PESQUISA VETERINÁRIA BRASILEIRA

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:

Medeiros J.M., Tabosa I.M., Simões S.V.D., Nóbrega Jr J. E., Vasconcelos J.S. & Riet-Correa F. 2005. [Perinatal mortality in kids in the semiarid region of Paraíba, Brazil.] Mortalidade perinatal em cabritos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(4):201-206. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-970 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal kid mortality were studied from May 2002 to August 2004 in the semiarid region of Paraíba. In 118 necropsied kids the frequency of different causes of death were neonatal infections (50%), distocia (12.71%), hypothermia/starvation (11.86%), malformations (7.62%), floppy kid (6.77%) and abortions (1.69%). Regarding the time of death, 1.69% of the kids died before parturition, 16.94% during the parturition and 81.34 % after birth. The high occurrence of neonatal infections, dystocias, and hypothermia/starvation is probably to due to factors related with error in the sanitary, reproductive and nutritional management. Arthrogryposis of the forelimbs was the main malformation observed. This defect is endemic in goat flocks in the semi-arid of Brazil. Most deaths occurred after birth (25.42%) and from the 4th to the 28th day of life (38.98%) suggesting that care with the kids during their first 28 days of life is important for the improvement of the survival rate.

• Perinatal mortality kids semiarid region Brazil.

Abstract in Portuguese:

Medeiros J.M., Tabosa I.M., Simões S.V.D., Nóbrega Jr J. E., Vasconcelos J.S. & Riet-Correa F. 2005. [Perinatal mortality in kids in the semiarid region of Paraíba, Brazil.] Mortalidade perinatal em cabritos no semi-árido da Paraíba. Pesquisa Veterinária Brasileira 25(4):201-206. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-970 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br The causes of perinatal kid mortality were studied from May 2002 to August 2004 in the semiarid region of Paraíba. In 118 necropsied kids the frequency of different causes of death were neonatal infections (50%), distocia (12.71%), hypothermia/starvation (11.86%), malformations (7.62%), floppy kid (6.77%) and abortions (1.69%). Regarding the time of death, 1.69% of the kids died before parturition, 16.94% during the parturition and 81.34 % after birth. The high occurrence of neonatal infections, dystocias, and hypothermia/starvation is probably to due to factors related with error in the sanitary, reproductive and nutritional management. Arthrogryposis of the forelimbs was the main malformation observed. This defect is endemic in goat flocks in the semi-arid of Brazil. Most deaths occurred after birth (25.42%) and from the 4th to the 28th day of life (38.98%) suggesting that care with the kids during their first 28 days of life is important for the improvement of the survival rate.

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:

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:

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:

Rech R.R., Schild A.L., Driemeier D., Garmatz S.L., Oliveira F.N., Riet-Correa F. & Barros C.S.L. 2005. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Epidemiology, clinical signs and pathology.] Febre catarral maligna em bovinos no Rio Grande do Sul: epidemiologia, sinais clínicos e patologia. Pesquisa Veterinária Brasileira 25(2):97-105. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical signs, necropsy and histopathological findings in cases of malignant catarrhal fever (MCF) occurring in cattle from 15 farms in Rio Grande do Sul, Brazil, from 1973 to 2003, are described. In 9 instances (60%) the disease occurred as sporadic cases affecting 1-3 cattle whereas in six farms (40%) MCF occurred as epizootics involving several cattle in each affected herd. Morbidity rates ranged from 2.4% to 20% and lethality rates were 83.3% and 100%. Cattle of all ages and both sexes were affected. Where the information was available (9 farms) sheep were in contact with affected cattle and cases of MCF occurred more frequently in spring and summer. Clinical courses were acute or subacute and clinical signs included fever, nasal and ocular discharges, conjunctivitis, drooling, hematuria, necrosis and blunting of buccal papillae, enlargement of lymph nodes, diarrhea and neurological disturbances. Necropsy findings included opaque corneas, reddening, erosions and ulcerations in several mucous membranes of the alimentary, respiratory and urogenital tracts, and the conjunctiva; enlargement and haemorrhage of lymph nodes and multiple white foci in the renal cortices and in the hepatic portal triads. Crustous dermatitis was observed in some cases. Main histopathological findings included vasculitis, necrosis of the surface epithelia and accumulation of inflammatory cells in several organs. Vasculitis were associated with fibrinoid necrosis of the medial layer of arteries and inflammatory cells included lymphoblasts, lymphocytes, plasma cells and macrophages.

• Infectious diseases epidemiology viral diseases diseases of cattle pathology.

Abstract in Portuguese:

Rech R.R., Schild A.L., Driemeier D., Garmatz S.L., Oliveira F.N., Riet-Correa F. & Barros C.S.L. 2005. [Malignant catarrhal fever in cattle in Rio Grande do Sul, Brazil: Epidemiology, clinical signs and pathology.] Febre catarral maligna em bovinos no Rio Grande do Sul: epidemiologia, sinais clínicos e patologia. Pesquisa Veterinária Brasileira 25(2):97-105. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical signs, necropsy and histopathological findings in cases of malignant catarrhal fever (MCF) occurring in cattle from 15 farms in Rio Grande do Sul, Brazil, from 1973 to 2003, are described. In 9 instances (60%) the disease occurred as sporadic cases affecting 1-3 cattle whereas in six farms (40%) MCF occurred as epizootics involving several cattle in each affected herd. Morbidity rates ranged from 2.4% to 20% and lethality rates were 83.3% and 100%. Cattle of all ages and both sexes were affected. Where the information was available (9 farms) sheep were in contact with affected cattle and cases of MCF occurred more frequently in spring and summer. Clinical courses were acute or subacute and clinical signs included fever, nasal and ocular discharges, conjunctivitis, drooling, hematuria, necrosis and blunting of buccal papillae, enlargement of lymph nodes, diarrhea and neurological disturbances. Necropsy findings included opaque corneas, reddening, erosions and ulcerations in several mucous membranes of the alimentary, respiratory and urogenital tracts, and the conjunctiva; enlargement and haemorrhage of lymph nodes and multiple white foci in the renal cortices and in the hepatic portal triads. Crustous dermatitis was observed in some cases. Main histopathological findings included vasculitis, necrosis of the surface epithelia and accumulation of inflammatory cells in several organs. Vasculitis were associated with fibrinoid necrosis of the medial layer of arteries and inflammatory cells included lymphoblasts, lymphocytes, plasma cells and macrophages.

Abstract in English:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

• Poisonous plants Baccharis coridifolia Asteraceae diseases of cattle pathology.

Abstract in Portuguese:

Rissi D.R., Rech R.R., Fighera R.A., Cagnini D.Q., Kommers G.D. & Barros C.S.L. 2005. [Spontaneous Baccharis coridifolia poisoning in cattle.] Intoxicação espontânea por Baccharis coridifolia em bovinos. Pesquisa Veterinária Brasileira 25(2):111-114. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Two outbreaks of Baccharis coridifolia poisoning in cattle in southern Brazil are described. Cases occurred when stressed, hungry and thirsty cattle brought from pastures free of B. coridifolia were placed into pastures heavily infested by this poisonous plant. In the two outbreaks morbidity was 21.73% and 22.51% and lethality was virtually 100%. Clinical signs included mild bloat, instability of hind limbs, muscle tremors, dry muzzle, dry feces or diarrhea, polydipsia and restlessness. Consistent necropsy findings included dehydration, large amounts of ruminal fluid, reddening and erosions of the mucosae of the forestomachs. Degeneration and necrosis of the lining epithelium of the forestomachs and of lymphoid tissue were the main histopathological changes encountered.

Abstract in English:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).

• Polioencephalomalacia cortical necrosis goats sheep sulfur poisoning thiamine deficiency.

Abstract in Portuguese:

Lima E.F., Riet-Correa F., Tabosa I.M., Dantas A.F.M., Medeiros J.M. & Sucupira Júnior G. 2005. [Polioencephalomalacia in goats and sheep in the semiarid region of northeastern Brazil.] Polioencefalomalacia em caprinos e ovinos na região semi-árida do Nordeste do Brasil. Pesquisa Veterinária Brasileira 25(1):9-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: riet@cstr.ufcg.edu.br Seven outbreaks of polioencephalomalacia in goats and 3 in sheep are reported from the semiarid region of northeastern Brazil. Animals of different ages were affected in various seasons of the year. In 5 outbreaks the animals were supplemented with concentrate ration and in 5 others they were only grazing on pastures. In one outbreak sheep were supplemented with an energy-protein-mineral mixture containing 1.3% of sulfur flower. Clinical signs were characterized by blindness, depression, head pressing, circling, grinding of the teeth, incoordination, spastic paralysis, ataxia, depression of the palpebral and pupillary reflexes, lateral strabismus, nystagmus, and dilated pupils. Nine affected animals were treated with thiamine and dexamethasone; 7 of them recovered but 2 died. The diagnosis of the disease was based on the recovered animals after treatment and/or on the histologic lesions. The clinical course varied from 2 to 15 days. On three animals post-mortem examination was made. One had herniation of the cerebellum through the Foramen magnum and softening of the cerebral cortex. The cut surface of the cerebral cortex showed cavitation and yellowish discoloration. Another animal had only cerebellar herniation. In a third animal no gross lesions were observed. Histological changes in the 3 animals were laminar necrosis of the cerebral cortex, and in 2 malacia of the thalamus and the rostral colliculi was also observed. In 9 outbreaks the cause of the disease was not determined, but one was probably due to sulfur toxicosis caused by the high sulfur content of the energy-protein-mineral mixture containing 1.3% of sulfur flower (96% sulfur) and 30% chicken litter (0.39% sulfur).