellum, respectively, which were demonstrated by hypersignal areas in the MRI. Therefore, the neurolocalization of the lesion based on neurologic examination and the MRI findings were related. The physicochemical and cytological evaluations of the cerebrospinal fluid, and dosage of thiamine and the concentration of hydrogen sulphide in the rumen were not performed. However, the response to thiamine treatment associated with the neurologic examination and MRI findings helped in determining the diagnosis. Additionally, MRI can be used as a useful tool for the ante mortem diagnosis of PEM.

Toxoplasmose encefálica em um gambá-de-orelha-branca (Didelphis albiventris) / Encephalic toxoplasm in a white-eared possum (Didelphis albiventris)

Background: Toxoplasmosis is caused by Toxoplasma gondii, an obligate intracellular protozoan that belongs to the Apicomplexa phylum, coccidian subclass, and affects all warm-blooded animals. The role of opossums in the epidemiology of toxoplasmosis in Brazil is not fully understood, and there are very few descriptions of toxoplasmosis lesions in these animals. This report describes the anatomopathological, molecular and immunohistochemical findings of a case of encephalic toxoplasmosis in free-living white-eared possum (Didelphis albiventris). Case: A young male opossum (D. albiventris), was treated at the Veterinary Hospital of Wild Animals of the University of Brasília, Federal District. The animal was apathetic, uncoordinated, reluctant to move, and had an exposed proximal fracture in the left radius and ulna with laceration of muscles and adjacent tendinous structures. Amputation on the left thoracic limb was performed followed by analgesia and antibiotic therapy. The environment is frequented by other wild animals, and stray cats have access to the patio of the building. Twenty-five days after arriving at the hospital, the animal was found dead in its cage. After death, a necropsy was performed. Organ fragments from the abdominal cavity, thoracic and central nervous system were collected, processed routinely for histology and stained with hematoxylin and eosin. Macroscopic lesions in the central nervous system were not observed. On microscopy, the brain showed moderate random glial nodules throughout the neuropil associated with the presence of spherical to elongated parasitic cysts of about 20 µm, with a thin wall and with its interior full of bradyzoites, consistent with Toxoplasma gondii. There was also moderate fibrinoid necrosis and moderate multifocal lymphoplasmacytic infiltrate surrounding the blood vessels (perivascular cuffs) To investigate the etiology of the brain injury, brain sections were subjected to immunohistochemistry (IHC) and real-time polymerase chain reaction (qPCR) technique for detection of T. gondii and Neospora caninum. Immunostaining for T. gondii in the cyst wall and in bradyzoites and negative immunostaining for N. caninum. qPCR was positive for T. gondii and negative for N. caninum. Discussion: Diagnosis of encephalic toxoplasmosis in a Didelphis albiventris was possible based on histopathological, immunohistochemical and molecular findings. The morphological classification of the brain lesion was important for the diagnosis. Brain toxoplasmosis in opossums usually results in focal areas of malacia on macroscopy and focally extensive necrosis on microscopy, neutrophil infiltrate, calcified necrotic material, and perivascular cuffs of lymphocytes and plasma cells. In the present case, similar histopathological lesions were noted, but no significant macroscopic changes were observed. The etiology here was defined by immunohistochemistry and qPCR, techniques proven to be useful and with good specificity for diagnosing toxoplasmosis in mammals. It is believed that the positive immunohistochemical and molecular result for Toxoplasma gondii together with the negative result for Neospora caninum were conclusive for the diagnosis. Thus, we demonstrate here a post mortem diagnosis of toxoplasmosis in a free-living synanthropic opossum and the use of anatomopathology, immunohistochemistry and real-time polymerase chain reaction as a diagnostic option for this disease in opossums.

First report of an outbreak of cerebral coenurosis in Dhofari goats in Oman / Primeiro relato de um surto de coenurose cerebral em cabras Dhofari em Omã

This study documented the first outbreak of cerebral coenurosis in goats in Salalah, southern Oman. Deaths of 130 (16.6%) adult native goats in a herd (n=780) were reported from January to June 2017. Affected goats showed various nervous signs ended by death. Investigations for thiamine deficiency, polioencephalomalacia, caprine arthritis encephalitis, and listeriosis were negative. Upon necropsy, multiple (1-4) thin-walled cysts 2-3.5 cm in diameter containing clear fluid with numerous clusters of protoscolices in the cerebrum and cerebellum had replaced the brain parenchyma, causing space-occupying lesions. Parasitologically, the recovered cysts were Coenurus cerebralis, based on the arrangement of protoscolices, and the number and size of their hooks. Morphologically, each protoscolex had four suckers and a rostellum with double-crown hooks. The large and small hooks were 157.7±0.5 µm and 115±0.6 µm in length, respectively. Histopathologically, the parasite destroyed the affected tissues associated with multifocal to diffuse lymphocytic, non-suppurative meningoencephalitis; ischemic neuronal necrosis; and malacia. This is the first report of cerebral coenurosis in livestock in Oman, which should alert the local public health authorities for the application of prevention and control measures.(AU)

Este estudo documentou o primeiro surto de coenurose cerebral em cabras em Salalah, Oman. A morte de 130 (16,6%) caprinos adultos nativos (n=780) foi relatada de janeiro a junho de 2017. As cabras afetadas mostraram distúrbios neurológicos, que culminaram em óbito. Investigações para deficiência de tiamina, polioencefalomalácia, encefalite por artrite caprina e listeriose foram negativas. Na necropsia, múltiplos (1-4) cistos de paredes finas com 2-3,5 cm de diâmetro contendo líquido claro com numerosos aglomerados de protoescólices no cérebro e no cerebelo haviam substituído o parênquima cerebral, causando compressão nas estruturas adjacentes. Os cistos recuperados foram identificados como sendo de Coenurus cerebralis, com base no arranjo dos protoescólices, e no número e tamanho de seus ganchos. Morfologicamente, cada protoescólice tinha quatro ventosas e um rostelo com dupla coroa de ganchos. Os ganchos grandes e pequenos tinham 157,7±0,5 µm e 115±0,6 µm de comprimento, respectivamente. Histopatologicamente, o parasita causou a destruição dos tecidos afetados associada à meningoencefalite linfocítica não-supurativa, que variou de multifocal a difusa, necrose neuronal isquêmica e malacia. Este é o primeiro relato de coenurose em ruminantes no Oman, o que deve servir de alerta para as autoridades locais da área de saúde para a aplicação de medidas de prevenção e controle.(AU)

Encefalomalacia nutricional por hipovitaminose E em Gallus gallus domesticus / Nutritional encephalomalacia by hypovitaminosis E in Gallus gallus domesticus

A encefalomalácia nutricional é um distúrbio metabólico caracterizado por sinais clínicos neurológicos e sua etiologia é atribuída à hipovitaminose E. Atinge frangos jovens acarretando altos prejuízos aos criadores e agroindústrias pela sua alta morbidade e mortalidade. O objetivo do presente estudo foi relatar as alterações macroscópicas e histopatológicas de um caso de encefalomalácia nutricional. Um frango de corte com quatro semanas de vida, foi encaminhado ao Laboratório de Patologia Animal da Universidade Federal de Rondônia. Ao exame físico apresentou escore corporal 1 e sinais neurológicos como, ataxia, andar em círculos, lateralização da cabeça, prostração e hiperestesia, caracterizada por espasmos corporais iniciados após estímulos como sons altos e toque físico. Após eutanásia, realizou-se exame necroscópico e exame histopatológico. Para isto, foram coletados fragmentos de órgãos e fixados em formalina tamponada a 10%. No exame necroscópico constatou-se necrose coliquativa no encéfalo, o qual apresentou-se extremamente friável, com coloração pálida. Na análise histopatológica foram observadas alterações como vacuolização citoplasmática, degeneração de células de Purkinje e malácia focal extensa na substância cinzenta cortical e da substância branca do cerebelo. Pela história clínica e as observações necroscópicas e histopatológicas, o caso foi diagnosticado como encefalomalácia nutricional por hipovitaminose E.

Nutritional encephalomalacia is a metabolic disorder characterized by clinical neurological signs and its etiology is attributed to hypovitaminosis E. It affects young chickens causing high losses to breeders and agroindustries due to their high morbidity and mortality. The aim of the present study was to report macroscopic and histopathological changes in a case of nutritional encephalomalacia. A young chicken with four weeks of life conducted to the Animal Pathology Laboratory of Federal University of Rondônia. Physical examination showed poor body score and neurological signs, such as ataxia, circling, head lateralization, prostration and hypersensitivity, characterized by body spasms initiated after stimuli such as loud sounds and physical touch. After euthanasia, necroscopic examination was performed, organ fragments were collected and fixed in 10% buffered formalin. Necroscopic examination revealed collictive necrosis in the brain, which was extremely friable, with a pale color. In histopathological analysis, changes such as cytoplasmic vacuolization, Purkinje cell degeneration and extensive focal malacia in the cortical gray matter and white matter of the cerebellum were observed. From the clinical history and necroscopic and histopathological observations, the case was diagnosed as nutritional encephalomalacia by hypovitaminosis E.

Encefalomalacia nutricional por hipovitaminose E em Gallus gallus domesticus / Nutritional encephalomalacia by hypovitaminosis E in Gallus gallus domesticus

A encefalomalácia nutricional é um distúrbio metabólico caracterizado por sinais clínicos neurológicos e sua etiologia é atribuída à hipovitaminose E. Atinge frangos jovens acarretando altos prejuízos aos criadores e agroindústrias pela sua alta morbidade e mortalidade. O objetivo do presente estudo foi relatar as alterações macroscópicas e histopatológicas de um caso de encefalomalácia nutricional. Um frango de corte com quatro semanas de vida, foi encaminhado ao Laboratório de Patologia Animal da Universidade Federal de Rondônia. Ao exame físico apresentou escore corporal 1 e sinais neurológicos como, ataxia, andar em círculos, lateralização da cabeça, prostração e hiperestesia, caracterizada por espasmos corporais iniciados após estímulos como sons altos e toque físico. Após eutanásia, realizou-se exame necroscópico e exame histopatológico. Para isto, foram coletados fragmentos de órgãos e fixados em formalina tamponada a 10%. No exame necroscópico constatou-se necrose coliquativa no encéfalo, o qual apresentou-se extremamente friável, com coloração pálida. Na análise histopatológica foram observadas alterações como vacuolização citoplasmática, degeneração de células de Purkinje e malácia focal extensa na substância cinzenta cortical e da substância branca do cerebelo. Pela história clínica e as observações necroscópicas e histopatológicas, o caso foi diagnosticado como encefalomalácia nutricional por hipovitaminose E.(AU)

Nutritional encephalomalacia is a metabolic disorder characterized by clinical neurological signs and its etiology is attributed to hypovitaminosis E. It affects young chickens causing high losses to breeders and agroindustries due to their high morbidity and mortality. The aim of the present study was to report macroscopic and histopathological changes in a case of nutritional encephalomalacia. A young chicken with four weeks of life conducted to the Animal Pathology Laboratory of Federal University of Rondônia. Physical examination showed poor body score and neurological signs, such as ataxia, circling, head lateralization, prostration and hypersensitivity, characterized by body spasms initiated after stimuli such as loud sounds and physical touch. After euthanasia, necroscopic examination was performed, organ fragments were collected and fixed in 10% buffered formalin. Necroscopic examination revealed collictive necrosis in the brain, which was extremely friable, with a pale color. In histopathological analysis, changes such as cytoplasmic vacuolization, Purkinje cell degeneration and extensive focal malacia in the cortical gray matter and white matter of the cerebellum were observed. From the clinical history and necroscopic and histopathological observations, the case was diagnosed as nutritional encephalomalacia by hypovitaminosis E.(AU)

Leukoencephalomalacia in horses associated with immature corn consumption / Surto de leucoencefalomalacia em equinos associado ao consumo de milho verde

Horse leukoencephalomalacia (ELEM) is a disease caused by the ingestion of mycotoxins (fumonisins) produced by fungi of the genus Fusarium that infect corn and/or its byproducts. This disease has been described by ingestion of mature corn with humidity above 15% at temperatures below 20°C. The aim of this paper was to report an outbreak of leukoencephalomalacia in horses fed with immature corn. Two horses out of three showed neurological signs approximately seven days after eating immature corn in its reproductive phase (R2, milky grains). Corn was harvested and administered directly to the animals, with no storage. Deaths occurred approximately 24 hours after the onset of clinical signs. Grossly, there were multifocal dark red to brown areas in the white matter of the telencephalon and hyppocampus and thalamus. Histologically, there was edema and hemorrhage in several areas of the telencephalon white matter, which corresponded to dark red to brown areas observed in the macroscopy. There was also foci of malacia with presence of reactive astrocytes with abundant eosinophilic cytoplasm and inflammatory cells. Diffuse capillary wall degeneration and endothelial cell swelling were also observed. Two ppm of fumonisin were detected by immunoaffinity column method (VICAM) in the immature corn sample. The water activity in this cereal, when the grain is still milky, is 0.98 and can predispose it to growth of mycotoxin-producing fungi. In the present case, fumonisin was found in milky grains in the beginning of the reproductive phase (R2), which suggested that even immature corn may be infected by Fusarium spp. and should not be administered to horses.(AU)

A leucoencefalomalácia dos equinos (ELEM) é uma doença causada pela ingestão de micotoxinas (fumonisinas) produzidas por fungos do gênero Fusarium que infectam o milho e/ou seus subprodutos. A doença tem sido descrita pela ingestão de milho maduro com umidade acima de 15% em temperatura ambiente abaixo de 20°C. O objetivo deste trabalho foi relatar um surto de leucoencefalomacia em equinos alimentados com milho verde. Dois equinos de três animais apresentaram sinais clínicos neurológicos aproximadamente sete dias após iniciarem a ingestão de milho verde na fase reprodutiva (R2, grãos leitosos) com palha e talos, colhido no máximo 24 horas antes de ser administrado. A morte ocorreu aproximadamente 24 horas após o início dos sinais clínicos. Macroscopicamente havia no sistema nervoso central áreas multifocais acinzentadas e amareladas na substância branca do telencéfalo, no hipocampo e no tálamo. Histologicamente observou-se edema e hemorragia em diversas áreas da substância branca do telencéfalo, que correspondiam às áreas acinzentadas observadas na macroscopia. Havia, também, próximo as áreas hemorrágicas, focos de malacia com presença de astrócitos reativos com abundante citoplasma eosinophilico e algumas células inflamatórias. Degeneração das paredes dos capilares e tumefação das células endoteliais também foram observadas. Na análise da amostra de milho pelo método de colunas de imunoafinidade (VICAM) foram detectados 2ppm de fumonisina. A atividade de água neste cereal, quando o grão ainda está leitoso, é de 0,98, o que predispõe ao crescimento de fungos produtores de micotoxinas. No presente caso fumonisina foi encontrada nos grãos leitosos no início da fase reprodutiva (R2), o que sugere que mesmo o milho ainda imaturo pode estar infectado por Fusarium spp. e não deve, também, ser administrado aos equinos.(AU)

Meningoencephalitis due to Naegleria fowleri in cattle in southern Brazil / Meningoencefalite por Naegleria fowleri em um bovino no sul do Brasil

Naegleria fowleri is a free-living amoeba commonly found in the environment, mainly in fresh water and soil. This protozoon is occasionally involved in cases of fatal central nervous system disease in humans and other animal species. We describe here a case of meningoencephalitis due to Naegleria fowleri in cattle, in southern Brazil. A four-year-old Angus cow presented a clinical history of initial mild neurological signs that progressed to paddling movements, opisthotonus and lateral recumbency after five days. This animal had been kept in an irrigated rice stubble paddock. Grossly, the main lesions consisted of multiple areas of malacia in the right olfactory bulb, piriform lobes, hippocampus, frontal lobe cortex and fornix, along with severe thickening of the mesencephalon and rhombencephalon leptomeninges. Microscopically, severe multifocal necrosuppurative and hemorrhagic meningoencephalitis associated with a large quantity of amoebic trophozoites was present. The latter were confirmed to be Naegleria spp., through immunohistochemistry. Based on the strong congruence with the histopathological data of known cases reported in the literature, a probable association with Naegleria fowleri was established. To our knowledge, this is only the second report of Naegleria fowleri-associated meningoencephalitis in cattle in South America, and it is the first in southern Brazil.(AU)

Naegleria fowleri é uma ameba de vida livre, comumente encontrada no meio ambiente, principalmente em água doce e no solo. Este protozoário é ocasionalmente associado a casos fatais de doença do sistema nervoso central em seres humanos e espécies animais. No presente trabalho, um caso de meningoencefalite por Naegleria fowleri em um bovino na região sul do Brasil é descrito. Uma vaca Angus, de quatro anos de idade apresentou histórico clínico caracterizado inicialmente por sinais neurológicos leves que progrediram para movimentos de pedalagem, opistótono e decúbito lateral após cinco dias. Este animal era mantido em um piquete em resteva de arroz irrigado. Macroscopicamente, as principais lesões foram caracterizadas por múltiplas áreas de malacia no bulbo olfatório direito, lobos piriformes, hipocampo, córtex do lobo frontal e no fórnix, bem como acentuado espessamento das leptomeninges do mesencéfalo e rombencéfalo. Microscopicamente, meningoencefalite necrossupurativa e hemorrágica associada à grande número de trofozoítos amebianos foram observadas. Estes foram confirmados como Naegleria spp. através de imuno-histoquímica. Baseado na forte congruência apresentada entre os dados histopatológicos provenientes de casos conhecidos publicados na literatura, uma provável associação com Naegleria fowleri foi estabelecida. O presente trabalho trata-se do segundo relato de meningoencefalite associada à Naegleria fowleri em bovinos na América do Sul e o primeiro na região sul do Brasil.(AU)

Neurological diseases of cattle in the state of Goiás, Brazil (2010-2017) / Doenças neurológicas de bovinos no estado de Goiás (2010-2017)

A retrospective study was conducted on neurological diseases of cattle in the state of Goiás, Brazil, from March 2010 to August 2017. Samples of three veterinary diagnostic laboratories were analyzed. Diagnosis was established in 170 out of 407 cattle with neurological signs. Epidemiological, clinical, and anatomic pathology features of each case were researched in the files. Main disorders included diseases caused by viruses (rabies 29.41%, meningoencephalitis by bovine herpesvirus 15.88%, and malignant catarrhal fever 1.76%), by bacteria (botulism 5.88%, suppurative meningitis 3.53%, encephalic abscesses 2.94%, listeriosis 1.76%, and thrombotic meningoencephalitis 1.76%), of metabolic origin (polioencephalomalacia 17.06%), of indefinite cause (lymphoplasmacytic meningoencephalitis 11.18%, traumatic hemorrhages 3.53%, and multifocal malacia with gliosis 1.18%), congenital (hydrocephaly 1.18% and multiple malformations 0.59%), toxic (urea poisoning 1.18% and insecticide poisoning 0.59%), and parasitic (meningoencephalitis associated with infection by Trypanosoma sp. 0.59%).(AU)

Foi realizado um estudo retrospectivo de doenças neurológicas de bovinos no estado de Goiás durante o período de março de 2010 a agosto de 2017, analisando amostras de três laboratórios de diagnóstico veterinário. De 407 bovinos que apresentaram sinais clínicos neurológicos, o diagnóstico foi estabelecido em 170 casos. Desses casos, foram pesquisadas nas fichas as características epidemiológicas, clínicas e anatomopatológicas. As principais doenças diagnosticadas foram causadas por vírus (raiva 29,41%, meningoencefalite por herpesvírus bovino 15,88% e febre catarral maligna 1,76%), de origem metabólica (polioencefalomalacia 17,06%), por bactérias (botulismo 5,88%, meningite supurativa 3,53%, abscessos encefálicos 2,94%, listeriose 1,76% e meningoencefalite trombótica 1,76%), sem causa definida (meningoencefalite linfoplasmocítica 11,18%, hemorragias traumáticas 3,53% e malacia multifocal com gliose 1,18%), congênitas (hidrocefalia 1,18% e malformações múltiplas 0,59%), tóxicas (intoxicação por ureia 1,18% e intoxicação por inseticida 0,59%), e parasitária (meningoencefalite associada à infecção por Trypanosoma sp. 0,59%).(AU)

Intoxicação por antibióticos ionóforos e leucoencefalomalácia concomitantes pelo consumo de ração comercial contaminada em equinos / Concurrent ionophore poisoning and leukoencephalomalacia by consumption of contaminated commercial ration in horses

Background: Equidae nutritional change increased the frequency of diseases due to inappropriate administration and storage of rations. Although there are reports of ionophore poisoning (IP) and leukoencephalomalacia (LEM) in equidae from Brazil, the concurrent occurrence of both diseases by the same contaminated commercial ration is unprecedented. Therefore, the present paper aims to describe the epidemiological, clinical, laboratorial and pathological findings of concurrent IP and LEM outbreaks in horses.Cases: Eleven farmers from seven different locations in Distrito Federal, Midwestern Brazil, reported sudden clinical signs in 27 horses after the ingestion of commercial pelleted ration. During the farm visits, it was found that the ration brand and batches were identical, and macroscopic evaluation revealed no abnormalities. Eight horses were clinically evaluated and presented hyporexia, apathy, hypermetria, ataxia, dehydration, dyspnea, tongue hypotonia, muscle tremors, tachycardia, facial hypoalgesia, dysphagia, and sporadic or permanent recumbence. Laboratorial changes were restricted to creatine phosphokinase (mean: 1,573.4 ± 16.9 IU/L) and gammaglutamyl transferase (mean: 34.85 ± 29.14 IU/L) serum increases. Pathological evaluation has performed in eight horses presenting pallor and whitish striations in the gluteal, longissimus dorsi, femoral quadriceps muscles and myocardium, varying from mild to moderate. One horse also showed a soft and yellowish focal area on the right temporal lobe white matter. Microscopically, alterations in skeletal and cardiac muscle tissues included striated muscle fibers and cardiomyocytes segmental necrosis, characterized by sarcoplasmic fragmentation with clusters of eosinophilic debris, cellular retraction and hypereosinophilia. Histological alterations in the central nervous system of one horse were characteristic of LEM.[...]

Neurological diseases of cattle in the state of Goiás, Brazil (2010-2017) / Doenças neurológicas de bovinos no estado de Goiás (2010-2017)

A retrospective study was conducted on neurological diseases of cattle in the state of Goiás, Brazil, from March 2010 to August 2017. Samples of three veterinary diagnostic laboratories were analyzed. Diagnosis was established in 170 out of 407 cattle with neurological signs. Epidemiological, clinical, and anatomic pathology features of each case were researched in the files. Main disorders included diseases caused by viruses (rabies 29.41%, meningoencephalitis by bovine herpesvirus 15.88%, and malignant catarrhal fever 1.76%), by bacteria (botulism 5.88%, suppurative meningitis 3.53%, encephalic abscesses 2.94%, listeriosis 1.76%, and thrombotic meningoencephalitis 1.76%), of metabolic origin (polioencephalomalacia 17.06%), of indefinite cause (lymphoplasmacytic meningoencephalitis 11.18%, traumatic hemorrhages 3.53%, and multifocal malacia with gliosis 1.18%), congenital (hydrocephaly 1.18% and multiple malformations 0.59%), toxic (urea poisoning 1.18% and insecticide poisoning 0.59%), and parasitic (meningoencephalitis associated with infection by Trypanosoma sp. 0.59%).(AU)

Foi realizado um estudo retrospectivo de doenças neurológicas de bovinos no estado de Goiás durante o período de março de 2010 a agosto de 2017, analisando amostras de três laboratórios de diagnóstico veterinário. De 407 bovinos que apresentaram sinais clínicos neurológicos, o diagnóstico foi estabelecido em 170 casos. Desses casos, foram pesquisadas nas fichas as características epidemiológicas, clínicas e anatomopatológicas. As principais doenças diagnosticadas foram causadas por vírus (raiva 29,41%, meningoencefalite por herpesvírus bovino 15,88% e febre catarral maligna 1,76%), de origem metabólica (polioencefalomalacia 17,06%), por bactérias (botulismo 5,88%, meningite supurativa 3,53%, abscessos encefálicos 2,94%, listeriose 1,76% e meningoencefalite trombótica 1,76%), sem causa definida (meningoencefalite linfoplasmocítica 11,18%, hemorragias traumáticas 3,53% e malacia multifocal com gliose 1,18%), congênitas (hidrocefalia 1,18% e malformações múltiplas 0,59%), tóxicas (intoxicação por ureia 1,18% e intoxicação por inseticida 0,59%), e parasitária (meningoencefalite associada à infecção por Trypanosoma sp. 0,59%).(AU)

Intoxicação por antibióticos ionóforos e leucoencefalomalácia concomitantes pelo consumo de ração comercial contaminada em equinos / Concurrent ionophore poisoning and leukoencephalomalacia by consumption of contaminated commercial ration in horses

Background: Equidae nutritional change increased the frequency of diseases due to inappropriate administration and storage of rations. Although there are reports of ionophore poisoning (IP) and leukoencephalomalacia (LEM) in equidae from Brazil, the concurrent occurrence of both diseases by the same contaminated commercial ration is unprecedented. Therefore, the present paper aims to describe the epidemiological, clinical, laboratorial and pathological findings of concurrent IP and LEM outbreaks in horses.Cases: Eleven farmers from seven different locations in Distrito Federal, Midwestern Brazil, reported sudden clinical signs in 27 horses after the ingestion of commercial pelleted ration. During the farm visits, it was found that the ration brand and batches were identical, and macroscopic evaluation revealed no abnormalities. Eight horses were clinically evaluated and presented hyporexia, apathy, hypermetria, ataxia, dehydration, dyspnea, tongue hypotonia, muscle tremors, tachycardia, facial hypoalgesia, dysphagia, and sporadic or permanent recumbence. Laboratorial changes were restricted to creatine phosphokinase (mean: 1,573.4 ± 16.9 IU/L) and gammaglutamyl transferase (mean: 34.85 ± 29.14 IU/L) serum increases. Pathological evaluation has performed in eight horses presenting pallor and whitish striations in the gluteal, longissimus dorsi, femoral quadriceps muscles and myocardium, varying from mild to moderate. One horse also showed a soft and yellowish focal area on the right temporal lobe white matter. Microscopically, alterations in skeletal and cardiac muscle tissues included striated muscle fibers and cardiomyocytes segmental necrosis, characterized by sarcoplasmic fragmentation with clusters of eosinophilic debris, cellular retraction and hypereosinophilia. Histological alterations in the central nervous system of one horse were characteristic of LEM.[...](AU)

Outbreak of bovine herpetic meningoencephalomyelitis in Southern Brazil

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells.[...]

Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil / Polioencefalomalácia em ruminantes na região semiárida do estado do Rio Grande do Norte, Brazil

The present study aimed to describe epidemiological, clinical, laboratorial, and pathological findings of polioencephalomalacia (PEM) in ruminants from the semi-arid region of Rio Grande do Norte, Brazil. A total of seven ruminants (five sheep, one cattle, and one goat) with pathological diagnosis of PEM were included. Four cases were associated with thiamine deficiency, on account of chronic ruminal acidosis caused by diets rich in carbohydrate, with mainly concentrates, ground soybean hulls, and melon. Three ruminants from an outbreak of petroleum poisoning presented macro and microscopic lesions consistent with changes of malacia and edema in deep structures of the brain, as described in ruminants with PEM associated with sulfur intoxication. Major macroscopic changes included congestion of cerebral vessels, edema, and herniation of the cerebellum. The most observed microscopic lesions, among all assessed cases, were laminar and segmental neuronal necrosis at different regions of the brain, spongiosis, nuclear pyknosis, and red nucleus neurons. Cerebrospinal fluid analysis revealed nonspecific alterations, requiring its association with epidemiological, clinical, and pathological findings, as the results described here are similar to those reported in toxic diseases with neurological manifestations, such as botulism.

O presente trabalho objetiva descrever os achados epidemiológicos, clínicos, laboratoriais e patológicos de casos de polioencefalomalácia (PEM) em ruminantes na região semiárida do Rio Grande do Norte. Sete ruminantes (cinco ovinos, um bovino e um caprino) com diagnóstico patológico de PEM foram incluídos. Quatro casos foram associados à deficiência de tiamina devido acidose láctica ruminal crônica por oferta de alimentação rica em carboidratos, destacando-se os concentrados, casca de soja triturada e melão. Três ruminantes de um surto de intoxicação por petróleo apresentaram lesões macro e microscópicas condizentes com alterações de malácia e edema em estruturas profundas do encéfalo, descritas em ruminantes com PEM associada à intoxicação por enxofre. As principais alterações macroscópicas incluíram congestão dos vasos cerebrais, edema e conificação do cerebelo. Em todos os casos avaliados, as lesões microscópicas mais observadas foram a necrose neuronal laminar e segmentar em diferentes regiões do encéfalo, espongiose, picnose nuclear e a presença de neurônios vermelhos. A análise do líquido cefalorraquidiano revelou alterações inespecíficas, sendo necessário sua associação aos achados epidemiológicos, clínicos e patológicos, pois os resultados aqui descritos são semelhantes aos relatados em doenças tóxicas com manifestações neurológicas, como o botulismo.

Ischemic myelopathy caused by fibrocartilaginous embolism in a horse / Mielopatia isquêmica associada a embolismo fibrocartilaginoso em um equino

This report described clinical, epidemiological, and pathological aspects of ischemic myelopathy caused by fibrocartilaginous embolism (FCE) in a 10-year-old, mixed breed gelding. Clinically, the horse presented acute hind limbs paralysis, with a clinical course of approximately 24 hours. At necropsy, no gross lesions were observed. Cross-sections of the spinal cord revealed focally extensive areas of malacia from the T10 to L4 segments. Focally extensive areas of liquefactive necrosis involving the gray matter and adjacent white matter were observed on histologic sections. The lumen of multiple blood vessels in the periphery of the necrotic areas was occluded by fibrocartilaginous emboli that strongly stained with alcian blue. Clinical signs, gross necropsy, and histological findings observed in this case were identical to those described in the literature for ischemic myelopathy caused by FCE in the horse and other species.(AU)

Este relato descreve os aspectos epidemiológicos, clínicos e anatomopatológicos de um caso de mielopatia isquêmica por embolismo fibrocartilaginoso (FCE) em um equino, macho castrado, sem raça definida, com 10 anos de idade. Clinicamente, o equino apresentou paralisia aguda dos membros pélvicos com evolução de aproximadamente 24 horas. Na necropsia não foram observadas alterações. Após serem realizados vários cortes transversais na medula espinhal, observou-se área focalmente extensa de malacia entre o segmento T10 até L4. Histologicamente haviam áreas focalmente extensas de necrose de liquefação envolvendo a substância cinzenta e a substância branca adjacente. Múltiplos vasos sanguíneos da periferia das áreas de necrose estavam ocluídos por êmbolos fibrocartilaginosos, que reagiram fortemente pela técnica de azul alciano. Os sinais clínicos, as lesões macroscópicas e os achados histológicos observados neste caso, são idênticos aos descritos na literatura para FCE em equinos e nas demais espécies.(AU)

Polioencephalomalacia in ruminants from the semi-arid region of Rio Grande do Norte, Brazil / Polioencefalomalácia em ruminantes na região semiárida do estado do Rio Grande do Norte, Brazil

The present study aimed to describe epidemiological, clinical, laboratorial, and pathological findings of polioencephalomalacia (PEM) in ruminants from the semi-arid region of Rio Grande do Norte, Brazil. A total of seven ruminants (five sheep, one cattle, and one goat) with pathological diagnosis of PEM were included. Four cases were associated with thiamine deficiency, on account of chronic ruminal acidosis caused by diets rich in carbohydrate, with mainly concentrates, ground soybean hulls, and melon. Three ruminants from an outbreak of petroleum poisoning presented macro and microscopic lesions consistent with changes of malacia and edema in deep structures of the brain, as described in ruminants with PEM associated with sulfur intoxication. Major macroscopic changes included congestion of cerebral vessels, edema, and herniation of the cerebellum. The most observed microscopic lesions, among all assessed cases, were laminar and segmental neuronal necrosis at different regions of the brain, spongiosis, nuclear pyknosis, and red nucleus neurons. Cerebrospinal fluid analysis revealed nonspecific alterations, requiring its association with epidemiological, clinical, and pathological findings, as the results described here are similar to those reported in toxic diseases with neurological manifestations, such as botulism.(AU)

O presente trabalho objetiva descrever os achados epidemiológicos, clínicos, laboratoriais e patológicos de casos de polioencefalomalácia (PEM) em ruminantes na região semiárida do Rio Grande do Norte. Sete ruminantes (cinco ovinos, um bovino e um caprino) com diagnóstico patológico de PEM foram incluídos. Quatro casos foram associados à deficiência de tiamina devido acidose láctica ruminal crônica por oferta de alimentação rica em carboidratos, destacando-se os concentrados, casca de soja triturada e melão. Três ruminantes de um surto de intoxicação por petróleo apresentaram lesões macro e microscópicas condizentes com alterações de malácia e edema em estruturas profundas do encéfalo, descritas em ruminantes com PEM associada à intoxicação por enxofre. As principais alterações macroscópicas incluíram congestão dos vasos cerebrais, edema e conificação do cerebelo. Em todos os casos avaliados, as lesões microscópicas mais observadas foram a necrose neuronal laminar e segmentar em diferentes regiões do encéfalo, espongiose, picnose nuclear e a presença de neurônios vermelhos. A análise do líquido cefalorraquidiano revelou alterações inespecíficas, sendo necessário sua associação aos achados epidemiológicos, clínicos e patológicos, pois os resultados aqui descritos são semelhantes aos relatados em doenças tóxicas com manifestações neurológicas, como o botulismo.(AU)

Outbreak of bovine herpetic meningoencephalomyelitis in Southern Brazil

Background: Herpetic meningoencephalitis is an infectious contagious disease worldwide distributed, most often caused by bovine alphaherpesvirus type 5 (BoHV-5), although bovine alphaherpesvirus type 1 (BoHV-1) may occasionally be the causative agent. The disease is characterized by subacute to acute clinical onset, often affecting animals submitted to stressful situations. Clinical signs are mainly neurologic due to meningoencephalitis and cortical necrosis. The involvement of the spinal cord has also been reported, however in BoHV-1 associated disease only. The aim of this report is to describe an outbreak of bovine meningoencephalomyelitis associated to BoHV-5.Case: In August 2017, nine 1-year-old calves died in a beef cattle farm with a flock of approximately 400 bovines. The animals presented neurological clinical signs characterized by excessive salivation, nasal and ocular discharges, incoordination, apathy, head tremors, head pressing, wide-based stance, recumbency followed by convulsions and paddling. According to the owner and referring veterinarian, affected animals displayed severe clinical signs with rapid progression and often leading to death in up to seven days. Four of these calves were submitted for necropsy, and gross lesions were present in the brain, characterized by mild to moderate multifocal hemorrhagic and soft areas. On cut surface, extensive areas of dark brown discoloration and malacia were observed. Histologically, lesions were characterized by extensive areas of liquefactive necrosis in the cerebral cortex grey matter, associated with inflammatory infiltrates composed of neutrophils, lymphocytes, plasma cells and foamy macrophages, as well as multifocal to coalescing areas of hemorrhage and fibrin deposition. Intranuclear eosinophilic inclusion bodies were rarely observed in neurons and astrocytes. On leptomeninges, there was diffuse inflammatory infiltrates of lymphocytes and plasma cells.[...](AU)

Polioencefalomalacia em ruminantes: aspectos etiológicos, clínicos e anatomopatológicos

Polioencefalomalacia é uma doença cosmopolita, multifatorial, que acomete bovinos,bubalinos, caprinos e ovinos. O termo polioencefalomalacia indica um diagnóstico morfológico deamolecimento por necrose (malacia) da substância cinzenta (pólio) do córtex cerebral. As causas de PEMsão variadas, no entanto possuem patogênese semelhante por promoverem alterações irreversíveis nometabolismo das células nervosas que invariavelmente evoluem para morte (necrose). As principaiscausas conhecidas são: deficiência de tiamina, intoxicação por enxofre, meningoencefalite porherpesvírus bovino tipo 5 (BoHV-5), intoxicação por sal associada a privação por água, intoxicação porchumbo, intoxicação por plantas que produzem tiaminases, amprólio e “Uva do Japão”.

Polioencephalomalacia is a cosmopolitan, multifactorial disease that affects cattle,buffaloes, goats and sheep. Polioencephalomalacia is a morphological diagnosis that means necrosis(malacia) in the cerebral cortex causing the softening of the gray matter (polio). Although the etiologicalagents are multiples, they have similar pathogenesis causing irreversible lesions in the metabolism ofnerve cells, leading to the cellular death. Among the main etiological agents are thiamine deficiency,sulfur intoxication, bovine herpesvirus type 5 (BHV-5) meningoencephalitis, salt intoxication associatedwith water deprivation, lead intoxication, intoxication by plants that produce thiaminases, amprolium andJapanese.

Lesões no sistema nervoso central e na pele de cães com cinomose submetidos à necropsia na região central do rio grande do sul, brasil

A cinomose é uma doença viral frequentemente fatal em cães, causada pelo vírus da cinomose canina (CDV). Muitos aspectos da cinomose permanecem pouco elucidados. O objetivo desse trabalho foi explorar formas de apresentação incomuns ou pouco exploradas na literatura. O primeiro artigo da tese teve o objetivo de caracterizar a distribuição e aspectos histopatológicos das lesões de medula espinhal em cães com a forma espontânea de leucoencefalomielite desmielinizante (LEMD). Foram estudados 17 cães com LEMD submetidos à necropsia no Laboratório de Patologia Veterinária da UFSM (2006-2008). Secções de medula foram submetidas a Hematoxilina e Eosina (H&E), Luxol Fast Blue e imuno-histoquímica para CDV. Setenta e duas das 231 secções de medula espinhal tinham lesões, que afetavam consistentemente a substância branca. A região lombossacra foi mais afetada (13/17), seguida de toracolombar (11/17), cervical (9/17) e cervicotorácica (9/17). As áreas mais afetadas foram funículos lateral (42/72) e dorsal (31/72). Desmielinização (17/17), astrocitose (17/17), microglioses (17/17), gemistócitos (11/17) e inflamação não supurativa (10/17) foram os achados mais comuns na substância branca. Alterações de substância cinzenta incluíram gliose (8/17), inflamação não supurativa (7/17) e malácia (5/17). Lesões agudas foram mais prevalentes (13/17), no entanto, era comum o mesmo cão apresentar lesões em diferentes estágios de evolução em regiões distintas da medula. As lesões de medula nem sempre se correlacionaram com os sinais clínicos apresentados. O segundo estudo teve o objetivo de caracterizar lesões de hiperceratose em coxim, plano nasal e outras regiões de pele em cães com cinomose. Foram investigados 12 cães submetidos à necropsia no LPV UFSM (2006-2018). Foi realizada reavaliação histológica das lesões de pele e imuno-histoquímica para antígenos do CDV. Os 23 focos de hiperceratose cutânea afetaram coxins (11/12), plano nasal (4/12), região periocular (2/12), abdômen ventral (2/12), pele hirsuta do focinho (2/12), escroto (1/12) e vulva (1/12). Das 22 amostras de pele, 17 foram submetidas à reavaliação histológica. A análise histopatológica revelou hiperceratose ortoceratótica em todos os casos, por vezes acompanhada de outras lesões, dentre as quais: inclusões intracitoplasmáticas (14/17), acantose (9/17) e degeneração hidrópica (6/17). Quinze secções histológicas de 11 cães foram positivas na imuno-histoquímica. A marcação foi mais comum na epiderme, seguida por glândulas sudoríparas e células endoteliais/perícitos dos vasos sanguíneos. Não houve diferenças nos achados histopatológicos e imuno-histoquímicos entre pele da região naso-digital e das demais regiões. Ressalta-se a importância do reconhecimento de lesões cutâneas, contribuindo para o diagnóstico precoce. Esse trabalho caracterizou lesões pouco exploradas no sistema nervoso central e pele de cães com cinomose. Espera-se que os presentes resultados possam auxiliar no diagnóstico clinicopatológico de casos de cinomose com lesões de pele e medula espinhal em cães, além de contribuir para futuros estudos de patogênese da doença.

Canine distemper is a frequently fatal viral disease of dogs caused by canine distemper virus (CDV). Many aspects of canine distemper remain poorly understood. The aim of this study was to explore unusual or poorly described presentations of distemper in the literature. The first study of this thesis aimed to characterize the distribution and histopathological aspects of spinal cord injuries in dogs with spontaneous demyelinating leucoencephalomyelitis (DLEM) induced by CDV. Seventeen dogs with DLEM submitted to necropsy at the Laboratory of Veterinary Pathology at UFSM (2006-2008) were studied. Spinal cord sections were subjected to hematoxylin and eosin (H&E), Luxol Fast Blue and immunohistochemistry for CDV. Seventy-two of 231 spinal cord sections from these animals had histological lesions, which consistently affected the white matter. The lumbosacral region was mostly affected (13/17), followed by the thoracolumbar (11/17), cervical (9/17) and cervicothoracic (9/17). Lesions were most common in the lateral (42/72) and dorsal funiculi (31/72). Demyelination (17/17), astrocytosis (17/17), microgliosis (17/17), gemistocytes (11/17) and non-suppurative inflammation (10/17) were frequent in the white matter. Grey matter changes were less common, and included gliosis (8/17), non-suppurative inflammation (7/17) and malacia (5/17). Acute lesions were most prevalent (13/17) but it was common (10/17) for the same dog to have lesions at different stages of evolution in distinct spinal cord regions. Spinal cord lesions did not always correlate with the reported clinical signs and some dogs did not present spinal cord-related clinical signs. The second study aimed to characterize hyperkeratosis in the footpads, nasal planum and other skin regions in dogs naturally infected with CDV. Twelve dogs with canine distemper and concomitant cutaneous hyperkeratosis submitted to necropsy at the Laboratory of Veterinary Pathology at UFSM (2006-2018) were retrospectively investigated. Paraffin blocks were retrieved and new skin sections were stained with H&E and submitted to immunohistochemistry for CDV antigens. Twenty-three foci of hyperkeratosis were described, affecting footpads (11/12), nasal planum (4/12), periocular region (2/12), ventral abdomen (2/12), haired skin from the snout (2/12), scrotum (1/12) and vulva (1/12). Histopathological analysis was performed in 17 skins and revealed orthokeratotic hyperkeratosis in all cases, sometimes accompanied by other lesions, including: intracytoplasmic inclusions (14/17 skins analyzed), acanthosis (9/17), hydropic degeneration (6/17) and parakeratotic hyperkeratosis (4/17). Fifteen histological sections from 11 dogs were positive by immunohistochemistry. Labelling was most common in the epidermis, followed by sweat glands and endothelial cells/pericytes of dermal blood vessels. No differences in histopathological and immunohistochemical findings between skin from the nasodigital region and non-nasodigital areas were evidenced. The importance of recognizing cutaneous lesions in distemper is highlighted, thus contributing to the early diagnosis. This investigation has characterized poorly explored cutaneous and spinal cord lesions in dogs with distemper. We hope our findings will facilitate the clinicopathologic diagnosis of future cases of distemper and contribute to future pathogenesis studies.

Clinical, pathological, and immunohistochemistry characterization of toxoplasmosis in dogs with distemper in the semiarid region of Paraíba, Brazil / Caracterização clínica, patológica e imuno-histoquímica da toxoplasmose em cães com cinomose no semiárido da Paraíba, Brasil

The objective of this study was to describe the clinical, pathological, and immunohistochemistry characteristics of five cases of toxoplasmosis, an infection often associated with distemper in dogs. From January 2000 to December 2012, a retrospective study was performed analyzed dogs with distemper in the semiarid region of Paraíba. We evaluated this sample to focus on individuals who presented with concomitant structures in protozoa characteristics, and performed immunohistochemistry (IHC) tests using polyclonal anti-Toxoplasma gondii antibody. In all cases, the clinical signs were similar including digestive changes, as well as respiratory, neurological, and ocular lesions, suggesting an infection of canine distemper virus. The diagnosis of distemper was confirmed on histopathological analysis depending on the presence of intranuclear and intracytoplasmic eosinophilic inclusion bodies in different tissues. Histopathological examination also revealed the characteristic presence of parasitic cysts T. gondii in the brain in four cases, and in the lung in one case. The brain cysts were associated with multifocal areas of malacia and lung there was alveolar septa thickening due to infiltration of macrophages, lymphocytes, and plasma cells, with moderate proliferation of type II pneumocytes and coalescing multifocal areas of necrosis. These cysts are characterized by round and strongly basophilic structures, measuring approximately 5 to 70 μm, delimited by thin wall, stained by hematoxylin and eosin, and immunomarked as brown by immunohistochemistry (IHC) using the chromogen DAB. The diagnosis of toxoplasmosis associated with infection by canine distemper virus in the five case studied was based on microscopic findings and confirmed by immunohistochemistry. Toxoplasmosis should be included in the differential diagnosis of dogs with severe progressive systemic signs, especially when respiratory and neurological involvement is suspected.(AU)

Objetivou-se com este trabalho descrever as características clínicas, patológicas e imuno-histoquímica de cinco casos de toxoplasmose associados à cinomose em cães no semiárido da Paraíba. Para isso, foi realizado um estudo retrospectivo durante o período de janeiro de 2000 a dezembro de 2012, sendo identificados e selecionados os casos de cães com cinomose. Destes, foram avaliados os que apresentavam concomitantemente estruturas características de protozoários e realizada a imuno-histoquímica (IHQ) com anticorpo policlonal anti-Toxoplasma gondii. Em todos os casos os sinais clínicos foram semelhantes e sugestivos de infecção pelo vírus da cinomose canina, variando de alterações digestivas, respiratórias, neurológicas e lesões oculares. O diagnóstico de cinomose foi confirmado na histopatologia através da presença de corpúsculos de inclusões virais eosinofílicos intranucleares e intracitoplasmáticos em diferentes tecidos. O exame histopatológico revelou ainda a presença dos cistos parasitários característicos de T. gondii no encéfalo em quatro casos e no pulmão em um caso. No encéfalo os cistos estavam associados a áreas multifocais de malacia e no pulmão havia espessamento dos septos alveolares por infiltrado de macrófagos, plasmócitos e linfócitos, com proliferação moderada de pneumócitos tipo II e áreas multifocais a coalescentes de necrose. Esses cistos caracterizaram-se por estruturas arredondadas fortemente basofílicas medindo aproximadamente de 5 a 70 μm, delimitadas por uma fina parede pela hematoxilina e eosina e na IHQ foram fortemente imunomarcados em marrom para T. gondii. O diagnóstico de toxoplasmose associado à infecção pelo vírus da cinomose nos cinco casos estudados foi baseado nos achados microscópicos e confirmado através da imuno-histoquímica. A toxoplasmose deve ser incluída no diagnóstico diferencial de cães com sinais sistêmicos progressivos severos, principalmente quando há envolvimento respiratório e neurológico.(AU)