Rabies in Cows (Bovis) | Vetlexicon
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Rabies

ISSN 2398-2993

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Synonym(s): rabid aggressive hypersalivation notifiable

Introduction

  • Cause: an infection caused by the rabies virus, which manifests as neurologic disease.
  • Notifiable disease in most countries, including UK, USA, Canada and Australia.
  • Zoonosis: fatal to humans.
  • Transmitted by bite or saliva contact (with broken skin or intact mucous membrane) from a rabid animal.
  • Signs: varied (see below).
  • Diagnosis: see below.
  • Treatment: none, but vaccines are available.
  • Prognosis: invariably fatal.

Presenting signs

  • In cattle, rabies usually manifests as:
    • Excessive salivation.
    • Behavioral changes.
    • Muzzle tremors, vocalization (bellowing).
    • Aggression or depression.
    • Hyperesthesia and/or hyperexcitability.
    • Paralysis of body parts (ear droop, limb paralysis, etc).
    • Pharyngeal paralysis.
    • Rumen bloat Ruminal bloat.
    • Straining.
  • Death usually occurs within 1 week of clinical signs.
  • The literature often describes forms as dumb or furious – this refers to the clinical signs observed, which in turn depend on the region of the nervous system most affected by the virus. This article does not distinguish between dumb or furious forms on the basis that clinical signs may vary widely between cases, and the diagnosis and prognosis is identical regardless of the symptoms seen.

Acute presentation

  • Acute onset neurological symptoms may include hypersalivation, muscle tremors, hyperesthesia and aggression.

Geographic incidence

  • Widely distributed throughout the world except in some European countries (inc UK), Australia, New Zealand, Japan, Antarctica and some Caribbean countries.
  • Rabies has been recognized for over 4000 years.

Age predisposition

  • All ages affected.

Breed/Species predisposition

  • All breeds susceptible.

Public health considerations

  • Notifiable disease in many countries.
  • Zoonosis:
    • Fatal to humans.
    • Rabies surveillance in the United States in 2000, found that of the domestic species, cattle were second only to cats in their incidence of rabies and thus cattle producers should be considered to be at increased risk from this disease.
  • Veterinarians, cattle owners, farm workers or other personnel exposed to confirmed or suspected case of bovine rabies should report to the appropriate authorities to determine their need for rabies treatment or prophylaxis:
    • If treatment (post-exposure prophylaxis) is deemed necessary, it should be initiated promptly.
    • Post-exposure prophylaxis consists of the combination of local wound cleansing, human rabies immune globulin (HRIG) and rabies vaccine.
    • Post-exposure treatment is effective in preventing the disease developing in humans providing it is administered promptly after a person has been exposed to infection and before clinical symptoms develop.
    • The rabies virus is inactivated rapidly by warm soapy water and basic detergents. Swift and thorough cleansing of the entry site with these is an effective first measure to reduce the risk of blood or saliva contamination of the wound and therefore infection.
    • Pre-exposure prophylaxis vaccination provides safe and effective protection for humans and animals (including companion animals and wildlife).

Cost considerations

  • Loss of affected animals.
  • Cost of vaccination.
  • Cost of controlling wildlife reservoirs and implementing biosecurity measures.
  • Cost of Post Exposure Prophylaxis (PEP) for humans

Special risks

  • Zoonotic risk to attending veterinarians / in contact farm staff.

Pathogenesis

Etiology

  • Rabies virus, a Lyssavirus, which infects all mammals and birds.

Predisposing factors

General

  • All cattle are susceptible to infection.

Specific

  • Cattle are usually infected by a bite wound inflicted by a rabid animal, such as a raccoon, skunk or fox. Bites are often around the face or muzzle.
  • Other methods of transmission (inhalation, oral inoculation, transplacental, or transmammary) are theoretically possible.

Pathophysiology

  • 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.
  • 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

  • Wildlife reservoirs include bats, foxes, raccoons and skunks (North America), red foxes (Europe), vampire bats (Latin America) and domestic / feral 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.
  • Rinchen et al (2018) Cross sectional survey on knowledge, attitude, practices and risk perception regarding rabies among cattle owners in two districts of Bhutan. Int J Infect Diseases 73, 226 Ijidonline
  • Tariku et al (2016) Incidence and economic impact of rabies in the cattle population of Ethiopia. Prevent Med 130, 67-76 ScienceDirect.
  • Krebs J W, Mondul A M, Rupprecht C E & Childs J E (2001) Rabies surveillance in the United States during 2000. JAVMA 219 (12), 1687-1699 Pubmed.
  • Martinez-Burnes et al (1997) An outbreak of vampire bat transmitted rabies in cattle in northeastern Mexico. Can Vet J 38 (3). 175-177 PubMed.
  • Hudson L C, Weinstock D, Jordan T & Bold-Fletcher N O (1996) Clinical features of experimentally induced rabies in cattle and sheep. J Vet Med 43, 85-95 PubMed.

Other sources of information

  • Department for Environment Food & Rural Affairs (2018) Rabies Control Strategy for Great Britain. Website: www.assets.publishing.service.gov.uk.
  • Brown, C M, Slavinski S, Ettestad P, Sidwa T J & Sorhage F E (2016) Compendium of Animal Rabies Prevention and Control NASPHV.
  • Dee Whittier W (2006) Rabies in Cattle a Continual Threat in Virginia. In: Virginia Cooperative Extension Livestock Newsletter. Website: www.sites.ext.
  • Rupprecht C E (1996) Rhabdoviruses: Rabies Virus. In: Medical Microbiology. 4th edn. Ed: Baron S. Elsevier, USA NCBI.
  • Centers for Disease Control and Prevention (CDC) Rabies. Website: www.cdc.gov.
  • Centers for Disease Control and Prevention (CDC) Compendium of Animal Rabies Prevention and Control. Website: www.cdc.gov.

Organisation(s)

  • Centers for Disease Control and Prevention (CDC) Website: www.cdc.gov.