Group Group V ((−)ssRNA) Family Paramyxoviridae | Order Mononegavirales Genus Morbillivirus | |
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Species Peste-des-petits-ruminants virus |
Ovine rinderpest, also commonly known as peste des petits ruminants (PPR), is a contagious disease primarily affecting goats and sheep in Central and Southern Africa, the Middle East, the Indian subcontinent, and, since June 2008, Morocco. The cases in Morocco indicate a crossing of the natural barrier of the Sahara. It is caused by a species of the Morbillivirus genus of viruses. The disease is highly contagious, and has roughly an 80 percent mortality rate in acute cases.
Contents
- Synonyms
- Signs and symptoms
- Hyperacute cases
- Acute cases at onset
- Evolution of acute cases
- Cause
- Origin and spread
- Geographical repartition
- Dissemination
- Post mortem lesions
- Diagnosis
- Treatment and control
- References
In 2017, it was reported that the disease was affecting saiga in Mongolia, causing near-catastrophic herd depletion for the endangered species.
Synonyms
Traditionally, the name kata was given to stomatitis and pneumoenteritis of the Nigerian dwarf goat. Peste des Petits Ruminants was the French name of a similar disease of sheep and goats first described in Côte d'Ivoire (Ivory Coast) in 1942. These diseases have been shown to be very close to each other.
Many authors prefer the name "Ovine Rinderpest". But official agencies such as the FAO and OIE use the French name "Peste des Petits Ruminants", "Peste Des Petits Ruminants", "Peste-des-Petits-Ruminants" or "Peste-des-petits-ruminants", even in English, although the phrase Goat Plague is becoming more widely used in the popular press. The French acronym, PPR, is commonly used among veterinary professionals in East Africa.
Signs and symptoms
They are similar to those of rinderpest in cattle and involves oral necrosis, mucopurulent nasal and ocular discharges and diarrhoea though they vary according to the previous immune status of the sheep (enzootic or newly infected country). They also vary according to the breed of sheep. However fever in addition to either diarrhoea or signs of oral discomfort is sufficient for the diagnosis.
Incubation period is two to six days.
Hyperacute cases
Hyperacute cases are found dead without previous symptoms. They die with a serous, foamy or haemorrhagic discharge coming out of the nose.
Acute cases at onset
In acute cases, animals are recumbent, sometimes in self-auscultation position.
Body temperature is high (40.5 to 41 °C.) in the beginning of the onset in acute cases.
The most typical signs are seen in the digestive tract. When entering an affected flock, one sees many animals with hind limbs stained by sticky faeces. Some sheep have an arched back and show pain when defecating. Tenesmus may be noticed when taking rectal temperature. Fluid faeces are olive green to brown.
Examination of the mouth shows ulceration of the buccal mucosae, especially on the inner face of the lips, and neighboring gum. There can be periodontitis.
There is serous nasal exudate and conjunctivitis.
Evolution of acute cases
Nasal discharge becomes mucopurulent and may obstruct the nose.
A dry, fitful coughing develops.
Death occurs from 5 to 10 days after the onset of the fever.
Some animals may recover, but a dry, stertorous coughing often persists for some days. Besides coughing, there is intensive labial dermatitis with scab formation, resembling orf.
Abortions may occur.
Cause
Ovine rinderpest is caused by a Morbillivirus – Peste-des-petits-ruminants virus – which is related to but distinct from Rinderpest virus. There are four genotypes (lineages) of the virus. The classification of genotypes is based on the fusion (F) protein gene. Lineage 1 and 2 viruses are only found in West Africa. Viruses of lineage 3 have are generally found in east Africa. The fourth lineage has more recently spread across the Middle East and the Asian sub-continent. Genotype 4 appears to be related to genotype 1.
Origin and spread
This virus appears to have evolved at the start of the 20th century in Nigeria. The extant genotypes subsequently appeared in West Africa (lineages I and II), East Africa and Arabia (lineage III) and Pakistan–India (lineage IV).
The first description of the disease was published in 1942 and relates to an outbreak in Côte d’Ivoire, West Africa in goats and sheep in 1940. It spread to East Africa and Arabia at the beginning of 1980s and to Pakistan and India in early 1990s (Calcutta goat markets) finally reaching Tibet in 2007. The first description of this virus in India was in 1987.
The outbreak in Burkina Faso in 1999 was caused by the lineage 1 group. Genotype 3 has caused outbreaks in Ethiopia (1996) and also in Arabia, southern India and in Tamil Nadu (1992). This lineage was found in Yemen in 2001. Genotype 4 has been isolated in Kuwait in 1999.
Geographical repartition
As of 2017 the disease is present in West Africa, part of Central Africa (Gabon, Central African Republic), East Africa (north of the Equator), the Middle East and the Indian subcontinent including Nepal and Myanmar. The disease is endemic in the Indian subcontinent and is a major threat to fast-growing goat husbandry in India, causing an annual loss of around 1800 million Indian rupees.
In North Africa, only Egypt was once hit. But since summer 2008, Morocco is suffering a generalized outbreak with 133 known cases in 129 provinces, mostly affecting sheep. The outbreak has precipitated the vaccination of a large number of the 17 million sheep and five million goats in the country.
Dissemination
The disease is transmitted by infected aerosols in situation of close contact of animals. The long distance spread is by sick animals. As the virus soon becomes inactive outside the body, indirect contamination is generally limited.
In an affected flock, even in pest-free regions, the disease does not progress very rapidly, in spite of the close contact between animals. New clinical cases may be observed daily for a one-month period.
Post-mortem lesions
The lesions are situated in the digestive tract. Quick post-mortem examination will lead to the discovery of many haemorrhagic patches on the serous membranes, and intense pneumonia. There is a risk that it may conclude with enzootic pneumonia, inability to open the mouth, and problems with the oesophagus and different parts of the intestine.
Erosions and inflammation are widespread on buccal mucosa. The same lesions are also present in pharynx, oesophagus, and on mucus-producing epithelia of the gut, from abomasum to rectum. Zebra-striped lesions on coecum and colon are said to be typical in some cases. Rarely, there are also petechiae on the rumen mucosa.
Diagnosis
History and clinical signs will enable a presumptive diagnosis to be made in endemic regions. The virus can be detected in acute cases from various swabs and blood samples, using PCR and ELISA. Antibodies can also be detected via ELISA.
Treatment and control
Antibiotics such as chloramphenicol, penicillin and streptomycin can be used and supportive treatment may be helpful.
A vaccine has been developed that may decrease death in the flock.
According to the country's policy, there may be movement restrictions, slaughter of affected flocks in an attempt to eradicate the disease.
A global eradication programme has been developed by the Food and Agriculture Organization of the United Nations and the World Organisation for Animal Health. More information can be found on FAO's website on the implementation of this global plan. It is considered feasible to eradicate ovine rinderpest in 15 years.