Perversely ... as one morbillivirus of farm animals ceases to be important, another moves to centre stage. Deaths among small ruminants due to PPRV continue to mount in the form of rolling epidemics moving across international borders to the extent that PPR is now regarded as the most constraining disease of small ruminant production across sub-Saharan Africa and the Indian subcontinent. (Taylor and Barrett, 2009).
Peste des petits ruminants (PPR) is an acute or sub-acute viral disease primarily of goats and sheep characterised by fever, a catarrhal ocular and nasal discharge, pneumonia, necrotic stomatitis, diarrhoea and high morbidity and mortality. It was first diagnosed in Cote-d'ivoire, West Africa in 1942 although the source may have been from Asia (Taylor and Barrett 2007). The disease, which can devastate sheep and goat populations, is now widespread across Africa, the near and Middle East and Asia (Figure 1). While it appears that the disease has spread rapidly, this may in part be a reflection of better diagnostic tools, increased awareness or even a change in the nature of the virus (FAO). It has been estimated that 62.5% of world's small stock are at risk from PPR.
The virus responsible for PPR is a morbillivirus closely related to rinderpest virus, distemper virus in candids and measles in humans. Some deer species may develop the disease while others may become infected sub-clinically. However, it does not affect people and while causing sero-conversion in cattle and pigs, produces no clinical disease (Taylor and Barrett 2007, AUSVETPLAN 2009).
The virus requires close contact to spread and does not survive long in the environment. As with the other morbilliviruses, vaccines are highly effective. Most outbreaks are associated with the recent introduction of infected livestock (Taylor and Barrett 2007).
Peste des petits ruminants virus (PPRV) attacks the alimentary, respiratory and lymphoid systems following initial multiplication in retropharyngeal mucosa and a viraemia. The clinical findings and pathology are referable to necrosis and in the case of the respiratory system, cellular proliferation (Radostits et al 2007).
After a short incubation (2 - 6 days), affected animals develop a marked fever (40 - 42°C), severe depression and anorexia. Some acute cases die suddenly. A few days after the onset of the disease animals develop a clear, watery ocular, nasal and oral discharge, which progresses to a thick purulent discharge following secondary bacterial infection. These discharges matt the eyelids and obstruct the nasal passages. The characteristic epithelial necrosis of the bucchal cavity (and sometimes the mucous membranes of the nose, vulva and vagina) then develops (Figure 2). In some cases, this produces a thick, cheesy, foul smelling exudate covering the oral membranes. Affected animals also develop a diarrhoea, which is initially soft, and then proceeds to become watery, foul smelling and may contain blood and necrotic intestinal casts. Dyspnoea and coughing is also a feature of the disease as animals develop pneumonia. Death may occur after an illness of 7-10 days but some recover after a lengthy convalescence (FAO).
In endemic areas, sheep and goats between 4 and 18-24 months of age are most likely to be affected. Goats are usually more severely affected than sheep.
Post-mortem findings relate to cellular necrosis of the tissues of the alimentary and lymphatic systems and proliferative lesions of the lungs. The nasal cavity is hyperaemic with erosions and thick mucus. There is a patchy to general pneumonia and the pulmonary and mesenteric lymph nodes are swollen. The abomasum and small intestines appear red, congested, and gastro-intestinal haemorrhages and 'zebra stripes' may be noted in the large intestine.
PPRV affects multiple organ systems. A veterinarian confronted with an outbreak of PPR in Australia would be alerted to the disease if faced with a syndrome of rapid onset fever, nasal and ocular secretions, respiratory signs and severe diarrhoea. However, in unusual or early cases only some of these symptoms might be present and the diagnosis missed.
The differential diagnosis of sick sheep or goats with diarrhoea and respiratory disease would include salmonellosis, lactic acidosis and pasteurellosis with concurrent gastro-intestinal parasitism or bacterial infection. Contagious Caprine Pleuropneumonia should be considered in a disease outbreak in goats but sheep would not be affected. Foot and mouth disease and bluetongue should both be on the differential list of disease causing oral lesions while coccidiosis and Nairobi Sheep Disease both cause diarrhoea. The differential diagnosis of facial lesions should include Sheep Pox, Orf and photosensitisation.
The virus can be isolated from swabs of the conjunctival sac and from the rectal, bucchal and nasal mucosa. Blood samples should be collected and lymph node and spleen samples considered (AUSVETPLAN, 2009).
As the PPR virus survives only briefly outside the host and Australia does not permit the importation of live sheep or goats, the risk of importing the virus is limited. However, the virus can survive in semen and embryos so their illegal importation poses a risk. An uncontrolled outbreak of PPR however would have serious consequences for the Australian sheep and goat industries. Our feral goat population could act as a reservoir and would need to be contained in this event. (AUSVETPLAN, 2009).
In some African countries, PPR is the single most important threat to sheep and goats. In Nigeria for example, with a petite ruminant population of 51 million head, PPR causes 'periodic outbreaks of disease (that) literally wipe out almost all of the stock of sheep and goats' (Dilli et al 2011). PPR has not yet spread to South Africa but remains an important threat (hence the title of this paper). With Australia's quarantine restrictions prohibiting the importation of live animals, PPR is less of a threat but its spread through Asia increases that risk.
In Australia's naive and highly susceptible small ruminant population, PPR should present as a distinct dramatic disease of high morbidity and mortality. It could become present with less obvious clinical signs in either sheep or goats. If the acute stage of an outbreak was missed, the chronic sequelae may be misleading. For example, the residual face lesions might be mistaken for Orf. In Turkey, PPRV was first officially reported in 1999 but could well have been present before then. It is now widespread. In most cases the disease presented with excessive ocular and nasal discharge, mild ulcerative stomatitis, dyspnoea and coughing. Severe mucosal lesions and diarrhoea were not a feature of the disease (Ozkul et al 2002).
PPR is the small ruminant version of rinderpest (with the important diagnostic distinction that rinderpest does not cause primary pneumonia, Brown et al 1991). It is a disease of great significance as it can destroy the livelihood of small-scale farmers in the developing world. However, the virus is readily prevented by vaccination and does not survive long in the environment. It could potentially join small pox and rinderpest as the only virus diseases eradicated from the world (see appendix below).
Appended is an interesting editorial comment from the ProMED moderator on PPR following a report of the disease in Tunisia, posted on 17 May 2011.
PPR is sometimes referred to as pseudorinderpest because its effect on sheep and goats has some parallels clinically and epidemiologically to rinderpest in cattle. PPR or pseudorinderpest is very disruptive to small ruminant populations and a major disease of sheep and goats in West Africa, although the kind of explosive outbreaks that characterize the classic pandemics of rinderpest of 18th and 19th century are not the rule for PPR in many places currently.
The analogous nature of Peste des petite ruminants and Rinderpest as well as the fact that OIE and FAO will declare worldwide freedom from Rinderpest disease later this month in Paris begs the questions of the potential for PPR eradication. Rinderpest eradication in cattle, following on the heels of smallpox eradication in humans, represents the second example of a successful viral disease eradication campaign.
Rinderpest is particularly closely tied to the history of the veterinary profession whose origins literally started with Rinderpest. In 1761, Claude Bourgelat managed to persuade King Louis XV of France of the need to train specialists to treat animal diseases. By decision of the King, the world's first veterinary school was established in Lyon, France. Bourgelat was a true visionary. He had secured the King's support because rinderpest was ravaging Europe's countryside and ruining the rural economy.
While the eradication of Rinderpest is a tremendous boon to animals, humans and societal well-being, it will be interesting to see if the momentum and veterinary infrastructure created by the Rinderpest Eradication campaign can then be leveraged to eliminate PPR or some other animal disease. Resources are critical but taking on Peste des petite ruminants may be just the challenge that is needed to keep the world's veterinary community sharp when it comes to disease control, prevention and eradication.