Resultado da pesquisa (331)

Termo utilizado na pesquisa C.S

#261 - Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil, p.1-14

Abstract in English:

ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.

Abstract in Portuguese:

ABSTRACT.- Santos J.C.A., Riet-Correa F., Simões S.V.D. & Barros C.S.L. 2008. [Pathogenesis, clinical signs and pathology of diseases caused by hepatotoxic plants in ruminants and horses in Brazil.] Patogênese, sinais clínicos e patologia das doenças causadas por plantas hepatotóxicas em ruminantes e eqüinos no Brasil. Pesquisa Veterinária Brasileira 28(1):1-14. Centro de Saúde e Tecnologia Rural, Universidade Federal de Campina Grande, Patos, PB 58700-000, Brazil. E-mail: franklin.riet@pq.cnpq.br Plants causing hepatic lesions in ruminants and horses constitute one important group of poisonous plants in Brazil. These plants can be placed in three major groups: plants causing acute liver necrosis; plants causing liver fibrosis; and plants causing hepatogenous photosensitization. For some of these plants the toxic principles are known. Cestrum parqui and Xanthium cavanillesi that cause acute liver necrosis contain carboxy-atractylosides. Senecio spp., Crotalaria spp., and Echium plantagineum that cause liver fibrosis contain pyrrolizidine alkaloids. As for the group of plants causing hepatogenous photosensibilization, Myoporum spp. contain furanosesquiterpenes, Lantana spp contain triterpenes, and Brachiaria spp. and Panicum spp. contain steroidal saponins. The clinical and pathologic features of the toxicosis caused by these phytotoxins, general mechanisms of production for the production of the clinical signs and the methods for diagnosis of hepatic failure in farm animals are reviewed.


#262 - Harpejamento em eqüinos no Rio Grande do Sul, p.23-28

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.

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.


#263 - Cirrose hepática em cães: 80 casos (1965-2003), p.471-480

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%]).

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%]).


#264 - Identificação e diferenciação de herpesvírus bovino tipos 1 e 5 isolados de amostras clínicas no Centro-Sul do Brasil, Argentina e Uruguai (1987-2006), p.403-408

Abstract in English:

ABSTRACT.- Silva M.S., Brum M.C.S., Weiblen R. & Flores E.F. 2007. [Identification and differentiation of herpesvirus types 1 and 5 isolated from clinical samples in central-southern Brazil, Argentina and Uruguay (1987-2006).] Identificação e diferenciação de herpesvírus bovino tipos 1 e 5 isolados de amostras clínicas no Centro-Sul do Brasil, Argentina e Uruguai (1987-2006). Pesquisa Veterinária Brasileira 27(10):403-408. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesviruses types 1 and 5 (BoHV-1; BoHV-5) are genetically and antigenically closely related such they can not be distinguished by routine diagnostic tests. As BoHV-1 has been historically associated with respiratory and genital disease, herpesviruses isolated from these clinical syndromes have been tentatively – and sometimes definitively - diagnosed as BoHV-1. Likewise, cases of herpetic neurological infection in cattle have been generally attributed to BoHV-5. This study reports the identification of 40 herpesvirus isolates from different clinical specimens and syndromes in central-southern Brazil, Argentina and Uruguay (1987-2006) by the use of a PCR able to differentiate between BoHV-1 and BoHV-5. BoHV-1 isolates (n=16) were identified in cases of respiratory disease (n=3), vulvovaginitis and/or balanoposthitis (n=3), in semen of healthy bulls (n=5) and in cases of neurological disease (n=5). Viruses identified as BoHV-5 (n=24) were isolated predominantly from cases of neurological disease (n=21), but also from semen of healthy bulls (n=2) and from a spleen of a calf with systemic disease (n=1). These results show that both BoHV-1 and BoHV-5 are not strictly associated with their respective diseases; yet are frequently involved in clinical conditions otherwise attributed to the other virus. These findings also reinforce the need of correctly identifying the herpesvirus isolates as to better understand their pathogenesis and epidemiology.

Abstract in Portuguese:

ABSTRACT.- Silva M.S., Brum M.C.S., Weiblen R. & Flores E.F. 2007. [Identification and differentiation of herpesvirus types 1 and 5 isolated from clinical samples in central-southern Brazil, Argentina and Uruguay (1987-2006).] Identificação e diferenciação de herpesvírus bovino tipos 1 e 5 isolados de amostras clínicas no Centro-Sul do Brasil, Argentina e Uruguai (1987-2006). Pesquisa Veterinária Brasileira 27(10):403-408. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesviruses types 1 and 5 (BoHV-1; BoHV-5) are genetically and antigenically closely related such they can not be distinguished by routine diagnostic tests. As BoHV-1 has been historically associated with respiratory and genital disease, herpesviruses isolated from these clinical syndromes have been tentatively – and sometimes definitively - diagnosed as BoHV-1. Likewise, cases of herpetic neurological infection in cattle have been generally attributed to BoHV-5. This study reports the identification of 40 herpesvirus isolates from different clinical specimens and syndromes in central-southern Brazil, Argentina and Uruguay (1987-2006) by the use of a PCR able to differentiate between BoHV-1 and BoHV-5. BoHV-1 isolates (n=16) were identified in cases of respiratory disease (n=3), vulvovaginitis and/or balanoposthitis (n=3), in semen of healthy bulls (n=5) and in cases of neurological disease (n=5). Viruses identified as BoHV-5 (n=24) were isolated predominantly from cases of neurological disease (n=21), but also from semen of healthy bulls (n=2) and from a spleen of a calf with systemic disease (n=1). These results show that both BoHV-1 and BoHV-5 are not strictly associated with their respective diseases; yet are frequently involved in clinical conditions otherwise attributed to the other virus. These findings also reinforce the need of correctly identifying the herpesvirus isolates as to better understand their pathogenesis and epidemiology.


#265 - Hepatite infecciosa canina: 62 casos, p.325-332

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%).

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%).


#266 - Meningoencephalitis by bovine herpesvirus-5, p. 251-260

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.

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.


#267 - Intoxicações por plantas e micotoxinas associadas a plantas em bovinos no Rio Grande do Sul: 461 casos, p.261-268

Abstract in English:

ABSTRACT.- Rissi D.R., Rech R.R., Pierezan F., Gabriel A.L., Trost M.E., Brum J.S., Kommers G.D. & Barros C.S.L. 2007. [Plant and plant-associated mycotoxins poisoning in cattle in Rio Grande do Sul, Brazil: 461 cases.] Intoxicações por plantas e micotoxinas associadas a plantas em bovinos no Rio Grande do Sul: 461 casos. Pesquisa Veterinária Brasileira 27(7):261-268. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br From 1990 to 2005, tissues from 2,912 cattle necropsies were examined at the Laboratory of Veterinary Pathology (LPV) of the Federal University of Santa Maria (UFSM), Brazil. These tissues came from necropsies performed by faculty members of the LPV or were mailed-in samples from necropsy performed by veterinarian practitioners. In 461 (15.83%) of these necropsies the cause of death was attributed to the ingestion of poisonous plants. In decreasing order of frequency poisoning by the following plants were registered: Senecio spp (56.14%), Pteridium aquilinum (12.06%), Ateleia glazioviana (10.31%), Solanum fastigiatum (5.04%), Baccharis coridifolia (3.29%), Xanthium cavanillesii (3.07%), Senna occidentalis (2.63%), Ramaria flavo-brunnescens (2.41%), Amaranthus spp (2.19%), Vicia villosa (1.54%), Ipomoea batatas, Prunus sellowii, cytrus pulp (0.44% each), Cestrum parqui, Claviceps paspali, Claviceps purpurea, Brachiaria spp and Lantana sp (0.22% each). In a given outbreak the number of affected cattle was substantially higher than the number of necropsies performed. The following aspects are discussed for each plant: geographical distribution; factors inducing ingestion; morbidity, mortality and lethality rates, clinical signs, necropsy findings, histopathology. For those plants in which information on the active principle and pathogenesis are available, these aspects are included in the discussion.

Abstract in Portuguese:

ABSTRACT.- Rissi D.R., Rech R.R., Pierezan F., Gabriel A.L., Trost M.E., Brum J.S., Kommers G.D. & Barros C.S.L. 2007. [Plant and plant-associated mycotoxins poisoning in cattle in Rio Grande do Sul, Brazil: 461 cases.] Intoxicações por plantas e micotoxinas associadas a plantas em bovinos no Rio Grande do Sul: 461 casos. Pesquisa Veterinária Brasileira 27(7):261-268. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br From 1990 to 2005, tissues from 2,912 cattle necropsies were examined at the Laboratory of Veterinary Pathology (LPV) of the Federal University of Santa Maria (UFSM), Brazil. These tissues came from necropsies performed by faculty members of the LPV or were mailed-in samples from necropsy performed by veterinarian practitioners. In 461 (15.83%) of these necropsies the cause of death was attributed to the ingestion of poisonous plants. In decreasing order of frequency poisoning by the following plants were registered: Senecio spp (56.14%), Pteridium aquilinum (12.06%), Ateleia glazioviana (10.31%), Solanum fastigiatum (5.04%), Baccharis coridifolia (3.29%), Xanthium cavanillesii (3.07%), Senna occidentalis (2.63%), Ramaria flavo-brunnescens (2.41%), Amaranthus spp (2.19%), Vicia villosa (1.54%), Ipomoea batatas, Prunus sellowii, cytrus pulp (0.44% each), Cestrum parqui, Claviceps paspali, Claviceps purpurea, Brachiaria spp and Lantana sp (0.22% each). In a given outbreak the number of affected cattle was substantially higher than the number of necropsies performed. The following aspects are discussed for each plant: geographical distribution; factors inducing ingestion; morbidity, mortality and lethality rates, clinical signs, necropsy findings, histopathology. For those plants in which information on the active principle and pathogenesis are available, these aspects are included in the discussion.


#268 - Intoxicação experimental por Senecio brasiliensis (Asteraceae) em eqüinos, p.287-296

Abstract in English:

ABSTRACT.- Pilati C. & Barros C.S.L. 2007. [Experimental poisoning by Senecio brasiliensis (Asteraceae) in horses.] Intoxicação experimental por Senecio brasiliensis (Asteraceae) em eqüinos. Pesquisa Veterinária Brasileira 27(7):287-296. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Fourteen 4 to 22-year-old mixed breed horses weighing 230-475 kg were experimentally fed the dried aerial parts of Senecio brasiliensis (Spreng.) collected in its sprouting stage. A 15-year-old horse served as non-plant-fed control. Small amounts of the dried plant material were admixed in the ration given to the horses; larger amounts were grounded, admixed with water and force fed through nasogastric intubation. Liver biopsies were periodically performed in 11 horses. Nine horses died with signs or lesions of the poisoning after having received amounts of the plant corresponding to 0.87%, 1.5% (single administrations), 1.74% (two weekly administrations), 3.0% (three daily administrations), 7.42% (17 weekly administrations), 8.9% (284 daily administrations), 9.66% (82 daily administrations) and 9.30% (43 weekly administrations) of their body weight. Two horses which received amounts of the plant corresponding to 15.0% (30 and 60 daily administrations) of their body weight died during the experiments due to unrelated causes. Three horses which received amounts of the plant corresponding to 0.5% and 1.0% (single administrations), and 15.0% (240 daily administrations) of their body weight, and the control horse survived without any clinical signs. The disease induced by the plant had a clinical course of 1-30 days and was characterized by anorexia, jaundice and neurological signs of hepatic encephalopathy. Weight loss was observed in the more protracted cases. Necropsy findings included marked enhancement of the lobular pattern of the livers or those were firm and dark-red. Hemorrhages were frequent and more conspicuous on the subcutis, serosal surfaces and in the gastrointestinal mucosa. Edema occurred in the submucosa of the gastrointestinal tract and in body cavities. Histologically, the livers of horses that ingested relatively larger amounts of the plant for short periods of time had zonal coagulative necrosis and centrilobular to massive hemorrhages. Moderate to marked hepatomegalocytosis and mild to moderate fibrosis were seen in 4 horses which ingested small amounts of the plant for longer periods. Cholestasis and hemosiderosis were observed in the liver of 8 horses, neutrophilic aggregates in 6 and acidophilic intranuclear pseudo-inclusion bodies in hepatocytes of 3 horses. Changes suggestive of hepatic encephalopathy were observed in the brain of 6 horses. The earliest detected change in the liver biopsies was vacuolization of hepatocyte nuclei followed by apoptotic loss of hepatocytes, hepatomegalocytosis, infiltration of neutrophils and centrolobular necrosis. Occasionally hepatocellular acidophilic intranuclear pseudo-inclusion bodies and, in more protracted cases, slight fibrosis were seen. No changes were observed in the liver biopsies of the 3 plant-fed horses that survived, nor on the 2 horses that died of unrelated causes. The control horse had no clinical signs.

Abstract in Portuguese:

ABSTRACT.- Pilati C. & Barros C.S.L. 2007. [Experimental poisoning by Senecio brasiliensis (Asteraceae) in horses.] Intoxicação experimental por Senecio brasiliensis (Asteraceae) em eqüinos. Pesquisa Veterinária Brasileira 27(7):287-296. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Fourteen 4 to 22-year-old mixed breed horses weighing 230-475 kg were experimentally fed the dried aerial parts of Senecio brasiliensis (Spreng.) collected in its sprouting stage. A 15-year-old horse served as non-plant-fed control. Small amounts of the dried plant material were admixed in the ration given to the horses; larger amounts were grounded, admixed with water and force fed through nasogastric intubation. Liver biopsies were periodically performed in 11 horses. Nine horses died with signs or lesions of the poisoning after having received amounts of the plant corresponding to 0.87%, 1.5% (single administrations), 1.74% (two weekly administrations), 3.0% (three daily administrations), 7.42% (17 weekly administrations), 8.9% (284 daily administrations), 9.66% (82 daily administrations) and 9.30% (43 weekly administrations) of their body weight. Two horses which received amounts of the plant corresponding to 15.0% (30 and 60 daily administrations) of their body weight died during the experiments due to unrelated causes. Three horses which received amounts of the plant corresponding to 0.5% and 1.0% (single administrations), and 15.0% (240 daily administrations) of their body weight, and the control horse survived without any clinical signs. The disease induced by the plant had a clinical course of 1-30 days and was characterized by anorexia, jaundice and neurological signs of hepatic encephalopathy. Weight loss was observed in the more protracted cases. Necropsy findings included marked enhancement of the lobular pattern of the livers or those were firm and dark-red. Hemorrhages were frequent and more conspicuous on the subcutis, serosal surfaces and in the gastrointestinal mucosa. Edema occurred in the submucosa of the gastrointestinal tract and in body cavities. Histologically, the livers of horses that ingested relatively larger amounts of the plant for short periods of time had zonal coagulative necrosis and centrilobular to massive hemorrhages. Moderate to marked hepatomegalocytosis and mild to moderate fibrosis were seen in 4 horses which ingested small amounts of the plant for longer periods. Cholestasis and hemosiderosis were observed in the liver of 8 horses, neutrophilic aggregates in 6 and acidophilic intranuclear pseudo-inclusion bodies in hepatocytes of 3 horses. Changes suggestive of hepatic encephalopathy were observed in the brain of 6 horses. The earliest detected change in the liver biopsies was vacuolization of hepatocyte nuclei followed by apoptotic loss of hepatocytes, hepatomegalocytosis, infiltration of neutrophils and centrolobular necrosis. Occasionally hepatocellular acidophilic intranuclear pseudo-inclusion bodies and, in more protracted cases, slight fibrosis were seen. No changes were observed in the liver biopsies of the 3 plant-fed horses that survived, nor on the 2 horses that died of unrelated causes. The control horse had no clinical signs.


#269 - Aspectos clinicopatológicos de 620 casos neurológicos de cinomose em cães, 215-220

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. [Clinicopathological features in 620 neurological cases of canine distemper.] Aspectos clinicopatológicos de 620 casos neurológicos de cinomose em cães. Pesquisa Veterinária Brasileira 27(5):215-220. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The files of 5,361 necropsies performed in dogs in the Veterinary Pathology Laboratory of the Federal University of Santa Maria during 1965-2006 were reviewed in search of cases of canine distemper. Six hundred and eighty three cases (12.7%) of the disease were found, 620 of which had neurological signs. From those 620, the following data on each case were retrieved: age, clinical signs, histopathology and concomitance or not of another disease. Age groups were classified as puppies (up to 1 year of age), adults (from 1 to 9 years) and aged (from 10 years on). In 565 out of the 620 (91.1%) neurological cases of canine distemper, histopathological brain changes were observed and in 554 of those 565 the age was registered in the files with following age group distribution: 45.9% of puppies, 51.4% of adults, and 2.7% of aged dogs. Neurological clinical signs encompassed a large spectrum of motor, postural and behavioral disturbances which could occur together or individually. Most frequent clinical signs were myoclonus (38.4%), motor incoordination (25.0%), seizures (18.5%), and paraplegia (13.4%). In 98.4% of the 565 dogs with histopathological changes in the brain demyelination, non-suppurative encephalitis or a combination of these two were found. Intranuclear eosinophilic inclusion bodies were observed in different brain cells of 343 of the 565 dogs with histopathological changes. In 170 (49.6%) the cellular type bearing the inclusions was not mentioned in the file and in the remaining cases the inclusions were seen in astrocytes (94.8% of the cases), neurons (3.5%), oligodendrocytes (1.1%), and ependyma cells (0.6%). Taking in consideration the type of lesions and the age groups, cases with combined demyelination and non-suppurative encephalitis occurred in 40.0% of the puppies, 51.2% of the adult dogs and 72.7% of the aged dogs. Demyelination alone occurred in 48.4% of the puppies, 41.3% of the adults and in 35.7% of the aged dogs. Non-suppurative encephalitis alone occurred 11.6% of the puppies, 7.5% of the adults and in 7.1% of the aged dogs.

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. [Clinicopathological features in 620 neurological cases of canine distemper.] Aspectos clinicopatológicos de 620 casos neurológicos de cinomose em cães. Pesquisa Veterinária Brasileira 27(5):215-220. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br The files of 5,361 necropsies performed in dogs in the Veterinary Pathology Laboratory of the Federal University of Santa Maria during 1965-2006 were reviewed in search of cases of canine distemper. Six hundred and eighty three cases (12.7%) of the disease were found, 620 of which had neurological signs. From those 620, the following data on each case were retrieved: age, clinical signs, histopathology and concomitance or not of another disease. Age groups were classified as puppies (up to 1 year of age), adults (from 1 to 9 years) and aged (from 10 years on). In 565 out of the 620 (91.1%) neurological cases of canine distemper, histopathological brain changes were observed and in 554 of those 565 the age was registered in the files with following age group distribution: 45.9% of puppies, 51.4% of adults, and 2.7% of aged dogs. Neurological clinical signs encompassed a large spectrum of motor, postural and behavioral disturbances which could occur together or individually. Most frequent clinical signs were myoclonus (38.4%), motor incoordination (25.0%), seizures (18.5%), and paraplegia (13.4%). In 98.4% of the 565 dogs with histopathological changes in the brain demyelination, non-suppurative encephalitis or a combination of these two were found. Intranuclear eosinophilic inclusion bodies were observed in different brain cells of 343 of the 565 dogs with histopathological changes. In 170 (49.6%) the cellular type bearing the inclusions was not mentioned in the file and in the remaining cases the inclusions were seen in astrocytes (94.8% of the cases), neurons (3.5%), oligodendrocytes (1.1%), and ependyma cells (0.6%). Taking in consideration the type of lesions and the age groups, cases with combined demyelination and non-suppurative encephalitis occurred in 40.0% of the puppies, 51.2% of the adult dogs and 72.7% of the aged dogs. Demyelination alone occurred in 48.4% of the puppies, 41.3% of the adults and in 35.7% of the aged dogs. Non-suppurative encephalitis alone occurred 11.6% of the puppies, 7.5% of the adults and in 7.1% of the aged dogs.


#270 - Epidemiologia e sinais clínicos da conidiobolomicose em ovinos no Estado do Piauí, p.184-190

Abstract in English:

ABSTRACT.- Silva S.M.M.S., Castro R.S., Costa F.A.L., Vasconcelos A.C., Batista M.C.S., Riet-Correa F. & Carvalho E.M.S. 2007. [Epidemiology and symptoms of conidiobolomycosis in sheep in the State of Piauí, Brazil.] Epidemiologia e sinais clínicos da conidiobolomicose em ovinos no Estado do Piauí. Pesquisa Veterinária Brasileira 27(4):184-190. Departamento de Clínica e Cirurgia, Centro de Ciências Agrárias, Universidade Federal do Piauí, Campus da Socopo s/n, Teresina, PI 64049-550, Brazil. E-mail: silvanammss@ufpi.br Conidiobolomycosis is reported in 25 farms, from January 2002 to December 2004, in the state of Piauí. The disease affects only sheep, mainly in April-June. The mean morbidity rate was 2.80%, but was higher in the first semester (2.1%), during the raining period, than in the second one (0.69%), during the dry period. Morbidity rate among flocks varied from 0.1-14.3%. Case fatality rate was 100%, and the clinical manifestation period varied from 1-5 weeks. Clinical signs were serous, mucous and/or bloody nasal secretion, respiratory distress, snoring respiration, cranium-facial asymmetry, exophthalmia, fever and progressive emaciation. Marked depression, sometimes with the head down or head pressing was observed in some cases. Gross, microscopic and ultrastructural lesions and identification of the agent are reported elsewhere. This is the first report of conidiobolomycosis in Brazil, which is endemic and has a high frequency in sheep in the State of Piauí, associated with high rainfalls (1000-1600mm annually) and high temperature (19-36°C).

Abstract in Portuguese:

ABSTRACT.- Silva S.M.M.S., Castro R.S., Costa F.A.L., Vasconcelos A.C., Batista M.C.S., Riet-Correa F. & Carvalho E.M.S. 2007. [Epidemiology and symptoms of conidiobolomycosis in sheep in the State of Piauí, Brazil.] Epidemiologia e sinais clínicos da conidiobolomicose em ovinos no Estado do Piauí. Pesquisa Veterinária Brasileira 27(4):184-190. Departamento de Clínica e Cirurgia, Centro de Ciências Agrárias, Universidade Federal do Piauí, Campus da Socopo s/n, Teresina, PI 64049-550, Brazil. E-mail: silvanammss@ufpi.br Conidiobolomycosis is reported in 25 farms, from January 2002 to December 2004, in the state of Piauí. The disease affects only sheep, mainly in April-June. The mean morbidity rate was 2.80%, but was higher in the first semester (2.1%), during the raining period, than in the second one (0.69%), during the dry period. Morbidity rate among flocks varied from 0.1-14.3%. Case fatality rate was 100%, and the clinical manifestation period varied from 1-5 weeks. Clinical signs were serous, mucous and/or bloody nasal secretion, respiratory distress, snoring respiration, cranium-facial asymmetry, exophthalmia, fever and progressive emaciation. Marked depression, sometimes with the head down or head pressing was observed in some cases. Gross, microscopic and ultrastructural lesions and identification of the agent are reported elsewhere. This is the first report of conidiobolomycosis in Brazil, which is endemic and has a high frequency in sheep in the State of Piauí, associated with high rainfalls (1000-1600mm annually) and high temperature (19-36°C).


Colégio Brasileiro de Patologia Animal SciELO Brasil CAPES CNPQ UNB UFRRJ CFMV