ISSN 2398-2977      

Rabies

pequis

Synonym(s): Lyssavirus


Introduction

  • Cause: an infection caused by the rabies virus Rabies virus, which manifests as neurologic disease.
  • Notifiable disease in most countries, including UK, USA, Canada and Australia.
  • Zoonosis.
  • Transmitted by bite of or saliva contact (with broken skin or intact mucous membrane) from a rabid animal.
  • Signs: neurologic signs with 'paralytic', 'dumb' and 'furious' forms.
  • Diagnosis: history, signs. Post-mortem examination.
  • Treatment: none.
  • Prognosis: invariably fatal, inactivated vaccine available.

Pathogenesis

Etiology

  • Rabies virus Rabies virus, a Lyssavirus, which infects all mammals and birds.
  • Several major and minor antigenic variants.
  • Variants associated with strain pathogenicity and host species specificity.

Predisposing factors

General

  • All mammals susceptible to infection.
  • Horses one of most susceptible of domestic species.

Specific

  • Infections in horses tend to coincide with presence of epizootics in wildlife reservoirs.
  • Horses kept at pasture are at particular risk.
  • Horses usually infected by bite wound inflicted by rabid animal, often around the face or muzzle.
  • Other methods of transmission (inhalation, oral inoculation, transplacental, or transmammary) not reported in horses.

Pathophysiology

  • Viral infection, transmitted by the bite of a rabid animal, and which is invariably fatal in horses.
  • Bite from a rabid animal → inoculation of rabies-infected saliva into sub-epithelium and striated muscle → virus replication at the site of bite wound → infection of motor and sensory nerves once sufficient concentration of virus is reached → centripetal spread from site of inoculation to spinal cord and CNS via neuronal axons.
  • Clinical signs dependent on sites of viral replication within CNS.
  • Paralytic form: replication in spinal cord.
  • Furious form: replication in cerebral cortex.
  • Dumb form: replication in brainstem.
  • From CNS virions move centrifugally in peripheral nerves to all highly innervated organs, including salivary glands → bud from plasma membranes of mucous cells and are released in high concentrations in saliva.

Timecourse

  • Incubation period is very variable and depends on:
    • Local replication of virus in muscle at wound site before migrating to nervous tissues (=latency).
    • Site of bite wound (proximity to CNS).
    • Dose of inoculated virus.
    • Pathogenicity of strain of inoculated virus.
  • Generally from 2-9 weeks, but can be several months.
  • Death usually occurs within 2-10 days after onset of clinical signs.

Epidemiology

  • Horses are extremely susceptible to infection and require lower dose of virus compared to other domestic species.
  • Wildlife reservoirs include bats, foxes, raccoons and skunks (North America), red foxes (Europe), vampire bats (Latin America) and domestic dogs and mongoose (Africa and Asia).
  • Higher incidence of rabies seen in late summer months in North America, when density of wildlife population has reached a peak.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Harvey A M, Watson J L, Brault S A et al (2016) Duration of serum antibody response to rabies vaccination in horses. J Am Vet Med Assoc 249 (4), 411-418 PubMed.
  • Green S L (1997) Rabies. Vet Clin North Am Equine Pract 13 (1), 1-11 PubMed.
  • Turner G S (1994) Equine rabies. Equine Vet Educ 6 (4), 197-199 VetMedResource.

Other sources of information

  • Gimenez T, Stafford K B & Johannessen D T (2003) How to Safely Manage a Potentially Rabid Equine. In: Proc 49th AAEP Convention. pp 274-279.

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