PESQUISA VETERINÁRIA BRASILEIRA

Abstract in English:

ABSTRACT.- Batista J.S., Bezerra F.S.B., Lira R.A., Carvalho J.R.G., Rosado Neto A.M., Petri A.A. & Teixeira M.M.G. 2008. [Clinical, epidemiological and pathological signs of natural infection in cattle by Trypanosoma vivax in Paraíba, Brazil.] Aspectos clínicos, epidemiológicos e patológicos da infecção natural em bovinos por Trypanosoma vivax na Paraíba. Pesquisa Veterinária Brasileira 28(1):63-69. Departamento de Ciências Animais, Universidade Federal Rural do Semi-árido, BR 110 Km 47, Caixa Postal 147, Mossoró, RN 59625-900, Brazil. E-mail: jaelsbatista@hotmail.com Two outbreaks of trypanosomiasis by Trypanosoma vivax, reported in cattle, occurred on two farms located in the state of Paraíba, northeastern Brazil. The epidemiology, clinical signs and pathology of the disease were studied from May 2005 to November 2006. T. vivax was identified morphologically and by polymerase chain reaction test (PCR). The affected cattle presented anorexia, depression, fever, anemia, weight loss, reduction in milk production, transitory blindness, abortion and some nervous signs as nystagmus, tetany and bruxism. All cattle that presented nervous signs died. Necropsy findings were enlarged lymph and spleen, serous atrophy of the fat depots, proeminence of the splenic white pulp, hydropericardium and pericardial petechiae and ecchymoses on the epicardium. Histologically there was meningoencephalitis. The treatment of the clinical cases with diminazena aceturate was efficient with clearance of the parasite from the blood or disappearance of clinical signs in up to 2 months after the beginning of the outbreak on the two farms studied. The epidemiologic factors favoring the occurrence of the outbreak were the abundance of mechanical vectors, as tabanids and Stomoxys sp., and the introduction into the herd of cattle from farms where the disease occurred. It is suggested that the semiarid of the Brazilian Northeast is an enzootic instability region for trypanosomiasis due to its prolonged periods of drought and high temperatures, constituting during most part of the year an unfavorable environment for the development of vectors.

• Trypanosoma vivax trypanosomiasis cattle outbreak Brazilian Northeast semi-arid

Abstract in Portuguese:

ABSTRACT.- Batista J.S., Bezerra F.S.B., Lira R.A., Carvalho J.R.G., Rosado Neto A.M., Petri A.A. & Teixeira M.M.G. 2008. [Clinical, epidemiological and pathological signs of natural infection in cattle by Trypanosoma vivax in Paraíba, Brazil.] Aspectos clínicos, epidemiológicos e patológicos da infecção natural em bovinos por Trypanosoma vivax na Paraíba. Pesquisa Veterinária Brasileira 28(1):63-69. Departamento de Ciências Animais, Universidade Federal Rural do Semi-árido, BR 110 Km 47, Caixa Postal 147, Mossoró, RN 59625-900, Brazil. E-mail: jaelsbatista@hotmail.com Two outbreaks of trypanosomiasis by Trypanosoma vivax, reported in cattle, occurred on two farms located in the state of Paraíba, northeastern Brazil. The epidemiology, clinical signs and pathology of the disease were studied from May 2005 to November 2006. T. vivax was identified morphologically and by polymerase chain reaction test (PCR). The affected cattle presented anorexia, depression, fever, anemia, weight loss, reduction in milk production, transitory blindness, abortion and some nervous signs as nystagmus, tetany and bruxism. All cattle that presented nervous signs died. Necropsy findings were enlarged lymph and spleen, serous atrophy of the fat depots, proeminence of the splenic white pulp, hydropericardium and pericardial petechiae and ecchymoses on the epicardium. Histologically there was meningoencephalitis. The treatment of the clinical cases with diminazena aceturate was efficient with clearance of the parasite from the blood or disappearance of clinical signs in up to 2 months after the beginning of the outbreak on the two farms studied. The epidemiologic factors favoring the occurrence of the outbreak were the abundance of mechanical vectors, as tabanids and Stomoxys sp., and the introduction into the herd of cattle from farms where the disease occurred. It is suggested that the semiarid of the Brazilian Northeast is an enzootic instability region for trypanosomiasis due to its prolonged periods of drought and high temperatures, constituting during most part of the year an unfavorable environment for the development of vectors.

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.- David N., Hubner S.O., Riet-Correa F., Halfen D. & Lemos R.A. 2007. Reactivation of latent bovine herpesvirus type 5 in cattle with polioencephalomalacia induced by ammonium sulphate. Pesquisa Veterinária Brasileira 27(10):435-441. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br In the state Mato Grosso do Sul, Brazil, outbreaks of meningoencephalitis by BoHV-5 and polioencephalomalacia (PEM) display similar epidemiological features, suggesting that meningoencephalitis may be associated with reactivation of a latent BoHV-5 infection, during the development of PEM. To test this hypothesis, four 7-8 months old steers negative for BoHV-5 antibodies were inoculated intranasally with BoHV-5 and received amprolium from day 35 to day 105 after inoculation. Because PEM was not produced during this period, ammonium sulphate was given from day 114 to day 180 after inoculation. Two uninfected control steers received amprolium and ammonium sulphate for the same periods. All inoculated cattle developed antibodies against BoHV-5 after inoculation and the virus was isolated from nasal swabs, indicating that they were infected. Two inoculated steers had clinical signs of PEM after 118 and 146 days after virus inoculation. One was euthanized after a clinical manifestation period of seven days and had severe lesions of PEM and meningoencephalitis. BoHV-5 was isolated from the central nervous system of this animal. The other animal recovered but continued to manifest chronic signs of PEM and was euthanatized. On histological examination, the cerebral cortex, caudate nucleus and thalamus had multifocal areas of malacia and mild meningoencephalitis of the cortex. BoHV-5 was not isolated from the brain. One uninfected control steer had signs of neurological disease on day 158 and had lesions of PEM without meningoencephalitis at necropsy. The simultaneous production of PEM and diffuse meningoencephalitis, with isolation of BoHV-5, in one steer treated with ammonium sulphate, 118 days after BoHV-5 inoculation, suggests that latent BoHV-5 was reactivated in this animal submitted to experimental induction of PEM.

• Polioencephalomalacia bovine herpesvirus type 5 viral reactivation cattle

Abstract in Portuguese:

ABSTRACT.- David N., Hubner S.O., Riet-Correa F., Halfen D. & Lemos R.A. 2007. Reactivation of latent bovine herpesvirus type 5 in cattle with polioencephalomalacia induced by ammonium sulphate. Pesquisa Veterinária Brasileira 27(10):435-441. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br In the state Mato Grosso do Sul, Brazil, outbreaks of meningoencephalitis by BoHV-5 and polioencephalomalacia (PEM) display similar epidemiological features, suggesting that meningoencephalitis may be associated with reactivation of a latent BoHV-5 infection, during the development of PEM. To test this hypothesis, four 7-8 months old steers negative for BoHV-5 antibodies were inoculated intranasally with BoHV-5 and received amprolium from day 35 to day 105 after inoculation. Because PEM was not produced during this period, ammonium sulphate was given from day 114 to day 180 after inoculation. Two uninfected control steers received amprolium and ammonium sulphate for the same periods. All inoculated cattle developed antibodies against BoHV-5 after inoculation and the virus was isolated from nasal swabs, indicating that they were infected. Two inoculated steers had clinical signs of PEM after 118 and 146 days after virus inoculation. One was euthanized after a clinical manifestation period of seven days and had severe lesions of PEM and meningoencephalitis. BoHV-5 was isolated from the central nervous system of this animal. The other animal recovered but continued to manifest chronic signs of PEM and was euthanatized. On histological examination, the cerebral cortex, caudate nucleus and thalamus had multifocal areas of malacia and mild meningoencephalitis of the cortex. BoHV-5 was not isolated from the brain. One uninfected control steer had signs of neurological disease on day 158 and had lesions of PEM without meningoencephalitis at necropsy. The simultaneous production of PEM and diffuse meningoencephalitis, with isolation of BoHV-5, in one steer treated with ammonium sulphate, 118 days after BoHV-5 inoculation, suggests that latent BoHV-5 was reactivated in this animal submitted to experimental induction of PEM.

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.- 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.

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.

• Poisonous plants epidemiology cattle diseases

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.

Abstract in English:

ABSTRACT.- Schons S.V., Kommers G.D., Pereira G.M., Raffi M.B. & Schild A.L. 2007. [Microscopic, immunohistochemical, and ultra-structural study of the lesions experimentaly induced by Ramaria flavo-brunnescens (Clavariaceae) in cattle.] Estudo histológico, imuno-histoquímico e ultra-estrutural das lesões induzidas experimentalmente por Ramaria flavo-brunnescens (Clavariaceae) em bovinos. Pesquisa Veterinária Brasileira 27(7):269-276. Laboratório Regional de Diagnóstico, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The objective of this study was to investigate the pathogenesis of the lesions observed in cattle experimentally poisoned by Ramaria flavo-brunnescens. The mushroom was given to three 9 to10-month-old Jersey calves immediately after harvesting. Daily doses were around 20g/kg of body weight during 7 (Calf 1) or 13 days (Calves 2-3), and the total doses of mushroom given were 140, 268, and 261g/kg of body weight, respectively. One calf (Calf 4) with same age and breed was used as control. Clinical signs were characterized by prostration, anorexia, hyperemia of oral mucosa, and loosening of long hairs of the tail tip under mild traction. The calves were submitted to euthanasia and necropsied on days 8 (Calf 1) and 15 (Calves 2-4) after the beginning of the experiment. Microscopically, there was smoothness of dorsal epithelium of tongue with absence of filiform papillae, vacuolation of keratinocytes, and loosening of the keratin layer. In the hooves, there was vacuolation and irregular keratinization of the laminar epidermis and hyperplasia of keratinocytes. Hyperkeratosis, vacuolation of the external root sheath, thickening of tricholemal keratin, and inflammatory infiltration around hair follicles were observed on the skin of the tail tip. Immunohistochemical results with anti-pancytoceratin and anti-Ki67 (cell proliferation marker) antibodies showed no differences between the tongue dorsal epithelium of the control and experimental calves. Ultrastructural study demonstrated decrease in tonofilaments and increased intercellular spaces of the spinous layer of the tongue dorsal epithelium. The results of this study favor the hypothesis of an interference with the epithelial keratinization mechanisms by the toxic principles of Ramaria flavo-brunnescens.

• Ramaria flavo-brunnecens mushroom poisoning cattle diseases pathology

Abstract in Portuguese:

ABSTRACT.- Schons S.V., Kommers G.D., Pereira G.M., Raffi M.B. & Schild A.L. 2007. [Microscopic, immunohistochemical, and ultra-structural study of the lesions experimentaly induced by Ramaria flavo-brunnescens (Clavariaceae) in cattle.] Estudo histológico, imuno-histoquímico e ultra-estrutural das lesões induzidas experimentalmente por Ramaria flavo-brunnescens (Clavariaceae) em bovinos. Pesquisa Veterinária Brasileira 27(7):269-276. Laboratório Regional de Diagnóstico, Universidade Federal de Pelotas, Campus Universitário s/n, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The objective of this study was to investigate the pathogenesis of the lesions observed in cattle experimentally poisoned by Ramaria flavo-brunnescens. The mushroom was given to three 9 to10-month-old Jersey calves immediately after harvesting. Daily doses were around 20g/kg of body weight during 7 (Calf 1) or 13 days (Calves 2-3), and the total doses of mushroom given were 140, 268, and 261g/kg of body weight, respectively. One calf (Calf 4) with same age and breed was used as control. Clinical signs were characterized by prostration, anorexia, hyperemia of oral mucosa, and loosening of long hairs of the tail tip under mild traction. The calves were submitted to euthanasia and necropsied on days 8 (Calf 1) and 15 (Calves 2-4) after the beginning of the experiment. Microscopically, there was smoothness of dorsal epithelium of tongue with absence of filiform papillae, vacuolation of keratinocytes, and loosening of the keratin layer. In the hooves, there was vacuolation and irregular keratinization of the laminar epidermis and hyperplasia of keratinocytes. Hyperkeratosis, vacuolation of the external root sheath, thickening of tricholemal keratin, and inflammatory infiltration around hair follicles were observed on the skin of the tail tip. Immunohistochemical results with anti-pancytoceratin and anti-Ki67 (cell proliferation marker) antibodies showed no differences between the tongue dorsal epithelium of the control and experimental calves. Ultrastructural study demonstrated decrease in tonofilaments and increased intercellular spaces of the spinous layer of the tongue dorsal epithelium. The results of this study favor the hypothesis of an interference with the epithelial keratinization mechanisms by the toxic principles of Ramaria flavo-brunnescens.

Abstract in English:

ABSTRACT.- Macêdo J.T.S.A., Riet-Correa F., Simões S.V.D., Dantas A.F.M. & Nobre V.M.T. 2007. [Malignant catarrhal fever in cattle in Paraíba, northeastern Brazil.] Febre catarral maligna em bovinos na Paraíba. Pesquisa Veterinária Brasileira 27(7):277-281. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br Six cases of malignant catarrhal fever (MCF) observed from 2000 to 2005, and one outbreak occurred from 1986 to 1987 are reported in the state of Paraíba, northeastern Brazil. In one case the disease was diagnosed clinically and in 5 cases also by histopathology consisting of diffuse vasculitis with fibrinoid degeneration and perivascular infiltration of mononuclear cells in many organs. In 5 cases only one cattle was affected, and in one, 2 out of 6 cattle were affected. Five cases occurred from May to August, at the end of the raining season during the lambing season. Clinical signs and pathology were characteristics of the disease. Four cattle died after a clinical manifestation period of 5-8 days, another was euthanized after 40 days, and another recovered. The outbreak reported in the municipality of Taperoá occurred from August 1986 to December 1987, with a morbidity rate of 8.22% and a fatality rate of 100%. The disease occurred after the introduction of a ram in the farm. The outbreak was controlled after the slaughter of all sheep in the farm. These results demonstrated that MCF is endemic in Paraíba, and outbreaks with high morbidity and fatality rates can also occur. As it was previously reported in the state of Rio Grande do Sul few affected cattle can recovered. Because the 6 cases of MCF represent 3.1% of the 190 cases of different diseases diagnosed by the Veterinary Hospital from 2000 to 2005, it can be estimated that the disease affects 0.125% of cattle population in the state of Paraíba.

• Malignant catarrhal fever vasculitis diseases of cattle viral diseases semiarid

Abstract in Portuguese:

ABSTRACT.- Macêdo J.T.S.A., Riet-Correa F., Simões S.V.D., Dantas A.F.M. & Nobre V.M.T. 2007. [Malignant catarrhal fever in cattle in Paraíba, northeastern Brazil.] Febre catarral maligna em bovinos na Paraíba. Pesquisa Veterinária Brasileira 27(7):277-281. Hospital Veterinário, CSTR, Universidade Federal de Campina Grande, Campus de Patos, 58700-000 Patos, PB, Brazil. E-mail: franklin.riet@pesquisador.cnpq.br Six cases of malignant catarrhal fever (MCF) observed from 2000 to 2005, and one outbreak occurred from 1986 to 1987 are reported in the state of Paraíba, northeastern Brazil. In one case the disease was diagnosed clinically and in 5 cases also by histopathology consisting of diffuse vasculitis with fibrinoid degeneration and perivascular infiltration of mononuclear cells in many organs. In 5 cases only one cattle was affected, and in one, 2 out of 6 cattle were affected. Five cases occurred from May to August, at the end of the raining season during the lambing season. Clinical signs and pathology were characteristics of the disease. Four cattle died after a clinical manifestation period of 5-8 days, another was euthanized after 40 days, and another recovered. The outbreak reported in the municipality of Taperoá occurred from August 1986 to December 1987, with a morbidity rate of 8.22% and a fatality rate of 100%. The disease occurred after the introduction of a ram in the farm. The outbreak was controlled after the slaughter of all sheep in the farm. These results demonstrated that MCF is endemic in Paraíba, and outbreaks with high morbidity and fatality rates can also occur. As it was previously reported in the state of Rio Grande do Sul few affected cattle can recovered. Because the 6 cases of MCF represent 3.1% of the 190 cases of different diseases diagnosed by the Veterinary Hospital from 2000 to 2005, it can be estimated that the disease affects 0.125% of cattle population in the state of Paraíba.

Abstract in English:

ABSTRACT.- Rozza D.B., Corrêa A.M.R., Leal J.S., Bandarra P.M., Guagnini F.S. & Djeison Lutier Raymundo D.L. & Driemeier D. 2007. [Experimental monensin poisoning in water buffaloes (Bubalus bubalis) and cattle.] Intoxicação experimental por monensina em búfalos e bovinos. Pesquisa Veterinária Brasileira 27(4):172-178. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Monensin is widely used as a feed additive to improve performance of livestock; however accidental poisoning by this ionophore compound has been reported in a number of animal species. Typical clinical signs and lesions of monensin poisoning were induced in water buffaloes dosed with single dosages of 15, 10, 7.5, and 5mg/kg of the compound. Only buffaloes dosed with 2.5 mg/kg (1 day) and 1mg/kg (7 days) survived. Clinical signs initiated about 6 h post-dosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the principal histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. In addition, this communication presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as health monitoring tools in the management of buffalo herds supplemented with monensin.

• Buffaloes cattle CK levels degenerative myopathy monensin toxicity monensin tolerance

Abstract in Portuguese:

ABSTRACT.- Rozza D.B., Corrêa A.M.R., Leal J.S., Bandarra P.M., Guagnini F.S. & Djeison Lutier Raymundo D.L. & Driemeier D. 2007. [Experimental monensin poisoning in water buffaloes (Bubalus bubalis) and cattle.] Intoxicação experimental por monensina em búfalos e bovinos. Pesquisa Veterinária Brasileira 27(4):172-178. Departamento de Patologia Clínica Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Monensin is widely used as a feed additive to improve performance of livestock; however accidental poisoning by this ionophore compound has been reported in a number of animal species. Typical clinical signs and lesions of monensin poisoning were induced in water buffaloes dosed with single dosages of 15, 10, 7.5, and 5mg/kg of the compound. Only buffaloes dosed with 2.5 mg/kg (1 day) and 1mg/kg (7 days) survived. Clinical signs initiated about 6 h post-dosing and included apathy, anorexia, diarrhea, drooling, muscular weakness, locomotion disorders, dyspnea, tachycardia, jugular distension and pulse, recumbency and death. The creatine kinase (CK) levels were highly augmented in blood samples of buffaloes dosed with monensin. Most prominent gross changes were ascites, hydrothorax, hydropericardium, cardiomegaly, hepatomegaly, and focal pale areas in the myocardium and in skeletal muscles. Degeneration and necrosis of myofibers were the principal histopathological findings. Conversely, no evidence of disease, neither change in CK levels were observed in the beef cattle steers dosed with same doses, confirming preliminary findings that buffaloes are more susceptible to monensin than cattle. In addition, this communication presents the minimal toxic dosage of monensin to buffaloes and suggests that CK tests may serve as health monitoring tools in the management of buffalo herds supplemented with monensin.

Abstract in English:

ABSTRACT.- Pissinatti T.A., Pissinatti A. & Burity C.H.F. 2007. Myocardial stereology in captive Callithrix kuhlii (Callitrichidae, Primates): healthy animals versus animals affected by wasting marmoset syndrome (WMS). Pesquisa Veterinária Brasileira 27(2):75-79. Setor de Morfologia, IBC, Universidade do Grande Rio (Unigranrio), Rua Prof. José de Souza Herdy 1160, uque de Caxias, RJ 25071-202, Brazil. E-mail: cburity@unigranrio.com.br This study comprised 12 hearts of Wied´s black-tufted-ear marmoset, Callithrix kuhlii (Coimbra-Filho 1985), 6 with Wasting Marmoset Syndrome (WMS) and 6 non-affected. Biometry was performed after death. After necropsy, the hearts were weighed, dissected, fixed in 10% formalin solution (pH 7.2), and processed for optical microscopy at 5µm sections stained with Haematoxylin-Eosin. Quantitative analysis was performed by stereological techniques. The statistical differences between the biometrical and stereological parameters were assessed by the Mann-Whitney test. The morphometric results showed that WMS causes a significant reduction in body and cardiac weights, and also in the volume density of vessels in those animals. Further studies are necessary to understand some of the results shown here.

• Wasting marmoset syndrome myocardium stereology Callithrix Callitrichidae

Abstract in Portuguese:

ABSTRACT.- Pissinatti T.A., Pissinatti A. & Burity C.H.F. 2007. Myocardial stereology in captive Callithrix kuhlii (Callitrichidae, Primates): healthy animals versus animals affected by wasting marmoset syndrome (WMS). Pesquisa Veterinária Brasileira 27(2):75-79. Setor de Morfologia, IBC, Universidade do Grande Rio (Unigranrio), Rua Prof. José de Souza Herdy 1160, uque de Caxias, RJ 25071-202, Brazil. E-mail: cburity@unigranrio.com.br This study comprised 12 hearts of Wied´s black-tufted-ear marmoset, Callithrix kuhlii (Coimbra-Filho 1985), 6 with Wasting Marmoset Syndrome (WMS) and 6 non-affected. Biometry was performed after death. After necropsy, the hearts were weighed, dissected, fixed in 10% formalin solution (pH 7.2), and processed for optical microscopy at 5µm sections stained with Haematoxylin-Eosin. Quantitative analysis was performed by stereological techniques. The statistical differences between the biometrical and stereological parameters were assessed by the Mann-Whitney test. The morphometric results showed that WMS causes a significant reduction in body and cardiac weights, and also in the volume density of vessels in those animals. Further studies are necessary to understand some of the results shown here.