Rinderpest

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.