PESQUISA VETERINÁRIA BRASILEIRA

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:

Karam F.S.C., Soares M.P., Haraguchi M., Riet-Correa F., Méndez M.C. & Jarenkow J.A. 2004. [Epidemiological aspects of seneciosis in southern Rio Grande do Sul, Brazil.] Aspectos epidemiológicos da seneciose na região sul do Rio Grande do Sul, Brasil. Pesquisa Veterinária Brasileira 24(4):191-198. Laboratório de Toxicologia, Faculdade de Medicina Veterinária, URCAMP, Bagé, RS 96400-110, Brazil. E-mail: fernando@alternet.com.br Seneciosis is the main cause of livestock mortality due to poisonous plants in the State of Rio Grande do Sul, Brazil. This paper presents epidemiological data of 24 outbreaks in cattle and one in horses, diagnosed by the Regional Diagnostic Laboratory at Pelotas University in southern Rio Grande do Sul, from 1998 to 2000. Additionally, data of 54 outbreaks which occurred in 1978-1997 were analyzed. The farms where outbreaks occurred in 1998-2000 were visited to obtain clinical and epidemiological data and to verify the presence of Senecio spp. Eleven outbreaks (45.83%) affected cattle up to 3 years of age, and 13 (54.16%) cattle over 3 years. Nine (37.5%) outbreaks affected females and 15 (62.5%) males. Ten (41.66%) outbreaks occurred in spring, 4 (16.66%) in summer, 5 (20.83%) in autumn, and 5 (20.83%) in winter. Morbidity rate was estimated with 4.92% and case fatality with 95.59%. The predomionating Senecio species were S. brasiliensis on 12 farms (57.14%), S. selloi on 10 (47.61%), S. oxyphyllus on 6 (28.57%), S. heterotrichius on 3 (14.28%), and S. leptolobus on 1 farm (4.76%). The main clinical signs were progressive emaciation, incoordination, diarrhea, tenesmus, rectal prolapse and aggressiveness. The clinical manifestation periods of affected cattle observed during the farm visits, or of cattle sent for post-mortem examination,were 24-96 hours in 4 outbreaks (16.66%), 4-7 days in 7 (29.16%), 1-2 weeks in 4 (16.66%), 2-3 weeks in 2 (8.33%), 1-2 months in 2 (8.33%), and 2-3 months in 1 outbreak (4.16%). In 4 outbreaks (16.66%) the clinical manifestation period was not established. In outbreaks with longer clinical manifestation periods some animals showed photosensitization. The main necropsy findings were a hard and enlarged liver, distended gall bladder, edema of the mesenterium and abomasum, and increased amount of liquid in the cavities. Histopathological findings were fibroplasia, megalocytosis and biliary ductal proliferation of the liver, and spongy degeneration of the cerebral white matter. Samples of different Senecio species, in different seasons, were analyzed for detection of pyrrolizidine alkaloids (PAs) by thin layer chromatography. Retrorsine was found in Senecio brasiliensis, S. heterotrichius, S. selloi and S. oxyphyllus. In S. brasiliensis and S. heterotrichius one and two more non-identified PAs were detected, respectively. The total PAs concentration by spectrophotometric method was 0.25% for S. brasiliensis, 0.19% for S. heterotrichius, 0.03% for S. oxyphyllus, and 0.03% for S. selloi. The highest PAs concentration occurred in winter (June/July). No alkaloids were found in samples of S. leptolobus. These results show that S. brasiliensis is the most important cause of seneciosis in southern Rio Grande do Sul. Additional data obtained dealt with 54 outbreaks of PAs poisoning in 1978-1997. During this period, 7 outbreaks (12.96%) affected cattle up to 3 years of age, 39 (72.22%) cattle over 3 years, and 3 outbreaks (5.55%) affected cattle of different ages. In 5 outbreaks (9.25%) the age was not informed. Seven outbreaks (12.96%) affected males, 39 (72.22%) females, 3 (5.55%) both sexes, and in 5 outbreaks (9.25%) the sex was not informed. Twenty-three outbreaks (42.59%) occurred in spring, 9 (16.66%) in summer, 9 (16.66%) in autumn, and 13 (24.07%) in winter. The greater number of outbreaks during 1998-2000 (24 outbreaks in 3 years) in regard to 1978-1997 (54 outbreaks in 20 years) is probably due to a decrease of more than 50% in the number of sheep in the region.

• Seneciosis epidemiology poisonous plants Senecio spp Asteraceae pyrrolizidine alkaloids cattle.

Abstract in Portuguese:

Karam F.S.C., Soares M.P., Haraguchi M., Riet-Correa F., Méndez M.C. & Jarenkow J.A. 2004. [Epidemiological aspects of seneciosis in southern Rio Grande do Sul, Brazil.] Aspectos epidemiológicos da seneciose na região sul do Rio Grande do Sul, Brasil. Pesquisa Veterinária Brasileira 24(4):191-198. Laboratório de Toxicologia, Faculdade de Medicina Veterinária, URCAMP, Bagé, RS 96400-110, Brazil. E-mail: fernando@alternet.com.br Seneciosis is the main cause of livestock mortality due to poisonous plants in the State of Rio Grande do Sul, Brazil. This paper presents epidemiological data of 24 outbreaks in cattle and one in horses, diagnosed by the Regional Diagnostic Laboratory at Pelotas University in southern Rio Grande do Sul, from 1998 to 2000. Additionally, data of 54 outbreaks which occurred in 1978-1997 were analyzed. The farms where outbreaks occurred in 1998-2000 were visited to obtain clinical and epidemiological data and to verify the presence of Senecio spp. Eleven outbreaks (45.83%) affected cattle up to 3 years of age, and 13 (54.16%) cattle over 3 years. Nine (37.5%) outbreaks affected females and 15 (62.5%) males. Ten (41.66%) outbreaks occurred in spring, 4 (16.66%) in summer, 5 (20.83%) in autumn, and 5 (20.83%) in winter. Morbidity rate was estimated with 4.92% and case fatality with 95.59%. The predomionating Senecio species were S. brasiliensis on 12 farms (57.14%), S. selloi on 10 (47.61%), S. oxyphyllus on 6 (28.57%), S. heterotrichius on 3 (14.28%), and S. leptolobus on 1 farm (4.76%). The main clinical signs were progressive emaciation, incoordination, diarrhea, tenesmus, rectal prolapse and aggressiveness. The clinical manifestation periods of affected cattle observed during the farm visits, or of cattle sent for post-mortem examination,were 24-96 hours in 4 outbreaks (16.66%), 4-7 days in 7 (29.16%), 1-2 weeks in 4 (16.66%), 2-3 weeks in 2 (8.33%), 1-2 months in 2 (8.33%), and 2-3 months in 1 outbreak (4.16%). In 4 outbreaks (16.66%) the clinical manifestation period was not established. In outbreaks with longer clinical manifestation periods some animals showed photosensitization. The main necropsy findings were a hard and enlarged liver, distended gall bladder, edema of the mesenterium and abomasum, and increased amount of liquid in the cavities. Histopathological findings were fibroplasia, megalocytosis and biliary ductal proliferation of the liver, and spongy degeneration of the cerebral white matter. Samples of different Senecio species, in different seasons, were analyzed for detection of pyrrolizidine alkaloids (PAs) by thin layer chromatography. Retrorsine was found in Senecio brasiliensis, S. heterotrichius, S. selloi and S. oxyphyllus. In S. brasiliensis and S. heterotrichius one and two more non-identified PAs were detected, respectively. The total PAs concentration by spectrophotometric method was 0.25% for S. brasiliensis, 0.19% for S. heterotrichius, 0.03% for S. oxyphyllus, and 0.03% for S. selloi. The highest PAs concentration occurred in winter (June/July). No alkaloids were found in samples of S. leptolobus. These results show that S. brasiliensis is the most important cause of seneciosis in southern Rio Grande do Sul. Additional data obtained dealt with 54 outbreaks of PAs poisoning in 1978-1997. During this period, 7 outbreaks (12.96%) affected cattle up to 3 years of age, 39 (72.22%) cattle over 3 years, and 3 outbreaks (5.55%) affected cattle of different ages. In 5 outbreaks (9.25%) the age was not informed. Seven outbreaks (12.96%) affected males, 39 (72.22%) females, 3 (5.55%) both sexes, and in 5 outbreaks (9.25%) the sex was not informed. Twenty-three outbreaks (42.59%) occurred in spring, 9 (16.66%) in summer, 9 (16.66%) in autumn, and 13 (24.07%) in winter. The greater number of outbreaks during 1998-2000 (24 outbreaks in 3 years) in regard to 1978-1997 (54 outbreaks in 20 years) is probably due to a decrease of more than 50% in the number of sheep in the region.

Abstract in English:

ABSTRACT.- Schild A.L, Soares M.P., Damé M.C., Portianski E.L. & Riet-Correa F. 2002. Arthrogryposis in Murrah buffaloes in southern .Brazil. Pesquisa Veterinária Brasileira 23(1):13-16. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Campus Universitário s/n, Pelotas, RS 96010-960, Brazil. Congenital arthrogryposis is described in a Murrah buffalo herd. The disease was characterized by curvature and multiple articular rigidity of the hindlimbs or of all limbs without associated clefects except for one case of brachygnatia. Histologically there was reduction of motor neurons from the ventral horns of the spinal cord and hypoplasia of the limb muscles. Analysis of the herd breeding records suggests that the disease is genetically transmitted by an autosomal recessive trait.

• Arthrogryposis buffalo Artrogripose búfalos.

Abstract in Portuguese:

RESUMO.- Schild A.L, Soares M.P., Damé M.C., Portianski E.L. & Riet-Correa F. 2002. Arthrogryposis in Murrah buffaloes in southern .Brazil. Pesquisa Veterinária Brasileira 23(1):13-16. [Artrogripose em búfalos Murrah no Sul do Rio Grande do Sul, Brasil.] Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Campus Universitário s/n, Pelotas, RS 96010-960, Brazil. Artrogripose congênita é descrita em um rebanho de búfalos da raça Murrah. A enfermidade caracterizou- se por curvatura e rigidez articular múltipla dos membros posteriores e/ou dos quatro membros sem associação com outros defeitos exceto por um búfalo que apresentou, também, braquignatia. Histologicamente observou-se diminuição dos neurônios motores nos cornos ventrais da medula espinhal e hipoplasia dos músculos dos membros. A análise genealógica dos animais sugere que a doença possa ser geneticamente transmitida por um gene recessivo autossômico.

Abstract in English:

ABSTRACT.- Marques A.P., Riet-Correa F., Soares M.P., Ortolani E.L. & Giuliodori M.J. 2003. (Sudden deaths in cattle associated with copper deficiency.] Mortes súbitas em bovinos associadas à carência de cobre. Pesquisa Veterinária Brasileira 23(1):21-32. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900, Pelotas, RS, Brazil. An outbreak of sudden death was observed in cattle in southern Brazil. No significant gross or microscopic lesions were found in 1 O cattle at post-mortem examination. To test if the sudden deaths were caused by a toxic plant, 13 weeds were collected and given to rabbits at a total of 440 to 600 g per kg body weight within 7 days. Results were negative. Mean copper levels of the tiver in 10 cattle were very low (3.6± 1.6 ppm-dry matter) suggesting Cu deficiency as the cause of the disease. Five samples of pasture collected during the outbreak had normal levels of Cu (8.4±0.8 ppm-d.m.) and S (0.2%±0.03-d.m.), but high levels of Fe (522± 122 ppm-d.m.). One group of 10 heifers was supplemented with Cu subcutaneously. This group and a similar control group were maintained in the sarne area where the outbreak occurred. Serum levels of Cu, S, Fe, Mo and ceruloplasmin were determined bimonthly in both groups during one year. Mean serum levels of Cu (1.76± 1.06 to 10.34±3.1 μmol/1 for the control group and 3.86± 1.53 to 10.61 ± 1.34 μmol/1 for the treated group) and ceruloplasmin (6.59±3.93 to 18.61±4.14 mg/1 for the control group and 10.31±5.48 to 32.49±6.05 mg/1 for the treated group) were significantly higher in the supplemented group (P=0.0046 for Cu and P=0.0001 for ceruloplasmin), but they were below normal levels in most samples of both groups. Serum levels of Cu and ceruloplasmin were correlated (r=0.67; P=00.5). ln both groups serum levels of Fe (40.09±5.25 to 78.48±28.23 μmol/1) were higher than normal levels. Samples of forage were collected bimonthly for determination of Cu, Mo, S, Fe and protein in 7 points of the paddock where the outbreak occurred. Levels of Cu (1.36±0.56 to 4.76±1.15 ppm-d.m.) were below the normal ranges. The concentration of Mo (0.17±0.06 to 0.96±0.47 ppm-d.m.) was within normal ranges. Levels of S (0.21 ±0.04% to 0.5±0.17%) and Fe (172.92±62.64 to 437.24±205.44 ppm-d.m.) were occasionally within toxic level. Levels of protein varied from 7.77±2.6% to 13.16±3.02%. Six samples of water and six of submersed pastures were collected at the end of the experiment when the paddock was flooded. High levels of iron (169.23±83.49 ppm-d.m.) and S (0.06±0.03%) were found in the water. Levels of Fe and S in the submerse pasture were of 469.3±218.28 ppm and 0.19 ±0.05%, respectively. The results obtained suggest that the sudden deaths are due to Cu deficiency. Three factors seem to be responsible for the Cu deficiency: 1) high levels of iron in pastures and water; 2) occasionally low levels of copper in the pastures; and 3) the ingestion of S above the requirements due to the levels occasionally high in pastures and high in water. The outbreak reported is similar to other outbreaks of sudden deaths associated with low liver copper previously reported during winter in the sarne region of southern Brazil. This area is characterized by acid sandy soils with frequent flooding during this season. ln periodically flooded acid soils iron is solubilized and absorbed by the plants, decreasing the Cu content and increasing the Fe content of forage. This seems to be the main reason for Cu deficiency in the region.

• Cattle copper deficiency sudden death iron molibdenum sulfur Bovinos deficiência de cobre morte súbita ferro molibdênio enxofre

Abstract in Portuguese:

RESUMO.- Marques A.P., Riet-Correa F., Soares M.P., Ortolani E.L. & Giuliodori M.J. 2003. [Sudden deaths in cattle associated with copper deficiency.] Mortes súbitas em bovinos associadas à carência de cobre. Pesquisa Veterinária Brasileira 23(1):21-32. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900, Pelotas, RS, Brazil. Foi estudado um surto de morte súbita em bovinos no sul do Rio Grande do Sul. Nos animais necropsiados não foram observadas lesões macroscópicas ou microscópicas significativas. Para testar se as mortes súbitas teriam sido causadas por plantas tóxicas, 13 espécies de plantas foram coletadas e administradas a coelhos num total de 440 a 600g/kg de peso vivo num período de 7 dias. Os resultados foram negativos. Os teores de cobre no fígado dos bovinos foram muito baixos (3,6±1,6 ppm-base seca) sugerindo que as mortes foram causadas por deficiência de cobre. Cinco amostras de pasto, coletadas no local do surto, apresentaram teores normais de Cu (8,4±0,8 ppm-bs) e S (0,2%±0,03%-bs), mas altos teores de Fe (522±122 ppm-bs). Um grupo de 10 novilhas foi suplementado com Cu subcutâneo. Este grupo e um grupo controle foram mantidos em área similar à da ocorrência do surto. Teores séricos de Cu, S, Fe, Mo e ceruloplasmina foram determinados bimensalmente durante um ano de experimento. Os teores médios de Cu (1,76±1,06 a 10,34±3,1 μmol/1 no grupo controle e 3,86± 1,53 a 10,61 ± 1,34 μmol/1 para o grupo suplementado) e ceruloplamina (6,59±3,93 a 18,61 ±4,14 mg/1 para o grupo controle e 10,35±5,48 a 32,49±6,05 mg/1 para o grupo suplementado) foram significativamente maiores no grupo suplementado (P=0,0046 para o Cu e P=0,0001 para a ceruloplasmina), mas a maioria das amostras tiveram teores abaixo do normal em ambos os grupos. Houve uma correlação entre os teores de Cu e os de ceruloplasmina (r=0,67, P=0,05). Em ambos os grupos os teores séricos de Fe (40,09±5,22 a 78,48±28,23 μmol/1) estiveram acima dos teores normais. Amostras de forragens foram coletadas bimensalmente em sete pontos do campo onde ocorreu o surto para determinação de Cu, Mo, S, Fe e proteína. Os teores de Cu (1,36±0,56 a 4,76±1,15 ppm-bs) estiveram abaixo dos requerimentos. Os teores de Mo (0,17±0,06 a 0,96±0,47 ppm-bs) estiveram dentro da normalidade. Valores de S (0,21 ±0,04% a 0,5±0, 17%) e Fe (172,92±62,64 a 437,24±205,44 ppm-bs) alcançaram, ocasionalmente, níveis tóxicos. Teores de proteína variaram de 7,77±2,6% a 13, 16±3,02%. Seis amostras de água e 6 amostras de pasto submerso foram coletadas no fim do experimento quando o campo estava inundado. Altos teores de Fe (169, 23±83,49 ppm) e S (0,06±0,03%) foram encontrados na água. Os teores de Fe e S no pasto submerso foram de 469,5±218,28 ppm e 0,19±0,05%, respectivamente. Os resultados obtidos sugerem que as mortes súbitas foram causadas por deficiência de Cu. Três fatores parecem ser responsáveis pela deficiência de Cu: 1) altos teores de Fe na pastagem e na água; 2) ocasionalmente baixos teores de Cu na pastagem; e 3) ingestão de S acima dos requerimentos, devido aos teores ocasionalmente altos na pastagem e na água. O surto descrito é similar a outros surtos de morte súbita em bovinos descritos no sul do Rio Grande do Sul durante o inverno, que foram, também, associados a baixos teores de cobre no fígado. As regiões onde ocorre a enfermidade são caracterizadas por solos arenosos e ácidos com inundações freqüentes durante o inverno. Em solos ácidos periodicamente inundáveis o ferro é solubilizado e absorvido pelas plantas, diminuindo o conteúdo de Cu na forragem e aumentando os teores de Fe. Esta parece ser a maior razão para a deficiência de cobre na região.