PESQUISA VETERINÁRIA BRASILEIRA

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.- 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.- Pescador C.A., Oliveira E.C., Pedroso P.M.O., Bandarra P.M., Okuda L.H., Corbellini L.G. & Driemeier D. 2007. [Reproductive losses linked to Toxoplasma gondii infection in goats in southern Brazil.] Perdas reprodutivas associadas com infecção por Toxoplasma gondii em caprinos no sul do Brasil. Pesquisa Veterinária Brasileira 27(4):167-171. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Toxoplasma gondii was implicated with reproductive losses in a goat herd in Rio Grande do Sul, Brazil. Gross changes were present in 2 out of 6 fetuses/offsprings submitted for diagnosis and included enlarged, pale mesenteric lymph nodes, and edematous, mottled red and tan lungs. Microscopic changes were observed in most fetuses and were especially characterized by lymphoplasmacytic infiltration in the brain and lungs. Other histological changes included lymphoplasmacytic interstitial nephritis, necrotizing lymphadenitis and periportal lympho-plasmacytic cell infiltrates. While bacteriological and direct immunofluorescent antibody tests for Leptospira sp. were negative in samples from all cases, immunohistochemical and PCR procedures for Toxoplasma gondii reacted positively in most of them. Antibody titles against T. gondii varying from 1:512 to 1:2048 were detected in serum samples from the mother goats of these aborted (1), stillborn (3) or dead newborn (2) kids. This paper describes the clinical, pathological, serological, molecular and immunohistochemical findings of a Toxoplasma gondii-infected goat flock.

• Abortion goat reproductive losses stillborn Toxoplasma gondii

Abstract in Portuguese:

ABSTRACT.- Pescador C.A., Oliveira E.C., Pedroso P.M.O., Bandarra P.M., Okuda L.H., Corbellini L.G. & Driemeier D. 2007. [Reproductive losses linked to Toxoplasma gondii infection in goats in southern Brazil.] Perdas reprodutivas associadas com infecção por Toxoplasma gondii em caprinos no sul do Brasil. Pesquisa Veterinária Brasileira 27(4):167-171. Departamento de Patologia Clínica Veterinária, Faculdade de Veterinária, Universidade Federal do Rio Grande do Sul, Av. Bento Gonçalves 9090, Porto Alegre, RS 91540-000, Brazil. E-mail: davetpat@ufrgs.br Toxoplasma gondii was implicated with reproductive losses in a goat herd in Rio Grande do Sul, Brazil. Gross changes were present in 2 out of 6 fetuses/offsprings submitted for diagnosis and included enlarged, pale mesenteric lymph nodes, and edematous, mottled red and tan lungs. Microscopic changes were observed in most fetuses and were especially characterized by lymphoplasmacytic infiltration in the brain and lungs. Other histological changes included lymphoplasmacytic interstitial nephritis, necrotizing lymphadenitis and periportal lympho-plasmacytic cell infiltrates. While bacteriological and direct immunofluorescent antibody tests for Leptospira sp. were negative in samples from all cases, immunohistochemical and PCR procedures for Toxoplasma gondii reacted positively in most of them. Antibody titles against T. gondii varying from 1:512 to 1:2048 were detected in serum samples from the mother goats of these aborted (1), stillborn (3) or dead newborn (2) kids. This paper describes the clinical, pathological, serological, molecular and immunohistochemical findings of a Toxoplasma gondii-infected goat flock.

Abstract in English:

ABSTRACT.- Domingues-F.L.M., Ferreira J., Lopes F.M., Tymoszczenko A. & Gioso M.A. 2007. The effect of timing temporary cements to treat induced pulp necrosis in the teeth of dogs. Revista Pesquisa Veterinária Brasileira 27(2):85-88. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando de Marques de Paiva 87, Bloco 8-superior, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: lesliedf@usp.br During endodontic therapy (pulpectomy, root canal debridement and root canal filling) microbiological management is a major concern. Bacteria present in dentine tubules, apical foramina and apical delta are causally related to failure of the procedure. Studies have shown that during single session endodontic treatment bacteria remain within dental structures. The aim of the present study was to evaluate endodontic treatment performed as two sessions, using temporary endodontic dressing materials for different periods in four groups of experimental dogs. A total of 80 roots of second and third upper premolar teeth and second, third and fourth lower premolar teeth were divided into four groups. The pulp chamber was opened with burrs and the pulp exposed for 60 days to induce pulpal inflammation and necrosis. Groups II, III and IV were treated with calcium hydroxide plus camphorated paramono-chlorophenol (PMCC) for 7, 15 and 30 days, respectively. In all groups, the root canals were filled with zinc oxide-eugenol and gutta-percha cones. Clinical and radiographical measurements were performed every 2 weeks. After 60 days a small block section containing the teeth, surrounding periapical tissues and the periodontium was removed for histological and microbiological study. Histological analysis revealed intense inflammatory response in all groups. Microbiological analysis showed microbial reduction inversely proportional to the period of time that the intracanal temporary medicament was left in place.

• Apical delta endodontic gutta-percha camphorated paramonochlorophenol microorganisms dogs

Abstract in Portuguese:

ABSTRACT.- Domingues-F.L.M., Ferreira J., Lopes F.M., Tymoszczenko A. & Gioso M.A. 2007. The effect of timing temporary cements to treat induced pulp necrosis in the teeth of dogs. Revista Pesquisa Veterinária Brasileira 27(2):85-88. Departamento de Cirurgia, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando de Marques de Paiva 87, Bloco 8-superior, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: lesliedf@usp.br During endodontic therapy (pulpectomy, root canal debridement and root canal filling) microbiological management is a major concern. Bacteria present in dentine tubules, apical foramina and apical delta are causally related to failure of the procedure. Studies have shown that during single session endodontic treatment bacteria remain within dental structures. The aim of the present study was to evaluate endodontic treatment performed as two sessions, using temporary endodontic dressing materials for different periods in four groups of experimental dogs. A total of 80 roots of second and third upper premolar teeth and second, third and fourth lower premolar teeth were divided into four groups. The pulp chamber was opened with burrs and the pulp exposed for 60 days to induce pulpal inflammation and necrosis. Groups II, III and IV were treated with calcium hydroxide plus camphorated paramono-chlorophenol (PMCC) for 7, 15 and 30 days, respectively. In all groups, the root canals were filled with zinc oxide-eugenol and gutta-percha cones. Clinical and radiographical measurements were performed every 2 weeks. After 60 days a small block section containing the teeth, surrounding periapical tissues and the periodontium was removed for histological and microbiological study. Histological analysis revealed intense inflammatory response in all groups. Microbiological analysis showed microbial reduction inversely proportional to the period of time that the intracanal temporary medicament was left in place.

Abstract in English:

ABSTRACT.- Cortez A., Heinemann M.B., Castro A.M.M.G., Soares M.S, Pinto A.M.V., Alfieri A.A., Flores E.F., Leite R.C. & Richtzenhain L.J. 2006. Genetic characterization of Brazilian bovine viral diarrhea virus isolates by partial nucleotide sequencing of the 5’-UTR region. Pesquisa Veterinária Brasileira 26(4):211-216. Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: leonardo@usp.br Nineteen isolates of bovine viral diarrhea virus (BVDV) from Brazil were genetically characterized through partial nucleotide sequencing and analysis of the 5’UTR region. The isolates were grouped as BVDV-1 (11/19), BVDV-2 (6/19) or “atypical” pestivirus (2/19). Among the BVDV-1, eight isolates were classified as subgenotype BVDV-1a, whereas most (4 out of 6) BVDV-2 belonged to subgenotype 2b. Two isolates from aborted fetuses were not classified into any genetic group, being considered atypical BVDVs. Genetic diversity among Brazilian BVDV isolates may be responsible for vaccination and diag-nostic failure and therefore may influence the control strategies for BVDV infection in the country.

• BVDV-1 BVDV-2 Pestivirus phylogenetic analysis

Abstract in Portuguese:

ABSTRACT.- Cortez A., Heinemann M.B., Castro A.M.M.G., Soares M.S, Pinto A.M.V., Alfieri A.A., Flores E.F., Leite R.C. & Richtzenhain L.J. 2006. Genetic characterization of Brazilian bovine viral diarrhea virus isolates by partial nucleotide sequencing of the 5’-UTR region. Pesquisa Veterinária Brasileira 26(4):211-216. Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof. Dr. Orlando Marques de Paiva 87, Cidade Universitária, São Paulo, SP 05508-000, Brazil. E-mail: leonardo@usp.br Nineteen isolates of bovine viral diarrhea virus (BVDV) from Brazil were genetically characterized through partial nucleotide sequencing and analysis of the 5’UTR region. The isolates were grouped as BVDV-1 (11/19), BVDV-2 (6/19) or “atypical” pestivirus (2/19). Among the BVDV-1, eight isolates were classified as subgenotype BVDV-1a, whereas most (4 out of 6) BVDV-2 belonged to subgenotype 2b. Two isolates from aborted fetuses were not classified into any genetic group, being considered atypical BVDVs. Genetic diversity among Brazilian BVDV isolates may be responsible for vaccination and diag-nostic failure and therefore may influence the control strategies for BVDV infection in the country.

Abstract in English:

Abstract.- Brocchi M., Ferreira A., Lancellotti M., Stehling E.G., Campos T.A., Nakazato G., Pestana de Castro A.F. & Silveira W.D. 2006. Typing of avian pathogenic Escherichia coli strains by REP-PCR. Pesquisa Veterinária Brasileira 26(2):69-73. Departamento de Microbiologia e Imunologia, Instituto de Biologia, Universidade de Campinas, Cx. Postal 6109, Campinas, SP 13081-862, Brazil. E-mail: wds@unicamp.br In the present study the repetitive extragenic palindromic (REP) polymerase chain reaction (PCR) technique was used to establish the clonal variability of 49 avian Escherichia coli (APEC) strains isolated from different outbreak cases of septicemia (n=24), swollen head syndrome (n=14) and omphalitis (n=11). Thirty commensal strains isolated from poultry with no signs of these illnesses were used as control strains. The purified DNA of these strains produced electrophoretic profiles ranging from 0 to 15 bands with molecular sizes varying from 100 bp to 6.1 kb, allowing the grouping of the 79 strains into a dendrogram containing 49 REP-types. Although REP-PCR showed good discriminating power it was not able to group the strains either into specific pathogenic classes or to differentiate between pathogenic and non-pathogenic strains. On the contrary, we recently demonstrated that other techniques such as ERIC-PCR and isoenzyme profiles are appropriate to discriminate between commensal and APEC strains and also to group these strains into specific pathogenic classes. In conclusion, REP-PCR seems to be a technique neither efficient nor universal for APEC strains discrimination. However, the population clonal structure obtained with the use of REP-PCR must not be ignored particularly if one takes into account that the APEC pathogenic mechanisms are not completely understood yet.

• Avian Escherichia coli typing REP-PCR.

Abstract in Portuguese:

Abstract.- Brocchi M., Ferreira A., Lancellotti M., Stehling E.G., Campos T.A., Nakazato G., Pestana de Castro A.F. & Silveira W.D. 2006. Typing of avian pathogenic Escherichia coli strains by REP-PCR. Pesquisa Veterinária Brasileira 26(2):69-73. Departamento de Microbiologia e Imunologia, Instituto de Biologia, Universidade de Campinas, Cx. Postal 6109, Campinas, SP 13081-862, Brazil. E-mail: wds@unicamp.br In the present study the repetitive extragenic palindromic (REP) polymerase chain reaction (PCR) technique was used to establish the clonal variability of 49 avian Escherichia coli (APEC) strains isolated from different outbreak cases of septicemia (n=24), swollen head syndrome (n=14) and omphalitis (n=11). Thirty commensal strains isolated from poultry with no signs of these illnesses were used as control strains. The purified DNA of these strains produced electrophoretic profiles ranging from 0 to 15 bands with molecular sizes varying from 100 bp to 6.1 kb, allowing the grouping of the 79 strains into a dendrogram containing 49 REP-types. Although REP-PCR showed good discriminating power it was not able to group the strains either into specific pathogenic classes or to differentiate between pathogenic and non-pathogenic strains. On the contrary, we recently demonstrated that other techniques such as ERIC-PCR and isoenzyme profiles are appropriate to discriminate between commensal and APEC strains and also to group these strains into specific pathogenic classes. In conclusion, REP-PCR seems to be a technique neither efficient nor universal for APEC strains discrimination. However, the population clonal structure obtained with the use of REP-PCR must not be ignored particularly if one takes into account that the APEC pathogenic mechanisms are not completely understood yet.

Abstract in English:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

• Bovine herpesvirus-5 BoHV-5 encephalitis diseases of cattle viral diseases neuropathology.

Abstract in Portuguese:

ABSTRACT.- Rissi D.R., Oliveira F.N., Rech R.R., Pierezan F., Lemos R.A.A. & Barros C.S.L. 2006. [Epidemiology, clinical signs and distribution of the encephalic lesions in cattle affected by meningoencephalitis caused by bovine herpesvirus-5.] Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5. Pesquisa Veterinária Brasileira 26(2):123-132. Departamento de Patologia, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Seven outbreaks and an isolated case of meningoencephalitis caused by bovine herpesvirus-5 (BoHV-5) in cattle in Rio Grande do Sul, Brazil, occurring in 2002-2004, are described. From a total population at risk of 1,359 cattle, 54 1-18-month-old calves from both sexes and several breeds were affected and 50 died spontaneously or were euthanatized while moribund. The highest frequency of cases was in recently weaned calves or calves submitted to other stressing factors. General rates of morbidity, mortality and lethality were respectively 3.97, 3.67 and 92.59%. Clinical courses varied from 3-10 days and included depression, nasal and ocular discharge, grinding of teeth, circling, blindness, fever, nistagmus, trembling, anorexia, dysphagia, drooling, incoordination, head pressing, rough hair coat, tachycardia, tachypnea, abdominal pain, melena, falls, recumbency, opisthotonus, convulsions and paddling. Nineteen calves were necropsied. Necropsy findings were characterized by hyperemia of leptomeninges, swollen rostral portions of the telencephalon, and flattening of frontal lobes gyri; frequently in these frontal areas there were segmental brown-yellow discoloration and softening (malacia) of the cortex. In cases with more protracted clinical courses there were extensive swelling, softening and hemorrhaging of the telencephalic frontal lobes. Microscopically, all affected cattle had a necrotizing non-suppurative meningoencephalitis with variable distribution among the 19 cases and among the various telencephalic regions of the same case. The severity of these changes were more marked, in decreasing order of intensity, in the telencephalic frontal cortex, basal ganglia (nuclei), thalamus, brain stem, parietal telencephalic cortex, occipital telencephalic cortex and cerebellum. Perivascular inflammatory infiltrate consisted predominantly of lymphocytes, plasm cells, and less frequently of neutrophils. Additional microscopic findings included variable degrees of gliosis, edema, neuronal necrosis in the telencephalic cortex characterized by shrinking and eosinophilia of perikaria and nuclear picnosis (red neuron); basophilic intranuclear inclusion bodies in astrocytes and neurons (21.05% of the cases); sattelitosis; and neuronophagia. The areas of softening in the cortical substance consisted of necrosis of the neuroctodermal elements with maintenance of mesenchymal structures (vessels and microglia), infiltrate of Gitter cells, and, in more severe cases, extensive hemorrhages. In chronic cases, only vascular structures and a few Gitter cells remained in the cortical area leaving a cavity between white matter and leptomeninges (residual lesion).

Abstract in English:

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

• Circovirus PMWS PCV2 immunohistochemistry swine.

Abstract in Portuguese:

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

Abstract in English:

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

• Meningoencephalitis polioencephalomalacia bovine herpesvirus-5 cattle.

Abstract in Portuguese:

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

Abstract in English:

Diel D.G., Fonseca E.T., Souza S.F., Mazzanti A., Bauermann F., Weiblen R. & Flores E.F. 2005. [Bovine herpesvirus 5 may use the olfactory and trigeminal pathways to invade the central nervous system of rabbits, depending upon the route of inoculation.] O Herpesvírus bovino tipo 5 (BoHV-5) pode utilizar as rotas olfatória ou trigeminal para invadir o sistema nervoso central de coelhos, dependendo da via de inoculação. Pesquisa Veterinária Brasileira 25(3):164-170. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesvirus type 5 (BoHV-5) is a major etiological agent of meningoencephalitis in cattle. Following replication in the nasal mucosa, viral invasion of the brain is thought to occur mainly by the olfactory pathway. To address the role of this pathway in the pathogenesis of neurological infection in a laboratory model, 30 days old rabbits had the main olfactory bulbs (MOBs) surgically removed and were subsequently inoculated intranasally (IN) or conjunctivally (IC) with a highly neurovirulent BoHV-5 strain (SV-507). Following IN inoculation, 10 out of 10 (100 %) control rabbits developed neurological disease. The clinical onset ranged from day 5 to 10 post-inoculation (pi, average 7.5 days); nine being euthanized in extremis and one recovering after a mild clinical course. In contrast, only one rabbit (9.1 %) of the group lacking the MOBs (n=11) developed neurological disease (onset at day 17 pi). Dexamethasone administration to the survivors (n=10) at day 50pi was followed by virus shedding in nasal and/or ocular secretions by 8 animals, demonstrating that the virus was able to reach the trigeminal ganglia (TG) during acute infection. These results demonstrate that the olfactory route provides the main, yet not the sole access to the brain of rabbits following IN inoculation. To address the role of a second pathway, groups of control (n=12) or MOB-lacking rabbits (n=12) were inoculated into the conjunctival sac (IC), following which the virus would be expected to use the ophtalmic branch of the trigeminal nerve to reach the brain. Ten control rabbits (83.3 %) developed neurological disease upon IC inoculation (onset 15.3 days [11 to 20]). Previous ablation of the MOBs did not affect the frequency and course of neurological disease: ten out of 12 rabbits (83.3 %) lacking the MOBs developed neurological disease (onset 9 to 15 dpi, average: 12.7 days) upon IC inoculation. These results demonstrate that both IN and IC routes may operate in the transport of BoHV-5 to the brain of experimentally infected rabbits, depending on the route of inoculation. IN inoculation results in a fast and efficient transport by the olfactory pathway, the trigeminal route providing an alternative, much slower and less efficient transport; IC inoculation results in efficient viral transport by the trigeminal route, yet with a delayed kinetics comparing to the transport provided by the olfactory pathway.

• Bovine herpesvirus type 5 BoHV-5 neurological infection rabbits.

Abstract in Portuguese:

Diel D.G., Fonseca E.T., Souza S.F., Mazzanti A., Bauermann F., Weiblen R. & Flores E.F. 2005. [Bovine herpesvirus 5 may use the olfactory and trigeminal pathways to invade the central nervous system of rabbits, depending upon the route of inoculation.] O Herpesvírus bovino tipo 5 (BoHV-5) pode utilizar as rotas olfatória ou trigeminal para invadir o sistema nervoso central de coelhos, dependendo da via de inoculação. Pesquisa Veterinária Brasileira 25(3):164-170. Departamento de Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: flores@ccr.ufsm.br Bovine herpesvirus type 5 (BoHV-5) is a major etiological agent of meningoencephalitis in cattle. Following replication in the nasal mucosa, viral invasion of the brain is thought to occur mainly by the olfactory pathway. To address the role of this pathway in the pathogenesis of neurological infection in a laboratory model, 30 days old rabbits had the main olfactory bulbs (MOBs) surgically removed and were subsequently inoculated intranasally (IN) or conjunctivally (IC) with a highly neurovirulent BoHV-5 strain (SV-507). Following IN inoculation, 10 out of 10 (100 %) control rabbits developed neurological disease. The clinical onset ranged from day 5 to 10 post-inoculation (pi, average 7.5 days); nine being euthanized in extremis and one recovering after a mild clinical course. In contrast, only one rabbit (9.1 %) of the group lacking the MOBs (n=11) developed neurological disease (onset at day 17 pi). Dexamethasone administration to the survivors (n=10) at day 50pi was followed by virus shedding in nasal and/or ocular secretions by 8 animals, demonstrating that the virus was able to reach the trigeminal ganglia (TG) during acute infection. These results demonstrate that the olfactory route provides the main, yet not the sole access to the brain of rabbits following IN inoculation. To address the role of a second pathway, groups of control (n=12) or MOB-lacking rabbits (n=12) were inoculated into the conjunctival sac (IC), following which the virus would be expected to use the ophtalmic branch of the trigeminal nerve to reach the brain. Ten control rabbits (83.3 %) developed neurological disease upon IC inoculation (onset 15.3 days [11 to 20]). Previous ablation of the MOBs did not affect the frequency and course of neurological disease: ten out of 12 rabbits (83.3 %) lacking the MOBs developed neurological disease (onset 9 to 15 dpi, average: 12.7 days) upon IC inoculation. These results demonstrate that both IN and IC routes may operate in the transport of BoHV-5 to the brain of experimentally infected rabbits, depending on the route of inoculation. IN inoculation results in a fast and efficient transport by the olfactory pathway, the trigeminal route providing an alternative, much slower and less efficient transport; IC inoculation results in efficient viral transport by the trigeminal route, yet with a delayed kinetics comparing to the transport provided by the olfactory pathway.