PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

Corrêa A.M.R., Pescador C.A., Schmitz M., Zlotowski P., Rozza D.B., Oliveira E.C., Barcellos D.E. & Driemeier D. 2006. [Clinical and pathological aspects of swine circovirosis in Rio Grande do Sul, southern Brazil.] Aspectos clínico-patológicos associados à circovirose suína no Rio Grande do Sul. Pesquisa Veterinária Brasileira 26(1):9-13. Setor de Patologia Veterinária, Faculdade de Veterinária, UFRGS, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br A total of 97 pigs, which had presented wasting, lymphadenomegaly, respiratory distress and pale or icteric mucosa, was necropsied over a 6-month period. Macroscopic lesions were characterized mostly by enlarged lymph nodes, non collapsed and round edged lungs with cranio-ventral areas of consolidation and interlobular edema. Kidneys had increased size, were pale, and presented numerous scattered white spots projecting from surface to the cortical area. Some kidneys also showed small red spots similar to petechial hemorrhage over the cortex. Main microscopic lesions were lympho-histiocytic infiltration in lymph nodes, lungs, and kidneys. Immunohistochemical probing with polyclonal antisera to type II swine circovirus stained positively in 50 out of the 56 cases tested (89.2%).

• Circovirus PMWS PCV2 immunohistochemistry swine.

Abstract in Portuguese:

Corrêa A.M.R., Pescador C.A., Schmitz M., Zlotowski P., Rozza D.B., Oliveira E.C., Barcellos D.E. & Driemeier D. 2006. [Clinical and pathological aspects of swine circovirosis in Rio Grande do Sul, southern Brazil.] Aspectos clínico-patológicos associados à circovirose suína no Rio Grande do Sul. Pesquisa Veterinária Brasileira 26(1):9-13. Setor de Patologia Veterinária, Faculdade de Veterinária, UFRGS, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br A total of 97 pigs, which had presented wasting, lymphadenomegaly, respiratory distress and pale or icteric mucosa, was necropsied over a 6-month period. Macroscopic lesions were characterized mostly by enlarged lymph nodes, non collapsed and round edged lungs with cranio-ventral areas of consolidation and interlobular edema. Kidneys had increased size, were pale, and presented numerous scattered white spots projecting from surface to the cortical area. Some kidneys also showed small red spots similar to petechial hemorrhage over the cortex. Main microscopic lesions were lympho-histiocytic infiltration in lymph nodes, lungs, and kidneys. Immunohistochemical probing with polyclonal antisera to type II swine circovirus stained positively in 50 out of the 56 cases tested (89.2%).

Abstract in English:

Rissi D.R., Rech R.R., Barros R.R., Kommers G.D., Langohr I.M., Pierezan F. & Barros C.S.L. 2006. [Listeric meningoencephalitis in goats.] Forma nervosa de listeriose em caprinos. Pesquisa Veterinária Brasileira 26(1):14-20. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A neurologic disease was observed in three young adult goats (indentified as A-C) from a herd of 100 goats during October-December, 2004. Clinical signs included head tilt, torticollis, nystagmus, staggering, falls and eventually recumbency and paddling, with stiff limbs. Treatment of Goat C with antibiotics resulted in a temporary remission of the clinical signs. The clinical courses where 5, 10 and 30 days respectively for Goats A, B and C. Goat A died spontaneously and the other two where euthanatized in extremis. No gross changes were observed. Histologic lesions were predominantly unilateral, with inflammatory and degenerative changes, extending from the medulla oblongata to the thalamus. In all 3 cases there were perivascular cuffings of one or more types of mononuclear cells (lymphocytes, plasma cells, activated macrophages) and occasionally neutrophils associated with areas of malacia where Gitter cells filled spaces of parenchymal loss. Additionally, Goat B had microabscesses in the medulla, pons, and mesencephalon and multifocal neutrophilic and lymphocytic infiltrates within the fascicles of the trigeminal nerve and in the cerebellar leptomeninges. In the brainstem of Goat C, there was multifocal granulomatous inflammation which included epithelioid macrophages and occasional multinucleated giant cells. Listeria sp antigen was detected by imunohistochemistry in routinely processed sections of mesencephalon from Goats A and C and of pons from Goat B.

• Listeria sp Listeria monocytogenes listeriosis encephalitis immunohistochemistry pathology diseases of goats.

Abstract in Portuguese:

Rissi D.R., Rech R.R., Barros R.R., Kommers G.D., Langohr I.M., Pierezan F. & Barros C.S.L. 2006. [Listeric meningoencephalitis in goats.] Forma nervosa de listeriose em caprinos. Pesquisa Veterinária Brasileira 26(1):14-20. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A neurologic disease was observed in three young adult goats (indentified as A-C) from a herd of 100 goats during October-December, 2004. Clinical signs included head tilt, torticollis, nystagmus, staggering, falls and eventually recumbency and paddling, with stiff limbs. Treatment of Goat C with antibiotics resulted in a temporary remission of the clinical signs. The clinical courses where 5, 10 and 30 days respectively for Goats A, B and C. Goat A died spontaneously and the other two where euthanatized in extremis. No gross changes were observed. Histologic lesions were predominantly unilateral, with inflammatory and degenerative changes, extending from the medulla oblongata to the thalamus. In all 3 cases there were perivascular cuffings of one or more types of mononuclear cells (lymphocytes, plasma cells, activated macrophages) and occasionally neutrophils associated with areas of malacia where Gitter cells filled spaces of parenchymal loss. Additionally, Goat B had microabscesses in the medulla, pons, and mesencephalon and multifocal neutrophilic and lymphocytic infiltrates within the fascicles of the trigeminal nerve and in the cerebellar leptomeninges. In the brainstem of Goat C, there was multifocal granulomatous inflammation which included epithelioid macrophages and occasional multinucleated giant cells. Listeria sp antigen was detected by imunohistochemistry in routinely processed sections of mesencephalon from Goats A and C and of pons from Goat B.

Abstract in English:

Méndez M.C., Elias F., Riet-Correa F., Gimeno E.J. & Portiansky E. 2006. [Experimental poisoning by fruits of Melia azedarach (Meliaceae) in pigs.] Intoxicação experimental com frutos de Melia azedarach (Meliaceae) em suínos. Pesquisa Veterinária Brasileira 26(1):26-30. Departamento de Clínicas Veterinárias, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. E-mail: nane@ufpel.tche.br Mature ground fruits of Melia azedarach were administered mixed with the food to 8 pigs at single doses of 5-20g/kg. Transient diarrhea was the only sign observed in the 2 pigs that ingested 5g/kg. Clinical signs observed in the pigs that ingested 10, 15 and 20 g/kg were incoordination, muscular tremors, difficulty to stand or to get up, sternal decubitus and hypothermia. The 2 pigs that ingested 20g/kg died. The gross lesions were congestion and necrosis of the small intestine and the stomach mucosa. The microscopic alterations were characterised by necrosis of the lymphatic tissues and skeletal muscles, congestion and necrosis of the stomach and small intestine, and moderate degenerative alterations of liver and kidneys. The serum levels of AST and CPK increased after the ingestion of the toxic fruits. High values of CPK were observed in the succumbing animals due to the muscle necrosis.These results demonstrate that the ingestion of high doses of Melia azedarach fruits by pigs may induce clinical signs of poisoning and cause lesions in several organs and even death.

• Poisonous plants plant poisoning Melia azedarach Meliaceae swine.

Abstract in Portuguese:

Méndez M.C., Elias F., Riet-Correa F., Gimeno E.J. & Portiansky E. 2006. [Experimental poisoning by fruits of Melia azedarach (Meliaceae) in pigs.] Intoxicação experimental com frutos de Melia azedarach (Meliaceae) em suínos. Pesquisa Veterinária Brasileira 26(1):26-30. Departamento de Clínicas Veterinárias, Faculdade de Veterinária, Universidade Federal de Pelotas, 96010-900 Pelotas, RS, Brazil. E-mail: nane@ufpel.tche.br Mature ground fruits of Melia azedarach were administered mixed with the food to 8 pigs at single doses of 5-20g/kg. Transient diarrhea was the only sign observed in the 2 pigs that ingested 5g/kg. Clinical signs observed in the pigs that ingested 10, 15 and 20 g/kg were incoordination, muscular tremors, difficulty to stand or to get up, sternal decubitus and hypothermia. The 2 pigs that ingested 20g/kg died. The gross lesions were congestion and necrosis of the small intestine and the stomach mucosa. The microscopic alterations were characterised by necrosis of the lymphatic tissues and skeletal muscles, congestion and necrosis of the stomach and small intestine, and moderate degenerative alterations of liver and kidneys. The serum levels of AST and CPK increased after the ingestion of the toxic fruits. High values of CPK were observed in the succumbing animals due to the muscle necrosis.These results demonstrate that the ingestion of high doses of Melia azedarach fruits by pigs may induce clinical signs of poisoning and cause lesions in several organs and even death.

Abstract in English:

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

• Experimental infection Trypanosoma vivax sheep semiarid.

Abstract in Portuguese:

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

Abstract in English:

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

• Meningoencephalitis polioencephalomalacia bovine herpesvirus-5 cattle.

Abstract in Portuguese:

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

Abstract in English:

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:

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:

Barbosa J.D., Oliveira C.M.C., Duarte M.D., Peixoto P.V. & Tokarnia C.H. 2005. [Experimental and natural poisoning by Ipomoea asarifolia (Convolvulaceae) in buffaloes and other ruminants.] Intoxicações experimental e natural por Ipomoea asarifolia (Convolvulaceae) em búfalos e outros ruminantes. Pesquisa Veterinária Brasileira 25(4):231-234. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br Ipomoea asarifolia R. et Schult. is a plant responsible for occasional outbreaks of poisoning in cattle, sheep and goats. Its oral administration to cattle and buffalos showed that the buffalo is as susceptible as cattle. One to 4 daily doses of 10-20g/kg caused similar symptoms in both species, as incoordination, muscular twiching and swaying of the head and anterior part of the body (pendular movement). In buffaloes the signs of incoordination were observed to a smaller extent. There is no report yet on natural poisoning by I. asarifolia in buffaloes, possibly because cases are not being noticed.

• Poisonous plants Ipomoea asarifolia Convolvulaceae plant poisoning buffaloes bovines sheep goats.

Abstract in Portuguese:

Barbosa J.D., Oliveira C.M.C., Duarte M.D., Peixoto P.V. & Tokarnia C.H. 2005. [Experimental and natural poisoning by Ipomoea asarifolia (Convolvulaceae) in buffaloes and other ruminants.] Intoxicações experimental e natural por Ipomoea asarifolia (Convolvulaceae) em búfalos e outros ruminantes. Pesquisa Veterinária Brasileira 25(4):231-234. Escola de Medicina Veterinária, Campus Castanhal, Universidade Federal do Pará, Rua Maximino Porpino 1000, Castanhal, PA 68743-080, Brazil. E-mail: tokarnia@ufrrj.br Ipomoea asarifolia R. et Schult. is a plant responsible for occasional outbreaks of poisoning in cattle, sheep and goats. Its oral administration to cattle and buffalos showed that the buffalo is as susceptible as cattle. One to 4 daily doses of 10-20g/kg caused similar symptoms in both species, as incoordination, muscular twiching and swaying of the head and anterior part of the body (pendular movement). In buffaloes the signs of incoordination were observed to a smaller extent. There is no report yet on natural poisoning by I. asarifolia in buffaloes, possibly because cases are not being noticed.

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:

Soto P., Echevarría H.M., Monteavaro C.E. & Catena M.C. 2005. Experimentally induced intravaginal Tritrichomonas foetus infection in a mouse model. Pesquisa Veterinária Brasileira 25(4):225-230. Laboratory of Clinical and Experimental Microbiology, Facultad de Ciencias Veterinarias, UNCPBA, Pinto 399, Tandil (7000), Buenos Aires, Argentina. E-mail: psoto@vet.unicen.ar The interest to develop research on the host-parasite relationship in bovine tritrichomonosis has accomplished the use of experimental models alternative to cattle. The BALB/c mouse became the most appropriate species susceptible to vaginal Tritrichomonas foetus infection requiring previous estrogenization. For the need of an experimental model without persistent estrogenization and with normal estrous cycles, the establishment and persistence of vaginal infection on BALB/c mouse with different concentrations of T. foetus in two experimental groups was evaluated. Group A was treated with 5mg of b-estradiol 3-benzoate to synchronize the estrous, 48 hours before the T. foetus vaginal inoculation, and Group B was inoculated in natural estrus. At 5-7 days after treatment, estrogenic effect decreased allowing all animals to cycle regularly during the experiment. From the first week post-infection, samples of vaginal mucus were taken from all animals during 34 weeks, in order to evaluate the course of infection and the stage of the estrus cycle. Group A showed 93.6% of infected animals, and Group B showed 38%. Different doses of T. foetus were assayed to establish the vaginal infection, with a persistence of 34 weeks. Although different behavior was observed in each subgroup belonging to either Group A or Group B, there were no significant differences among the infecting doses used. The b-estradiol 3-benzoate treatment had a favorable effect on the establishment of the infection (P<0.0001), but it did not influence its persistence (P=0.1097). According to the results, an experimental mouse model is presented, appropriate for further studies on mechanisms of pathogenicity, immune response, protective evaluation of immunogen and therapeutic effect of drugs.

• Tritrichomonas foetus mouse model experimental tritrichomonosis.

Abstract in Portuguese:

Soto P., Echevarría H.M., Monteavaro C.E. & Catena M.C. 2005. Experimentally induced intravaginal Tritrichomonas foetus infection in a mouse model. Pesquisa Veterinária Brasileira 25(4):225-230. Laboratory of Clinical and Experimental Microbiology, Facultad de Ciencias Veterinarias, UNCPBA, Pinto 399, Tandil (7000), Buenos Aires, Argentina. E-mail: psoto@vet.unicen.ar The interest to develop research on the host-parasite relationship in bovine tritrichomonosis has accomplished the use of experimental models alternative to cattle. The BALB/c mouse became the most appropriate species susceptible to vaginal Tritrichomonas foetus infection requiring previous estrogenization. For the need of an experimental model without persistent estrogenization and with normal estrous cycles, the establishment and persistence of vaginal infection on BALB/c mouse with different concentrations of T. foetus in two experimental groups was evaluated. Group A was treated with 5mg of b-estradiol 3-benzoate to synchronize the estrous, 48 hours before the T. foetus vaginal inoculation, and Group B was inoculated in natural estrus. At 5-7 days after treatment, estrogenic effect decreased allowing all animals to cycle regularly during the experiment. From the first week post-infection, samples of vaginal mucus were taken from all animals during 34 weeks, in order to evaluate the course of infection and the stage of the estrus cycle. Group A showed 93.6% of infected animals, and Group B showed 38%. Different doses of T. foetus were assayed to establish the vaginal infection, with a persistence of 34 weeks. Although different behavior was observed in each subgroup belonging to either Group A or Group B, there were no significant differences among the infecting doses used. The b-estradiol 3-benzoate treatment had a favorable effect on the establishment of the infection (P<0.0001), but it did not influence its persistence (P=0.1097). According to the results, an experimental mouse model is presented, appropriate for further studies on mechanisms of pathogenicity, immune response, protective evaluation of immunogen and therapeutic effect of drugs.