PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.

• Poisonous plants Tetrapterys multiglandulosa Malpighiaceae plant poisoning cardiomiopathy abortion diseases of cattle pathology

Abstract in Portuguese:

ABSTRACT.- Carvalho N.M., Alonso L.A., Cunha T.G., Ravedutti J., Barros C.S.L. & Lemos R.A.A. 2006. [Poisoning of cattle by Tetrapterys multiglandulosa in Mato Grosso do Sul, Brazil.] Intoxicação de bovinos por Tetrapterys multiglandulosa (Malpighiaceae) em Mato Grosso do Sul. Pesquisa Veterinária Brasileira 26(3):139-146. Departamento de Medicina Veterinária, Universidade Federal de Mato Grosso do Sul, Avenida Senador Filinto Müller 2443, Caixa Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br Two outbreaks of poisoning by Tetrapterys multiglandulosa in cattle and the experimental reproduction of the toxicosis in sheep are described. Both outbreaks occurred on the same farm in the municipality of Bataiporã, state of Mato Grosso do Sul, Brazil. The first outbreak occurred in July-October 2004 and involved a cattle population at risk of 290 pregnant cows, which were introduced into a 60 hectare pasture with a legal reservation area heavily infested by T. multiglandulosa. Of these, 230 cows (79.3%) aborted, had stillbirths or delivered weak calves that died few days after birth. Seven cows died, and one cow and a 10-day-old calf were necropsied. The second outbreak occurred in September-October 2005, 40 days after 285 2-year-old heifers were introduced into the same pasture infested by T. multiglandulosa and where the first outbreak had occurred in the previous year. Nine heifers got sick and died, and three of then were necropsied. Clinical signs of affected cattle, including a 10-day-old calf, were marked lethargy, loss of weight with distension of the abdomen (ascites), subcutaneous dependant edema, distended and pulsating jugular veins, dyspnea and cardiac arrhythmia. Necropsy findings included a round and dilated heart with whitish and firm areas in the myocardium, and changes related to cardiac failure such as cavitary edema, nutmeg liver, pulmonary edema, a large blood clot in the left ventricle. Histopathological changes included necrosis and fibrosis in the myocardium, chronic passive hepatic centrolobular congestion, pulmonary edema, and spongy degeneration in the white matter of the brain. Experimental sheep died 29 (Sheep 1) and 35 (Sheep 2) days after being fed average daily doses of T. multiglandulosa corresponding to 14g/kg (Sheep 1) and 7,5 g/kg (Sheep 2) per day. Clinical signs were observed from the 7th day (Sheep1) and the 4th day (Sheep 2) of the experiment and included tachycardia, arrhythmia, lethargy and head pressing. Necropsy and histopathologic findings in both experimental sheep were very similar to those observed in affected cattle of the two spontaneous outbreaks.

Abstract in English:

ABSTRACT.- Almeida A.P.M.G., Kommers G.D., Nogueira A.P.A., Júnior L.G.B., Marques B.M.F.P. & Lemos R.A.A. 2006. [Evaluation of the toxicity of Leucaena leucocephala (Leg. Mimosoi-deae) in sheep.] Avaliação do efeito tóxico de Leucaena leucocephala (Leg.Mimosoideae) em ovinos. Pesquisa Veterinária Brasileira 26(3):190-194. Departamento de Medicina Veterinária, Faculdade de Medicina Vetetinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Av. Senador Filinto Müller 2443, Cx.Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br An experiment was performed to evaluate the toxicity of Leucaena leucocephala for sheep. Two ewes and six lambs were divided into seven treatments and fed the plant. The adult ewes did not show clinical signs of poisoning. The 4 to 5-month-old lambs presented partial wool loss 6 days after beginning of the administration of the plant and total wool loss after 12 or 20 days. The age of the sheep in this experiment suggests resistance of adult ewes and susceptibility of young lambs to L. leucocaephala poisoning.

• Poisonous plants Leucaena leucocephala Leguminosae Mimosoideae plant poisoning sheep diseases pathology

Abstract in Portuguese:

ABSTRACT.- Almeida A.P.M.G., Kommers G.D., Nogueira A.P.A., Júnior L.G.B., Marques B.M.F.P. & Lemos R.A.A. 2006. [Evaluation of the toxicity of Leucaena leucocephala (Leg. Mimosoi-deae) in sheep.] Avaliação do efeito tóxico de Leucaena leucocephala (Leg.Mimosoideae) em ovinos. Pesquisa Veterinária Brasileira 26(3):190-194. Departamento de Medicina Veterinária, Faculdade de Medicina Vetetinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Av. Senador Filinto Müller 2443, Cx.Postal 549, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br An experiment was performed to evaluate the toxicity of Leucaena leucocephala for sheep. Two ewes and six lambs were divided into seven treatments and fed the plant. The adult ewes did not show clinical signs of poisoning. The 4 to 5-month-old lambs presented partial wool loss 6 days after beginning of the administration of the plant and total wool loss after 12 or 20 days. The age of the sheep in this experiment suggests resistance of adult ewes and susceptibility of young lambs to L. leucocaephala poisoning.

Abstract in English:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

• Bovine herpesvirus-5 BoHV-5 encephalitis diseases of cattle viral diseases neuropathology.

Abstract in Portuguese:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

Abstract in English:

RESUMO.- Brum K.B., Purisco E., Lemos R.A.A. & Riet-Correa F. 2002. [Intoxication by Vernonia rubricaulis in cattle in Mato Grosso do Sul.] Intoxicação por Vernonia rubricaulis em bovinos no Mato Grosso do Sul. Pesquisa Veterinária Brasileira 22(3):119-128. Depto Medicina Veterinária, UFMS, Cx. Postal 549, Campo Grande, MS 79070-900. E-mail: rlemos@nin.ufms.br Descrevem-se surtos de intoxicação por Vernonia rubricoulis em bovinos em nove fazendas no Estado de Mato Grosso do Sul, entre setembro de 1999 e maio de 2001. No total morreram pelo menos 954 animais. Alguns fatores foram aparentemente importantes para a ocorrência da intoxicação: a utilização de técnicas que favorecem a brotação da planta incluindo a utilização da roçadeira ("trilho") para o controle de plantas invasoras, assim como a queima ou o desmatamento do campo; o transporte de animais procedentes de outras fazendas ou de outros piquetes da mesma fazenda, com ou sem manejo de animais no curral; e a superlotação de piquetes. O curso clínico variou de 12 a 48 horas. Os sinais clínicos foram, principalmente, agressividade ou depressão, salivação, cegueira, gemidos, incoordenação, retração de abdômen, fezes ressecadas com muco e estrias de sangue, focinho seco e decúbito. A letalidade foi de 100%. Os principais achados de necropsia foram observados no fígado. As lesões hepáticas variavam num mesmo animal e entre diferentes animais. Áreas focais vermelhas de hemorragias com tamanhos variando entre 1 mm e 25cm, foram observadas em meio ao tecido hepático amarelado em alguns casos. Fígados inteiros ou áreas hepáticas com aspecto de noz-moscada e fígados difusamente amarelados com ou sem hemorragias petequiais, também foram observados. Ocorriam, também, hemorragias em diferentes tecidos e órgãos. As principais alterações histológicas caracterizaram-se por necrose centrolobular com vacuolização dos hepatócitos das áreas periportais e intermediárias ou necrose massiva e vacuolização difusa dos hepatócitos. A intoxicação foi reproduzida experimentalmente em três bovinos. A menor dose que causou morte foi de 3g/kg da planta verde fresca em fase de brotação. Os sinais clínicos e as lesões macro e microscópicas observadas foram semelhantes às apresentadas pelos animais intoxicados naturalmente.

• Toxic plants Vernonia rubricaulis liver necrosis cattle Plantas tóxicas necrose hepática bovinos.

Abstract in Portuguese:

RESUMO.- Brum K.B., Purisco E., Lemos R.A.A. & Riet-Correa F. 2002. [Intoxication by Vernonia rubricaulis in cattle in Mato Grosso do Sul.] Intoxicação por Vernonia rubricaulis em bovinos no Mato Grosso do Sul. Pesquisa Veterinária Brasileira 22(3):119-128. Depto Medicina Veterinária, UFMS, Cx. Postal 549, Campo Grande, MS 79070-900. E-mail: rlemos@nin.ufms.br Descrevem-se surtos de intoxicação por Vernonia rubricoulis em bovinos em nove fazendas no Estado de Mato Grosso do Sul, entre setembro de 1999 e maio de 2001. No total morreram pelo menos 954 animais. Alguns fatores foram aparentemente importantes para a ocorrência da intoxicação: a utilização de técnicas que favorecem a brotação da planta incluindo a utilização da roçadeira ("trilho") para o controle de plantas invasoras, assim como a queima ou o desmatamento do campo; o transporte de animais procedentes de outras fazendas ou de outros piquetes da mesma fazenda, com ou sem manejo de animais no curral; e a superlotação de piquetes. O curso clínico variou de 12 a 48 horas. Os sinais clínicos foram, principalmente, agressividade ou depressão, salivação, cegueira, gemidos, incoordenação, retração de abdômen, fezes ressecadas com muco e estrias de sangue, focinho seco e decúbito. A letalidade foi de 100%. Os principais achados de necropsia foram observados no fígado. As lesões hepáticas variavam num mesmo animal e entre diferentes animais. Áreas focais vermelhas de hemorragias com tamanhos variando entre 1 mm e 25cm, foram observadas em meio ao tecido hepático amarelado em alguns casos. Fígados inteiros ou áreas hepáticas com aspecto de noz-moscada e fígados difusamente amarelados com ou sem hemorragias petequiais, também foram observados. Ocorriam, também, hemorragias em diferentes tecidos e órgãos. As principais alterações histológicas caracterizaram-se por necrose centrolobular com vacuolização dos hepatócitos das áreas periportais e intermediárias ou necrose massiva e vacuolização difusa dos hepatócitos. A intoxicação foi reproduzida experimentalmente em três bovinos. A menor dose que causou morte foi de 3g/kg da planta verde fresca em fase de brotação. Os sinais clínicos e as lesões macro e microscópicas observadas foram semelhantes às apresentadas pelos animais intoxicados naturalmente.

Abstract in English:

ABSTRACT.- Nakano L., Lemos R.A.A. & Riet-Correa F. 2000. [Polioencephalomalacia in cattle in the states of Mato Grosso do Sul and São Paulo.] Polioencefalomalacia em bovinos nos estados de Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 20(3):119-125. Depto Patologia, Fac. Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. Thirty outbreaks of polioencephalomalacia (PEM) were diagnosed from August 1993 to October 1997. Twenty nine occurred in the state of Mato Grosso do Sul and one in São Paulo. The disease affected cattle from 4 months to 7 years of age. Morbidity rates ranged from 0.02% to 14.28% and case fatalities from 42.5 % to 100%. The disease was not seasonal. All outbreaks occurred in cattle grazing Brachiaria spp, except one affecting feedlot cattle. Only neurologic signs were observed, and the course of the disease varied from 12 hours to 4 days in untreated cattle. Most animals treated with thiamine anel dexamethazone recovered. Moderate cerebral edema was observed at necropsy. Cell changes were characterized by laminar necrosis and gitter cells. In two cases moderate cortical anel submeningeal hemorrhages were observed. Nine cases had perivascular anel submeningeal infiltrations by eosinophils. Sodium ion concentration of the cerebrospinal fluid was elevated in one case. The cause of PEM in the region was not determined, but the results suggest that in some cases sodium chloride intoxication/water deprivation could play a role in the etiology of the disease. PEM represents 4.78% of cattle disease diagnosed at the Pathology Laboratory of the Federal University of Mato Grosso do Sul.

• Polioencephalomalacia cerebrocortical necrosis cattle thiamine salt Polioencefalomalacia necrose cerebrocortícal bovino tiamina sal.

Abstract in Portuguese:

RESUMO.- Nakano L., Lemos R.A.A. & Riet-Correa F. 2000. [Polioencephalomalacia in cattle in the states of Mato Grosso do Sul and São Paulo.] Polioencefalomalacia em bovinos nos estados de Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 20(3):119-125. Depto Patologia, Fac. Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. Trinta focos de polioencefalomalacia (PEM) foram diagnosticados no período de agosto de 1993 a outubro de 1997. Vinte e nove focos ocorreram no estado de Mato Grosso do Sul (MS) e um no estado de São Paulo (SP). Foram afetados bovinos de 4 a 84 meses de idade. A morbidade dos rebanhos afetados variou ele 0,02% a 14,28% e a letalidade de 42,5% a 100%. A doença não apresentou uma sazonalidade e ocorreu em vários municípios do MS. Em todos os focos estudados os animais afetados eram criados em regimes de criação extensiva, com exceção de um foco. Os sinais clínicos observados foram exclusivamente nervosos e a evolução dos casos variou de 12 horas a 4 dias. A maioria dos animais tratados com tiamina e dexametasona recuperou-se. Histologicamente, as lesões consistiam de necrose laminar do córtex cerebral. Adicionalmente em 2 casos observaram-se hemorragias submeningeanas e corticais, e em 9 casos presença ele infiltrado de eosinófilos. A dosagem de sódio no líquor apresentou-se elevada em um caso. A etiologia da PEM não está esclarecida, porém em alguns casos a intoxicação por cloreto de sódio/privação de água pode estar envolvida na etiologia da enfermidade. A PEM representa 4,78% dos casos ele enfermidades de bovinos diagnosticadas no Laboratório de Anatomia Patológica da UFMS. Com bases nos resultados, verifica-se a importância da enfermidade no diagnóstico diferencial de outras doenças com quadro clínico neurológico no MS, principalmente a raiva, a meningoencefalite por herpesvírus bovino tipo 5 (HVB-5) e o botulismo.

Abstract in English:

ABSTRACT.- Salvador S.C., Lemos R.A.A., Riet-Correa F., Roehe P.M. & Osório A.L.A.R. 1998. [Meningoencephalitis in cattle caused by bovine herpesvirus-5 in Mato Grosso do Sul and São Paulo.] Meningoencefalite em bovinos causada por herpesvírus bovino-5 no Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 18(2):76-83. Depto Medicina Veterinária, Universidade Federal do Mato Grosso do Sul, Cx. Postal 649, Campo Grande, MS 79070-900, Brazil. Fifteen outbreaks of bovine herpesvirus-type 5 (BHV-5) infection were diagnosed from August 1993 to December 1996. Fourteen outbreaks occurred in the State of Mato Grosso do Sul and one in the State of São Paulo. Cattle 6 to 60 months old were affected. Morbidity reached 0.05% to 5% and case fatality rate was nearly 100%. The disease occurred in diferente municipalities and at different times of the yea1: Clinical signs were exclusively nervous, and the clinical course varied from 1 to 15 days. The main histologic lesions were meningitis, diffuse encephalitis and necrosis of the cerebral cortex with intranuclear inclusion bodies in astrocytes and neurons. BHV-5 was isolated from 11 out of 12 brains of infected animals inoculated in calf testis cells and MDBK cells. The vírus was identified by immunoperoxidase stainingwith use of monoclonal specific antibodies. Outbreaks of infection by BHV-5 represent 5% of the total number of bovine cases submitted for diagnosis to the Clinical Hospital of the University of Mato Grosso do Sul. These results indicate the importance of the disease in Mato Grosso do Sul and the need for its differentiation from other diseases which affect the nervous system.

• Meningoencephalitis bovine herpesvirus-5 BHV-5 cortical cerebral necrosis cattle Mato Grosso do Sul Meningoencefalite herpesvírus bovino-5 polioencefalomalacia bovinos Mato Grosso do Sul.

Abstract in Portuguese:

RESUMO.- Salvador S.C., Lemos R.A.A., Riet-Correa F., Roehe P.M. & Osório A.L.A.R. 1998. [Meningoencephalitis in cattle caused by bovine herpesvirus-5 in Mato Grosso do Sul and São Paulo.] Meningoencefalite em bovinos causada por herpesvírus bovino-5 no Mato Grosso do Sul e São Paulo. Pesquisa Veterinária Brasileira 18(2):76-83. Depto Medicina Veterinária, Universidade Federal do Mato Grosso do Sul, Cx. Postal 649, Campo Grande, MS 79070-900, Brazil. Quinze focos de meningoencefalite por herpesvírus bovino-5 (BHV-5) foram diagnosticados entre agosto de 1993 e dezembro de 1996, sendo 14 provenientes do estado do Mato Grosso do Sul e um do estado de São Paulo. A doença ocorreu em diversos municípios e em diferentes épocas do ano. Foram afetados bovinos de 6 a 60 meses de idade, com uma morbidade de 0,05% a 5% e letalidade próxima a 100%. Os sinais clínicos foram exclusivamente nervosos e o curso da enfermidade variou de 1 a 15 dias. As principais lesões histológicas detectadas foram meningite e encefalite difusa com malacia do córtex cerebral e presença de corpúsculos de inclusão intranucleares em astrócitos e neurônios. O vírus foi isolado do cérebro de 11 de um total de 12 animais, e sua identidade confirmada por imunoperoxidase, utilizando-se anticorpos monoclonais específicos. Os surtos de encefalite por BHV-5 representam 5% dos diagnósticos realizados em bovinos pelo Hospital Veterinário da Universidade Federal do Mato Grosso do Sul. Os resultados deste trabalho evidenciam a importância da doença no Mato Grosso do Sul e indicam a necessidade de incluir a encefalite por BHV-5 no diagnóstico diferencial de outras doenças do sistema nervoso de bovinos frequentes no Estado.