PESQUISA VETERINÁRIA BRASILEIRA

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., 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:

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

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

Abstract in Portuguese:

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

Abstract in English:

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:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

• Trypanosomiasis Trypanosoma evansi infectious diseases encephalitis hematology pathology diseases of horses.

Abstract in Portuguese:

Rodrigues A., Fighera R.A., Souza T.M., Schild A.L., Soares M.P., Milano J. & Barros C.S.L. 2005. [Outbreaks of trypanosomiasis in horses by Trypanosoma evansi in the state of Rio Grande do Sul, Brazil: epidemiological, clinical, hematological, and pathological aspects.] Surtos de tripanossomíase por Trypanosoma evansi em eqüinos no Rio Grande do Sul: aspectos epidemiológicos, clínicos, hematológicos e patológicos. Pesquisa Veterinária Brasileira 25(4):239-249. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Cases of trypanosomiasis by Trypanosoma evansi were diagnosed in horses in the state of Rio Grande do Sul, Brazil, between 2003 and 2004. In one stud farm (Farm A) with 125 horses, 52 died. Additionally, around 80 mares were sent to Farm A to be bred. Of those, 66 became ill and 56 died after being returned to their farms of origin. Twenty one horses clinically affected by the disease were observed. Clinical signs included loss of weight (despite voracious appetite), lethargy, incoordination and instability of hindlimbs, atrophy of the large muscles of the hindlimbs, muscle weakness and paleness of mucosae. Specimens of T. evansi were detected in the blood drawn from four affected horses. Normocytic normochromic anemia with PCVs ranging from 15 to 31%, leucocytosis due to lymphocytosis associated to large atypical lymphocytes was observed in several affected horses. High levels of antibodies against T. evansi were detected in the serum of six horses from Farm A. Eight horses presented encephalic neurological signs such as circling, ataxia, blindness, excitation, falls, listlessness, proprioception deficits and head tilt. One horse assumed a “dog-seating position”. Necropsy findings included muscle atrophy, enlargement and lymphoid hyperplasia of the spleen and lymphnodes, edema and softening of the white and grey matter of the brain. Histologically, an overwhelming necrotizing panencephalitis was observed in the seven horses with encephalic signs. This panencephalitis was characterized by marked edema, demyelination and necrosis and perivascular infiltrates of 6-10 layers of lymphocytes and plasm cells affecting both the white and gray matter. Several plasm cells in the inflammatory infiltrate contained numerous eosinophilic globules in their cytoplasm (Mott cells). Similar histological lesions were observed in the spinal cord of the horse with the “dog-seating position”. The brains of five horses with the encephalic signs were submitted to immunohistochemistry stain by the streptavidin-biotin technique. In all of those five brains moderate to abundant specimens of T. evansi in the perivascular spaces and neuropile were marked by the specific antibody. Epidemiological, clinical, hematological, and pathological aspects of equine trypanosomiasis caused by T. evansi are discussed.

Abstract in English:

Elias F., Schild A.L. & Riet-Correa F. 2004. [Bovine herpesvirus type-5 meningoencephalitis and malacia: histological lesions distribution in the central nervous system of naturally infected cattle.] Meningoencefalite e encefalomalacia por Herpesvírus bovino-5: distribuição das lesões no sistema nervoso central de bovinos naturalmente infectados. Pesquisa Veterinária Brasileira 24(3):123-131. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx. Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The distribution of the histological lesions in the central nervous system (CNS) of cattle naturally infected by bovine herpes virus type-5 (BHV-5) was determined in 12 affected calves from 10 outbreaks of the disease diagnosed by the Regional Diagnostic Laboratory (LRD) at Pelotas University, from 1986 to 2003. The epidemiological data, clinical signs and duration of clinical course were obtained from the files of LRD. Transversal sections were performed at different levels in 10% formalin-fixed CNS. The sections were made in the frontal, parietal, temporal e occipital lobes of the telencephalic hemispheres, basal ganglia and internal capsule, thalamus, anterior colliculus, pons, cerebellar peduncles, cerebellum, medulla oblongata and cervical spinal cord. Paraffin embedded tissues were sectioned and stained with hematoxylin and eosin. The severity and distribution of the inflammatory and malacic lesions were evaluated in all sections. These lesions were related with the epidemiological and clinical aspects of the disease. The outbreaks of the disease were observed in different seasons of the year. Affected animals were 2 to 24-month-old, of different breeds and both sexes. Gross lesions characterized by yellow and depressed areas in the cerebral cortex were observed in five calves. In two of them, similar lesions were additionally observed in thalamus, basal nuclei, and internal capsule. Congestion and multifocal hemorrhages were observed in most cases. The histological lesions were characterized by non-suppurative meningoencephalitis in all sections of CNS, but more severe in the frontal cortex. Focal or widespread malacia with infiltration of Gitter cells were observed in all sections of cerebral cortex, basal ganglia, internal capsule, and thalamus. In some cases mild malacia was also observed in the rostral colliculi, pons, medulla, cerebellum and cervical spinal cord. Intranuclear inclusion bodies were seen in all cases studied; they were frequent in regions of the cerebral cortex near mild to moderate inflammatory or malacic lesions. In two cases the inclusion bodies were also seen in the basal ganglia and thalamus. The severity of the histological lesions was not proportional with the clinical course of the disease. The presence of lesions of malacia in different regions of the CNS, an aspect not mentioned in most reports of BHV-5 infections, could be due to variable pathogenicity of different virus isolates. Alternatively, it is possible that BHV-5 encephalitis occurs due to the reactivation of the virus in cattle previously affected by polioencefalomacia; this last sequence of events was already demonstrated experimentally by our research group.

• Bovine herpesvirus type-5 BHV-5 cattle meningoencephalitis polioencephalomalacia.

Abstract in Portuguese:

Elias F., Schild A.L. & Riet-Correa F. 2004. [Bovine herpesvirus type-5 meningoencephalitis and malacia: histological lesions distribution in the central nervous system of naturally infected cattle.] Meningoencefalite e encefalomalacia por Herpesvírus bovino-5: distribuição das lesões no sistema nervoso central de bovinos naturalmente infectados. Pesquisa Veterinária Brasileira 24(3):123-131. Laboratório Regional de Diagnóstico, Faculdade de Veterinária, UFPel, Cx. Postal 354, Pelotas, RS 96010-900, Brazil. E-mail: alschild@terra.com.br The distribution of the histological lesions in the central nervous system (CNS) of cattle naturally infected by bovine herpes virus type-5 (BHV-5) was determined in 12 affected calves from 10 outbreaks of the disease diagnosed by the Regional Diagnostic Laboratory (LRD) at Pelotas University, from 1986 to 2003. The epidemiological data, clinical signs and duration of clinical course were obtained from the files of LRD. Transversal sections were performed at different levels in 10% formalin-fixed CNS. The sections were made in the frontal, parietal, temporal e occipital lobes of the telencephalic hemispheres, basal ganglia and internal capsule, thalamus, anterior colliculus, pons, cerebellar peduncles, cerebellum, medulla oblongata and cervical spinal cord. Paraffin embedded tissues were sectioned and stained with hematoxylin and eosin. The severity and distribution of the inflammatory and malacic lesions were evaluated in all sections. These lesions were related with the epidemiological and clinical aspects of the disease. The outbreaks of the disease were observed in different seasons of the year. Affected animals were 2 to 24-month-old, of different breeds and both sexes. Gross lesions characterized by yellow and depressed areas in the cerebral cortex were observed in five calves. In two of them, similar lesions were additionally observed in thalamus, basal nuclei, and internal capsule. Congestion and multifocal hemorrhages were observed in most cases. The histological lesions were characterized by non-suppurative meningoencephalitis in all sections of CNS, but more severe in the frontal cortex. Focal or widespread malacia with infiltration of Gitter cells were observed in all sections of cerebral cortex, basal ganglia, internal capsule, and thalamus. In some cases mild malacia was also observed in the rostral colliculi, pons, medulla, cerebellum and cervical spinal cord. Intranuclear inclusion bodies were seen in all cases studied; they were frequent in regions of the cerebral cortex near mild to moderate inflammatory or malacic lesions. In two cases the inclusion bodies were also seen in the basal ganglia and thalamus. The severity of the histological lesions was not proportional with the clinical course of the disease. The presence of lesions of malacia in different regions of the CNS, an aspect not mentioned in most reports of BHV-5 infections, could be due to variable pathogenicity of different virus isolates. Alternatively, it is possible that BHV-5 encephalitis occurs due to the reactivation of the virus in cattle previously affected by polioencefalomacia; this last sequence of events was already demonstrated experimentally by our research group.

Abstract in English:

Rech R.R, Fighera R.A., Oliveira F.N. & Barros C.S.L. 2004. [Granulomatous meningoencephalitis in cattle grazing vetch (Vicia spp).] Meningoencefalite granulomatosa em bovinos em pastoreio de ervilhaca (Vicia spp). Pesquisa Veterinária Brasileira 24(3): 169-172. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Granulomatous meningoencephalitis was observed in 7 out of 8 adult dairy cows affected by vetch-associated systemic granulomatous disease, although there was no neurological signs associated with the condition. The cellular inflammatory infiltrates were located in the leptomeninges and as perivascular cuffings within the brain and consisted of epithelioid macrophages, lymphocytes, plasm cells and eosinophils. These inflammatory changes varied from mild to severe from animal to animal and among different brain regions of the same animal. Perivascular cuffings were usually more marked than the leptomeningeal infiltrates. Affected brain regions, in decreasing order of intensity, included diencephalon through the level of massa intermedia, mesencephalon at the level of rostral colliculi, pons and cerebellar peduncles, medulla at the level of obex, frontal lobe at the level of the genu of the corpus callosum, and cerebellum. The character and the distribution of the inflammatory changes are emphasized regarding the differential diagnosis with other diseases and lesions of the bovine central nervous system in the context of the Brazilian surveillance program for bovine spongiform encephalopath.

• Diseases of cattle diseases of the central nervous system meningoencephalitis plant poisoning Vicia spp pathology.

Abstract in Portuguese:

Rech R.R, Fighera R.A., Oliveira F.N. & Barros C.S.L. 2004. [Granulomatous meningoencephalitis in cattle grazing vetch (Vicia spp).] Meningoencefalite granulomatosa em bovinos em pastoreio de ervilhaca (Vicia spp). Pesquisa Veterinária Brasileira 24(3): 169-172. Depto Patologia, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil. E-mail: claudioslbarros@uol.com.br Granulomatous meningoencephalitis was observed in 7 out of 8 adult dairy cows affected by vetch-associated systemic granulomatous disease, although there was no neurological signs associated with the condition. The cellular inflammatory infiltrates were located in the leptomeninges and as perivascular cuffings within the brain and consisted of epithelioid macrophages, lymphocytes, plasm cells and eosinophils. These inflammatory changes varied from mild to severe from animal to animal and among different brain regions of the same animal. Perivascular cuffings were usually more marked than the leptomeningeal infiltrates. Affected brain regions, in decreasing order of intensity, included diencephalon through the level of massa intermedia, mesencephalon at the level of rostral colliculi, pons and cerebellar peduncles, medulla at the level of obex, frontal lobe at the level of the genu of the corpus callosum, and cerebellum. The character and the distribution of the inflammatory changes are emphasized regarding the differential diagnosis with other diseases and lesions of the bovine central nervous system in the context of the Brazilian surveillance program for bovine spongiform encephalopath.

Abstract in English:

ABSTRACT.- Spilki F.R., Esteves P.A., Franco A.C., Lima M., Holz C.L., Batista H.B.C.R., Driemeier D., Flores E.F., Weiblen R. & Roehe P.M. 2002. [Neurovirulence and neuroinvasiveness of bovine herpesvirus type 1 and 5 in rabbits.] Neurovirulência e neuroinvasividade de Herpesvírus bovinos tipos 1 e 5 em coelhos. Pesquisa Veterinária Brasileira 22(2):58-63. Centro de Pesquisas Veterinárias Desidério Finamor, Estrada do Conde 6000, Cx. Postal 47, Eldorado do Sul, RS 92990-000, Brazil. E-mail: proehe@orion.ufrgs.br In order to determine the capacity of bovine herpesvirus type 1 and 5 (BHV-1 and BHV-5) to invade, multiply and spread along the central nervous system (CNS) (neuroinvasiveness), as well as their potential to induce neurological illness (neurovirulence), 30 to 35 days old rabbits were inoculated with the BHV-5 strain EVI 88 / 95 and Los Angeles and Cooper BHV-1 strains, by the intrathecal (IT) and intranasal (IN) routes. The BHV-5 strain induced severe neurological clinical signs in 100% (12/12) of the rabbits inoculated by both routes. Histopathological examination revealed multifocal non-suppurative meningoencephalitis, characterized by multifocal gliosis and perivascular cuffing. Virus was recovered from many parts of the brain. Both BHV-1 strains, when inoculated via 1T route, were not neurovirulent. The strain Los Angeles, after IN inoculation, induced signs of severe respiratory disease (7/7), as well as signs of neurological impairment, indistinguishable from those induced by BHV-5, in 57% (4/7) of the infected rabbits. However, the rabbits with nervous signs revealed at histopathology vasculitis and thrombosis in lungs and brain, the latter with foci of neuronal necrosis, but no lesions indicative of encephalitis, suggesting that neural damage was probably consequent to tissue anoxia. The BHV-1 strain Cooper, after IN inoculation, induced only mild signs of respiratory disease. These findings indicate that the BHV-5 strain was both neuroinvasive and neurovirulent, since it was capable of invading, spreading and multiplying in the rabbits brains by both routes of inoculation, yet causing neurological disease, apparently consequent to vírus induced neural damage. The BHV-1 Los Angeles strain was not neuroinvasive, whereas its neurovirulence was probably consequent to tissue anoxia, which histologically seemed not to be related to direct viral pathogenic effect. The BHV-1 strain Cooper was neither neurovirulent nor neuroinvasive for rabbits. It is possible that these observations bear relationship with the frequent association of BHV-5 with encephalitis in cattle, as opposed to BHV-1 encephalitis, which is a rare event in nature.

• Infectious bovine rhinotracheitis IBR BHV-1 bovine encephalitis herpesvirus BHV-5 Rinotraqueíte infecciosa bovina herpesvírus da encefalite bovina.

Abstract in Portuguese:

RESUMO.- Spilki F.R., Esteves P.A., Franco A.C., Lima M., Holz C.L., Batista H.B.C.R., Driemeier D., Flores E.F., Weiblen R. & Roehe P.M. 2002. [Neurovirulence and neuroinvasiveness of bovine herpesvirus type 1 and 5 in rabbits.] Neurovirulência e neuroinvasividade de Herpesvírus bovinos tipos 1 e 5 em coelhos. Pesquisa Veterinária Brasileira 22(2):58-63. Centro de Pesquisas Veterinárias Desidério Finamor, Estrada do Conde 6000, Cx. Postal 47, Eldorado do Sul, RS 92990-000, Brazil. E-mail: proehe@orion.ufrgs.br Com o objetivo de avaliar a capacidade dos herpesvírus bovinos tipos 1 e 5 (BHV-1 e BHV-5) de invadir e replicar no sistema nervoso central (SNC) (neuroinvasividade), bem como sua capacidade de induzir doença neurológica (neurovirulência), coelhos com 30 a 35 dias de idade foram inoculados com uma amostra do Herpesvírus da Encefalite Bovina (BHV-5; amostra EVI 88/95) ou com amostras de BHV-1 (Los Angeles ou Cooper), pelas vias intratecal (IT) e intranasal (IN). A inoculação da amostra de BHV-5, tanto pela via 1T como IN, induziu sinais clínicos neurológicos em 100% (12/12) dos coelhos inoculados. Os exames histopatológicos revelaram um quadro de meningoencefalite não-purulenta multifocal, caracterizada por gliose multifocal e infiltrados perivasculares. O vírus foi isolado de várias áreas do SNC desses animais. As amostras de BHV-1, quando inoculadas pela via IT, não foram neurovirulentas. A amostra Los Angeles de BHV-1, quando administrada pela via IN, induziu sinais respiratórios severos, além de sinais neurológicos em 57% (4/7) dos animais inoculados. Entretanto, o exame histopatológico destes quatro animais revelou vasculite e trombose no pulmão e cérebro, este último apresentando focos de necrose neuronal, porém sem lesões indicativas de encefalite. Isso sugere que os sinais neurológicos foram, provavelmente, consequentes a prejuízos no fluxo sangüíneo encefálico, e não a danos neuronais provocados pela inoculação desse vírus. A amostra Cooper de BHV-1, quando inoculada pela via IN, induziu apenas sinais leves de infecção respiratória. Estes resultados indicam que apenas a amostra de BHV-5 foi capaz de invadir e replicar no encéfalo dos coelhos quando inoculada tanto por via IN como IT, apresentando neuroinvasividade e neurovirulência. É possível que estas observações tenham relação com o fato de amostras de BHV-5 freqüentemente causarem encefalites, em contraposição a infecções pelo BHV-1, onde encefalites são raramente observadas.

Abstract in English:

ABSTRACT.- Callado A.K.C., Castro R.S. & Teixeira M.F.S. 2001. [Lentiviruses of small ruminants (CAEV and Maedi-Visna): a review and perspectives] Lentivírus de pequenos ruminantes (CAEV e Maedi-Visna): revisão e perspectivas. Pesquisa Veterinária Brasileira 21(3):87-97. Depto Medicina Veterinária, Universidade Federal Rural de Pernambuco, Rua Dom Manoel de Medeiros s/n, Dois Irmãos, Recife, PE 55171-000, Brazil. E-mail: callado@altavista.net Small ruminant lentiviruses (SRLV), whose prototypes are Caprine Arthritis-Encephalitis virus (CAEV) and Maedi-Visna virus, are the causative agents of slow progressive degenerative diseases of goats and sheep (infected animals), responsible for significant economic losses. These viruses cause persistent infections with long periods of incubation and induce inflammatory and degenerative lesions. The lesions are induced in target organs of the host such as joints, CNS, lungs and mammary glands dueto viral replication in cells of the monocyte/macrophage lineage which is the main target cell. Infections occur particularly in the young and are acquired through ingestion of virus in milk or colostrum from infected does or ewes. The induction of immune response is variable and does not protect against the infection. Diagnosis is primarily based on the presence of SRLV antibodies usually detected by agar gel immunodiffusion (AGID) or enzyme linked immunosorbent assays (ELISA). As no vaccine is available, most often employed schemes to prevent spread of SRLV are based on segregation or/and culling of positive animals associated with management practices, especially the offspring. The strategies of SRLV for dealing with the immune system make difficult to accomplish diagnosis of infection, control or prevention of the viral spread. This review shows aspects of SRLV based on their phylogenetic studies of fields isolates, clinical, and immunopathological features.

• Small ruminant lentiviruses caprine arthritis-encephalitis virus maedi-visna retroviruses phylogenetic analysis epidemiology goat sheep Lentivírus de pequenos ruminantes vírus da artrite-encefalite caprina retrovírus análises filogenéticas epidemiologia caprino ovino.

Abstract in Portuguese:

RESUMO.- Callado A.K.C., Castro R.S. & Teixeira M.F.S. 2001. [Lentiviruses of small ruminants (CAEV and Maedi-Visna): a review and perspectives] Lentivírus de pequenos ruminantes (CAEV e Maedi-Visna): revisão e perspectivas. Pesquisa Veterinária Brasileira 21(3):87-97. Depto Medicina Veterinária, Universidade Federal Rural de Pernambuco, Rua Dom Manoel de Medeiros s/n, Dois Irmãos, Recife, PE 55171-000, Brazil. E-mail: callado@altavista.net Os lentivírus de pequenos ruminantes (SRLV), cujos protótipos são os vírus da Artrite-Encefalite Caprina (CAEV) e Maedi-Visna, são patógenos amplamente distribuidos, os quais causam doenças degenerativas progressivas lentas em caprinos e ovinos, determinando importantes perdas econômicas. Estes vírus causam infecções persistentes com período de incubação longo e causam inflamatórias e degenerativas. As lesões são induzidas em tecidos específicos do hospedeiro como articulações, pulmões, CNS e glândulas mamárias devido à replicação virai em células da linhagem monocítico-fagocitária que são as principais células-alvo. A infecção ocorre principalmente durante os primeiros meses de vida, através da ingestão de vírus no leite ou colostro de cabras ou ovelhas infectadas. A indução da resposta imunológica é variável e não protege contra a infecção. O diagnóstico é baseado primariamente na detecção de anticorpos para SRLV, geralmente por imunodifusão em gel de agar (AGID) e enzyme linked immunosorbent assay (ELISA). O diagnóstico e separação ou descarte dos animais soropositivos associado ao uso de certas práticas de manejo, especialmente das crias, são os principais meios implementados para prevenir a disseminação de SRLV, uma vez que ainda não existe vacina contra o vírus. As estratégias adotadas pelos SRLV para enfrentar o sistema imune dificultam o diagnóstico da infecção, controle ou prevenção da disseminação de SRLV. Esta revisão apresenta alguns aspectos das lentivíroses de pequenos ruminantes baseadas em estudos filogenéticos de amostras isoladas, aspectos clínicos e imunopatológicos.

Abstract in English:

ABSTRACT.- Beltrão, N., Flores E.F., Weiblen R., Silva A.M., Roehe, P.M. & lrigoyen L.F. 2000. [Acute infection and neurological disease by bovine herpesvirus type-5 (BHV-5): Rabbits as an experimental model.] Infecção aguda e enfermidade neurológica pelo herpesvírus bovino tipo 5 (BHV-5): coelhos como modelo experimental. Pesquisa Veterinária Brasileira 20(4):144-150. Depto Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brazil. Rabbits are susceptible to bovine herpesvirus type 5 (BHV-5) infection and often develop an acute and fatal neurological disease upon intranasal inoculation. The kinetics of viral infection of the central nervous system (CNS) was investigated by testing serial brain sections for infectivity at intervals after virus inoculation. The virus was first detected in the main olfactory bulb at 48h, followed by the olfactory cortex at 48/72h. At 72/96h infectivity was also detected in the trigeminal ganglia, pons and cerebral cortex. Two experiments were conducted to investigate the role of the olfactory system in the invasion of the rabbits’ CNS by BHV-5. In the first experiment, rabbits were inoculated with two BHV-5 isolates in the conjunctival sac. Rabbits inoculated by this route developed the neurological disease, yet with a reduced frequency and delayed clinical course. In a second experiment, twelve rabbits were submitted to surgical removal of the olfactory bulb and subsequently inoculated intranasally with BHV-5. Eleven out of 12 (91.6%) of the control rabbits developed the disease, against four out of 12 (33.3%) of the animals lacking the olfactory bulb. These results suggest that the olfactory system is the main pathway utilized by BHV-5 to reach the CNS of rabbits after intranasal inoculation. Nevertheless, the development of neurological infection in rabbits inoculated in the conjunctival sac and in rabbits lacking the olfactory bulb indicate that BHV- 5 may utilize an alternative route to invade the CNS, probably the sensory and autonomic fibers of the trigeminal nerve. The effects of immunization with homologous (BHV-5) and heterologous (BHV-1) strains in prevention of neurological disease by BHV-5 were investigated. Five out of 10 rabbits (50%) immunized with BHV-5 showed mild and transient neurological signs and one died upon challenge. Interestingly, the degree of protection against BHV-5 challenge was higher in rabbits immunized with BHV-1: only two rabbits showed transiente neurological signs and subsequently recovered. Thus, prevention of neurological disease by BHV-5 in rabbits may be achieved by immunization with either BHV-5 or BHV-1, likely reflecting the extensive serological cross-reactivity between these viruses. Further studies in rabbits may help in understanding the pathogenesis and immune response to BHV-5 infection.

• Bovine herpesvirus type 5 (BHV-5) meningo-encephalitis rabbits experimental model Herpesvírus Bovino tipo 5 meningoencefalite coelhos modelo experimental.

Abstract in Portuguese:

RESUMO.- Beltrão, N., Flores E.F., Weiblen R., Silva A.M., Roehe, P.M. & lrigoyen L.F. 2000. [Acute infection and neurological disease by bovine herpesvirus type-5 (BHV-5): Rabbits as an experimental model.] Infecção aguda e enfermidade neurológica pelo herpesvírus bovino tipo 5 (BHV-5): coelhos como modelo experimental. Pesquisa Veterinária Brasileira 20(4):144-150. Depto Medicina Veterinária Preventiva, Universidade Federal de Santa Maria, 97105- 900 Santa Maria, RS, Brazil. Coelhos são susceptíveis à infecção pelo herpesvírus bovino tipo 5 (BHV-5) e freqüentemente desenvolvem enfermidade neurológica aguda fatal após inoculação intranasal. A cinética da invasão do sistema nervoso central (SNC) de coelhos pelo BHV-5 foi estudada através de pesquisa de vírus em secções do SNC a diferentes intervalos pósinoculação. Após inoculação intranasal, o vírus foi inicialmente detectado no bulbo olfatório às 48h, seguido do córtex olfatório às 48/72h. Às 72/96h o vírus foi detectado também no gânglio trigêmeo, ponte e córtex cerebral. Dois experimentos foram realizados para avaliar a importância do sistema olfatório na invasão do SNC de coelhos pelo BHV-5. No primeiro experimento, coelhos foram inoculados com duas amostras do BHV-5 no saco conjuntival. Coelhos inoculados por essa via também desenvolveram a enfermidade neurológica, porém com menor freqüência com curso clínico tardio. No segundo experimento, doze coelhos foram submetidos à ablação cirúrgica do bulbo olfatório e posteriormente inoculados com o BHV-5 pela via intranasal. Onze de 12 coelhos controle (91,6%), não submetidos à cirurgia, desenvolveram a doença neurológica, contra quatro de 12 (33,3%) dos animais submetidos à remoção cirúrgica do bulbo olfatório. Esses resultados demonstram que o sistema olfatório constitui-se na principal via de acesso do BHV-5 ao encéfalo de coelhos após inoculação intranasal. No entanto, o desenvolvimento de infecção neurológica em coelhos inoculados pela via conjuntival e em coelhos sem o bulbo olfatório indica que o BHV-5 pode utilizar outras vias para invadir o SNC, provavelmente as. fibras sensoriais e autonômicas que compõe o nervo trigêmeo. Os efeitos da imunização com vírus homólogo (BHV-5) e heterólogo (BHV-1) na proteção à infecção neurológica foram investigados. Cinco entre 10 coelhos (50%) imunizados com o BHV-5 apresentaram sinais neurológicos discretos e transitórios e um morreu após o desafio com o BHV-5. Curiosamente, o grau de proteção foi superior nos coelhos imunizados com o BHV-1: apenas dois animais apresentaram sinais clínicos passageiros e recuperaram-se. Portanto, proteção da enfermidade neurológica pelo BHV-5 em coelhos pode ser obtida por imunização com o BHV-5 ou BHV-1, provavelmente devido à extensa reatividade sorológica cruzada entre esses vírus. Estudos adicionais em coelhos podem auxiliar no esclarecimento da patogênese e resposta imunológica a infecção pelo BHV-5.