Etiology
This is caused by paramyxovirus which is antigenically related to PPR, canine distemper and human measles virus.
Distribution
The disease is endemicin tropical Africa and Asia. It has been reported in Middle East.
Transmission
Transmission is by contact between infected/carrier animals and healthy ones. The virus is present in nasal and oral secretions, urine, faeces and expired air. Infected droplets are inhaled and the virus enters the body through the upper respiratory mucosa. Infection can be acquired by ingestion of contaminated feed and water.
Epidemiology
Cattle are susceptible to the disease but also pigs, bufallos, camels, sheep and goats. The later animals are relatively resistant but do not contract the disease in the field. Faeces, urine and discharges from the infected animals are infectious and transmission readily occurs. Close contact of infected and susceptible animals is necessary for transmission; aerosols and insects are most unlikely method of spread. Contaminated premises may be infectious for 6-8 hours after removal of affected animals. Contaminated urine without ventilation or sunlight may remain infective for 96 hours because rinderpest virus is very sensitive to environmental conditions and easily killed by heat and drying and by most disinfectants. After natural infection, animal develop protective immunity for a long time but the immunity is not lifelong. Other infected animals like camels, sheep, goats and bufallos may spread the infection to cattle if they are together.
Clinical signs
The signs observed in cattle are mild in sheep and goat. They are as follows:
High temperature about 107oF
Serous to mucopurulent nasal discharge and conjunctivitis
Anorexia
Reduction of milk production in lactating animals
Muscle is cracked, dry and necrotic erosions on mucous membrane of the mouth, inside lips,, hard palate, dental pad, ventral surface of tongue.
Necrosis may spread inside the nostrils, turbinates and mucopurulent nasal discharge may develop.
Diarrhea commonly occurs.
Congestion of vaginal mucous membrane and mucous membrane of the prepuce of the male occur.
Gray spots with the size of the pin head appear on the gum, lips and under the tongue and these mature into ulcers which may increase and coalesce.
Lips and gums swell and the animal salivate freely. Affected mucous membrane may be covered with an exudation and the same changes takes place in vagina/prepuce.
Faeces are soft, mucus covered and thin, turn black or may be blood stained.
The animal is depressed, grind its teeth, become debilitated, waste away and die from 2-8 days after the fever first occurs.
Abortion happens in pregnant animals. Convalescence occurs early. Mouth lesions start to heal 3-5 days after the appearance. Buccal papillae may remain reddened and eroded up to the end of second week of clinical reaction. Morbidity may reach 100% and mortality may be greater than 90%.
Post-mortem findings/lesions
The mouth is ulcerated and necrotized. The abdomen is congested and shows ulceration. Lymphoid patches of intestine become necrotic and this may be extensive enough to cause sloughing of the underlying epithelium leaving deep ulcers outlined clearly by clotted blood. Small intestine are inflamed and ulcerated. Kidneys and urinary bladder may show haemorrhages and gall bladder ulcerated. Respiratory tract is inflamed with some mucous haemorrhages in nose and trachea together with mucopurulent discharges. There may be haemorrhages and ulcerations in the uterus and vagina.
Diagnosis
This is based on clinical signs, post-mortem findings and lesions, epidemiology; isolation and recognition of the virus.
Differential diagnosis
Foot and mouth disease
Blue tongue
Sheep and goat pox
PPR
Coccidiosis
Orf
Salmonellosis
Bovine malignant catarrhal fever
Infectious bovine rhinotracheitis
Bovine papular stomatitis
Immunity
Immunity of long duration may be conferred on animals after natural infection. Young animals born to immune mothers are passively protected via ingestion of colostrums. Duration of this passive immunity is 4-12 months
Attenuated tissue culture vaccine is available. It produces a durable immunity.
Prevention and control
Of all the major disease of domestic livestock, rinderpest is considered to be the most readily controlled. It is well established that following introduction of rinderpest in disease free countries, effective control could be achieved by policy of slaughter and quarantine. The strategy for controlling rinderpest in disease free countries depends on whether they are geographically remote from or bordering enzootic regions. In either case, the most common route of introduction is by movement of large infected or carrier animals. In countries remote from enzootic areas, it is generally the policy to ban the importation of large animals and unprocessed animal products from rinderpest infected countries. Animals must be held on isolation in an area of exporting countries free from rinderpest and for a similar period of isolation on arrival at importing country. If there is a breakdown, it is essential that the national veterinary department must have legislative authority to immediately slaughter infected ruminants and pigs and to destroy or bury the carcasses. Animal houses and enclosures in infected zone must be isolated and disinfected and the movement of livestock, meat/hides prohibited.
In high risk countries, it is customary to minimize the whole cattle population or create a barrier zone of immunized cattle in regions adjacent to countries where rinderpest is enzootic. In these areas, cattle are vaccinated followed by annual vaccination. The principal strategy for control in enzootic region is by mass vaccination. It has been the policy to vaccinate all cattle each year for 3 consecutive years. Following the initial phase of annual vaccination, it is essential to maintain the annual vaccination of the previous years’ calf crop. Adequate quarantine and surveillance must be maintained.
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