Bovis ISSN 2398-2993

Rinderpest

Synonym(s): Cattle plague, Steppe murrain

Contributor(s): Belal Hossain , Mike Reynolds

Introduction

  • Rinderpest is caused by a negative-strand RNA virus of the Morbillivirus genus within the family Paramyxoviridae.
  • The world was officially declared free from rinderpest in 2011 in the course of the 79th OIE General Session.
  • Rinderpest is a highly contagious viral disease of livestock.
  • It can cause illness in cloven-hooved (two-toed) animals, particularly water buffalo (Bubalus bubalis); European cattle (Bos primigenius taurus) and zebu breeds (Bos primigenius indicus).
  • Most wild and domestic cloven-footed animals can become infected: zebu, sheep and goats, pigs, and wild ungulates in contact with cattle.
  • There was also variation in susceptibility to clinical disease between breeds, especially cattle. Most European cattle breeds (Bos taurus) were more susceptible than Bos indicus breeds. African humpless cattle, such as the Ankole in East Africa, were notoriously susceptible in comparison to East African zebus.

Pathogenesis

Predisposing factors

  • Large herd size.
  • Mixing of affected and non affected animals.
  • Drinking of contaminated water.
  • Sneezing of animals.
  • Improper disposal of manure and urine.

Pathophysiology

  • The virus can get entry to the susceptible animal through droplets, secretion or excretion and close contact with suspected and infected animals.
  • After gaining entry, the virus passes through the epithelium of the upper and less frequently the lower portion of the tract to establish foci of proliferation in the draining lymph nodes, from which it disseminates via the blood to other lymphoid tissues.
  • In the blood, the virus is intimately associated with the leucocytes and only small portions being free in the plasma rendering it filterable.
  • Virus titres are detected high in gastrointestinal tract.
  • The virus appeared in the turbinate mucosa and can also be detected in the lungs.
  • Researchers have found that a proportion of infected cattle showed slight lymphocytosis before the onset of pyrexia. This was followed by marked lymphopenia, caused by lymphoid necrosis.
  • During convalescence, lymphocyte levels slowly returned to normal over a period of days to weeks.
  • Eosinophils may also have disappeared from the blood during the early stages of clinical disease, returning to normal levels some 2 to 3 weeks later.
  • In severe cases the excessive loss of water caused hemoconcentration.
  • Serum aspartate transaminase and blood urea nitrogen levels increased during severe cases of disease.
  • Serum chloride levels fell markedly in terminal illness.
  • Blood clotting may have been impaired in severely affected animals and serum protein levels lowered.
  • The lesions of rinderpest were a direct result of virus-induced cytopathology.
  • Generally, the severity of the lesions was directly related to the virulence of the strain of virus involved.
  • Complications may have arisen during convalescence through re-activation of latent pathogens, especially protozoa.

Timecourse

  • The incubation period varies from 3-15 days but 4-5 days is typical.

Epidemiology

  • It has been suggested that rinderpest originated in central Asia.
  • Over the centuries, the disease swept through Asia and was subsequently introduced into Africa, resulting in “the great African rinderpest pandemic of the twentieth century.
  • Apart from an isolated outbreak in Brazil in 1920 and one in Australia in 1923, rinderpest has not affected countries in the Americas or Australia.
  • Between 2002 and 2011, there were no reported field cases of rinderpest. The eradication campaign concluded in 2011 with an international declaration of global freedom from rinderpest.
  • For more recent, detailed information on the occurrence of this disease worldwide, see the OIE World Animal Health Information Database (WAHID) Interface or refer to the latest issues of the World Animal Health and the OIE Bulletin.
  • Recent data on sero surveillance of ruminants to Rinderpest virus is limited. However in a serological survey conducted in Tanzania in wildlife and small ruminants found seropositive animals despite there being no reported cases.
  • Age predisposition:
    • Age has no influence on susceptibility, however in highly susceptible populations, rinderpest behaved in epidemic fashion with the virus infecting virtually all susceptible individuals and causing severe clinical disease in most age groups.
    • Endemic rinderpest however, was much milder and was maintained by young animals usually less than two years old that had lost their maternal immunity.

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

Other sources of information

  • World Organisation for Animal Health (2012) Terrestrial Animal Health Code. OIE, Paris.
  • World Organization for Animal Health (2012) Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. OIE, Paris.
  • Barrett T, Pastoret P P & Taylor W (2006) Rinderpest and peste des petits ruminants. London: Academic Press. pp 86–104.
  • Spinage C A (2003) Cattle plague. New York: Kluwer Academic/Plenum. pp 43–59, 497–551.
  • Anderson E C, Jago M, Mlengeya T, Timms C, Payne A & Hirji K (1990) A serological survey of rinderpest antibody in wildlife and sheep and goats in northern Tanzania. Epidemiology and Infection. 105 (1), 203-214.
  • Merck Veterinary Manual. Merck & Co. Inc. and Merial Ltd.


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