Definition
Peste des petits ruminants (PPR) is an acute or subacute viral
disease of goats and sheep characterized by fever, erosive stomatitis, conjunctivitis,
gastroenteritis, and pneumonia. Goats are usually more severely affected than sheep.
Etiology (1,2,9,16)
Peste des petits ruminants is caused by a paramyxovirus of the Morbillivirus genus. Other members of the genus include rinderpest virus (RPV), measles virus (MV),
canine distemper virus (CDV), and phocid distemper virus (PDV) of sea mammals (seals). For
many years, PPR virus was considered a variant of RPV, specifically adapted for goats and
sheep, that had lost its virulence for cattle. It is now known that the two viruses are
distinct though closely related antigenically.
Host Range (8)
Peste des petits ruminants is primarily a disease of goats and
sheep. However, there is one report of naturally occurring PPR in captive wild ungulates
from three families: Gazellinae (dorcas gazelle), Caprinae (Nubian
ibex and Laristan sheep), and Hippotraginae (gemsbok). Experimentally, the American
white-tailed deer (Odocoileus virginianus) is fully susceptible. The role of
wildlife on the epizootiology of PPR in Africa remains to be investigated. Cattle and pigs
are susceptible to infection with PPRV, but they do not exhibit clinical signs. Such
subclinical infections result in seroconversion, and cattle are protected from challenge
with virulent RPV. Cattle and pigs do not, however, play a role in the epizootidogy of PPR
because they are apparently unable to transmit the disease to other animals.
Geographic Distribution (7,12,13,21)
Presently, PPR occurs in most African countries situated in a wide
belt between the Sahara and Equator, the Middle East (Arabian Peninsula, Israel, Syria,
Iraq, Jordan), and the Indian subcontinent.
Transmission
Peste des petits ruminants is not very contagious and transmission
requires close contact. Ocular, nasal, and oral secretions and feces are the sources of
virus. Contact infection occurs mainly through inhalation of aerosols produced by sneezing
and coughing. Fomites such as bedding may also contribute to the onset of an outbreak. As
in rinderpest (RP), there is no known carrier state. Infected animals may transmit the
disease during the incubation period.
Incubation Period
Peste des petits ruminants has an incubation period of 4 to 5
days.
Clinical Signs (11,12,14,15,21)
The disease usually appears in the acute form, with an incubation
period of 4 to 5 days followed by a sudden rise in body temperature to 104-106° F
(40-41° C). The temperature usually remains high for about 5 to 8 days before slowly
returning to normal preceeding recovery or dropping below normal before death. Affected
animals appear ill and restless and have a dull coat, dry muzzle, and depressed appetite.
Accompanying these nonspecific signs are a series of changes that make up a highly
characteristic syndrome. From the onset of fever, most animals have a serous nasal
discharge, which progressively becomes mucopurulent. The discharge may remain slight or
may progress, resulting in a profuse catarrhal exudate, which crusts over and occludes the
nostrils. At this stage, animals have respiratory distress, and there is much sneezing in
an attempt to clear the nose. Small areas of necrosis may be seen on the visible nasal
mucous membranes. The conjunctiva usually becomes congested, and the medial canthus may
have some crusting. As with the nose, there may be profuse catarrhal conjunctivitis
resulting in matting of the eyelids (Fig. 88).
Necrotic stomatitis is common. It starts as small, roughened, red,
superficial necrotic foci on the gum below the incisor teeth. These areas may resolve
within 48 hours or progressively increase to involve the dental pad, the hard palate,
cheeks and their papillae, and the dorsum of the anterior part of the tongue. Necrosis may
result in shallow irregular nonhemorrhagic erosions in the affected areas of the mouth and
deep fissures on the tongue. Necrotic debris may collect at the oral commissures, and
scabs may form along the mucocutaneous junction of the lips. There may be excessive
salivation but not to the extent of drooling.
At the height of development of oral lesions, most animals
manifest severe diarrhea, often profuse but not hemorrhagic. As it progresses, there is
severe dehydration, emaciation, and dyspnea followed by hypothermia, and death usually
occurs after a course of 5 to 10 days. Bronchopneumonia, evidenced by coughing, is a
common feature in the later stages of PPR. Pregnant animals may abort.
Secondary latent infections may be activated and complicate the
clinical picture.
Gross Lesions (4,5,11,17)
The pathology caused by PPR is dominated by inflammatory and
necrotic lesions in the mouth and the gastrointestinal tract. Unlike RP, there is also a
definite, albeit inconstant, respiratory system component; hence, the synonym
stomatitis-pneumoenteritis complex.
Emaciation, conjunctivitis, erosive stomatitis involving the
inside of the lower lip and adjacent gum, cheeks near the commissures, and the free
portion of the tongue are frequent lesions. In severe cases, lesions may also be found on
the hard palate, pharynx, and upper third of the esophagus (Fig. 89). The necrotic lesions do not evolve into ulcers because
the basal layer of the squamous epithelium is rarely penetrated.
The rumen, reticulum, and omasum rarely have lesions. Sometimes,
there may be erosions on the pillars of the rumen. The abomasum is a common site of
regularly outlined erosions and often oozes blood.
Lesions in the small intestine are generally moderate, being
limited to small streaks of hemorrhages and, sometimes, erosions in the first portion of
the duodenum and the terminal ileum. Peyer's patches are the site of extensive necrosis,
which may result in severe ulceration. The large intestine is usually more severely
affected with congestion around the ileocecal valve, at the ceco-colic junction, and in
the rectum. In the posterior part of the colon and the rectum, discontinuous streaks of
congestion ("zebra stripes") form on the crests of the mucosal folds.
In the respiratory system, small erosions and petechiae may be
visible on the nasal mucosa, turbinates, larynx, and trachea. Bronchopneumonia may be
present, usually confined to the anteroventral areas and is characterized by consolidation
and atelectasis. There may be pleuritis, which may become exudative and results in
hydrothorax.
The spleen may be slightly enlarged and congested. Most lymph
nodes throughout the body are enlarged, congested, and edematous. Erosive vulvovaginitis
similar to the lesions in the oral mucocutaneous junction may be present.
Morbidity and Mortality (13,21)
The incidence of PPR in an enzootic area may be similar to that of
rinderpest (RP) in that a low rate of infection exists continuously. When the susceptible
population builds up, periodic epizootics (outbreaks) occur, that receive more attention
than usual. Such epizootics may be characterized by almost 100 percent mortality among
affected goat and sheep populations.
The prognosis of acute PPR is usually poor. The severity of the
disease and outcome in the individual is correlated with the extent of mouth lesions.
Prognosis is good in cases where the lesions resolve within 2 to 3 days. It is poor when
extensive necrosis and secondary bacterial infections result in an unpleasant, fetid odor
from the animal's breath. Respiratory involvement is also a poor prognostic sign. A
morbidity rate of 80-90 percent and a casefatality rate of 50-80 percent are not uncommon
— particularly in goats.
Young animals (4 to 8 months) have more severe disease, and
morbidity and mortality are higher. Both field and laboratory observations indicate that
PPR is less severe in sheep than in goats. Nevertheless, field outbreaks have been
reported in the humid zones of west Africa in which no distinction could be made between
the mortality rates in sheep and in goats. Poor nutritional status, stress of movement,
and concurrent parasitic and bacterial infections enhance the severity of clinical signs.
Diagnosis (7,9,13,19-22)
Field Diagnosis
In the field, a presumptive diagnosis can be made on the basis of
clinical, pathological, and epizootiological findings.
Laboratory confirmation is an absolute requirement —
particularly in areas or countries where PPR has not previously been reported.
Specimens for Laboratory
Specimens to submit include blood in EDTA anticoagulant, clotted
blood or serum (if possible, paired sera), mesenteric lymph nodes, spleen, lung, tonsils,
and sections of the ileum and large intestine.
Swabs of serous nasal and lachrymal discharges may also be useful.
All samples should be shipped fresh (not frozen) on ice within 12 hours after collection.
Laboratory Diagnosis
A wide range of laboratory procedures have been described for
detecting virus or viral antigen, viral nucleic acid, and antibody.
Differential Diagnosis (1)
Rinderpest. Clinical RP is rare in goats and sheep in Africa. In
India, these species are quite often involved in RP outbreaks. Clinically, RP and PPR are
similar, but the former should be the prime suspect if the disease involves both cattle
and small ruminants.
Confirmation requires virus isolation and cross-neutralization.
Pasteurellosis. Enzootic pneumonia or the septicemic form of
pasteurellosis is characterized by obvious respiratory signs, infrequent diarrhea, and a
fatality rate rarely exceeding 10 percent.
Contagious caprine pleuropneumonia. There is no digestive system
involvement, and the clinical signs and lesions are confined to the respiratory system and
pericardium.
Bluetongue. Swelling of the lips, muzzle, and oral mucosa,
together with edema of the head region, should serve to differentiate bluetongue from PPR.
Coronitis, common in bluetongue, is not a feature of PPR. Also, sheep are more affected
than goats.
Heartwater. There is often central nervous system involvement,
including convulsions. There is no diarrhea.
Contagious ecthyma (contagious pustular dermatitis, orf). The orf
virus causes proliferative, not necrotic lesions, that involve the lips rather than the
whole oral cavity. The absence of nasal discharges and diarrhea also distinguish orf from
PPR.
Foot-and-mouth disease. This condition is comparatively mild, and
the most characteristic clinical sign, lameness, is not a feature of PPR.
Nairobi sheep disease. Sheep are more severely affected than
goats. It is limited geographically to parts of east and central Africa (Kenya, Uganda,
Tanzania, Ethiopia, Somalia and Congo [formerly Zaire]). Diagnosis requires isolation and
serologic identification of the virus.
Coccidiosis. There is no upper digestive tract and respiratory
system involvement.
Plant or mineral poisoning. Several plants and minerals may cause
severe intestinal lesions. Case history and absence of fever should distinguish poisoning
from PPR.
Treatment
There is no specific treatment for PPR. However, drugs that
control bacterial and parasitic complications may decrease mortality.
Vaccination
The tissue culture rinderpest vaccine at a dose of 102.5 TCID50 protects goats for at least 12 months against PPR. The vaccine is currently used in many
African countries for vaccination against PPR. The efficacy notwithstanding, its wide use
is disadvantageous for the ongoing Pan-African rinderpest campaign (PARC) because it is
impossible to determine if seropositive small ruminants have been vaccinated or naturally
infected with RPV. A homologous attenuated PPR vaccine is being tested and may soon be
commercially available.
Control and Eradication (3,6,13,21)
Eradication is recommended when PPR appears in new areas. Methods
that have been successfully applied for RP eradication in many areas would be appropriate
for PPR. These should include quarantine, slaughter, and proper disposal of carcasses and
contact fomites, decontamination, and restrictions on importation of sheep and goats from
affected areas.
Public Health
Peste des petits ruminants is not infectious for humans.
GUIDE TO THE LITERATURE
1. APPEL, M.J.G., GIBBS, E.P.J., MARTIN, S.J., TER MEULEN, V.,
RIMA, B.K., STEPHENSON, J.R. and TAYLOR, W.P. 1981. Morbillivirus Diseases of Animals and
Man. In Comparative Diagnosis of Viral Diseases IV, E. Kurstak and C. Kurstak, eds.
New York:Acad. Press, pp. 235-297.
2. BOURDIN, P., and LAURENT-VAUTIER, A. 1967. Note sur la
structure du virus de la peste des petits ruminants. Rev. Elev. Med. Vet. Pays Trop., 20:
383-386.
3. BOURDIN, P., RIOCHE, M., and LAURENT, A. 1970. Emploi d'un
vaccin antibovipestique produit sur cultures cellulaires dans la prophylaxie de la peste
des petits ruminants au Dahomey. Rev. Elev. Med. Vet. Pays Trop., 23: 295-300.
4. BROWN, C.C., MARINER, J.C., and OLANDER, H.J. 1991. An
immunohistochemical study of the pneumonia caused by peste des petits ruminants virus.
Vet. Pathol., 28: 166-170.
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and BECKER, S.A.W.E. 1988. Experimental peste des petits ruminants (goat plague) in goats
and sheep. Can. J. Vet. Res., 52: 46-52.
6. DIALLO, A., TAYLOR, W.P., LEFEVRE, P.C., and PROVOST, A. 1989.
Attenuation d'une souche du virus de la peste des petits ruminants: candidat pour un
vaccin homologue vivant. Rev. Elev. Med. Vet. Pays Trop., 42: 311-319.
7. EL HAG ALI, and TAYLOR, W.P. 1983. The isolation of pests des
petits ruminants virus (PPRV) from the Sudan. Res. Vet. Sci., 36: 14.
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9. GIBBS, E.P.J., TAYLOR, W.P., LAWMAN, M.J.P., and BRYANT, J.
1979. Classification of peste des petits ruminants virus as the fourth member of the genus
Morbillivirus. Intervirol., 11: 268-274.
10. GILBERT, Y., and MONNIER, J. 1962. Adaptation du virus de la
peste des petits ruminants aux cultures cellulaires. Rev. Elev. Med. Vet. Pays Trop., 4:
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11. HAMDY, F.M., DARDIRI, A.H., NDUAKA, O., BREESE, S.S., and
IHEMELANDU, E.C. 1976. Etiology of the stomatitis pneumoenteritis complex in Nigerian
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bovipestique des ovins et caprins (Synthese bibliographique). Institut d'Elevage et de
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13. LEFEVRE, P. C., and DIALLO, A. 1990. Peste des petits
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14. MORNET, P., ORUE, J., GILBERT, Y., THIERRY, G., and SOW, M.
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and Derived Savanna Zones. In: Peste des petits ruminants
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Ethiopia:International Livestock Center for Africa, 1983. pp. 14-21.
16. OSTERHAUS, A.D.M.E. 1992. Studies on Virus Infections of Wild
Aquatic Mammals. In The Ciba-Geigy Prize for Research in Animal Health, 1991.
Switzerland:Ciba-Geigy Ltd, Basel. 27pp.
17. ROWLAND, A.C., SCOTT, G.R., RAMACHANDRAN, S., and HILL, D.H.
1971. A comparative study of peste des petits ruminants and kata in West African dwarf
goats. Trop. Anim. Hlth. Prod., 3: 241245.
18. SCOTT, G.R. 1988. Rinderpest and peste des petits ruminants.
In Vrus diseases of food animals, vol. II, Gibbs EPJ, ed., London:Academic Press,
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19. SALIKI, J.T., HOUSE, J. A., MEBUS, C.A., and DUBOVI, E.J.
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for detection of peste des petits ruminants virus in goat tissues and secretions. J. Clin.
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20. SALIKI, J.T., LIBEAU, G., HOUSE, J. A., MEBUS, C.A., and
DUBOVI, E.J. 1993. Monoclonal antibody-based blocking ELISA for specific detection and
titration of peste des petits ruminants virus antibody in caprine and ovine sera. J. Clin.
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21. TAYLOR, W.P. 1984. The distribution and epidemiology of peste
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J.T. Saliki, D.V.M., Ph.D., Oklahoma State University, Stillwater,
OK
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