PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Ferreira L.C.L., Flores E.F., Driemeier D., Melo O. & Lemos R.A.A. 2008. [Mucosal disease associated with generalized dermatitis in cattle, Mato Grosso do Sul, Brazil.] Doença das mucosas associada à dermatite generalizada em bovinos, Mato Grosso do Sul. Pesquisa Veterinária Brasileira 28(6):285-292. Departamento de Medicina Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Av. Senador Filinto Müller 2443, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br This paper reports epidemiological, clinical, pathological and laboratory diagnostic aspects of a form of dermatitis associated with mucosal disease (MD) in cattle. It also focuses on the methods used for identifying persistently infected (PI) animals and on the impact of the disease on fertility and weaning rates in the affected herd. Cases of dermatitis associated with MD were diagnosed in two 12 and 24-month-old Nelore calves belonging to a beef cattle farm that operates the full cycle of production (calving, rearing, finishing) in Mato Grosso do Sul, Midwest Brazil. The clinical signs exhibited by affected cattle 0included slow, progressive weight loss; formation of diffuse skin crusts in multiple body areas; skin dryness; multiple ulcerations on the gums and dorsal surface of the tongue which evolved to longitudinal fissures; formation of keratinized projections; and detachment of hoof horn. In addition, diarrhea affected one animal in the late stage of the disease. Necropsies also revealed longitudinal erosions in the esophagus. Histological examination showed coagulation necrosis foci in esophageal and lingual mucosae, with neutrophil and lymphocyte infiltration. Skin lesions consisted of epidermal coagulation necrosis associated with neutrophil infiltration and hyperkeratosis. In both cases, clinical diagnosis was confirmed by the isolation and identification of cytopathic and noncytopathic biotypes of the bovine viral diarrhea virus (BVDV) and immunohistochemical detection of viral antigens in formalin fixed tissues. Out of 300 cattle that had contact with the affected animals, 38 were found to be seropositive - in high neutralizing titers - to BVDV. Blood samples from 1,025 young animals and 40 bulls from the farm were examined for the presence of BVDV to identify potential PI animals. The virus was isolated from blood of three calves in the initial test and, 12 months later, from two of them which had remained on the farm. Only one of these calves was found to be BVDV-positive by immuno-histochemical testing performed on ear-tissue samples. In the year following the birth of PI calves, the herd underwent decreases in fertility and weaning rates, which later returned to their previous levels. The resulting data demonstrate the presence of BVDV infection in beef herds in Mato Grosso do Sul and provide evidence as to include the disease in the differential diagnosis of causes of generalized dermatitis in cattle.

• Bovine viral diarrhea virus mucosal disease cattle diseases viral diseases dermatitis

Abstract in Portuguese:

ABSTRACT.- Ferreira L.C.L., Flores E.F., Driemeier D., Melo O. & Lemos R.A.A. 2008. [Mucosal disease associated with generalized dermatitis in cattle, Mato Grosso do Sul, Brazil.] Doença das mucosas associada à dermatite generalizada em bovinos, Mato Grosso do Sul. Pesquisa Veterinária Brasileira 28(6):285-292. Departamento de Medicina Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Federal de Mato Grosso do Sul, Av. Senador Filinto Müller 2443, Campo Grande, MS 79070-900, Brazil. E-mail: eqrural@nin.ufms.br This paper reports epidemiological, clinical, pathological and laboratory diagnostic aspects of a form of dermatitis associated with mucosal disease (MD) in cattle. It also focuses on the methods used for identifying persistently infected (PI) animals and on the impact of the disease on fertility and weaning rates in the affected herd. Cases of dermatitis associated with MD were diagnosed in two 12 and 24-month-old Nelore calves belonging to a beef cattle farm that operates the full cycle of production (calving, rearing, finishing) in Mato Grosso do Sul, Midwest Brazil. The clinical signs exhibited by affected cattle 0included slow, progressive weight loss; formation of diffuse skin crusts in multiple body areas; skin dryness; multiple ulcerations on the gums and dorsal surface of the tongue which evolved to longitudinal fissures; formation of keratinized projections; and detachment of hoof horn. In addition, diarrhea affected one animal in the late stage of the disease. Necropsies also revealed longitudinal erosions in the esophagus. Histological examination showed coagulation necrosis foci in esophageal and lingual mucosae, with neutrophil and lymphocyte infiltration. Skin lesions consisted of epidermal coagulation necrosis associated with neutrophil infiltration and hyperkeratosis. In both cases, clinical diagnosis was confirmed by the isolation and identification of cytopathic and noncytopathic biotypes of the bovine viral diarrhea virus (BVDV) and immunohistochemical detection of viral antigens in formalin fixed tissues. Out of 300 cattle that had contact with the affected animals, 38 were found to be seropositive - in high neutralizing titers - to BVDV. Blood samples from 1,025 young animals and 40 bulls from the farm were examined for the presence of BVDV to identify potential PI animals. The virus was isolated from blood of three calves in the initial test and, 12 months later, from two of them which had remained on the farm. Only one of these calves was found to be BVDV-positive by immuno-histochemical testing performed on ear-tissue samples. In the year following the birth of PI calves, the herd underwent decreases in fertility and weaning rates, which later returned to their previous levels. The resulting data demonstrate the presence of BVDV infection in beef herds in Mato Grosso do Sul and provide evidence as to include the disease in the differential diagnosis of causes of generalized dermatitis in cattle.

Abstract in English:

ABSTRACT.- Fighera R.A., Souza T.M., Silva M.C., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2008. [Causes of death and reasons for euthanasia in dogs from the midland region of the Midwest of Rio Grande do Sul State, Brazil (1965-2004).] Causas de morte e razões para eutanásia de cães da Mesorregião do Centro Ocidental Rio-Grandense (1965-2004). Pesquisa Veterinária Brasileira 28(4):223-230. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: anemiaveterinaria@yahoo.com.br The main objective of this study was to investigate the prevalence of diseases culminating with death or motivating euthanasia of dogs from the midland region of the Midwest of Rio Grande do Sul State, Brazil. The necropsy files of the Laboratório de Patologia Veterinária (LPV) of the Universidade Federal de Santa Maria (UFSM) were accessed and necropsy protocols of dogs necropsied between January 1965 and December 2004 were reviewed. During this period 4,844 reports of canine necropsies were filed at the LPV-UFSM. The case distribution in relation to the disease categories diagnosed was as follows: infectious and parasitic diseases (1,693 [35.0%]); neoplasms (378 [7.8%]); disorders caused by physical agents (369 [7.6%]); degenerative diseases (342 [7.1%]); poisonings and toxinfections (112 [2.3%]); euthanasia due to convenience (101 [2.1%]); metabolic and endocrinological diseases (97 [2.0%]); iatrogenic disorders (83 [1.7%]); developmental disorders (25 [0.5%]); immune mediate diseases (10 [0.2%]); and nutritional disorders (6 [0.1%]). Other disorders, including multifactorial or idiopathic diseases contributed 80 (1.6%) cases. In 1,548 (32.0%) out of the 4,844 cases it was not possible to establish either cause of death or reason for euthanasia. Infectious and parasitic diseases (mainly canine distemper, parvoviral enteritis and intestinal parasitism), neoplasia (mainly mammary neoplasms and lymphoma), disorders caused by physical agents (mainly accidents caused by automotive vehicles) and degenerative diseases (mainly chronic renal failure, cirrhosis, and congestive heart failure) were the main disease categories causing death or motivating euthanasia in dogs of this midland region. However, when cases were evaluated in relation with the age of the dog, the disease prevalence differed. The main causes of death in puppies were infectious and parasitic disease (mainly parvoviral enteritis, canine distemper, and intestinal parasitism). In adult dogs the most important causes of death were canine distemper, neoplasia and trauma. In age dogs, approximately half of the deaths could be attributed to neoplasia and degenerative disease.

• Diseases of dogs causes of death reasons for euthanasia

Abstract in Portuguese:

ABSTRACT.- Fighera R.A., Souza T.M., Silva M.C., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2008. [Causes of death and reasons for euthanasia in dogs from the midland region of the Midwest of Rio Grande do Sul State, Brazil (1965-2004).] Causas de morte e razões para eutanásia de cães da Mesorregião do Centro Ocidental Rio-Grandense (1965-2004). Pesquisa Veterinária Brasileira 28(4):223-230. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: anemiaveterinaria@yahoo.com.br The main objective of this study was to investigate the prevalence of diseases culminating with death or motivating euthanasia of dogs from the midland region of the Midwest of Rio Grande do Sul State, Brazil. The necropsy files of the Laboratório de Patologia Veterinária (LPV) of the Universidade Federal de Santa Maria (UFSM) were accessed and necropsy protocols of dogs necropsied between January 1965 and December 2004 were reviewed. During this period 4,844 reports of canine necropsies were filed at the LPV-UFSM. The case distribution in relation to the disease categories diagnosed was as follows: infectious and parasitic diseases (1,693 [35.0%]); neoplasms (378 [7.8%]); disorders caused by physical agents (369 [7.6%]); degenerative diseases (342 [7.1%]); poisonings and toxinfections (112 [2.3%]); euthanasia due to convenience (101 [2.1%]); metabolic and endocrinological diseases (97 [2.0%]); iatrogenic disorders (83 [1.7%]); developmental disorders (25 [0.5%]); immune mediate diseases (10 [0.2%]); and nutritional disorders (6 [0.1%]). Other disorders, including multifactorial or idiopathic diseases contributed 80 (1.6%) cases. In 1,548 (32.0%) out of the 4,844 cases it was not possible to establish either cause of death or reason for euthanasia. Infectious and parasitic diseases (mainly canine distemper, parvoviral enteritis and intestinal parasitism), neoplasia (mainly mammary neoplasms and lymphoma), disorders caused by physical agents (mainly accidents caused by automotive vehicles) and degenerative diseases (mainly chronic renal failure, cirrhosis, and congestive heart failure) were the main disease categories causing death or motivating euthanasia in dogs of this midland region. However, when cases were evaluated in relation with the age of the dog, the disease prevalence differed. The main causes of death in puppies were infectious and parasitic disease (mainly parvoviral enteritis, canine distemper, and intestinal parasitism). In adult dogs the most important causes of death were canine distemper, neoplasia and trauma. In age dogs, approximately half of the deaths could be attributed to neoplasia and degenerative disease.

Abstract in English:

ABSTRACT.- Rodrigues A., De La Corte F.D., Graça D.L., Rissi D.R., Schild A.L., Kommers G.D. & Barros C.S.L. 2008. [Stringhalt in horses from the state of Rio Grande do Sul, Brazil.] Harpejamento em eqüinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 28(1):23-28. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical, gross and histological findings of cases of stringhalt occurring in horses from eight farms in six counties in the State of Rio Grande do Sul, Brazil from 2000-2005 are reported. At least 10 horses were affected. Ages of affected horses were 1-13 years (average 6.2 years) and 1-2 horses were affected in each farm. Factors that might have influenced the appearance of the disease included dearth of forage due to insufficient rainfall. The presence of the plant Hypochaeris radicata, often implicated as a cause of stringhalt in horses, was observed in the pasture of three out of five evaluated farms and in six of these farms the pasture was poor due to scarse precipitation. Estimated morbidity was 17.3% and lethality was close to zero although two horses were euthanatized for necropsy. Characteristic clinical signs included excessive flexion of the stifle and hock joints, impaired ambulation and bunny hop-type of gait. Clinical disease was graded by number scores from 1-5, higher numbers indicating increasing severity. Three horses were graded as 1, one horse as 2, three horses as 3, one horse as 4 and two horses as 5. Treatment with phenytoin in two horses and with phenytoin and tenectomy in another one did not result in amelioration of the clinical signs. Four out of ten clinical examined horses with stringhalt recovered with no treatment within 2-4 months of clinical disease and four affected horses did not recover even after 9-17 months of clinical disease, when they were lastly examined. Necropsy findings included atrophy of skeletal muscle of the large muscular groups which was confirmed histologically. Histological evaluation of peripheral nerves of one of the euthanatized horses revealed reduction or absence of myelinated fibers. Ultrastructural findings included signs of demyelination, regeneration and remyelination of peripheral nerves.

• Neuropathy toxic neuropathy diseases of horses

Abstract in Portuguese:

ABSTRACT.- Rodrigues A., De La Corte F.D., Graça D.L., Rissi D.R., Schild A.L., Kommers G.D. & Barros C.S.L. 2008. [Stringhalt in horses from the state of Rio Grande do Sul, Brazil.] Harpejamento em eqüinos no Rio Grande do Sul. Pesquisa Veterinária Brasileira 28(1):23-28. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The epidemiology, clinical, gross and histological findings of cases of stringhalt occurring in horses from eight farms in six counties in the State of Rio Grande do Sul, Brazil from 2000-2005 are reported. At least 10 horses were affected. Ages of affected horses were 1-13 years (average 6.2 years) and 1-2 horses were affected in each farm. Factors that might have influenced the appearance of the disease included dearth of forage due to insufficient rainfall. The presence of the plant Hypochaeris radicata, often implicated as a cause of stringhalt in horses, was observed in the pasture of three out of five evaluated farms and in six of these farms the pasture was poor due to scarse precipitation. Estimated morbidity was 17.3% and lethality was close to zero although two horses were euthanatized for necropsy. Characteristic clinical signs included excessive flexion of the stifle and hock joints, impaired ambulation and bunny hop-type of gait. Clinical disease was graded by number scores from 1-5, higher numbers indicating increasing severity. Three horses were graded as 1, one horse as 2, three horses as 3, one horse as 4 and two horses as 5. Treatment with phenytoin in two horses and with phenytoin and tenectomy in another one did not result in amelioration of the clinical signs. Four out of ten clinical examined horses with stringhalt recovered with no treatment within 2-4 months of clinical disease and four affected horses did not recover even after 9-17 months of clinical disease, when they were lastly examined. Necropsy findings included atrophy of skeletal muscle of the large muscular groups which was confirmed histologically. Histological evaluation of peripheral nerves of one of the euthanatized horses revealed reduction or absence of myelinated fibers. Ultrastructural findings included signs of demyelination, regeneration and remyelination of peripheral nerves.

Abstract in English:

ABSTRACT.- Furlan F.H., Lucioli J., Veronezi L.O., Traverso S. D. & Gava A. 2008. [Experimental poisoning by Sida carpinifolia (Malvaceae) in cattle.] Intoxicação experimental por Sida carpinifolia (Malvaceae) em bovinos. Pesquisa Veterinária Brasileira 28(1):57-62. Departamento de Clínica e Patologia, Centro de Ciências Agroveterinárias, Universidade do Estado de Santa Catarina, Lages, SC 88520-000, Brazil. E-mail: a2ag@cav.udesc.br Clinical and pathological findings of experimental poisoning by Sida carpinifolia in cattle are described. A neurologic disease was observed in cattle on farms of the Alto Vale do Itajaí region of the Brazilian state of Santa Catarina. For the experimental reproduction of the disease, fresh green leaves, weekly harvested in the same region where spontaneous case occurred, were force-fed to five cattle at doses of 10 and 20g/kg for 120 days, 40g/kg for 30 days, and 30 and 40g/kg body weight for 150 days. One animal died and the others were euthanatized at the end of the experiment. Clinical signs and lesions varied from mild to severe in the experimentally poisoned cattle and depended on dose and length of the period of consumption. Main histological and ultrastructural lesions consisted of vacuolation and distension of neuronal perikarya (mainly of Purkinje cells), and of the cytoplasm of acinar pancreatic cells and thyroid follicular cells. It is concluded that ingestion of even small amounts S. carpinifolia for prolonged periods of time cause lisosomal storage disease in cattle.

• Poisonous plants Sida carpinifolia Malvaceae cattle storage disease alpha-mannosidosis

Abstract in Portuguese:

ABSTRACT.- Furlan F.H., Lucioli J., Veronezi L.O., Traverso S. D. & Gava A. 2008. [Experimental poisoning by Sida carpinifolia (Malvaceae) in cattle.] Intoxicação experimental por Sida carpinifolia (Malvaceae) em bovinos. Pesquisa Veterinária Brasileira 28(1):57-62. Departamento de Clínica e Patologia, Centro de Ciências Agroveterinárias, Universidade do Estado de Santa Catarina, Lages, SC 88520-000, Brazil. E-mail: a2ag@cav.udesc.br Clinical and pathological findings of experimental poisoning by Sida carpinifolia in cattle are described. A neurologic disease was observed in cattle on farms of the Alto Vale do Itajaí region of the Brazilian state of Santa Catarina. For the experimental reproduction of the disease, fresh green leaves, weekly harvested in the same region where spontaneous case occurred, were force-fed to five cattle at doses of 10 and 20g/kg for 120 days, 40g/kg for 30 days, and 30 and 40g/kg body weight for 150 days. One animal died and the others were euthanatized at the end of the experiment. Clinical signs and lesions varied from mild to severe in the experimentally poisoned cattle and depended on dose and length of the period of consumption. Main histological and ultrastructural lesions consisted of vacuolation and distension of neuronal perikarya (mainly of Purkinje cells), and of the cytoplasm of acinar pancreatic cells and thyroid follicular cells. It is concluded that ingestion of even small amounts S. carpinifolia for prolonged periods of time cause lisosomal storage disease in cattle.

Abstract in English:

ABSTRACT.- Silva M.C., Fighera R.A., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2007. [Hepatic cirrhosis in dogs: 80 cases (1965-2003).] Cirrose hepática em cães: 80 casos (1965-2003). Pesquisa Veterinária Brasileira 27(11):471-480. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A retrospective study in 80 cases of canine hepatic cirrhosis was carried out at the Veterinary Pathology Laboratory of the Federal University of Santa Maria, Rio Grande do Sul, Brazil. Considering those cases in which the sex and age of the dogs were informed in the necropsy reports, males comprised 53.8% of the cases and 46.2% were females; while 50.0% of these dogs were aged, 48.6% were adults and 1.4% were puppies. The main observed clinical signs include ascites (39/80 [48.8%]), icterus (19/80 [23.8%]), anorexia (13/80 [16.2%]), neurological disturbances (12/80 [15.0%]), dyspnea (12/80 [15.0%]) and subcutaneous edema (10/80 [12.5%]). In 63 dogs for which there was a description of gross morphology in the necropsy reports, 76.2% had macronodular and 23.8% had micronodular cirrhosis. In 14 cases in which the histopathology of the liver was reviewed different degrees of fibrosis were observed: mild in 57.2%, moderate in 21.4%, or marked in 21.4%; in these cases there were no correlation with the degree of fibrosis and other associated histological changes such as lipidosis, biliary ducts hyperplasia, inflammation, bilestasis, hemosiderosis and random hepatocellular necrosis. Extra hepatic changes included ascites (39/63 [61.9%]), icterus (19/63 [30.2%]), status spongiosus (15/63 [23.8%]), hydrothorax (12/63 [19.0%]), subcutaneous edema (10/63 [15.9%]), portosystemic shunts (11/63 [17.5%]), gastric our duodenal ulceration (11/63 [17.5%]) and cholemic nephrosis (4/63 [6.3%]).

• Diseases of dogs cirrhosis fibrosis nodular regeneration pathology diseases of the liver

Abstract in Portuguese:

ABSTRACT.- Silva M.C., Fighera R.A., Brum J.S., Graça D.L., Kommers G.D., Irigoyen L.F. & Barros C.S.L. 2007. [Hepatic cirrhosis in dogs: 80 cases (1965-2003).] Cirrose hepática em cães: 80 casos (1965-2003). Pesquisa Veterinária Brasileira 27(11):471-480. Departamento de Patologia, Universidade Federal de Santa Maria, Camobi, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br A retrospective study in 80 cases of canine hepatic cirrhosis was carried out at the Veterinary Pathology Laboratory of the Federal University of Santa Maria, Rio Grande do Sul, Brazil. Considering those cases in which the sex and age of the dogs were informed in the necropsy reports, males comprised 53.8% of the cases and 46.2% were females; while 50.0% of these dogs were aged, 48.6% were adults and 1.4% were puppies. The main observed clinical signs include ascites (39/80 [48.8%]), icterus (19/80 [23.8%]), anorexia (13/80 [16.2%]), neurological disturbances (12/80 [15.0%]), dyspnea (12/80 [15.0%]) and subcutaneous edema (10/80 [12.5%]). In 63 dogs for which there was a description of gross morphology in the necropsy reports, 76.2% had macronodular and 23.8% had micronodular cirrhosis. In 14 cases in which the histopathology of the liver was reviewed different degrees of fibrosis were observed: mild in 57.2%, moderate in 21.4%, or marked in 21.4%; in these cases there were no correlation with the degree of fibrosis and other associated histological changes such as lipidosis, biliary ducts hyperplasia, inflammation, bilestasis, hemosiderosis and random hepatocellular necrosis. Extra hepatic changes included ascites (39/63 [61.9%]), icterus (19/63 [30.2%]), status spongiosus (15/63 [23.8%]), hydrothorax (12/63 [19.0%]), subcutaneous edema (10/63 [15.9%]), portosystemic shunts (11/63 [17.5%]), gastric our duodenal ulceration (11/63 [17.5%]) and cholemic nephrosis (4/63 [6.3%]).

Abstract in English:

ABSTRACT.- Barbosa R.C., Riet-Correa F., Lima E.F., Medeiros R.M.T., Guedes K.M.R, Gardner D.R., Molyneux R.J. & Melo L.E.H. 2007. Experimental swainsonine poisoning in goats ingesting Ipomoea sericophylla and Ipomoea riedelii (Convolvulaceae). Pesquisa Veterinária Brasileira 27(10):409-414. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande. Campus de Patos, 58700-000 Patos, Paraíba, Brazil. E-mail: franklin.riet@pq.cnpq.br Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05% and 0.01% swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004% of the dry matter in goats ingesting 1.5% bw of the dry matter. For goats ingesting 2%-2.5% bw of dry matter this dose would be 0.00024%-0.0003% of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean corpuscular volume, and serum levels of glucose, total protein, and albumin, and the serum activities of gamma glutamyl transferase and aspartate aminotransferase. Swainsonine concentration of 0.05% in I. sericophylla and 0.01% in I. riedelii are different from samples of these plants used in previous experiments, which contained 0.14% and 0.5% swainsonine, respectively, demonstrating a wide variation in the toxicity of different samples.

• Poisonous plants plant poisoning lysosomal storage disease swainsonine goats Ipomoea sericophylla Ipomoea riedelii

Abstract in Portuguese:

ABSTRACT.- Barbosa R.C., Riet-Correa F., Lima E.F., Medeiros R.M.T., Guedes K.M.R, Gardner D.R., Molyneux R.J. & Melo L.E.H. 2007. Experimental swainsonine poisoning in goats ingesting Ipomoea sericophylla and Ipomoea riedelii (Convolvulaceae). Pesquisa Veterinária Brasileira 27(10):409-414. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande. Campus de Patos, 58700-000 Patos, Paraíba, Brazil. E-mail: franklin.riet@pq.cnpq.br Ipomoea sericophylla and Ipomoea riedelii cause a glycoprotein storage disease in goats. This paper reports the experimental poisoning in goats by dried I. sericophylla and I. riedelii containing 0.05% and 0.01% swainsonine, respectively. Three groups with four animals each were used. Group 1 received daily doses of 2g/kg body weight (bw) of dried I. sericophylla (150mg of swainsonine/kg). Goats from this group had clinical signs 36-38 days after the start of ingestion. Group 2 received dried I. riedelii daily doses of 2g/kg of I. riedelii (30mg of swainsonine/kg) for 70 days. No clinical signs were observed, therefore the swainsonine dose was increased to 60mg/kg for another 70 days. Goats from Group 2 had clinical signs 26-65 days after increase in swainsonine dose to 60mg/kg. Group 3 was used as control. In these experiments the minimum toxic dose was 60mg/kg which represents 0.0004% of the dry matter in goats ingesting 1.5% bw of the dry matter. For goats ingesting 2%-2.5% bw of dry matter this dose would be 0.00024%-0.0003% of the dry matter. After the end of the experiment two goats were euthanized and another six were observed for recovery of clinical signs. Four goats that continued to consume swainsonine containing plant for 39-89 days after the first clinical signs had non reversible signs, while two goats that ingested the plant for only 15 and 20 days after the first clinical signs recovered completely. These and previous results indicate that irreversible lesions due to neuronal loss occur in goats that continue to ingest the plants for about 30 days after the first clinical signs. Clinical signs and histological lesions were similar to those reported previously for goats poisoned by swainsonine containing plants. No significant alterations were found in packed cell volume, red and white blood cell counts, hemoglobin and mean corpuscular hemoglobin concentrations, mean corpuscular volume, and serum levels of glucose, total protein, and albumin, and the serum activities of gamma glutamyl transferase and aspartate aminotransferase. Swainsonine concentration of 0.05% in I. sericophylla and 0.01% in I. riedelii are different from samples of these plants used in previous experiments, which contained 0.14% and 0.5% swainsonine, respectively, demonstrating a wide variation in the toxicity of different samples.

Abstract in English:

ABSTRACT.- Antoniassi N.A.B., Ferreira E.V., Santos C.E.P., Campos J.L.E., Nakazato L. & Colodel E.M. 2007. [Spontaneous Ipomoea carnea subsp. fistulosa (Convolvulaceae) poisoning of cattle in the Brazilian Pantanal.] Intoxicação espontânea por Ipomoea carnea subsp. fistulosa (Convol-vulaceae) em bovinos no Pantanal Matogrossense. Pesquisa Veterinária Brasileira 27(10):415-418. Departamento de Clínica Médica Veterinária, Faculdade de Agronomia e Medicina Veterinária, Universidade Federal de Mato Grosso, Cuiabá, MT 78068-900, Brazil. E-mail: moleta@ufmt.br A spontaneous Ipomoea carnea subsp. fistulosa (canudo, algodoeiro) poisoning of cattle in the county of Poconé, Brazilian Pantanal, is reported. The investigation began after 12 cattle had died from a flock of 500 animals maintained in an extensive area intensely infested by I. carnea subsp. fistulosa with scarce availability of other fodder plants. The deaths occurred from June to September of 2006. Clinical signs were loss of weight and neurological deficits with hypermetry and incoordination. No significant gross lesions were observed at postmortem examination of one bovine. Histological changes comprised widespread cytoplasmic vacuolation of neurons, cells of the thyroid, kidney and pancreas. Cattle with similar clinical picture, that had been removed from the area invaded by I. carnea subsp. fistulosa and placed into areas with native and Brachiaria sp. pasture, recovered clinically within 15 days.

• Poisonous plants Ipomoea carnea subsp. fistulosa plant poisoning storage diseases cattle

Abstract in Portuguese:

ABSTRACT.- Antoniassi N.A.B., Ferreira E.V., Santos C.E.P., Campos J.L.E., Nakazato L. & Colodel E.M. 2007. [Spontaneous Ipomoea carnea subsp. fistulosa (Convolvulaceae) poisoning of cattle in the Brazilian Pantanal.] Intoxicação espontânea por Ipomoea carnea subsp. fistulosa (Convol-vulaceae) em bovinos no Pantanal Matogrossense. Pesquisa Veterinária Brasileira 27(10):415-418. Departamento de Clínica Médica Veterinária, Faculdade de Agronomia e Medicina Veterinária, Universidade Federal de Mato Grosso, Cuiabá, MT 78068-900, Brazil. E-mail: moleta@ufmt.br A spontaneous Ipomoea carnea subsp. fistulosa (canudo, algodoeiro) poisoning of cattle in the county of Poconé, Brazilian Pantanal, is reported. The investigation began after 12 cattle had died from a flock of 500 animals maintained in an extensive area intensely infested by I. carnea subsp. fistulosa with scarce availability of other fodder plants. The deaths occurred from June to September of 2006. Clinical signs were loss of weight and neurological deficits with hypermetry and incoordination. No significant gross lesions were observed at postmortem examination of one bovine. Histological changes comprised widespread cytoplasmic vacuolation of neurons, cells of the thyroid, kidney and pancreas. Cattle with similar clinical picture, that had been removed from the area invaded by I. carnea subsp. fistulosa and placed into areas with native and Brachiaria sp. pasture, recovered clinically within 15 days.

Abstract in English:

ABSTRACT.- Lucioli J., Furlan F.H., Mezaroba S., Traverso S. D. & Gava A. 2007. [Spontaneous and experimental poisoning by Eupatorium tremulum (Asteraceae) in cattle.] Intoxicação espon-tânea e experimental por Eupatorium tremulum (Asteraceae) em bovinos. Pesquisa Veterinária Brasi-leira 27(10):442-445. Departamento de Clínica e Patologia, Centro de Ciências Agroveterinárias, Univer-sidade do Estado de Santa Catarina, Lages, SC 88520-000, Brazil. E-mail: a2ag@cav.udesc.br The spontaneous and experimental poisoning by Eupatorium tremulum in cattle is described. Spontaneous cases were diagnosed in a herd of 19 cattle in the municipality of Lages, Santa Catarina, Brazil. Three of the animals were found dead after having been transferred to a pasture with abundant quantities of E. tremulum. On two of them postmortem examination was performed and several internal organs were sampled for histological examination. Green leaves of E. tremulum were force-fed orally to 5 calves in single doses of 23-32g/kg body weight. Three calves showed clinical signs and two died. The main clinical signs included anorexia, apathy, absence of rumen movements, diarrhea and a flabby abdominal wall. Gross changes were restricted to the fore stomachs and were identical to those observed in the cases of natural poisoning. Rumen and reticulum were slightly reddish from outside; the corneal layer of their internal lining was loosely attached to a markedly red mucosa. The histological examination of rumen and reticulum from spontaneous and experimental cases revealed necrosis and vesicle formation in the epithelium; in some segments of the ruminal mucosa there was detachment of the epithelial covering and infiltration by neuthophils. Poisoning by E. tremulum has clinical course, gross lesions and histopathology very similar to those observed in poisoning caused by ingestion of the plants Baccharidastrum triplinervium, Baccharis coridifolia and Baccharis megapotamica var. weirii. The diagnosis of the spontaneous cases here described was confirmed by epidemiological data and the experimental reproduction of characteristic gross lesions and histopathology.

• Poisonous plants plant poisoning Eupatorium tremulum Asteraceae diseases of cattle digestive tract

Abstract in Portuguese:

ABSTRACT.- Lucioli J., Furlan F.H., Mezaroba S., Traverso S. D. & Gava A. 2007. [Spontaneous and experimental poisoning by Eupatorium tremulum (Asteraceae) in cattle.] Intoxicação espon-tânea e experimental por Eupatorium tremulum (Asteraceae) em bovinos. Pesquisa Veterinária Brasi-leira 27(10):442-445. Departamento de Clínica e Patologia, Centro de Ciências Agroveterinárias, Univer-sidade do Estado de Santa Catarina, Lages, SC 88520-000, Brazil. E-mail: a2ag@cav.udesc.br The spontaneous and experimental poisoning by Eupatorium tremulum in cattle is described. Spontaneous cases were diagnosed in a herd of 19 cattle in the municipality of Lages, Santa Catarina, Brazil. Three of the animals were found dead after having been transferred to a pasture with abundant quantities of E. tremulum. On two of them postmortem examination was performed and several internal organs were sampled for histological examination. Green leaves of E. tremulum were force-fed orally to 5 calves in single doses of 23-32g/kg body weight. Three calves showed clinical signs and two died. The main clinical signs included anorexia, apathy, absence of rumen movements, diarrhea and a flabby abdominal wall. Gross changes were restricted to the fore stomachs and were identical to those observed in the cases of natural poisoning. Rumen and reticulum were slightly reddish from outside; the corneal layer of their internal lining was loosely attached to a markedly red mucosa. The histological examination of rumen and reticulum from spontaneous and experimental cases revealed necrosis and vesicle formation in the epithelium; in some segments of the ruminal mucosa there was detachment of the epithelial covering and infiltration by neuthophils. Poisoning by E. tremulum has clinical course, gross lesions and histopathology very similar to those observed in poisoning caused by ingestion of the plants Baccharidastrum triplinervium, Baccharis coridifolia and Baccharis megapotamica var. weirii. The diagnosis of the spontaneous cases here described was confirmed by epidemiological data and the experimental reproduction of characteristic gross lesions and histopathology.

Abstract in English:

ABSTRACT.- Inkelmann M.A., Rozza D.B., Fighera R.A., Kommers G.D., Graça D.L., Irigoyen L.F. & Barros C.S.L. 2007. [Infectious canine hepatitis: 62 cases.] Hepatite infecciosa canina: 62 casos. Pesquisa Veterinária Brasileira 27(8):325-332. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Necropsy reports from 5,361 dogs necropsied over a 43-year period (1964-2006) were reviewed in search for cases of infectious canine hepatitis (ICH). Sixty two (1.2%) cases of the disease were found. Most of the 62 affected dogs (91.9%,) were 2-year-old or less. Clinical signs were recorded in the necropsy files of 45 ICH affected dogs and included anorexia (55.6%), apathy (35.6%), diarrhea (35.6%) (often with blood [43,8%]), neurological signs (33.3%), vomiting (26.7%), petechiae and echymosis in the mucous membranes and/or skin (24.4%), hypothermia (20.0%), abdominal pain (15.6%), icterus (13.3%), enlargement and congestion of the tonsils (11.1%), fever (11.1%) and ascites (6.7%). The clinical courses lasted from few hours to 15 days. The most frequent necropsy findings included hepatic changes (87.1%), edematous, congested and hemorrhagic lymph nodes (51.6%), bloodstained fluid, clear fluid or whole blood in the abdominal cavity (35.5%), and petechial or paint-brush hemorrhages over the pleural (27.4%) and gastrointestinal (24.2%) serosal surfaces. In 12.9% of the cases there was a granularity to the intestinal serosa. Hemorrhages in the leptomeninges and in the substance of the brain were observed in 9.7% of the cases. Hepatic gross changes included moderately enlarged and more friable livers with marked lobular pattern, congestion and multifocal pale or hemorrhagic foci of necrosis. Films and strands of fibrin covered the hepatic surface in 20.4% of the cases and in 27.8% of the cases the gall bladder was thickened by edema. Zonal or randomly distributed multifocal hepatic necrosis (93.5%) associated with intranuclear inclusion bodies were the most consistent microscopic findings. Intranuclear inclusion bodies were found in the liver in every case and their detection was the criterium for confirmation of the diagnosis. The most significant microscopic extra-hepatic lesions included hemorrhages and intranuclear inclusion bodies in endothelial and reticuloendothelial cells of the renal glomeruli (50.0%) lymph nodes (47.8%), brain (27.8%), tonsils (25.0%) and spleen (10.0%).

• Liver diseases viral diseases infectious diseases pathology diseases of dogs infectious canine hepatitis

Abstract in Portuguese:

ABSTRACT.- Inkelmann M.A., Rozza D.B., Fighera R.A., Kommers G.D., Graça D.L., Irigoyen L.F. & Barros C.S.L. 2007. [Infectious canine hepatitis: 62 cases.] Hepatite infecciosa canina: 62 casos. Pesquisa Veterinária Brasileira 27(8):325-332. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Necropsy reports from 5,361 dogs necropsied over a 43-year period (1964-2006) were reviewed in search for cases of infectious canine hepatitis (ICH). Sixty two (1.2%) cases of the disease were found. Most of the 62 affected dogs (91.9%,) were 2-year-old or less. Clinical signs were recorded in the necropsy files of 45 ICH affected dogs and included anorexia (55.6%), apathy (35.6%), diarrhea (35.6%) (often with blood [43,8%]), neurological signs (33.3%), vomiting (26.7%), petechiae and echymosis in the mucous membranes and/or skin (24.4%), hypothermia (20.0%), abdominal pain (15.6%), icterus (13.3%), enlargement and congestion of the tonsils (11.1%), fever (11.1%) and ascites (6.7%). The clinical courses lasted from few hours to 15 days. The most frequent necropsy findings included hepatic changes (87.1%), edematous, congested and hemorrhagic lymph nodes (51.6%), bloodstained fluid, clear fluid or whole blood in the abdominal cavity (35.5%), and petechial or paint-brush hemorrhages over the pleural (27.4%) and gastrointestinal (24.2%) serosal surfaces. In 12.9% of the cases there was a granularity to the intestinal serosa. Hemorrhages in the leptomeninges and in the substance of the brain were observed in 9.7% of the cases. Hepatic gross changes included moderately enlarged and more friable livers with marked lobular pattern, congestion and multifocal pale or hemorrhagic foci of necrosis. Films and strands of fibrin covered the hepatic surface in 20.4% of the cases and in 27.8% of the cases the gall bladder was thickened by edema. Zonal or randomly distributed multifocal hepatic necrosis (93.5%) associated with intranuclear inclusion bodies were the most consistent microscopic findings. Intranuclear inclusion bodies were found in the liver in every case and their detection was the criterium for confirmation of the diagnosis. The most significant microscopic extra-hepatic lesions included hemorrhages and intranuclear inclusion bodies in endothelial and reticuloendothelial cells of the renal glomeruli (50.0%) lymph nodes (47.8%), brain (27.8%), tonsils (25.0%) and spleen (10.0%).

Abstract in English:

ABSTRACT.- Rissi D.R., Rech R.R., Flores E.F., Kommers G.D. & Barros C.S.L. 2007. [Meningoencephalitis by bovine herpesvirus-5.] Meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 27(7):251-260. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) is an often fatal, acute or subacute infectious disease that affects mainly young cattle under stressing conditions. The disease has been recognized in several Brazilian regions and in other parts of the world. BoHV-5 is a double stranded DNA virus member of the Herpesviridae family and subfamily Alphaherpesvirinae. The virus is characterized by rapid and lytic replication in cell cultures and by the ability to establish lifelong latent infection in sensory nerve ganglia of the host. BoHV-5 is transmitted mainly by direct and indirect contact and replicates acutely in the oral, nasal, oropharingeal or ocular mucosae. After primary replication, the virus invades nerve endings and is transported to the neuron cell bodies of the sensory ganglia where it replicates actively and/or establishes latency. Viral invasion of the brain may result in massive virus replication and production of neurological disease. Virtually all cattle developing neurological disease die of meningoencephalitis; yet the infection may be subclinical in some animals. These animals recover and become latently infected. Viral dissemination within a herd is facilitated by conditions such as crowding, introduction of cattle from other herds and weaning of calves in ages that coincide with decrease of passive immunity. Certain natural or induced conditions may reactivate the latent virus and favor its transmission and dissemination to other susceptible individuals. The disease may occur as outbreaks or as sporadic cases, with morbidity rates ranging of 0.05%-5%; lethality is almost always 100%. Clinical signs include depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, paddling movements, disphagia, abdominal pain, nystagmus, muscle tremors, drooling, incoordinated gait, opisthotonus, head pressing, falls and convulsions. Clinical course is usually 1-15 days. Necropsy findings may be absent but often there is swollen of the rostral portions of the cerebral cortex and flattening of gyri, with softening and segmental yellow discoloration (malacia). As the disease progresses the affected areas become gelatinous and grey and, in advanced cases, there is segmental loss of the cerebral cortex of the frontal lobe of the brain (residual lesion). In several cases there is malacia of the basal nuclei and of the thalamus. Histologically, there is necrotizing non-suppurative meningoencephalitis affecting mainly the cerebral cortex of the frontal lobe associated with eosinophilic intranuclear inclusion bodies in neurons and astrocytes, although the frequency of the inclusion bodies is inconsistent. The diagnosis of meningoencephalitis by BoHV-5 should be based on epidemiology, clinical signs, necropsy and histological findings. The diagnosis should be confirmed by viral isolation in cell culture and/or by detection of viral antigens in brain sections or in exfoliated cells from nasal secretions. The identification and characterization of BoHV-5 can be done by the use of monoclonal antibodies, polymerase chain reaction (PCR) and/or by restriction enzyme analysis of the viral genome. There is no specific treatment for the disease. As BoHV-1 and BoHV-5 are antigenically related, vaccination using BoHV-1 vaccines may be recommended as a means of reducing the losses caused by BoHV-5 infection, mainly during outbreaks of neurologic disease. Additionally, measures such as serologic testing of new additions to the herd; and management practices to prevent stress and to reduce conditions for virus dissemination among animals may help in reducing the incidence and the consequences of BoHV-5 infection and disease.

• Bovine herpesvirus-5 BoHV-5 BHV-5 meningoencephalitis viral diseases diseases of cattle neuropathology

Abstract in Portuguese:

ABSTRACT.- Rissi D.R., Rech R.R., Flores E.F., Kommers G.D. & Barros C.S.L. 2007. [Meningoencephalitis by bovine herpesvirus-5.] Meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 27(7):251-260. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) is an often fatal, acute or subacute infectious disease that affects mainly young cattle under stressing conditions. The disease has been recognized in several Brazilian regions and in other parts of the world. BoHV-5 is a double stranded DNA virus member of the Herpesviridae family and subfamily Alphaherpesvirinae. The virus is characterized by rapid and lytic replication in cell cultures and by the ability to establish lifelong latent infection in sensory nerve ganglia of the host. BoHV-5 is transmitted mainly by direct and indirect contact and replicates acutely in the oral, nasal, oropharingeal or ocular mucosae. After primary replication, the virus invades nerve endings and is transported to the neuron cell bodies of the sensory ganglia where it replicates actively and/or establishes latency. Viral invasion of the brain may result in massive virus replication and production of neurological disease. Virtually all cattle developing neurological disease die of meningoencephalitis; yet the infection may be subclinical in some animals. These animals recover and become latently infected. Viral dissemination within a herd is facilitated by conditions such as crowding, introduction of cattle from other herds and weaning of calves in ages that coincide with decrease of passive immunity. Certain natural or induced conditions may reactivate the latent virus and favor its transmission and dissemination to other susceptible individuals. The disease may occur as outbreaks or as sporadic cases, with morbidity rates ranging of 0.05%-5%; lethality is almost always 100%. Clinical signs include depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, paddling movements, disphagia, abdominal pain, nystagmus, muscle tremors, drooling, incoordinated gait, opisthotonus, head pressing, falls and convulsions. Clinical course is usually 1-15 days. Necropsy findings may be absent but often there is swollen of the rostral portions of the cerebral cortex and flattening of gyri, with softening and segmental yellow discoloration (malacia). As the disease progresses the affected areas become gelatinous and grey and, in advanced cases, there is segmental loss of the cerebral cortex of the frontal lobe of the brain (residual lesion). In several cases there is malacia of the basal nuclei and of the thalamus. Histologically, there is necrotizing non-suppurative meningoencephalitis affecting mainly the cerebral cortex of the frontal lobe associated with eosinophilic intranuclear inclusion bodies in neurons and astrocytes, although the frequency of the inclusion bodies is inconsistent. The diagnosis of meningoencephalitis by BoHV-5 should be based on epidemiology, clinical signs, necropsy and histological findings. The diagnosis should be confirmed by viral isolation in cell culture and/or by detection of viral antigens in brain sections or in exfoliated cells from nasal secretions. The identification and characterization of BoHV-5 can be done by the use of monoclonal antibodies, polymerase chain reaction (PCR) and/or by restriction enzyme analysis of the viral genome. There is no specific treatment for the disease. As BoHV-1 and BoHV-5 are antigenically related, vaccination using BoHV-1 vaccines may be recommended as a means of reducing the losses caused by BoHV-5 infection, mainly during outbreaks of neurologic disease. Additionally, measures such as serologic testing of new additions to the herd; and management practices to prevent stress and to reduce conditions for virus dissemination among animals may help in reducing the incidence and the consequences of BoHV-5 infection and disease.