Rinderpest (Etiology, transmission, pathogenesis, clinical signs, diagnosis, differential diagnosis, treatment, and control)

Synonyms: Cattle plague


  • Rinderpest or cattle plague is an acute, highly contagious virus disease, primarily of cattle and to a lesser degree of sheep, goats, and wild ruminants.
  • This disease is characterized by necrosis and erosions of the mucosa in the respiratory and digestive tracts.
  • Early constipation, usually preceded by dehydration and prostration, is followed by diarrhea.


• Rinderpest is caused by a negative-strand RNA virus of the Morbili virus genus within the family Paramyxoviridae.

• Rinderpest is enzootic in northern equatorial Africa, the Middle East countries. Rinderpest was eradicated in India.

• The virus strains are of a single serotype but represent various pathotypes, i.e. they vary in virulence, pathogenicity.

• The virus is immunologically related to measles, and canine distemper viruses.


• The virus is usually transmitted from sick to susceptible animals in aerosols and normally the contact has to be close because the infectious droplets are large and short-lived.

• Transmission through ingestion of virus-contaminated food or water is rare.

Clinical signs

• In enzootic areas, where most animals could have been exposed to the virus and develop a certain degree of immunity, it may be longer.

• It is an acute febrile disease with morbidity in susceptible populations reaching 100% and mortality 90-100%.

• The normal route of infection is through nasopharyngeal mucosa.

• The course of the disease comprises 4 stages.

I stage: Incubation period

• 2-9 days. It depends according to the strain and dose of the virus.

• The virus multiplies rapidly in the lymphoid tissue, lungs, bone marrow, and intestines.

• Active proliferation of the virus in the tissue results in fever.

II stage: Prodromal phase

• There is first rise in temperature – 105-107°C (41-42°C) and lasts for about 3-5 days until the appearance of lesions in the mouth.

• Animal shows depression, restlessness, and anorexia.

• Muzzle is dry, starry coat and initial constipation noticed, Leucopenia with the onset of fever and persists till death.

III stage: Mucosal phase

• Mouth lesions on the inner lips and adjacent gums. Visible mucous membranes are congested.

• The mouth lesions are greyish foci with necrotic centers and shallow erosions with bleeding.

• Ulcers with bran-like deposits were noticed. Smacking as in FMD is not common. The animal is restless and shows excess thirst.

• Temperature is high and recedes after that diarrhea begins.

• Rapid dehydration marked weakness and severe progressive emaciation lead to death.

IV stage: Diarrhoeic phase

• About three days after the appearance of the mucosal ulcers fever regresses and profuse diarrhea develops.

• The dark fluid feces often contain mucus, necrotic debris, and blood. Dehydration and wasting soon become evident.

• Severely affected animals may collapse and die within 12 days of the onset of clinical signs.

• In surviving animals convalescence lasts several weeks.

V stage: Convalescent phase

• Mouth lesions start healing. Rapid regeneration of the affected epithelium is noticed.

• Slow recuperation of general health. Mortality in cattle, sheep, and goats, and pigs are 90%.



• Spleen, pre scapular or mesenteric lymph nodes, ocular or nasal secretions of acutely infected animals

• Based on clinical signs

• Isolation and identification of the virus – Isolation of the virus from leukocyte fraction of whole blood that has been collected into heparin or EDTA (ethylene diamine tetraacetic acid), a monolayer of primary calf kidney, B95a marmoset lymphoblastoid, or African green monkey kidney (Vero) cells.

• Glycerol should not be used as a preservative for the Rinderpest virus.

• Serological tests – AGID, VNT (virus neutralization test), Competitive ELISA


• Cell culture

The virus grows in sheep, goats, rabbits, hamsters, and white mice. It can be grown in chick embryos by intravenous or CAM route.

• Cytopathogenic effect (CPE) is produced by the virus in susceptible cells from cattle, sheep, goats, chick embryos, pigs, hamsters, and men.

• Cytopathogenic effect consists of large, well-defined multinucleated giant cells known as “syncytia”.

• Infected cell cultures have stellate or spindle-shaped cells with large fine anastomosing intracellular processes.

• The virus multiplies in the cytoplasm of the host cells like Vero cells (African green monkey kidney cells).

• Both intracytoplasmic and intranuclear inclusion bodies are present.

Differential diagnosis

• Haemorrhagic septicemia


• Mucosal disease

• Bovine Viral Diarrhoea

Prevention and control


• Laprinised vaccine: Immunity last for 1-7 years

• Goat tissue vaccine: Immunity last for 13 years or lifelong

• In countries where Rinderpest is exotic, confirmed outbreaks are controlled by the slaughter and disposal of all affected and in-contact animals, as well as by appropriate quarantine and animal movement controls

• All outbreaks of rinderpest in virgin areas have been due to the importation of live infected animals.

• Prevention in such areas is therefore largely dependent upon vigilant control of the introduction of live animals from potentially infected areas

• Contaminated areas should be physically cleaned of all animal waste and soiled bedding and treated with disinfection solutions of high (>10) or low (<3) pH containing solvents to destroy the virus envelope. Solutions of caustic soda and Lysol have the highest virucidal activity against viruses contaminated with organic matter

• Attenuated tissue culture (bovine kidney cells, Vero cells) Kabete “O” strain of RPV produced a safe and effective attenuated virus which has been the principal vaccine used to combat rinderpest throughout the world during the past 40 years. It induces a lifelong immunity, is inexpensive and simple to produce, and is stable in freeze-dried form.

• The only drawback of the vaccine is that after reconstitution in normal saline it has a working life of only a few hours in the hot climates

• Recombinant vaccines in which genes expressing RPV immunizing antigen are incorporated into more thermostable poxviruses have been developed and used for differentiating vaccinated animals with the infected animals and thus helps in the eradication of disease

• In endemic areas calves at the age of 6-12 months were vaccinated for RP. Annual vaccination of all cattle will produces the highest levels of herd immunity.