Rinderpest

Also know as: Cattle Plague — RV

Rinderpest has now been eradicated
Rinderpest is the first animal disease to have been eradicated. Small pox in humans is the only other disease that has achieved the same status. For more information see FAO website.

Introduction

Rinderpest (RV) was an acute to subacute contagious viral disease of ruminants and pigs that could cause morbidity and mortality rates in excess of ninety per cent.

It was caused by a morbillivirus, a member of a group of enveloped viruses forming a separate genus within the family Paramyxoviridae. Other viruses in this genus include peste des petits ruminants virus (PPRV) infecting sheep and goats, canine distemper virus (CDV) and human measles virus (MV), and other members in marine mammals.

In terms of economic losses in domestic animals, Rinderpest was the most important member of the group. It was eradicated from the UK in 1877, but continued to be endemic in Africa and Asia until very recently. It was present in Sudan and Somalia until the 1994. Global Rinderpest Eradication Programme (GREP) succeeded in its goal in 2011.

Distribution

Spread of RV was achieved almost exclusively by contact between infected and susceptible animals. Infected animals excreted infectious virus in their ocular, nasal, oral and vaginal secretions and faeces. Excretion was highest when epithelial lesions were developing maximally, during the early stages. Excretion began 1 or 2 days before the onset of fever, the first clinical sign, and continued for 9 to 10 days after the start of pyrexia. Recovered cows may have aborted an infected foetus some weeks after apparent recovery, with virus excretion in their uterine and vaginal discharges.

There was no carrier state of Rinderpest.

The fragility of the virus ensured that most infectivity survived for only a few hours outside the host.

Transmission by infected aerosols probably only occurred under ideal conditions of close proximity and gentle air currents, i.e. amongst housed animals.

Wildlife also played an important role in rinderpes, particularly in Africa due to its greater population sizes and densities and larger number of susceptible species. However, wildlife could not maintain the virus alone and disease in wild species disappeared when it was eradicated from domestic cattle.

Vectors and intermediate hosts were not involved in the transmission of rinderpest.

Signalment

Cattle and buffallo showed the most severe clinical signs of Rinderpest Virus.

Sheep, goats and Asiatic pigs were also susceptible and may develop clinical disease.

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. European breeds of pig underwent subclinical infection. Infection of wild ruminants varied massively.

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 2 years old that had lost their maternal immunity.

Clinical Signs

The disease was characterised by necrosis and erosions in the gastrointestinal tract that resulted in severe diarrhoea and dehydration.

The animal would at first become pyrexic, dull and depressed. Oral lesions included ulcers, vesicles and erosions on the tongue and oral mucosa, causing ptyalism, smacking of the lips and bruxism due to pain.

There was also very commonly diarrhoea +/- blood and mucous. Diarrhoea and breath would usually have a foul odour. Generally the animal would be weak, lethargic and be reluctant to eat. There may have been signs of weight loss or reduced weight gain and if in milk, the yield would be severely reduced.

There may have been ocular signs such as excess lacrimation, blepharospasm and reddened conjunctiva.

The animal may have also exhibited respiratory distress with dyspnoea, tachypnoea, coughing and nasal discharge.

Diagnosis

History, clinical signs and signalment/region etc were suggestive of the disease. A presumptive diagnosis of Rinderpest could be therefore made on the basis of the clinical signs and gross pathology and measures be taken immediately. However, in countries where the disease was not prevalent, and especially in regions dependent on livestock exports, it was essential to obtain laboratory confirmation of the diagnosis as soon as possible.

The most commonly used assay was the agar-gel immunodiffusion test (AGID) which was simple, easy to read, and highly specific. Counter-immunoelectrophoresis was quicker and more sensitive than AGID but required more sophisticated equipment. Immunofluorescence and immunoperoxidase staining were very sensitive but also need more equipment than AGID. A range of ELISAs were also developed.

The virus could also be identified by inoculating sample materials into tubes containing antiserum to RV or by using immunofluorescent or immunoperoxidase techniques.

If antigen detection and virus isolation were negative then convalescent animals should have been bled again 2 to 4 weeks later.

The collection of adequate quantities of appropriate specimens greatly increased the chances of an accurate laboratory diagnosis. An ideal sample collection would have included whole blood for serum antibody assay, and in anti-coagulant for virus isolation from leukocytes, a biopsy from a superficial lymph node, debris from oral lesions, and ocular and nasal swabs for virus isolation and antigen or nucleic acid detection. If possible, two or more animals would be killed for necropsy examination and collection of spleen and mesenteric lymph nodes kept cool on ice (but not frozen). Glycerol should not be used as a preservative because it inactivates RV.

Later on, PCR offered the advantage of providing amplified viral RNA for nucleotide sequencing in order to establish the virus sub-type or lineage for epidemiological purposes.

The differentiation of Peste des Petits Ruminants from rinderpest was more difficult. The virus cross-reacted serologically with RV but monoclonal antibodies and nucleic-acid techniques that clearly distinguish between PPR virus and RV are now available.

Pathology

A proportion of infected cattle showed slight lymphocytosis before the onset of pyrexia. This was followed by marked lymphopaenia, 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 haemoconcentration.

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.

The overall appearance at necropsy was similar for most species that died of typical severe rinderpest. The carcass was dehydrated, emaciated, and usually soiled with fluid faeces. The eyes were sunken and often encrusted with mucopurulent discharge and the cheeks may have shown signs of epiphora. Erosions were most common on the gums, lips, buccal papillae, dorsal and ventral aspects of the tongue and the soft palate.

The folds of the abomasum were congested and oedematous and often showed necrosis and erosions along the edges. The fundus of the abomasum may have had small discrete erosions that increased in size towards the pylorus where whole areas of mucosa may have become desquamated. The early necrotic lesions were pale-greyish, whereas the erosions were often red due to congestion. Small intestine usually showed less involvement.

The Peyer's patches, being lymphoid tissue, were severely affected and swollen, dark red to almost black as a result of haemorrhage and may have sloughed completely leaving deep ulcer-like areas. In the large intestine, marked oedema and congestion accompanied by petechiae or larger haemorrhages, particularly along the crests of the longitudinal folds could be very striking, meriting the description zebra striping.

Congestion and erosions may also have been seen in the reproductive and urinary tracts.

The mucosa of the upper respiratory tract, including the larynx, was congested and usually covered with mucopurulent exudate. Petechiae were frequent and necrotic, erosive lesions may have extended from the nares to the larynx. The tracheal mucosa was frequently congested.

Skin lesions were seen rarely and consisted of exudative dermatitis which would develop from macular to pustular lesions.

Although RV had a predilection for lymphoid tissues, there were usually few visible changes to the superficial and visceral lymph nodes. These may have shown congestion, oedema, and a few petechiae. The nodes of animals that died after a prolonged clinical course may have bene shrunken and showed greyish radial streaks in the cortex, presumably due to haemorrhage. The spleen and haemolymph nodes appeared normal or slightly enlarged.

The essential histopathology of rinderpest was widespread necrosis of lymphocytes throughout the lymphoid tissues, together with syncytia and intracytoplasmic and (less frequently) intranuclear inclusion bodies. Lytic destruction of lymphoid tissues, especially germinal centres, sometimes accompanied an increase in the numbers of macrophages. Lesions in the squamous epithelium of the digestive tract became necrotic and sloughed off, leaving clearly demarcated erosions.

Treatment

Rinderpest was a viral disease and there was no specific therapeutic treatment.

Symptomatic treatment for diarrhoea and supportive antibiotic and fluid replacement therapy might conceivably have been useful in preventing the death or aiding recovery of important individual animals. However, in practice few animals were treated.

Control

The development of live attenuated vaccines against morbillivirus diseases was the key to achieving effective control of Rinderpest, because the immunity they generated was long lived and cell-mediated. In the early 1960s a cell-culture-attenuated vaccine was introduced which was completely safe and relatively easy to produce and induced no clinical signs following inoculation into domestic animals. In addition, the virus did not replicate at epithelial surfaces and could not be transmitted by contact. They did however have a short shelf-life.

This was the main weapon which succeeded in eradicating Rinderpest.

Rinderpest Learning Resources
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References

OIE Handistatus, (2004) World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE, (2009) World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. OIE

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 5 April 2011.