Difference between revisions of "Bovine Herpesvirus 5"

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'''Subacute''' disease causes calves to be depressed, anorexic and ataxic and suppresses [[Rumen - Anatomy & Physiology#Ruminoreticular contraction|rumenal motility]]. The '''dyspnoea is more pronounced than in acute infection due to the longer disease course''' and is almost always fatal. Those that recover become latent carriers.  
 
'''Subacute''' disease causes calves to be depressed, anorexic and ataxic and suppresses [[Rumen - Anatomy & Physiology#Ruminoreticular contraction|rumenal motility]]. The '''dyspnoea is more pronounced than in acute infection due to the longer disease course''' and is almost always fatal. Those that recover become latent carriers.  
  
Calves that acquire infection '''after vaccination for BHV-1 and those that have been previously infected''' by either virus become '''silently infected and the virus becomes latent'''. Sites of latency include the '''CNS and mucosae of the nose and trachea'''. The virus can then recrudesce with stress and/or immunosuppression, but usually produces '''no clinical signs'''; it is however shed into the nasal secretions providing a source of infection.  
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Calves that acquire infection '''after vaccination for BHV-1 and those that have been previously infected''' by either virus become '''silently infected and the virus becomes latent'''. Sites of latency include the trigeminal ganglia of the '''CNS and mucosae of the nose and trachea'''. The virus can then recrudesce with stress and/or immunosuppression, but usually produces '''no clinical signs'''; it is however shed into the nasal secretions providing a source of infection.
  
 
==Diagnosis==
 
==Diagnosis==

Revision as of 17:58, 31 August 2011

Caused By: BHV-5 — Bovine Encephalitis Virus — Bovine Encephalitis Herpesvirus

Introduction

Bovine Herpesvirus 5 is another potentially pathogenic member of the herpesvirus family, causing respiratory and neurological disease in cattle and sheep.

The virus is very similar to BHV-1, which is responsible for the major bovine disease, IBR. Although BHV-1 can cause neurological signs, BHV-5 demonstrates increased neurotropism.

Distribution

South America, USA, Australia, Germany and Hungary.

Signalment

Young calves up to ten months old are most commonly affected. Nervous disease is usually acute.

Clinical Signs

BHV-5 causes tachycardia and tachypnoea with pyrexia, dyspnoea, mucoid nasal discharge, gasping and abnormal lung sounds. Infected animals often hypersalivate and abdominal pain may be observed.

Affected animals are also often generally lethargic, anorexic, display various signs of pain and discomfort and may be recumbent.

Signs of acute neurological infection include opisthotonus, hyperaesthesia, dullness, abnormal behaviour, ataxia, head tilt, head pressing, conjunctivitis, blindness, coma and seizures. Proprioceptive deficits may also develop suddenly and acutely. Disease in neonatal animals causes rapid generalised viraemia and sudden death.

Subacute disease causes calves to be depressed, anorexic and ataxic and suppresses rumenal motility. The dyspnoea is more pronounced than in acute infection due to the longer disease course and is almost always fatal. Those that recover become latent carriers.

Calves that acquire infection after vaccination for BHV-1 and those that have been previously infected by either virus become silently infected and the virus becomes latent. Sites of latency include the trigeminal ganglia of the CNS and mucosae of the nose and trachea. The virus can then recrudesce with stress and/or immunosuppression, but usually produces no clinical signs; it is however shed into the nasal secretions providing a source of infection.

Diagnosis

Specific monoclonal antibodies are available for BHV-5 and can be used with immunoperoxidase staining on formalin fixed brain tissue for confirmatory identification. PCR is also available.

Antibodies against BHV-5 can be detected using most ELISA kits designed for BHV-1 due to their close relationship.

On post-mortem examination, a non-suppurative meningoencephalitis and evident perivascular cuffing. Lesions are more pronounced in white matter. Necrosis, oedema and spongiosis may also be recognisable. In some cases, satellitosis also develops.

Treatment

There is no treatment for infected individuals.

Control

No vaccination is available for BHV-5 but some cross-protection appears to be granted from some BHV-1 vaccines. This needs to be proven for each available vaccine.


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References



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This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 1 August 2011.