In endemic areas, most of the sick and dying animals are over four months and up to 18 to 24 months of age.

Clinical signs

Clinical signs appear an average of two to six days after natural infection with the virus (the incubation period). This is followed by the sudden onset of fever with rectal temperature of at least 40° to 41oC. Affected animals are markedly depressed and appear sleepy. Their hair stands erect giving them a bloated appearance, especially the short-haired breeds. Soon after this stage, a clear watery discharge starts to issue from the eyes, nose and mouth, later becoming thick and yellow as a result of secondary bacterial infection (Figure 1). The discharges wet the chin and the hair below the eye; they tend to dry, causing matting together of the eyelids, obstruction of the nose and difficulty in breathing.

One to two days after fever has set in, the mucous membranes of the mouth and eyes become very reddened (Figure 2). Then epithelial necrosis causes small pin-point greyish areas to appear on the gums, dental pad, palate, lips, inner aspects of the cheeks and upper surface of the tongue. These areas increase in number and size and join together. The lining of the mouth is changed in appearance. It becomes pale and coated with dying cells (Figure 3) and, in some cases, the normal membrane may be completely obscured by a thick cheesy material (Figure 4). Underneath the dead surface cells there are shallow erosions. In mild cases these changes may not be severe and will require careful examination to be seen. Gentle rubbing across the gum and palate with a finger may yield a foul-smelling material containing shreds of epithelial tissue. Similar changes may also be seen in the mucous membranes of the nose, the vulva and the vagina. The lips tend to swell and crack and become covered with scabs (Figure 5).

As the disease progresses, a characteristic foul smell exudes from the mouth. Affected animals resist attempts to open their mouths because of the pain.

Diarrhoea commonly appears about two to three days after the onset of fever (Figure 6) although, in early or mild cases, it may not be obvious. The faeces are initially soft and then watery, foul-smelling and may contain blood streaks and pieces of dead gut tissue. Where diarrhoea is not an obvious presenting sign, the insertion of a cotton wool swab into the rectum may reveal evidence of soft faeces which may be stained with blood.

Affected animals breathe fast, sometimes so fast that they exhibit rocking movements with both the chest and abdominal walls moving as the animal breathes. Severely affected cases show difficult and noisy breathing marked by extension of the head and neck, dilation of the nostrils, protrusion of the tongue and soft painful coughs - they have obvious signs of pneumonia.

Such victims may eventually become dehydrated with sunken eyeballs, and death often follows within seven to ten days from onset of the clinical reaction. Other animals will recover after a protracted convalescence.

A common feature in later stages of the disease is the formation of small nodular lesions in the skin on the outside of the lips around the muzzle (Figure 7). The exact cause of these is not known (possibly Dermatophilus infection or reactivation of a latent contagious ecthyma infection - orf or "sore mouth") but they cause confusion because of their similarity to the symptoms of primary contagious ecthyma or even sheep/goat pox.

Up to 100 percent of the animals in a flock may be affected in a PPR outbreak with between 20 and 90 percent dying. These proportions are usually lower in endemic areas where older animals have survived earlier infection. Pregnant animals may abort.

In summary, suspect PPR if you see any combination of:

• the sudden onset of a febrile illness affecting sheep and/or goats; eye, nose and mouth discharges with sores in the mouth, with or without scabs or nodules around the mouth;
• pneumonia;
• a significant death rate.

Post mortem findings

The carcass of an affected animal is usually emaciated, the hindquarters soiled with soft/watery faeces and the eyeballs sunken. The eyes and nose contain dried-up discharges. The following changes may be seen:

Mouth

Dirty-white, false membranes; erosions on the gums, soft and hard palates, tongue and cheeks and into the oesophagus.

Lips

Swollen; erosions and possibly scabs or nodules in late cases.

Nasal cavity

Congested (reddened) lining; clear or creamy yellow exudates; erosions.

Lungs

Dark red or purple areas; firm to the touch, mainly in the anterior and cardiac lobes (evidence of pneumonia) (Figures 8 and 9).

Lymph nodes (associated with the lungs and the intestines)

Soft and swollen. Abomasum Congested (reddened) lining; haemorrhages.

Small intestines

Congested (reddened) lining; haemorrhages; some erosions.

Large intestines (caecum, colon and rectum)

Small red haemorrhages along the folds of the lining, joining together as time passes and becoming darker, even green/black in stale carcasses (Figure 10).

Differential diagnosis

PPR is frequently confused with other diseases that present fever and grossly similar clinical signs, especially when it is newly introduced. When carrying out an investigation, examination of the way the disease behaves in the herd or flock is as important as the findings on a single goat or sheep. The most frequent sources of confusion are:

Mouth lesions

Could be a symptom of: rinderpest, foot-and-mouth disease, bluetongue or contagious ecthyma (orf or "sore mouth").

Difficult breathing

Could be a symptom of: pneumonic pasteurellosis or contagious caprine pleuropneumonia (CCPP).

Diarrhoea

Could be a symptom of: coccidiosis or gastro-intestinal helminth infestations. Pneumonia is usually a very obvious presenting sign in PPR so, without doubt, pneumonic pasteurellosis and CCPP have caused the most difficulty in differential diagnosis.

Pneumonic pasteurellosis

is a purely respiratory disease of sheep and goats caused by the bacterium Pasteurella haemolytica. Dark red/purple areas, firm to the touch, are evident mainly in the anterior and cardiac lobes of the lung (Figure 9). There are no oral lesions or diarrhoea. The numbers of affected and dead animals are usually lower than for PPR except under exceptional conditions of stress and crowding such as can occur when large numbers of sheep are assembled for trade. The main problem of differentiation arises when oral lesions and diarrhoea are either absent or not very obvious in PPR, as is sometimes the case. Using appropriate culture media, Pasteurella haemolytica bacteria are easily isolated in pure and profuse culture from pneumonic lungs of sheep, even from the lungs of PPR-affected animals. Isolation of Pasteurella haemolytica bacteria from the lungs of sheep, therefore, neither confirms a diagnosis of primary pneumonic pasteurellosis nor rules out the presence of PPR. Diagnostic tests for detecting PPRV should be carried out in all suspected cases of pneumonic pasteurellosis where there is a risk of PPR.

Contagious caprine pleuropneumonia (CCPP)

is a disease of goats (sheep are not affected) caused by a Mycoplasma sp. Like PPR, it is characterized by fever, difficult/abnormal breathing and coughing, but there mouth lesions or diarrhoea are not present in CCPP. At post mortem examination, the lung lesions in CCPP are more diffuse and a fibrinous fluid is found in the chest cavity. Fibrin deposits cover the lungs and are frequently connected to the chest wall by fibrinous strands (Figure 11). In PPR high-risk areas it is advisable to rule out PPR by laboratory testing of, at least, serum samples from convalescent flocks, even if CCPP is suspected.

Rinderpest disease

in small ruminants has been described primarily in Asia. Generally, this disease occurs in small ruminants only when they are in contact with affected cattle or buffaloes, so it is important during investigations to examine all species. Confirmation requires the resources of a specialist laboratory (see Sources of assistance). The samples required for laboratory confirmation of both rinderpest and PPR are identical. As the Global Rinderpest Eradication Programme (GREP) progresses, it becomes increasingly important that PPR and rinderpest be differentiated because, at this stage of the programme, any outbreak of rinderpest anywhere represents an international emergency.

Foot-and-mouth disease (FMD)

is more commonly seen in sheep than goats. The most important distinguishing features of FMD, other than the appearance of the lesions, are the absence of breathing problems and diarrhoea, and the presence of lameness (often marked). Sudden death of very young lambs without other signs often occurs. The oral lesions when present are often very small and difficult to see; the mouth does not exude such a foul odour as in PPR. Bluetongue, like PPR, is characterized by fever, discharges and oral lesions (Figure 12). However, it differs from PPR in: the presence of oedema of the head region; bluish discoloration of the oral cavity, the coronary band of the hooves and the less hairy parts of the body; and lameness.

Bluetongue

virus infection is endemic throughout the regions of the world affected by PPR. Clinical disease is, however, not generally experienced in indigenous breeds in these countries, being mainly restricted to exotic introduced animals. The presence of antibody to bluetongue viruses in single samples does not confirm a provisional diagnosis of bluetongue.

Contagious ecthyma (orf, "sore mouth", contagious pustular dermatitis)

is often confused with PPR because of the nodules and thick scabs sometimes seen on the lips in the late stages of PPR. Confusion is especially likely to arise in severe cases of orf where lesions extend into the mouth and nose. In uncomplicated orf, there is usually no oral necrosis, diarrhoea or pneumonia.

Diagnosis of PPR

The International Office of Epizootics (OIE) Manual of Standards for Diagnostic Tests and Vaccines contains guidelines on the collection of samples and the diagnostic techniques for diagnosis of PPRV infection. A provisional diagnosis of PPR can be made from epidemiological and clinical features. A disease characterized by discharges, diarrhoea, and deaths with breathing problems in sheep and/or goats, but not in-contact cattle, with mainly adolescents being affected and dying must arouse a suspicion of PPR. The observation of characteristic post mortem changes would further strengthen the provisional diagnosis.

Laboratory confirmation

Because of the necessity to detect PPR amid a number of other acute diseases with grossly similar presenting signs, and to differentiate it from rinderpest, some laboratory tests need to be carried out. These tests may detect the virus itself, evidence of the presence of the virus (virus antigen or genetic material) or antibodies against the virus found in blood serum.

Detection of virus antigens by the agar gel immunodiffusion test (AGIDT) is a relatively simple, fast and cheap process. It is extremely useful as an initial test, but it does not discriminate between PPR and rinderpest viruses and further tests are needed to do this. Histopathology combined with immunohistochemical staining (e.g. immunoperoxidase) is a useful procedure because it is performed on formalin-fixed material and can discriminate between PPR and rinderpest when performed with specific monoclonal antibodies. Virus antigens can also be detected by immunocapture ELISA (ICE) which is rapid and sensitive, and differentiates between PPR and rinderpest. Standardized reagent kits are commercially available for AGIDT and ICE.

Detection of virus genetic material is performed by the reverse transcriptase polymerase chain reaction (RT PCR) which requires specialist facilities and expertise. Despite its high cost, it is now one of the tests used most frequently in reference centres, together with enzyme linked immunosorbent assay(ELISA), because it is rapid, accurate, highly sensitive and can discriminate between PPR and rinderpest. Combining this test with nucleotide sequencing provides virus characterization information that is useful in epidemiological studies. Detection of the virus is done by isolation of the PPR virus in cultured cells. This method of diagnosis can be very valuable as it provides live virus for biological characterization studies. If facilities are available, it should always be attempted and isolated viruses stored for later studies.

Detection of antibodies for diagnosis requires the collection of two blood samples, three weeks apart, from the same animals, which is not always feasible in the field. Exceptionally, in a country that can be certain that it was free from PPR, testing single samples taken late in the course of the disease (at least a week after the appearance of clinical signs) can be diagnostic. Surveys for antibodies are very useful to determine the presence or absence of infection and its extent in a population. Competitive ELISA has now largely replaced the virus neutralization test.

Samples required for laboratory testing

The chances of a successful laboratory confirmation of the clinical diagnosis increase as the numbers of samples examined and animals sampled increase. There are several important points to observe when using the services of a laboratory:

1. Provide epidemiological and clinical details with the samples.
2. Always sample several animals in an outbreak.
3. Keep samples cool during transfer to the laboratory (preferably on melting ice) and reduce the time in transit to the minimum.
4. Mark sample bottles carefully with an indelible pen and record details of each sample's origin for submission to the laboratory.

The samples required are:

Tears

Cotton buds or swabs of absorbent cotton wool are inserted into the conjunctival sac and swirled around to collect tears. The bud/swab is broken off into a container and about 150 microlitres of sterile phosphate-buffered saline (PBS pH 7.2 to 7.6) are added (if available).

Gum debris

This material can be collected by a spatula or finger rubbed across the gum and inside the upper and lower lips. The material collected is then scraped into a container and 150 microlitres of PBS are added (if available).

Tissues

It is recommended that the following tissues be collected during post mortem examination: lymph nodes found around the lungs (mediastinal) and alimentary tract (mesenteric); portions of the spleen and the lungs.

Two sets of each tissue are required; one set is chilled but not frozen, and the other is put in 10 percent formalin solution to preserve the samples. Where cold storage is a problem, as is often the case, formalin can be used to preserve the samples when they are sent to the laboratory.

Unclotted blood

This is needed for virus isolation and should be collected in bottles containing anticoagulants (heparin or ethylenediamine tetracetic acid [EDTA]).

Clotted blood or serum

These are needed for antibody detection.

National laboratories will provide guidance about exactly which samples are required, but it is advisable to collect as many of the samples listed above as possible when dealing with an outbreak.

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Control of PPR

Control of PPR outbreaks relies on movement control (quarantine) combined with the use of focused ("ring") vaccination and prophylactic immunization in high-risk populations. Until recently, the most practical vaccination against PPR made use of tissue culture rinderpest vaccine. Recently, a homologous PPR vaccine has been developed and the vaccine seed is available through the Pan African Veterinary Vaccine Centre (PANVAC) at Debre Zeit, Ethiopia, for Africa, or CIRAD-EMVT at Montpellier, France, for other areas. This vaccine of choice is becoming increasingly available. The vaccines can protect small ruminants against PPR for at least three years.

The use of rinderpest vaccine to protect small ruminants against PPR is now contraindicated because its use produces antibodies to rinderpest which compromise serosurveillance for rinderpest, and thereby the Global Rinderpest Eradication Programme.

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Sources of assistance

Differentiating between rinderpest and PPR to obtain a definitive identification of PPR can be difficult, especially when the disease is encountered for the first time and national laboratories lack adequate facilities. Samples for diagnostic confirmation can be submitted to either the FAO World Reference Laboratory for Rinderpest at the Institute for Animal Health, Pirbight Laboratory, United Kingdom or the FAO Collaborating Centre at the International Cooperation Centre on Agrarian Research and Development, Department of Breeding and Tropical Veterninary Medicine (CIRAD-EMVT) Laboratory, Montpellier, France, which can assist with the diagnosis of PPR. Addresses are given below.

It should be noted that submission of samples to any laboratory outside the country of origin is always subject to prior agreement with the recipient and transportation in containers meeting International Air Transport Association (IATA) regulation standards. Detailed instructions for the collection and dispatch of rinderpest samples (which are also applicable to PPR samples) are contained in the publication Collection and submission of diagnostic specimens to the FAO World Reference Laboratory for Rinderpest, which can be obtained from FAO EMPRES; it can also be supplied electronically as an attachment to e-mail or by fax on request.

FAO World Reference Laboratory for Rinderpest, Reference Laboratory for PPR  
Institute for Animal Health Pirbright Laboratory Ash Road Pirbright ,Woking, Surrey GU24 0NF, United Kingdom,
Tel. +44 1483 232441 Fax + 44 1483 232448 E-mail [email protected]

FAO Reference Laboratory for PPR  
CIRAD-EMVT Campus international de Baillarguet Montferrier-sur-Lez BP 5034 34032 Montpellier Cedex 1 France
Tel. +33 4 67593705 Fax +33 4 67593798 E-mail [email protected]

FIGURE 1: PPR in a goat: purulent eye and nose discharges Discharges from the nose and eyes in advanced PPR infection; the hair below the eyes is wet and there is matting together of the eyelids as well as partial blockage of the nostrils by dried-up purulent discharges.

FIGURE 2: PPR in a goat: inflamed (reddened) eye membranes Reddening of the mucous membranes of the eye (the conjunctiva) in the early stages of infection. Note the purulent eye discharges.

FIGURE 3: PPR in a goat: early mouth lesions showing areas of dead cells Early pale, grey areas of dead cells on the gums.

FIGURE 4: PPR in a goat: later mouth lesions The membrane lining the mouth is completely obscured by a thick cheesy material; shallow erosions are found underneath the dead surface cells.

FIGURE 5: PPR in a goat: swollen, eroded lips The lips are swollen, oedematous and show areas of erosion.

FIGURE 6: PPR in a goat: signs of diarrhoea The hindquarters are soiled with liquid faeces.

FIGURE 7: PPR in a goat: nodular lesions around the mouth Such nodules are a common finding in the later stages of PPR infection.

FIGURE 8: PPR in a goat: the early lesions of pneumonia Note the small, red, solid areas of lung tissue caused directly by PPR virus infection.

FIGURE 9: PPR in a sheep: advanced pneumonia Note the extensive, dark red/purple areas, firm to the touch, in the anterior and cardiac lobes of the lungs. Although such pneumonia is commonly seen in PPR, it is caused by secondary bacterial infection, most commonly Pasteurella haemolytica. These lesions are typical of pneumonic pasteurellosis.

FIGURE 10: PPR in a goat: "zebra striping" in the large intestine Note the lines of haemorrhage along the tips of the folds of the lining of the caecum and colon. Later, the individual haemorrhages join up and, after death, turn black.

FIGURE 11: Typical lesions of contagious caprine pleuropneumonia (CCPP) in a goat Note the yellowish, fibrinous deposit on the surface of the lungs and adhesions to the inside of the rib cage.

FIGURE 12: Bluetongue disease in a sheep Note the bluish discoloration of the coronary bands of the hoof. The lips will usually be found to be swollen and discoloured blue at the same time.