Meningoencephalomyelitis in Horses Associated with Equine Herpesvirus 1 Infection

Charlton, Kenneth; Mitchell, D.; Girard, A.; Corner, A. H.

doi:10.1177/030098587601300107

Cited by 60 publications

(24 citation statements)

References 6 publications

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“…The ability, for example, to clear the viraemia would be of great clinical significance if it is reflected in the equine host. This is because viraemia and the associated replication of virus in the endothelial cells of the vessels is thought to predispose to the development of neurological signs (Charlton et al, 1976) and to the infection of the foetus, leading to abortion (Allen & Bryans, 1986). These findings concerning the efficacy of inhibitors of EHV-1 in the murine model will be the subject of a further publication.…”

Section: Discussionmentioning

confidence: 99%

“…In particular there is no evidence in the horse of direct replication of virus in neurons or establishment of neurological latency; the site of latency and molecular state of the virus have yet to be defined. Viraemia appears to be a crucial feature of the pathogenesis and severe and prolonged viraemia may correlate with spread across the placenta to the foetus and the production of neurological signs associated with virus replication in the endothelial cells in the small blood vessels of the central nervous system (CNS) (Charlton et al, 1976), Natural immunity to infection by EHV-1 appears to be incomplete or short-lived and reinfection with the same or related strains with the production of clinical signs is documented (Bryans, 1969;von Steinhagen, 1988) and confirmed in this laboratory (Y.-C. Chong, H. J. Field & P. H. Duffus unpublished).…”

Section: Introductionmentioning

confidence: 99%

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The Pathogenesis of Equine Herpesvirus Type 1 in the Mouse: A New Model for Studying Host Responses to the Infection

Awan

Chong

Field

1990

Journal of General Virology

113

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An infection was established in adult BALB/c mice by means of intranasal inoculation of the AB4 strain of equine herpesvirus type 1 (EHV-1). The acute infection was confined to the respiratory tract and blood. Virus was shown to replicate in the nasal mucosa, trachea and lung for several days producing clinical signs of disease. Viraemia was also detected and a small proportion of peripheral blood cells contained virus at the peak of the infection. Histological and electron microscopic evidence were obtained which proved that productive virus replication occurred in the ciliated epithelial cells lining the bronchi and in pneumocytes in the lung, resulting in the destruction of these cells. Both humoral and cell-mediated responses to the infection were detected and monitored. By means of immunoprophylaxis or chemotherapy it was possible to modify the course of the infection. This infection model has many striking features in common with that observed in the natural host and the observations suggest that the mouse is a convenient and relevant model in which to study both host responses to EHV-1 infection and modification of the pathogenesis by means of immunoprophylaxis or therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Pathogenesis of Equine Herpesvirus Type 1 in the Mouse: A New Model for Studying Host Responses to the Infection

Awan

Chong

Field

1990

Journal of General Virology

113

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“…The histopathological changes caused by EHV-9 were partially resembled to those of EHV-1 infected horses showing paresis [1,3,9,12,13,23]. Common features between EHV-9 encephalitis and EHV-1-associated meningoencephalomyelitis were cellular reaction including perivascular cuffing and glial reaction.…”

mentioning

confidence: 99%

“…Common features between EHV-9 encephalitis and EHV-1-associated meningoencephalomyelitis were cellular reaction including perivascular cuffing and glial reaction. However, the neuropathology of EHV-9 inoculated horses lacked vasculitis which is the most prominent histopathological finding of EHV-1-associated meningoencephalomyelitis [1,3,9,12,13,23]. Furthermore, EHV-9 encephalitis was characterized by localization of neuropathological lesions i n t h e b r a i n , t h o u g h E H V -1 -a s s o c i a t e d meningoencephalomyelitis showed diffuse vasculitis, most prominent in the brain and spinal cord, and also affecting the endometrium, lungs and uveal vessels.…”

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confidence: 99%

Pathogenicity of a New Neurotropic Equine Herpesvirus 9(Gazelle Herpesvirus 1) in Horses.

Taniguchi

Fukushi

Matsumura

et al. 2000

The Journal of Veterinary Medical Science

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ABSTRACT. Pathogenicity of equine herpesvirus 9 (EHV-9), a new type of equine herpesvirus isolated from Gazella thomsoni, in horses was investigated by intranasal inoculation of EHV-9 (10 7 pfu) to two conventionally reared 8-months old half-bred weanling horses. Fever higher than 39°C was recorded. Virus was recovered from nasal swabs and peripheral blood mononuclear cells. Both horses developed neutralizing antibody to EHV-9. Perivascular infiltration of mononuclear cells and glial reaction were found in the olfactory and limbic systems. The results suggested that EHV-9 has a pathogenicity in horses.-KEY WORDS: equine, gazelle, herpesvirus.J. Vet. Med. Sci. 62(2): 215-218, 2000 describe the experimental infection of horses with EHV-9. The working seed of EHV-9 P19 [11] was prepared by propagation in fetal horse kidney (FHK) cells from the original stock of the third passage in Madin-Darby bovine kidney (MDBK) cells. The titration of viruses was conducted by plaque formation using MDBK cells and methylcellulose medium for overlay [17]. The reference viruses used were 89c25 for EHV-1 [18,19] and TH-20 for .Two half-bred weanling horses aged 8 months (H1 and H2) were used for inoculation of EHV-9. Ten ml of virus solution containing 10 7 plaque forming units (pfu) were inoculated intranasally using a nebulizer as described previously [17]. The inoculated horses were kept in a P3-level specific pathogen free facility of the Japan Racing Association, Tochigi, Japan.Rectal temperatures were recorded twice a day throughout the experiment. Fever higher than 39°C was recorded at 2, 4 and 5, and 1, 6 and 8 days post infection in H1 and H2, respectively. Other clinical symptoms were not observed. Leukocyte counts of both horses were normal during the experiment. Nasal swab and peripheral blood samples were collected daily for the first week and every other day for the second week after inoculation in order to investigate virus secretion and viremia. Viral isolation was conducted immediately after sample collection without freezing as described elsewhere [17]. A nasal swab was suspended in 2.0 ml phosphate buffered saline containing antibiotics. Approximately 10 6 mononuclear cells fractionated using Lymphoprep (Nycomed, Oslo, Norway) and 0.5 ml of nasal suspension were co-cultured with FHK cells in 25-cm 2 flasks (Nalge Nunc International Inc., Tokyo, Japan). The flasks were incubated at 37°C and observed for cytopathic effect for a week. Virus was recovered from nasal swabs from both horses on days 1 to 4, and from peripheral blood mononuclear cells in horse H1 on days 1 and 3 to 6 post infection. The recovered virus was identified as EHV-9 by A new herpesvirus was isolated from the epizootic encephalitis of Thomson's gazelles (Gazella thomsoni) kept at a zoological garden [11,25]. The outbreak occurred in a herd of ten gazelles in the fall of 1993. Seven gazelles died with or without apparent neurological symptoms. All dead gazelles had nonsuppurative encephalitis characterized by necrosis and degeneration of neuron...

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“…Equine herpesvirus type 1 (EHV-1) causes an important infection in horses associated with a variety of clinical problems including respiratory distress, abortion (Bryans & Allen, 1989) and neurological signs (Charlton et al, 1976;Chowdury et al, 1986). The serologically related but distinct virus, EHV-4, also causes a common infection and both EHV-1 and EHV-4 establish latent infections in horses from which they may be reactivated.…”

mentioning

confidence: 99%

Cell-mediated antiviral response to equine herpesvirus type 1 demonstrated in a murine infection model by means of adoptive transfer of immune cells

Lila

Field

1993

Journal of General Virology

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Protection against equine herpesvirus type 1 (EHV-1) infection in a mouse model has been studied by means of delayed-type hypersensitivity (DTH) and adoptive transfer of immune spleen cells. Mice were found to develop a positive DTH response to EHV-1 antigen which was sustained for several months after primary inoculation. The response was found to cross-react with EHV-4-derived antigen. Immune cells (from mice primed with live or heat-inactivated EHV-1) conferred an enhanced DTH response on recipients; however, only the immune cells that were previously primed with live EHV-1 gave protection against re-infection. The degree of protection was also dependent on the number of spleen cells transferred. Immune cells from mice primed with heatinactivated EHV-1 appeared to enhance virus replication following subsequent inoculation. The serum antibody response to EHV-1 appeared to be slightly suppressed in recipients of spleen cells from mice primed with either live or heat-inactivated virus. These results support the important role for cell-mediated responses in protective immunity to EHV-1 and provide clues to the nature of protection and immunopathology in the natural host.

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Meningoencephalomyelitis in Horses Associated with Equine Herpesvirus 1 Infection

Cited by 60 publications

References 6 publications

The Pathogenesis of Equine Herpesvirus Type 1 in the Mouse: A New Model for Studying Host Responses to the Infection

The Pathogenesis of Equine Herpesvirus Type 1 in the Mouse: A New Model for Studying Host Responses to the Infection

Pathogenicity of a New Neurotropic Equine Herpesvirus 9(Gazelle Herpesvirus 1) in Horses.

Cell-mediated antiviral response to equine herpesvirus type 1 demonstrated in a murine infection model by means of adoptive transfer of immune cells

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