Peste des Petits Ruminants (PPR)

Last updated April 7, 2003

Agent
Hosts
Epidemiology
PPR As a Biological Weapon
Clinical Features
Differential Diagnosis
Laboratory Diagnosis
Treatment
Prevention
Outbreak Control
Public Health Issues
References

Agent

Peste des petits ruminants (PPR), also known as goat plague, is caused by a paramyxovirus of the Morbillivirus genus. It was first described in 1942 in Cote d'Ivoire, West Africa (see References: Dhar 2002) and is closely related to rinderpest virus, canine distemper virus, and human measles virus. The virus has the following characteristics (see References: OIE 2002):

May survive at 600C for 60 minutes
Stable from pH 4.0 to 10.0
Killed by alcohol, ether, and detergents as well as by most disinfectants (eg, phenol, sodium hydroxide)
Long survival time in chilled and frozen tissues

Hosts

PPR is primarily a disease of sheep and goats. There have been several reports of PPR occurring in other species, particularly in captive wild ungulates from three families:

Gazellinae (dorcas gazelle)
Caprinae (nubian ibex and laristan sheep)
Hippotraginae (gemsbok)

The American white-tailed deer (Odocoileus virginianus) has been infected experimentally (see References: Saliki 2002). Cattle, buffaloes, camels, and pigs are also susceptible to infection but do not exhibit clinical signs and are unable to transmit the disease to other animals (see References: EMPRES 1999).

PPR is not infectious to humans.

Epidemiology

Transmission

For PPR to spread, close contact between infected and susceptible animals is needed (see References: Ozkul 2002). There are several means of transmission between animals (see References: Saliki 2002):

Inhalation of aerosols produced by sneezing and coughing of infected animals

Outbreaks are more frequent during the rainy season or the dry, cold season (see References: OIE 2002).

Direct contact with ocular, nasal, or oral secretions
Direct contact with feces
Fomites such as bedding, water, and feed troughs
No carrier state is known to exist

Occurrence

PPR has been found in parts of sub-Saharan Africa for several decades and in the Middle East and southern Asia since 1993. It has been reported in Sudan, Kenya, Uganda, and Ethiopia. It was first reported in southern India in 1987. The Arabian Peninsula, the Middle East, and the rest of the Indian Subcontinent reported PPR incidents during 1993-1995. The disease has remained endemic in these areas. It has also occurred in Turkey (1996), Iraq (2000), Iran (1994), Bangladesh (1993 and 2000), and Nepal (1995) (see References: Dhar 2002).

In India, PPR was first confirmed in March 1987 in sheep suspected of having rinderpest. It is now believed that many outbreaks in India previously attributed to rinderpest were actually PPR. The virus was isolated four more times by 1992, and major epidemics occurred in the state of Andhra Pradesh in 1994-1995 and 1997-1998 (see References: Taylor 2002).
In Africa and Asia, the disease is particularly devastating, as these countries often use small ruminants as components of agricultural food production (see References: EMPRES 1999).

PPR As a Biological Weapon

PPR virus is considered a potential biological weapon because:

Morbidity and mortality can be as high as 100% and 90%, respectively. When associated with other diseases such as capripox, mortality can be 100% (see References: Dhar 2002).
Aerosol transmission would enable the disease to spread rapidly in large groups of animals.

Clinical Features

Susceptibility to infection rises with age; however, the disease is rapidly fatal in the young animals (see References: Ozkul 2002). The clinical signs imitate those of rinderpest, but changes can occur faster. Specific clinical signs are outlined in the table below:

Clinical Features of Petit des Pestis Ruminants
*Feature/Disease Form*	*Characteristics*
Incubation period	2-10 days, most commonly 4-5
Acute	Most common form Sudden high fever (400-410C), remaining high for 5-8 days; will return to normal before recovery or drop below normal before death Serous nasal discharge, becoming mucopurulent; can crust over and occlude nostrils Purulent ocular discharge with congested conjunctiva; can encrust, cementing eyelids together Bronchopneumonia Necrosis and ulceration of mucous membrane and inflammation of gastrointestinal tract leading to severe, nonhemorrhagic diarrhea Respiratory distress, including dyspnea and sneezing in an attempt to clear nose Excessive salivation but not to point of drooling Anorexia Severe dehydration and emaciation followed by hypothermia Death usually occurs after 5-10 days Abortion Mortality rate can reach 100% Secondary infections may be activated and complicate clinical signs
Peracute	Frequent in goats
Subacute and chronic	Pneumonia Develops over 10-15 days Inconsistent symptoms
Adapted from DEFRA, Dhar 2002, EMPRES 1999, Saliki 1998, OIE 2002R, Ozkul 2000 (see References).

The prognosis of acute PPR is usually poor, especially when lesions do not resolve within 2 to 3 days or when extensive necrosis and bacterial infection give the animal's breath an unpleasant, fetid odor. Young animals (4 to 8 months) often have more severe disease. Also, poor nutrition, stress of movement, and concurrent parasitic and bacterial infections worsen clinical signs (see References: Saliki 1998).

Necropsy Lesions

In addition to the signs mentioned above, characteristic necropsy lesions often occur. These lesions are usually seen in the digestive and respiratory systems, but can be seen in other systems as well.

Necropsy Features of Peste des Petits Ruminants
Digestive system	Inflammatory and necrotic lesions in mouth and gastrointestinal tract (see References: DEFRA 2005) Erosive stomatitis in inside of lower lip and adjacent gum Lesions on hard palate, pharynx, and upper third of esophagus in severe cases Rumen, reticulum, and omasum rarely have lesions Erosions on pillars of rumen Abomasum often oozes blood Small intestine lesions usually moderate Extensive necrosis of Peyer's patche, resulting in severe ulceration [References: Saliki 1998]) Large intestine features congestion around iliocecal valve, at cecocolic junction, and in rectum (see References: DEFRA 2005) "Zebra stripes" (discontinuous streaks of congestion) in posterior part of colon and rectum and on crests of mucosal folds
Respiratory system	Small erosions and petechiae visible on nasal mucosa, turbinates, larynx, and trachea Pleuritis, resulting in hydrothorax
Other systems	Slightly enlarged and congested spleen Enlarged, congested, and edematous lymph nodes throughout body Erosive vulvovaginitis may exist
Adapted from Saliki 1998 (see References).

Differential Diagnosis

In addition to rinderpest, other conditions that should be considered in differential diagnoses include (see References: Saliki 1998, EMPRES 1999):

Pasteurellosis
Contagious caprine pleuropneumonia
Bluetongue
Heartwater
Contagious ecthyma (contagious pustular dermatitis)
Foot-and-mouth disease
Nairobi sheep disease
Coccidiosis
Gastrointestinal helminth infestations
Plant or mineral poisoning

Laboratory Diagnosis

The following samples should be submitted for evaluation, shipped fresh (not frozen) on ice within 12 hours after collection (see References: Saliki 1998):

Blood in EDTA anticoagulant
Clotted blood or serum
Mesenteric lymph nodes
Spleen
Lung
Tonsils
Sections of the ileum and large intestine
Swabs of serous nasal and lacrimal discharges

The above samples should be collected in the acute phase of the disease, when clinical signs are readily apparent. Ideally, samples should be collected from several animals in an outbreak. Epidemiologic and clinical details should be provided with the samples, and each sample bottle should be marked carefully with an indelible pen. Details of each sample's origin should be recorded for submission to the laboratory (see References: EMPRES 1999).

Tthe following tests may be used to detect antigens (see References: OIE 2000):

Immunocapture enzyme-linked immunosorbent assay (ELISA)
Counterimmunoelectrophoresis (CIEP): Most rapid test for detecting viral antigen
Agar gel immunodiffusion (AGID): Very simple and inexpensive and gives results within 1 day, but not sensitive to mild forms of PPR
Polymerase chain reaction (PCR)
Culture and isolation in lamb kidney or African green monkey cell tissue cultures

Routine serologicl tests include (see References: OIE 2000):

Competitive ELISA

Sensitivity 99.4%
Specificity 94.5%

Virus neutralization test

Prescribed test for international trade
Cross-neutralization with rinderpest virus must be completed, so the test can be time-consuming
Highly sensitive and specific

Other serologic tests have been described, but not widely adopted:

CIEP
AGID
Precipitinogen inhibition test
Indirect fluorescent antibody test

Treatment

There is no treatment for PPR. However, mortality rates may be decreased by the use of drugs that control the bacterial and parasitic complications. Specifically, oxytetracycline and chlortetracycline are recommended to prevent secondary pulmonary infections (see References: OIE 2000).

Prevention

In the past, the rinderpest vaccine has been used. However, this practice is being phased out to avoid confusion during retrospective serologic studies. A homologous PPR vaccine is now available and gives strong immunity. There are also genetically engineered recombinant vaccines undergoing limited field trials (see References: OIE 2002).

Outbreak Control

Methods applied for rinderpest eradication may be appropriate for PPR. These include the following (see References: Saliki 1998):

Quarantine
Slaughter
Proper disposal of carcasses and contact fomites
Decontamination of facilities and equipment
Restrictions on importation of sheep and goats from infected areas

Public Health Issues

PDP does not cause infection in humans; therefore, there are no public health issues to be considered.

References

DEFRA (Department for Environment, Food, and Rural Affairs). Disease surveillance and control, peste des petits ruminants. Nov 2001 [Web page]

DEFRA (Department for Environment Food and Rural Affairs). Animal health and welfare. Peste des petits ruminants: pictures. May 24, 2005 [Web page]

Dhar P, Sreenivasa BP, Barrett T, et al. Recent epidemiology of peste des petits ruminants virus (PPRV). Vet Microbiol 2002 Aug 25;88(2):153-9 [Abstract]

EMPRES (Emergency Prevention System for Transboundary Animal and Plant Pests and Diseases). Recognizing peste des petits ruminants: a field manual. Rome, Italy: FAO (Food and Agriculture Organization of the United Nations), 1999 [Full text]

OIE (Office International des Epizooties/World Organization for Animal Health). Peste des petits ruminants. In: Manual of standards for diagnostic tests and vaccines. Ed 4. Chap 2.1.5. Paris: OIE, 2000 [Full text]

OIE (Office International des Epizooties/World Organization for Animal Health). Peste des petits ruminants. Technical disease card database. Apr 22, 2002 [Full text]

Ozkul A, Akca Y, Alkan F, et al. Prevalence, distribution, and host range of peste des petits ruminants virus, Turkey. Emerg Infect Dis 2002 Jul;8(7):708-12 [Full text]

Saliki JT. Peste des petits ruminants. In: US Animal Health Association, Committee on Foreign Animal Disease. Foreign animal diseases: the gray book. Ed 6. Part IV. Richmond, VA: US Animal Health Assoc, 1998 [Full text]

Taylor WP, Diallo A, Gopalakrishna S, et al. Peste des petits ruminants has been widely present in southern India since, if not before, the late 1980s. Prev Vet Med 2002 Jan 22;52(3-4):305-12 [Abstract]


Home	Mission & Activities	About Us	Center Support	Contact Us