PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Gomes M., Uieda W. & Latorre M.R.D.O. 2006. [Influence of sex differences in the same colony for chemical control of vampire Desmodus rotundus (Phyllostomidae) populations in the state of São Paulo, Brazil.] Influência do sexo de indivíduos da mesma colônia no controle químico das populações do morcego hematófago Desmodus rotundus (Phyllstomidae) no Estado de São Paulo. Pesquisa Veterinária Brasileira 26(1):38-43. Coordenadoria de Defesa Agropecuária/SP, Regional Mogi das Cruzes, Av. Cândido X.A.Sousa 35, Mogi das Cruzes, SP 08780-210, Brazil. E-mail: murilong@usp.br The aim of this study was to verify the fidelity to the diurnal roosts by the genders of the vampire bat Desmodus rotundus, and to analyse the Warfarin gel 2% effectiveness for reduction of the size of vampire bat colonies, when individuals of different sexes were treated. In 1999 and 2000, 626 vampire bats were mist netted while leaving at night 12 diurnal roosts in the state of São Paulo. They were marked, and 10% of the roost population received the Warfarin gel 2% treatment. In Test I only males were treated, in Test II only females were treated, and in Test III 5% of males and females were treated. After 5 and 10 days, the dead and the survivors were counted. Females were more loyal to the roosts (p<0,01) and better wide spreader of the Warfarin gel (p<0,01).

• Rabies vampire bats Desmodus rotundus Warfarin gel.

Abstract in Portuguese:

Gomes M., Uieda W. & Latorre M.R.D.O. 2006. [Influence of sex differences in the same colony for chemical control of vampire Desmodus rotundus (Phyllostomidae) populations in the state of São Paulo, Brazil.] Influência do sexo de indivíduos da mesma colônia no controle químico das populações do morcego hematófago Desmodus rotundus (Phyllstomidae) no Estado de São Paulo. Pesquisa Veterinária Brasileira 26(1):38-43. Coordenadoria de Defesa Agropecuária/SP, Regional Mogi das Cruzes, Av. Cândido X.A.Sousa 35, Mogi das Cruzes, SP 08780-210, Brazil. E-mail: murilong@usp.br The aim of this study was to verify the fidelity to the diurnal roosts by the genders of the vampire bat Desmodus rotundus, and to analyse the Warfarin gel 2% effectiveness for reduction of the size of vampire bat colonies, when individuals of different sexes were treated. In 1999 and 2000, 626 vampire bats were mist netted while leaving at night 12 diurnal roosts in the state of São Paulo. They were marked, and 10% of the roost population received the Warfarin gel 2% treatment. In Test I only males were treated, in Test II only females were treated, and in Test III 5% of males and females were treated. After 5 and 10 days, the dead and the survivors were counted. Females were more loyal to the roosts (p<0,01) and better wide spreader of the Warfarin gel (p<0,01).

Abstract in English:

Lima V.M.F., Biazzono L., Silva A.C., Correa A.P.F.L. & Luvizotto M.C.R. 2005. Serological diagnosis of visceral leishmaniasis by an enzyme immunoassay using protein A in naturally infected dogs. Pesquisa Veterinária Brasileira 25(4):215-218. Departamento de Clínica, Cirurgia e Reprodução Animal, Faculdade de Medicina Veterinária, Universidade Estadual Paulista, Rua Clóvis Pestana 793, Araçatuba, SP 16050-680, Brazil. E-mail: vmflima@fmva.unesp.br A rapid indirect enzyme-linked immunosorbent assay (ELISA) was developed for measuring antibodies against Leishmania chagasi using total antigen from lysed promastigotes. Fifty symptomatic mixed breed dogs from a region of high incidence of visceral leishmaniasis in Brazil were examined. The results showed that in the positive animals, diagnosed by cytological examination, the ELISA using protein A assay system (mean optical density ± SD / 2.078 ± 0.631) detected more antibodies than the anti-IgG assay (mean optical density ± SD / 1.008 ± 0.437), while in the negative animals, the results by both systems were similar. These results suggest that the ELISA assay using protein A peroxidase conjugated could be useful to detect early infected animals in endemic areas, and thus help to control the spread of the infection.

• Leishmania chagasi visceral leishmaniasis protein A dogs.

Abstract in Portuguese:

Lima V.M.F., Biazzono L., Silva A.C., Correa A.P.F.L. & Luvizotto M.C.R. 2005. Serological diagnosis of visceral leishmaniasis by an enzyme immunoassay using protein A in naturally infected dogs. Pesquisa Veterinária Brasileira 25(4):215-218. Departamento de Clínica, Cirurgia e Reprodução Animal, Faculdade de Medicina Veterinária, Universidade Estadual Paulista, Rua Clóvis Pestana 793, Araçatuba, SP 16050-680, Brazil. E-mail: vmflima@fmva.unesp.br A rapid indirect enzyme-linked immunosorbent assay (ELISA) was developed for measuring antibodies against Leishmania chagasi using total antigen from lysed promastigotes. Fifty symptomatic mixed breed dogs from a region of high incidence of visceral leishmaniasis in Brazil were examined. The results showed that in the positive animals, diagnosed by cytological examination, the ELISA using protein A assay system (mean optical density ± SD / 2.078 ± 0.631) detected more antibodies than the anti-IgG assay (mean optical density ± SD / 1.008 ± 0.437), while in the negative animals, the results by both systems were similar. These results suggest that the ELISA assay using protein A peroxidase conjugated could be useful to detect early infected animals in endemic areas, and thus help to control the spread of the infection.

Abstract in English:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

• Trypanosomiasis Trypanosoma evansi infectious diseases encephalitis hematology pathology diseases of horses.

Abstract in Portuguese:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

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:

Amorim S.L., Medeiros R.M.T. & Riet-Correa F. 2005. [Experimental poisoning by Manihot glaziovii (Euphorbiaceae) in goats.] Intoxicação experimental por Manihot glaziovii (Euphorbiaceae) em caprinos. Pesquisa Veterinária Brasileira 25(3):179-187. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufcg.edu.br Samples of fresh, dried and partially dried leaves of Manihot glaziovii Muell. Arg. were administered orally to Moxotó goats in single doses up to 12g/kg body weight (bw). The cyanide content of the plant samples was determined by the picrosodic paper test. The plant was collected from January to June 2004. When the goats with clinical signs were in lateral recumbency, they were treated intravenously with 50ml/100kg/bw of a 20% aqueous solution of sodium tiosulfate. Three experiments were performed. In Experiment 1, the plant was given immediately after collection to six goats; two ingested the plant after been ground and four ingested the plant without having been ground. In Experiment 2, the plant was maintained in the shade, in open air or inside plastic bags. The plastic bags were changed daily. The plant kept in plastic bags was given to 18 goats, 4, 8, 12, 16, 20, 24, 48, 72, 96 and 120 hours after collection. The plant kept in the open air was given to 13 goats, 4, 24, 48, 72 and 96 hours and 9, 10, 23 and 30 days after collection. In Experiment 3, the previously ground plant kept in the open air or inside plastic bags was administered 4, 8, 12, 16, 20, 24, 48, 72 and 96 hours after collection. Seventeen goats received the plant kept in plastic bags, and 16 goats the plant left in the open air. In Experiments 2 and 3, two or three goats were used for each period after collection, and the plant was given until the loss of its toxicity. Forty goats were used as controls for evaluation of the cardiac and respiratory frequencies. In Experiment 1, the ground and not ground plant had similar toxicity. In Experiment 2, the plant kept in the open air maintained its toxicity during the whole experiment (30 days), and the plant kept inside the plastic bags was toxic until 96 hours after collection. In Experiment 3, the ground plant, left in the open air or kept inside plastic bags, was toxic for 72 hours after collection. In all experiments clinical signs were characteristic of cyanide poisoning. All poisoned goats were treated successfully. In conclusion, Manihot glaziovii, which is used as forage in northeastern Brazil, should be ground and left for at least 96 hours in the open air before feeding to animals. The plant for preparing hay should be previously ground, and the hay should be given to animals also only 96 hours after its preparation.

• Poisonous plants plant poisoning Manihot glaziovii Euphorbiaceae cyanogenic plants hydrocyanic acid goats.

Abstract in Portuguese:

Amorim S.L., Medeiros R.M.T. & Riet-Correa F. 2005. [Experimental poisoning by Manihot glaziovii (Euphorbiaceae) in goats.] Intoxicação experimental por Manihot glaziovii (Euphorbiaceae) em caprinos. Pesquisa Veterinária Brasileira 25(3):179-187. Centro de Saúde e Tecnologia Rural, UFCG, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: rmtmed@cstr.ufcg.edu.br Samples of fresh, dried and partially dried leaves of Manihot glaziovii Muell. Arg. were administered orally to Moxotó goats in single doses up to 12g/kg body weight (bw). The cyanide content of the plant samples was determined by the picrosodic paper test. The plant was collected from January to June 2004. When the goats with clinical signs were in lateral recumbency, they were treated intravenously with 50ml/100kg/bw of a 20% aqueous solution of sodium tiosulfate. Three experiments were performed. In Experiment 1, the plant was given immediately after collection to six goats; two ingested the plant after been ground and four ingested the plant without having been ground. In Experiment 2, the plant was maintained in the shade, in open air or inside plastic bags. The plastic bags were changed daily. The plant kept in plastic bags was given to 18 goats, 4, 8, 12, 16, 20, 24, 48, 72, 96 and 120 hours after collection. The plant kept in the open air was given to 13 goats, 4, 24, 48, 72 and 96 hours and 9, 10, 23 and 30 days after collection. In Experiment 3, the previously ground plant kept in the open air or inside plastic bags was administered 4, 8, 12, 16, 20, 24, 48, 72 and 96 hours after collection. Seventeen goats received the plant kept in plastic bags, and 16 goats the plant left in the open air. In Experiments 2 and 3, two or three goats were used for each period after collection, and the plant was given until the loss of its toxicity. Forty goats were used as controls for evaluation of the cardiac and respiratory frequencies. In Experiment 1, the ground and not ground plant had similar toxicity. In Experiment 2, the plant kept in the open air maintained its toxicity during the whole experiment (30 days), and the plant kept inside the plastic bags was toxic until 96 hours after collection. In Experiment 3, the ground plant, left in the open air or kept inside plastic bags, was toxic for 72 hours after collection. In all experiments clinical signs were characteristic of cyanide poisoning. All poisoned goats were treated successfully. In conclusion, Manihot glaziovii, which is used as forage in northeastern Brazil, should be ground and left for at least 96 hours in the open air before feeding to animals. The plant for preparing hay should be previously ground, and the hay should be given to animals also only 96 hours after its preparation.

Abstract in English:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

• Poisonous plants plant poisoning Aeschynomene indica Leguminosae Papilionoideae pathology diseases of the central nervous system diseases of swine.

Abstract in Portuguese:

Oliveira F.N., Rech R.R., Rissi D.R., Barros R.R. & Barros C.S.L. 2005. [Poisoning in swine from the ingestion of Aeschynomene indica (Leg.Papilionoideae) seeds.] Intoxica-ção em suínos pela ingestão de sementes de Aeschynomene indica (Leg. Papilionoideae). Pesquisa Veterinária Brasileira 25(3):135-142. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A spontaneous outbreak of a neurological disease in swine caused by the ingestion of Aeschynomene indica seeds and the reproduction of the disease in the same animal species are reported. The natural outbreak occurred in a pig-raising facility in the central region of the state of Rio Grande do Sul, Brazil. On the premises there were 100 pigs (20 breeding sows and 80 young weaned pigs from several categories) that were fed a ration made by mixing 50% of corn bran, 25% of soybean bran, 5% of a commercial mix of vitamins and minerals, and 20% of broken rice contaminated with 40% of A. indica seeds. Although all pigs apparently ingested the same ration, only 45-day-old pigs were affected; morbidity, mortality and lethality rates were respectively 25%-40%, 8.5%-20%; and 25%-66%. Clinical signs appeared 24 hours after the beginning of feeding of A. indica seeds contaminated ration and included variable degrees of incoordinated gait, falls, sternal recumbency with the hind limbs in a wide base stance, lateral recumbency and death. It was not possible to ascertain how many pigs recovered nor the time frame of recovery. One pig was euthanatized and necropsied in the premises. The poisoning was reproduced in 5 young pigs (A-E) which were fed a ration containing 10% (Pig A), 15% (Pig B) and 20% (Pigs C-E) of A. indica seeds, and in one older pig (Pig F) which was fed a ration with 16.5% of A. indica seeds. Pigs A, B and F were euthanatized and Pigs C-E died of an acute disease respectively 16, 21 and 24 hours after the beginning of the experiment. Clinical signs were similar to those observed in pigs of the spontaneous outbreak. Necropsy findings included marked hyperemia of the encephalic leptomeninges of all pigs; there were large amounts of A. indica seeds in the stomach and reddening of the intestinal wall and bloody intestinal content in Pigs C-E. A hematoma was observed in the lungs of Pig C. The histopathological findings in the brain of pigs fed rations with larger concentrations (20%) of A. indica seeds (C-E) included congestion, edema and hemorrhage and swollen vascular endothelia with focal symmetrical distribution in several brain nuclei and in the telencephalic cortex. In Pigs A and B, and in Pig F, the case which received the lower dosage of the seeds of A. indica, and in the pig from the spontaneous outbreak, histopathological changes in the brain consisted of discrete focal symmetrical areas of malacia in which closely packed Gitter cells and astrocytosis, and capillaries with swollen endothelium obliterated the normal neuropil. The symmetrical malacic foci caused by the ingestion of A. indica seeds in swine affected cerebellar and vestibular nuclei, putamen, and the mesencephalic oculomotor and red nuclei. This indicates that the A. indica seeds ingestion was responsible for the neurological condition, that it may be fatal and seems to affect equally young and older swine. The clinical outcome and pathological changes were dose-dependent, and the brain lesions progressed from damaged blood vessels to vasogenic edema, hemorrhage and malacia.

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.

Abstract in English:

Diel D.G., Fonseca E.T., Souza S.F., Mazzanti A., Bauermann F., Weiblen R. & Flores E.F. 2005. [Bovine herpesvirus 5 may use the olfactory and trigeminal pathways to invade the central nervous system of rabbits, depending upon the route of inoculation.] O Herpesvírus bovino tipo 5 (BoHV-5) pode utilizar as rotas olfatória ou trigeminal para invadir o sistema nervoso central de coelhos, dependendo da via de inoculação. Pesquisa Veterinária Brasileira 25(3):164-170. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesvirus type 5 (BoHV-5) is a major etiological agent of meningoencephalitis in cattle. Following replication in the nasal mucosa, viral invasion of the brain is thought to occur mainly by the olfactory pathway. To address the role of this pathway in the pathogenesis of neurological infection in a laboratory model, 30 days old rabbits had the main olfactory bulbs (MOBs) surgically removed and were subsequently inoculated intranasally (IN) or conjunctivally (IC) with a highly neurovirulent BoHV-5 strain (SV-507). Following IN inoculation, 10 out of 10 (100 %) control rabbits developed neurological disease. The clinical onset ranged from day 5 to 10 post-inoculation (pi, average 7.5 days); nine being euthanized in extremis and one recovering after a mild clinical course. In contrast, only one rabbit (9.1 %) of the group lacking the MOBs (n=11) developed neurological disease (onset at day 17 pi). Dexamethasone administration to the survivors (n=10) at day 50pi was followed by virus shedding in nasal and/or ocular secretions by 8 animals, demonstrating that the virus was able to reach the trigeminal ganglia (TG) during acute infection. These results demonstrate that the olfactory route provides the main, yet not the sole access to the brain of rabbits following IN inoculation. To address the role of a second pathway, groups of control (n=12) or MOB-lacking rabbits (n=12) were inoculated into the conjunctival sac (IC), following which the virus would be expected to use the ophtalmic branch of the trigeminal nerve to reach the brain. Ten control rabbits (83.3 %) developed neurological disease upon IC inoculation (onset 15.3 days [11 to 20]). Previous ablation of the MOBs did not affect the frequency and course of neurological disease: ten out of 12 rabbits (83.3 %) lacking the MOBs developed neurological disease (onset 9 to 15 dpi, average: 12.7 days) upon IC inoculation. These results demonstrate that both IN and IC routes may operate in the transport of BoHV-5 to the brain of experimentally infected rabbits, depending on the route of inoculation. IN inoculation results in a fast and efficient transport by the olfactory pathway, the trigeminal route providing an alternative, much slower and less efficient transport; IC inoculation results in efficient viral transport by the trigeminal route, yet with a delayed kinetics comparing to the transport provided by the olfactory pathway.

• Bovine herpesvirus type 5 BoHV-5 neurological infection rabbits.

Abstract in Portuguese:

Diel D.G., Fonseca E.T., Souza S.F., Mazzanti A., Bauermann F., Weiblen R. & Flores E.F. 2005. [Bovine herpesvirus 5 may use the olfactory and trigeminal pathways to invade the central nervous system of rabbits, depending upon the route of inoculation.] O Herpesvírus bovino tipo 5 (BoHV-5) pode utilizar as rotas olfatória ou trigeminal para invadir o sistema nervoso central de coelhos, dependendo da via de inoculação. Pesquisa Veterinária Brasileira 25(3):164-170. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesvirus type 5 (BoHV-5) is a major etiological agent of meningoencephalitis in cattle. Following replication in the nasal mucosa, viral invasion of the brain is thought to occur mainly by the olfactory pathway. To address the role of this pathway in the pathogenesis of neurological infection in a laboratory model, 30 days old rabbits had the main olfactory bulbs (MOBs) surgically removed and were subsequently inoculated intranasally (IN) or conjunctivally (IC) with a highly neurovirulent BoHV-5 strain (SV-507). Following IN inoculation, 10 out of 10 (100 %) control rabbits developed neurological disease. The clinical onset ranged from day 5 to 10 post-inoculation (pi, average 7.5 days); nine being euthanized in extremis and one recovering after a mild clinical course. In contrast, only one rabbit (9.1 %) of the group lacking the MOBs (n=11) developed neurological disease (onset at day 17 pi). Dexamethasone administration to the survivors (n=10) at day 50pi was followed by virus shedding in nasal and/or ocular secretions by 8 animals, demonstrating that the virus was able to reach the trigeminal ganglia (TG) during acute infection. These results demonstrate that the olfactory route provides the main, yet not the sole access to the brain of rabbits following IN inoculation. To address the role of a second pathway, groups of control (n=12) or MOB-lacking rabbits (n=12) were inoculated into the conjunctival sac (IC), following which the virus would be expected to use the ophtalmic branch of the trigeminal nerve to reach the brain. Ten control rabbits (83.3 %) developed neurological disease upon IC inoculation (onset 15.3 days [11 to 20]). Previous ablation of the MOBs did not affect the frequency and course of neurological disease: ten out of 12 rabbits (83.3 %) lacking the MOBs developed neurological disease (onset 9 to 15 dpi, average: 12.7 days) upon IC inoculation. These results demonstrate that both IN and IC routes may operate in the transport of BoHV-5 to the brain of experimentally infected rabbits, depending on the route of inoculation. IN inoculation results in a fast and efficient transport by the olfactory pathway, the trigeminal route providing an alternative, much slower and less efficient transport; IC inoculation results in efficient viral transport by the trigeminal route, yet with a delayed kinetics comparing to the transport provided by the olfactory pathway.