PESQUISA VETERINÁRIA BRASILEIRA

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:

Rozza D.B., Raymundo D.L., Corrêa A.M.R., Seitz A.L., Driemeier D. & Colodel E.M. 2006. [Spontaneous Baccharis coridifolia (Compositae) poisoning in sheep.] Intoxicação espontânea por Baccharis coridifolia (Compositae) em ovinos. Pesquisa Veterinária Brasileira 26(1):21-25. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br An outbreak of Baccharis coridifolia (Compositae) poisoning in sheep is reported, which occurred in November 2004 in the county of Caxias do Sul, Rio Grande do Sul (RS), southern Brazil. From a herd of 212 sheep, coming from a Baccharis coridifolia free area, in the county of Jaguarão, RS, 35 sheep died until 5 days after the arrival in the new area where the plant was found with abundance. The clinical signs began 8 hours after introduction of the animals into the new pasture and included apathy, anorexia, abdominal retraction or mild distension, weakness of hind limbs, dry feces, sternal ou lateral decumbency, struggling movements, coma and death. Clinical evolution was from 5 to 48 hours. Other sheep that were already before on the pasture were not affected. Main necropsy findings were in the gastrointestinal tube, with wall and serosal oedema, mainly in the reticulo-ruminal fold and of the abomasum, reddening and detachment of the mucosa of forestomachs, and intense hemorrhage in the submucosa. Histopathological findings were degeneration and necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration associated with bacterial colonies, congestion, hemorrhage and oedema, and lymphoid tissue necrosis.

• Poisonous plants Baccharis coridifolia Compositae plant poisoning diseases of sheep pathology.

Abstract in Portuguese:

Rozza D.B., Raymundo D.L., Corrêa A.M.R., Seitz A.L., Driemeier D. & Colodel E.M. 2006. [Spontaneous Baccharis coridifolia (Compositae) poisoning in sheep.] Intoxicação espontânea por Baccharis coridifolia (Compositae) em ovinos. Pesquisa Veterinária Brasileira 26(1):21-25. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Cx. Postal 15094, Porto Alegre, RS 91540-000, Brazil. E-mail: moleta@terra.com.br An outbreak of Baccharis coridifolia (Compositae) poisoning in sheep is reported, which occurred in November 2004 in the county of Caxias do Sul, Rio Grande do Sul (RS), southern Brazil. From a herd of 212 sheep, coming from a Baccharis coridifolia free area, in the county of Jaguarão, RS, 35 sheep died until 5 days after the arrival in the new area where the plant was found with abundance. The clinical signs began 8 hours after introduction of the animals into the new pasture and included apathy, anorexia, abdominal retraction or mild distension, weakness of hind limbs, dry feces, sternal ou lateral decumbency, struggling movements, coma and death. Clinical evolution was from 5 to 48 hours. Other sheep that were already before on the pasture were not affected. Main necropsy findings were in the gastrointestinal tube, with wall and serosal oedema, mainly in the reticulo-ruminal fold and of the abomasum, reddening and detachment of the mucosa of forestomachs, and intense hemorrhage in the submucosa. Histopathological findings were degeneration and necrosis of the epithelium of the forestomachs with polymorphonuclear infiltration associated with bacterial colonies, congestion, hemorrhage and oedema, and lymphoid tissue necrosis.

Abstract in English:

Batista J.S., Riet-Correa F., Barbosa R.C. & Guerra J.L. 2006. [Experimental infection by Trypanosoma vivax in sheep.] Infecção experimental por Trypanosoma vivax em ovinos. Pesquisa Veterinária Brasileira 26(1):31-37. Hospital Veterinário, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br This paper has the objective to report clinical signs, hematologic changes, and macroscopic and microscopic alterations in sheep infected experimentally with Trypanosoma vivax, isolated from an outbreak in cattle in the semiarid region of the state of Paraíba, northeastern Brazil. Four Santa Inês sheep were inoculated intravenously with 1ml of blood containing 1.85x105 trypomastigotes. Other 4 sheep were used as control. The presence of trypanosomes in the blood and the temperature were recorded daily during the first 30 days and fortnightly from day 31 to day 90 after infection. Also fortnightly, the sheep were weighed and blood samples were obtained for hematological analysis. One inoculated sheep died 75 days after inoculation. The other 3 inoculated and the 4 control sheep were killed 90 days after the beginning of the experiment. T. vivax was observed constantly in the blood of the inoculated sheep from 4-15 days after inoculation. From day 16 to day 30 the parasitemia was lower and irregular. No trypanosomes were observed in the blood after 30 days of infection. A positive linear correlation [Y=0.027x + 38.515, R2=0.944 (P<0.05)] was found between the number of trypanosomes in the blood and body temperature. Significant differences were observed in body weight between inoculated and non-inoculated sheep from day 30 to day 90 after the experiment. From day 30 to day 90 after inoculation trypanosomes were absent or only in low numbers in the blood, and the animals showed anemia and leucopenia. Gross alterations were pale carcasses, enlarged lymph nodes and spleen, and augmented liquid in the peritoneal and pericardiac cavities. Multifocal lymphocytic myocarditis was observed histologically. It is concluded that the isolate is pathogenic to sheep. It is suggested that the semiarid region, where the outbreak occurred, is non-endemic (marginal) for trypanosomosis, and that the disease may occur if the parasite is introduced through vectors.

• Experimental infection Trypanosoma vivax sheep semiarid.

Abstract in Portuguese:

Batista J.S., Riet-Correa F., Barbosa R.C. & Guerra J.L. 2006. [Experimental infection by Trypanosoma vivax in sheep.] Infecção experimental por Trypanosoma vivax em ovinos. Pesquisa Veterinária Brasileira 26(1):31-37. Hospital Veterinário, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br This paper has the objective to report clinical signs, hematologic changes, and macroscopic and microscopic alterations in sheep infected experimentally with Trypanosoma vivax, isolated from an outbreak in cattle in the semiarid region of the state of Paraíba, northeastern Brazil. Four Santa Inês sheep were inoculated intravenously with 1ml of blood containing 1.85x105 trypomastigotes. Other 4 sheep were used as control. The presence of trypanosomes in the blood and the temperature were recorded daily during the first 30 days and fortnightly from day 31 to day 90 after infection. Also fortnightly, the sheep were weighed and blood samples were obtained for hematological analysis. One inoculated sheep died 75 days after inoculation. The other 3 inoculated and the 4 control sheep were killed 90 days after the beginning of the experiment. T. vivax was observed constantly in the blood of the inoculated sheep from 4-15 days after inoculation. From day 16 to day 30 the parasitemia was lower and irregular. No trypanosomes were observed in the blood after 30 days of infection. A positive linear correlation [Y=0.027x + 38.515, R2=0.944 (P<0.05)] was found between the number of trypanosomes in the blood and body temperature. Significant differences were observed in body weight between inoculated and non-inoculated sheep from day 30 to day 90 after the experiment. From day 30 to day 90 after inoculation trypanosomes were absent or only in low numbers in the blood, and the animals showed anemia and leucopenia. Gross alterations were pale carcasses, enlarged lymph nodes and spleen, and augmented liquid in the peritoneal and pericardiac cavities. Multifocal lymphocytic myocarditis was observed histologically. It is concluded that the isolate is pathogenic to sheep. It is suggested that the semiarid region, where the outbreak occurred, is non-endemic (marginal) for trypanosomosis, and that the disease may occur if the parasite is introduced through vectors.

Abstract in English:

Riet-Correa G., Duarte M.D., Barbosa J.D., Oliveira C.M.C., Cerqueira V.D., Brito M.F. & Riet-Correa F. 2006. [Meningoencephalitis and polioencephalomalacia caused by Bovine herpesvirus-5 in the state of Pará, northern Brazil.] Meningoencefalite e polioencefalomalacia causadas por Herpesvírus bovino-5 no Estado do Pará. Pesquisa Veterinária Brasileira 26(1):44-46. Central de Diagnóstico Veterinário, Universidade Federal do Pará, Maximino Porpino 1000, Castanhal, PA 68740-080, Brazil. E-mail: griet@ufpa.br Four outbreaks of meningoencephalitis in 1 to 2 years old cattle caused by Bovine herpesvirus-5 are reported in four municipalities in the state of Pará, northern Brazil. In three outbreaks only one animal was affected, in another 3 cattle were affected. Main clinical signs were incoordination, dullness, blindness, recumbence, and opisthotonus. Death occurred after a clinical manifestation period of 3-4 days. Softening and yellowish areas were observed grossly in the cerebral cortex. The histology revealed poliencephalomalacia in the cerebral cortex, thalamus and basal nuclei, and non suppurative encephalitis and meningitis, and eosinophilic intranuclear inclusion bodies in astrocytes. The diagnosis was based on the typical microscopic lesions.

• Meningoencephalitis polioencephalomalacia bovine herpesvirus-5 cattle.

Abstract in Portuguese:

Riet-Correa G., Duarte M.D., Barbosa J.D., Oliveira C.M.C., Cerqueira V.D., Brito M.F. & Riet-Correa F. 2006. [Meningoencephalitis and polioencephalomalacia caused by Bovine herpesvirus-5 in the state of Pará, northern Brazil.] Meningoencefalite e polioencefalomalacia causadas por Herpesvírus bovino-5 no Estado do Pará. Pesquisa Veterinária Brasileira 26(1):44-46. Central de Diagnóstico Veterinário, Universidade Federal do Pará, Maximino Porpino 1000, Castanhal, PA 68740-080, Brazil. E-mail: griet@ufpa.br Four outbreaks of meningoencephalitis in 1 to 2 years old cattle caused by Bovine herpesvirus-5 are reported in four municipalities in the state of Pará, northern Brazil. In three outbreaks only one animal was affected, in another 3 cattle were affected. Main clinical signs were incoordination, dullness, blindness, recumbence, and opisthotonus. Death occurred after a clinical manifestation period of 3-4 days. Softening and yellowish areas were observed grossly in the cerebral cortex. The histology revealed poliencephalomalacia in the cerebral cortex, thalamus and basal nuclei, and non suppurative encephalitis and meningitis, and eosinophilic intranuclear inclusion bodies in astrocytes. The diagnosis was based on the typical microscopic lesions.

Abstract in English:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

• Poisonous plants Baccharidastrum triplinervium Asteraceae plant poisoning diseases of cattle pathology.

Abstract in Portuguese:

Langohr I.M., Gava A. & Barros C.S.L. 2005. [Poisoning in cattle by Baccharidastrum triplinervium (Asteraceae).] Intoxicação por Baccharidastrum triplinervium (Asteraceae) em bovinos. Pesquisa Veterinária Brasileira 25(4):235-238. Animal Disease Diagnostic Laboratory, Purdue University, 406 South University, West Lafayette, IN 47907, Estados Unidos. E-mail: ilangohr@purdue.edu An outbreak of poisoning by Baccharidastrum triplinervium in cattle from Paraná, Brazil, is described. The disease occurred during a severe drought in early summer. The onset of clinical signs was two days after 50 cows and 8 heifers had been introduced into a pasture with high density of B. triplinervium that showed signs of having been consumed by the animals. Fifteen animals (9 cows and 6 heifers) got sick. Of these 15, two cows and four heifers died after a clinical course of 12-60 hours. Clinical signs included depression, ruminal atony, moderate bloat, marked dehydration, mild diarrhea and anorexia. The animals were restless, laying down and getting up constantly, remaining progressively longer periods in sternal recumbency. Once in that position, the animals had an extended head or the head turned to one of the sides of the body, and were groaning. Additionally, the cows had an abrupt fall in milk yield. The remaining affected cattle presented milder clinical signs and were partially back to their feed on the day following the onset of the clinical signs. The milk production was back to normal values within one week. The main gross lesions observed in two necropsied cows were in the forestomachs and abomasum, consisting of edema of the ruminal wall, as well as of diffuse reddening of the mucosae of the rumen, reticulum, abomasum and of some of the omasal folds. The main histological lesions included multifocal ballooning degeneration and necrosis of the lining epithelium of the rumen, associated with neutrophilic infiltrate. The diagnosis was based on the epidemiological data and on the experimental reproduction of the disease by force-feeding 3 bovine with the aeral fresh parts (20 and 30g/kg) of B. triplinervium. Chemical analysis of dried material from B. triplinervium harvested at the site of the outbreak was negative for macrocyclic trichothecenes.

Abstract in English:

Zlotowski P., Nakazato L., Dutra V., Barros S.S., Gimeno E.J., Göcks M., Colodel E.M. & Driemeier D. 2005. [Inherited glycogenosis in Brahman cattle in Brazil.] Glicogenose hereditária em bovinos Brahman no Brasil. Pesquisa Veterinária Brasileira 25(4):210-214. Setor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Bairro Agronomia, Cx. Postal 15094, Porto Alegre, RS 91540-000. Brazil. E-mail: davetpat@ufrgs.br An inherited disease of cattle, characterized by lysosomal storage of glycogen in several tissues, is reported. The disease was diagnosed in a Brahman herd in the municipality of Porto Lucena, Rio Grande do Sul, Brazil. Affected calves, after one month of age, showed progressive difficulty to follow their mother, retarded growth, muscular weakness and tremors, lethargy and poor body condition. All affected calves were sired by the same bull. Necropsy was performed on three affected calves. The only gross lesion detected was paleness of the skeletal muscles of the trunk and limbs. Cytoplasmic vacuoles, the main histological lesion, were particularly evident in skeletal muscles, myocardium and Purkinje fibers, in neurons of the brain and spinal cord. Large amounts of periodic acid Schiff (PAS) positive granules were also observed in these most severely affected tissues. Pretreatment with diastase completely abolished the PAS reactivity. The 1057?TA, a lethal mutation in the gene of the acid alpha-glucosidase, which causes generalized glycogenosis in Brahman cattle, was detected by PCR in paraffin embedded tissues of affected animals on which post-mortem examination was performed. Clinical, histological and molecular findings were similar to previous descriptions of generalized glycogenosis in Brahman cattle in Australia. No previous indexed reports about generalized glycogenosis of Brahman cattle in Brazil could be found.

• Glycogenosis inherited disease Brahman cattle.

Abstract in Portuguese:

Zlotowski P., Nakazato L., Dutra V., Barros S.S., Gimeno E.J., Göcks M., Colodel E.M. & Driemeier D. 2005. [Inherited glycogenosis in Brahman cattle in Brazil.] Glicogenose hereditária em bovinos Brahman no Brasil. Pesquisa Veterinária Brasileira 25(4):210-214. Setor de Patologia Veterinária, Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Bairro Agronomia, Cx. Postal 15094, Porto Alegre, RS 91540-000. Brazil. E-mail: davetpat@ufrgs.br An inherited disease of cattle, characterized by lysosomal storage of glycogen in several tissues, is reported. The disease was diagnosed in a Brahman herd in the municipality of Porto Lucena, Rio Grande do Sul, Brazil. Affected calves, after one month of age, showed progressive difficulty to follow their mother, retarded growth, muscular weakness and tremors, lethargy and poor body condition. All affected calves were sired by the same bull. Necropsy was performed on three affected calves. The only gross lesion detected was paleness of the skeletal muscles of the trunk and limbs. Cytoplasmic vacuoles, the main histological lesion, were particularly evident in skeletal muscles, myocardium and Purkinje fibers, in neurons of the brain and spinal cord. Large amounts of periodic acid Schiff (PAS) positive granules were also observed in these most severely affected tissues. Pretreatment with diastase completely abolished the PAS reactivity. The 1057?TA, a lethal mutation in the gene of the acid alpha-glucosidase, which causes generalized glycogenosis in Brahman cattle, was detected by PCR in paraffin embedded tissues of affected animals on which post-mortem examination was performed. Clinical, histological and molecular findings were similar to previous descriptions of generalized glycogenosis in Brahman cattle in Australia. No previous indexed reports about generalized glycogenosis of Brahman cattle in Brazil could be found.

Abstract in English:

Lima E.F., Riet-Correa F., Castro R.S., Gomes A.A.B. & Lima F.S. 2005. [Clinical signs, distribution of the lesions in the central nervous system and epidemiology of rabies in northeastern Brazil.] Sinais clínicos, distribuição das lesões no sistema nervoso e epidemiologia da raiva em herbívoros na região Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(4):250-264. Centro de Saúde e Tecnologia Rural, Campus de Patos, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: riet@cstr.ufcg.br Twenty four outbreaks of rabies in cattle, 4 in horses, 2 in sheep, and 2 in goats are reported in northeastern Brazil. All outbreaks occurred in the state of Paraíba, except one in horses that occurred in the state of Rio Grande do Norte. All outbreaks, except one in sheep, were probably transmitted by vampire-bats, but the transmission by foxes (Dusicyon vetulus) is also possible. Clinical signs were characteristic for distribution of the lesions in the central nervous system (CNS). In cattle, signs were mainly of the paralytic form of rabies, caused by lesions on the spinal cord, brain stem and cerebellum; but some animals showed also depression, excitation and other signs due to cerebral lesions. In 3 out of 5 horses, the main clinical signs were due to lesions in the cerebrum, and 2 had the paralytic form. From 4 sheep and 2 goats affected, 4 showed clinical signs of the paralytic form; but in 1 goat and 1 sheep the main clinical signs were caused by cerebral lesions. All affected animals, except 1 goat, had a clinical manifestation period of 2-8 days. The only gross lesions were distention of the urinary bladder in 4 cattle and distention of the rectum in 2 others. Two horses had skin lesions due to traumatic injury. Histologic lesions were diffuse non-suppurative encephalomyelitis and meningitis. In the horses, and in one goat with a clinical manifestation period of 35 days, the lesions were more severe, with neuronal necrosis, neuronophagia, and presence of axonal spheroids. Negri bodies were found in 87% (20/23) of the cattle cases examined histologically. In small ruminants Negri bodies were found in 83% (5/6) of the cases. In sheep, goats and cattle, Negri bodies were more frequent in the cerebellum, but they were found also in brain stem, spinal cord and cerebrum. In horses, Negri bodies were found in small amounts only in the cortex of one animal, and in the cortex and hippocampus of another. Histologic lesions and Negri bodies in the trigeminal ganglia were less frequent than in the CNS. These results show that in rabies of herbivores, clinical signs and distribution of lesions in the CNS are variable, so that for the diagnosis and adequate clinical evaluation and the histologic study of different areas of the CNS are necessary. This also suggests that when the fluorescent antibody test and mouse inoculation test are negative, they should be repeated with samples from different areas of the brain and spinal cord. Frequency data of diseases from 4 diagnostic laboratories were used to estimate cattle deaths due to rabies in 3 Brazilian states. In Paraíba, with a population of 918,262 cattle, the annual death rate is estimated in 8,609 heads. In Mato Grosso do Sul, with a population of 23 millions cattle, deaths caused by rabies are estimated in 149,500 heads, and in Rio Grande do Sul, with a cattle population of 13 millions, cattle deaths due to rabies are estimated in 13,000 to 16,250 heads. If these data are used to estimate cattle losses in Brazil, with a cattle population of 195 millions, it can be estimated that 842,688 deaths are caused annually by rabies.

• Rabies cattle sheep goats horses pathology clinical signs economical impact.

Abstract in Portuguese:

Lima E.F., Riet-Correa F., Castro R.S., Gomes A.A.B. & Lima F.S. 2005. [Clinical signs, distribution of the lesions in the central nervous system and epidemiology of rabies in northeastern Brazil.] Sinais clínicos, distribuição das lesões no sistema nervoso e epidemiologia da raiva em herbívoros na região Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(4):250-264. Centro de Saúde e Tecnologia Rural, Campus de Patos, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: riet@cstr.ufcg.br Twenty four outbreaks of rabies in cattle, 4 in horses, 2 in sheep, and 2 in goats are reported in northeastern Brazil. All outbreaks occurred in the state of Paraíba, except one in horses that occurred in the state of Rio Grande do Norte. All outbreaks, except one in sheep, were probably transmitted by vampire-bats, but the transmission by foxes (Dusicyon vetulus) is also possible. Clinical signs were characteristic for distribution of the lesions in the central nervous system (CNS). In cattle, signs were mainly of the paralytic form of rabies, caused by lesions on the spinal cord, brain stem and cerebellum; but some animals showed also depression, excitation and other signs due to cerebral lesions. In 3 out of 5 horses, the main clinical signs were due to lesions in the cerebrum, and 2 had the paralytic form. From 4 sheep and 2 goats affected, 4 showed clinical signs of the paralytic form; but in 1 goat and 1 sheep the main clinical signs were caused by cerebral lesions. All affected animals, except 1 goat, had a clinical manifestation period of 2-8 days. The only gross lesions were distention of the urinary bladder in 4 cattle and distention of the rectum in 2 others. Two horses had skin lesions due to traumatic injury. Histologic lesions were diffuse non-suppurative encephalomyelitis and meningitis. In the horses, and in one goat with a clinical manifestation period of 35 days, the lesions were more severe, with neuronal necrosis, neuronophagia, and presence of axonal spheroids. Negri bodies were found in 87% (20/23) of the cattle cases examined histologically. In small ruminants Negri bodies were found in 83% (5/6) of the cases. In sheep, goats and cattle, Negri bodies were more frequent in the cerebellum, but they were found also in brain stem, spinal cord and cerebrum. In horses, Negri bodies were found in small amounts only in the cortex of one animal, and in the cortex and hippocampus of another. Histologic lesions and Negri bodies in the trigeminal ganglia were less frequent than in the CNS. These results show that in rabies of herbivores, clinical signs and distribution of lesions in the CNS are variable, so that for the diagnosis and adequate clinical evaluation and the histologic study of different areas of the CNS are necessary. This also suggests that when the fluorescent antibody test and mouse inoculation test are negative, they should be repeated with samples from different areas of the brain and spinal cord. Frequency data of diseases from 4 diagnostic laboratories were used to estimate cattle deaths due to rabies in 3 Brazilian states. In Paraíba, with a population of 918,262 cattle, the annual death rate is estimated in 8,609 heads. In Mato Grosso do Sul, with a population of 23 millions cattle, deaths caused by rabies are estimated in 149,500 heads, and in Rio Grande do Sul, with a cattle population of 13 millions, cattle deaths due to rabies are estimated in 13,000 to 16,250 heads. If these data are used to estimate cattle losses in Brazil, with a cattle population of 195 millions, it can be estimated that 842,688 deaths are caused annually by rabies.

Abstract in English:

Caron L., Brum M.C.S., Moraes M.P., Golde W.T., Arns C.W. & Grubman M.J. 2005. Granulocyte-macrophage colony-stimulating factor does not increase the potency or efficacy of a foot-and-mouth disease virus subunit vaccine. Pesquisa Veterinária Brasileira 25(3):150-158. USDA, ARS, PIADC-FMD Research Unit, PO.Box 848, Greenport, NY 11944 0848, USA. E-mail: mgrubman@piadc.ars.usda.gov Foot-and-mouth disease (FMD) is one of the most feared diseases of livestock worldwide. Vaccination has been a very effective weapon in controlling the disease, however a number of concerns with the current vaccine including the inability of approved diagnostic tests to reliably distinguish vaccinated from infected animals and the need for high containment facilities for vaccine production, have limited its use during outbreaks in countries previously free of the disease. A number of FMD vaccine candidates have been tested and a replication-defective human adenovirus type 5 (Ad5) vector containing the FMDV capsid (P1-2A) and 3C protease coding regions has been shown to completely protect pigs against challenge with the homologous virus (FMDV A12 and A24). An Ad5-P1-2A+3C vaccine for FMDV O1 Campos (Ad5-O1C), however, only induced a low FMDV-specific neutralizing antibody response in swine potency tests. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been successfully used to stimulate the immune response in vaccine formulations against a number of diseases, including HIV, hepatitis C and B. To attempt to improve the FMDV-specific immune response induced by Ad5-O1C, we inoculated swine with Ad5-O1C and an Ad5 vector containing the gene for porcine GM-CSF (pGM-CSF). However, in the conditions used in this trial, pGM-CSF did not improve the immune response to Ad5-O1C and adversely affected the level of protection of swine challenged with homologous FMDV.

• Foot-and-mouth disease virus O1 Campos Adenovirus Granulocyte-macrophage colony-stimulating factor.

Abstract in Portuguese:

Caron L., Brum M.C.S., Moraes M.P., Golde W.T., Arns C.W. & Grubman M.J. 2005. Granulocyte-macrophage colony-stimulating factor does not increase the potency or efficacy of a foot-and-mouth disease virus subunit vaccine. Pesquisa Veterinária Brasileira 25(3):150-158. USDA, ARS, PIADC-FMD Research Unit, PO.Box 848, Greenport, NY 11944 0848, USA. E-mail: mgrubman@piadc.ars.usda.gov Foot-and-mouth disease (FMD) is one of the most feared diseases of livestock worldwide. Vaccination has been a very effective weapon in controlling the disease, however a number of concerns with the current vaccine including the inability of approved diagnostic tests to reliably distinguish vaccinated from infected animals and the need for high containment facilities for vaccine production, have limited its use during outbreaks in countries previously free of the disease. A number of FMD vaccine candidates have been tested and a replication-defective human adenovirus type 5 (Ad5) vector containing the FMDV capsid (P1-2A) and 3C protease coding regions has been shown to completely protect pigs against challenge with the homologous virus (FMDV A12 and A24). An Ad5-P1-2A+3C vaccine for FMDV O1 Campos (Ad5-O1C), however, only induced a low FMDV-specific neutralizing antibody response in swine potency tests. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been successfully used to stimulate the immune response in vaccine formulations against a number of diseases, including HIV, hepatitis C and B. To attempt to improve the FMDV-specific immune response induced by Ad5-O1C, we inoculated swine with Ad5-O1C and an Ad5 vector containing the gene for porcine GM-CSF (pGM-CSF). However, in the conditions used in this trial, pGM-CSF did not improve the immune response to Ad5-O1C and adversely affected the level of protection of swine challenged with homologous FMDV.

Abstract in English:

Nóbrega Jr J.E., Riet-Correa F., Nóbrega R.S., Medeiros J.M., Vasconcelos J.S., Simões S.V.D. & Tabosa I.M. 2005. [Perinatal mortality of lambs in the semi-arid region of Paraíba, Brazil.] Mortalidade perinatal de cordeiros no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(3):171-178. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal lamb mortality were studied, from March 2002 to October 2004, on 27 farms in the semiarid region of Paraíba, northeastern Brazil. In 90 lambs necropsied the following frequency of different causes of death was found: neonatal infections (41.1%), malformations (23.3%), dystocia (10%), starvation/hypothermia (10%), abortion (4.4%), and predation (2.2%). Regarding the time of death, 4.4% of the lambs died before parturition, 10% during parturition, 30% on the first day after parturition, 20% between the second and the third day, and 35.6% between the 4th and the 28th day after parturition. The assistance during parturition, umbilical disinfection of the neonates, colostrum ingestion between 2 and 6 hours after parturition, and keeping the ewes in healthy environmental conditions during and after parturition could improve lamb surviving. The high frequency of malformations in different breeds suggests that malformations are due to a toxic plant. The main defects were permanent flexure of the front legs, brachygnathia, cleft palate, and other head malformations. In a recent report the authors demonstrated the teratogenic effects of Mimosa tenuiflora, a very common plant in the semiarid region, which is probably the cause of those malformations. Lambs which died due to starvation/hypothermia and had low birth weight (1.37 ± 0.70kg), suggesting that a better nutrition of the ewe during the last trimester of gestation is a way to control this cause of lamb mortality. Considering that in the northeastern region, in most farms, the rams stay with the ewes during the whole year, the adoption of a breeding season would help to control the different causes of perinatal lamb mortality.

• Lamb mortality newborn lambs sheep production perinatal mortality.

Abstract in Portuguese:

Nóbrega Jr J.E., Riet-Correa F., Nóbrega R.S., Medeiros J.M., Vasconcelos J.S., Simões S.V.D. & Tabosa I.M. 2005. [Perinatal mortality of lambs in the semi-arid region of Paraíba, Brazil.] Mortalidade perinatal de cordeiros no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(3):171-178. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal lamb mortality were studied, from March 2002 to October 2004, on 27 farms in the semiarid region of Paraíba, northeastern Brazil. In 90 lambs necropsied the following frequency of different causes of death was found: neonatal infections (41.1%), malformations (23.3%), dystocia (10%), starvation/hypothermia (10%), abortion (4.4%), and predation (2.2%). Regarding the time of death, 4.4% of the lambs died before parturition, 10% during parturition, 30% on the first day after parturition, 20% between the second and the third day, and 35.6% between the 4th and the 28th day after parturition. The assistance during parturition, umbilical disinfection of the neonates, colostrum ingestion between 2 and 6 hours after parturition, and keeping the ewes in healthy environmental conditions during and after parturition could improve lamb surviving. The high frequency of malformations in different breeds suggests that malformations are due to a toxic plant. The main defects were permanent flexure of the front legs, brachygnathia, cleft palate, and other head malformations. In a recent report the authors demonstrated the teratogenic effects of Mimosa tenuiflora, a very common plant in the semiarid region, which is probably the cause of those malformations. Lambs which died due to starvation/hypothermia and had low birth weight (1.37 ± 0.70kg), suggesting that a better nutrition of the ewe during the last trimester of gestation is a way to control this cause of lamb mortality. Considering that in the northeastern region, in most farms, the rams stay with the ewes during the whole year, the adoption of a breeding season would help to control the different causes of perinatal lamb mortality.

Abstract in English:

Brito M.F., Seixas J.N., Jabour F.F., Andrade G.B., Cunha B.R.M., França T.N. & Peixoto P.V. 2005. [About an outbreak of cumarin poisoning in cattle.] Sobre um surto de envenenamento por derivado cumarínico em bovinos. Pesquisa Veterinária Brasileira 25(3):143-149. Depto Epidemiologia e Saúde Pública, Instituto de Veterinária, UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: marilene@ufrrj.br An outbreak of cumarin poisoning which occurred in feedlot cattle in the county of Seropédica, Rio de Janeiro, is described. Three from 43 animal died. The main manifestations included bloody diarrhea, apathy, anorexia, sialorrhoe, incoordenation and dyspnoe. At post-mortem examinations there were mainly hemorrhages of varies forms and intensity in several organs, which also were seen at histopathological examination. Analysis for cumarin derivates of rumen, reticulum, omasum and abomasum contents, of liver and kidney samples, as well as of food collected from the trough, resulted positive for cumarin compounds which included warfarin, bromadiolone and brodifacoum. Feeding experiments with food stored at the property resulted negative. An intentional or accidental act could not be excluded. Animals that did not feed from the same trough did not get sick.

• umarin poisoning cattle.

Abstract in Portuguese:

Brito M.F., Seixas J.N., Jabour F.F., Andrade G.B., Cunha B.R.M., França T.N. & Peixoto P.V. 2005. [About an outbreak of cumarin poisoning in cattle.] Sobre um surto de envenenamento por derivado cumarínico em bovinos. Pesquisa Veterinária Brasileira 25(3):143-149. Depto Epidemiologia e Saúde Pública, Instituto de Veterinária, UFRRJ, Seropédica, RJ 23890-000, Brazil. E-mail: marilene@ufrrj.br An outbreak of cumarin poisoning which occurred in feedlot cattle in the county of Seropédica, Rio de Janeiro, is described. Three from 43 animal died. The main manifestations included bloody diarrhea, apathy, anorexia, sialorrhoe, incoordenation and dyspnoe. At post-mortem examinations there were mainly hemorrhages of varies forms and intensity in several organs, which also were seen at histopathological examination. Analysis for cumarin derivates of rumen, reticulum, omasum and abomasum contents, of liver and kidney samples, as well as of food collected from the trough, resulted positive for cumarin compounds which included warfarin, bromadiolone and brodifacoum. Feeding experiments with food stored at the property resulted negative. An intentional or accidental act could not be excluded. Animals that did not feed from the same trough did not get sick.