Diseases

PRRS

Download as PDF Download as XLS Download summary

Chapter select

Control Tools

  • Diagnostics availability

  • Commercial diagnostic kits available worldwide

    Kits are available for use in main laboratories, one serological kit is validated for suids and camelids in addition to small ruminants.

    List of commercially available diagnostic kits (Diagnostics for animals).

    GAPS

    • Kits are available although costs are relatively high for developing countries, which has an effect on capacity and quality of diagnostics in some of these countries.
    • POC tests that are sensitive and affordable are not widely available. Lateral flow devices are available, but field validation is limited, and training and protocols on how to use any such tests for surveillance and testing need to be proposed.
    • Issue with investment in deployment of the kits in the field (logistics including transport and shipment to central labs).
    • New kits are being commercialized without proper validation, increasing the risk of misdiagnosis. Labs need to get information and training as necessary from reference lab and WOAH manual before purchasing a new kit.
    • Existing serological kits need to be validated for relevant atypical and wild hosts
  • Diagnostic kits validated by International, European or National Standards

    None. Penside tests, immunocapture kits for PPR antigen detection and competitive ELISA tests for PPR indicated in WOAH Manual but none yet validated according to WOAH standards.

    GAPS

    Penside tests, Immunocapture kits for PPR antigen detection and competitive ELISA tests for PPR antibodies indicated in WOAH Manual but none yet validated according to WOAH standards.

  • Diagnostic method(s) described by International, European or National standards

    Methods are described in the WOAH Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2022: Identification of the agent
    • RT-PCR
    • Real-Time RT-PCR
    • Virus isolation in cell culture
    • Immunocapture ELISA
    • Penside test /lateral flow device (LFD)
    • AGID
    • Counter immune-electrophoresis
    Detection of immune response
    • Virus neutralisation
    • Competitive ELISA
    • AGID
    • Counter immune-electrophoresis
    Validated protocols available through website of EURL (https://eurl-ppr.cirad.fr/)

  • Commercial potential for diagnostic kits worldwide

    The disease emerged in Europe in 2024. There is a risk of further spread of the disease in Europe. All national and regional laboratories need to purchase kits or reagents to be prepared in case of emergence, and veterinary services must be prepared to test more regularly on suspicion.

    GAP

    We need much better understanding of the potential market for products before we invent new ones.

  • DIVA tests required and/or available

    Not available, but some DIVA tests and some DIVA vaccine prototypes and companion ELISA tests are under development. These tests will be important to help epidemiological surveillance where the virus is circulating or in naïve countries with borders with countries vaccinating. This will be especially important for the last stages of the eradication programme, and for countries to have confidence to cease vaccination ahead of official freedom recognition, and at the post-eradication stage. It will provide wider options of preventive vaccination in PPR-free zones at risk from neighbours.

    GAP

    DIVA tests and DIVA vaccine and companion tests useful. Development of these tests need to be completed. Tests need to be fully validated before use.

  • Vaccines availability

  • Commercial vaccines availability (globally)

    Live attenuated PPRV vaccine is available from more than 20 vaccine production companies and government laboratories in Africa, the Middle East, Asia and Turkey. Vaccine banks are kept by the EU and other national and international institutions. Several multivalent vaccines (i.e. protecting against PPR in combination with other pathogens) were recently developed. PPR/SGP is in use and a new PPR/SGP/CCPP now has market authorisation ‘Thermotolerant’ vaccines are also now on the market, with thermotolerant property defined and validated within QC by AU-PANVAC

    GAPS

    Maintain the long-term vaccine banks to ensure the availability of sufficient stocks (emergency or global strategy) as supply is subject to supplier’s rapidity in response. In addition, independent certified quality of the batches used for vaccine banks and vaccination programmes needs to be ensured. Notably, only vaccine strains recognized by WOAH and quality controlled by independent institutions such as AU-PANVAC or EURL should be purchased and used. Vaccine producers need information on demand for the vaccines by countries well ahead of time (the stock may be there but, if there is no demand, then useless) i.e. forecasting of demand. A long-term strategy for the post eradication era needs to be put in place (official vaccine holding facilities, contingency plan in case of re-emergence). Ideally a properly validated DIVA vaccine and companion test is required for the post eradication era. Clear WOAH guidelines concerning PPR thermostable vaccines (thermostable in lyophilised form) to clarify to countries how and when to use them. Availability depends on information about the benefits of vaccination and level of access in remote regions. Increase awareness of existence of vaccines and better connections with remote communities and women need to be put in place notably through establishment of networks of community animal health workers. Impact of vaccination on trade should be carefully explained to stakeholders (traders, livestock owners, …) when developing control strategies

  • Marker vaccines available worldwide

    None, but DIVA vaccine prototypes are under development. This will be especially important for the last stages of the eradication programme, and for countries to have confidence to cease vaccination ahead of official freedom recognition, and at the post-eradication stage. It will provide wider option of preventive vaccination in PPR-free zones at risk of PPR incursion from neighbours.

    GAPS

    DIVA tests and DIVA vaccine and companion tests useful. Development of these tests needs to be completed. Tests need to be scientifically validated before use.
  • Effectiveness of vaccines / Main shortcomings of current vaccines

    Animals vaccinated once with the current live attenuated vaccines for PPR have a good immunity which lasts for at least 3 years but cannot be distinguished serologically from infected animals. A cold chain is required for the transport and storage of conventional PPR vaccines, although ‘thermotolerant’ vaccine preparations are now on the market. The stability of vaccines in lyophilized form and when resuspended varies among producers. Vaccines highly stable in lyophilized form are being tested in the field. Most vaccines are effective for only 2-3 h after resuspension. Not all vaccines on the market go through strict quality control procedures, so effectiveness of vaccines may vary.

    GAPS

    Risks associated with PPR vaccine quality control need to be evaluated. Strict standardised quality controls are needed for all vaccines produced. Buyers need to be informed of the issues with quality control so they can ask for information from producers.

    Buyers need to know about thermostability of vaccines so they can purchase vaccines most appropriate to their regional conditions, and consider use of thermotolerant vaccines.

    Some commercialised vaccines are based on strains which are not recognised by WOAH as their safety and efficacy data are incomplete.

    Given the variable quality of vaccines from different producers, there is a need to promote animal serology after vaccination (Post-Vaccination Monitoring (PVM)) to provide assurance of vaccination field efficacy.

    Identification of vaccinated animals is needed to avoid vaccine wastage and facilitate PVM.

    Farners need to be provided the right information about vaccination including timing and frequency of vaccination. Understand the benefits of marking.

    Vaccine acceptance (willingness-to-vaccinate and willingness-to-pay) by farmers needs to be studied and strong communication campaigns need to be implemented to avoid vaccine rejection and to combat misinformation regarding vaccinated animals developing illness (due to other or past infections)
  • Commercial potential for vaccines

    More than 20 producers of PPR vaccines but all out of Europe. High commercial potential due to the on-going eradication campaign. Member states affected by PPR incursion and not able to control following EU regulations can opt for and prepare a vaccination strategy to be submitted to and validated by the EC. EU has a PPR vaccine bank kept in case of emergency Some member states may prepare their own vaccine bank as well. Although no vaccine has yet been authorized, use of PPR vaccines could be authorized in infected and at-risk European countries, as for LSD or other diseases.

    GAPS

    Capacity of national vaccine manufacturers in low- and middle-income countries should be built.
  • Regulatory and/or policy challenges to approval

    DIVA vaccines are genetically modified viruses, so these products have to go through strict regulatory challenges before approval.

  • Commercial feasibility (e.g manufacturing)

    Adequate

  • Opportunity for barrier protection

    In principle it is possible to use vaccination as a barrier between free and endemic countries or zones although the movement of sheep and goats may render this unsuccessful. Availability of DIVA vaccines would make this option more likely, as WOAH could consider reviewing its manual and allow countries using preventive DIVA vaccination not to lose their disease-free status.

    GAPS

    Border vaccination strategy should be explored based on risk-based analyses performed on animal movement data. Contingency plans of PPR-free countries with porous borders with countries vaccinating should take into account the possibility of vaccinated animals entering their country.

  • Pharmaceutical availability

  • Current therapy (curative and preventive)

    There is no specific therapy for PPR. Fluid replacement and similar supportive care may help in severe disease. Supportive care and treatment of bacterial and parasitic coinfections may decrease mortality. Antibiotics may prevent secondary pulmonary infections (oxytetracycline, chlortetracycline). Deworming before or at the time of vaccination can boost immunity and then boost vaccine response. Offering deworming also increases vaccine acceptance in communities who will see directly a positive effect of the service offered.

    GAPS

    Integrate deworming, or prophylaxis of other diseases, in PPR vaccination efforts according to local contexts and socio-economic analyses.
  • Future therapy

    None.

    GAPS

    Use of antibiotics with fluid therapy and vaccination has been suggested to reduce the morbidity and mortality that result from PPR induced immunosuppression and development of secondary bacterial infections. Vitamin supplementation has proved useful for other morbillivirus infections.
  • Commercial potential for pharmaceuticals

    None

  • Regulatory and/or policy challenges to approval

    Potential for pharmaceuticals is nil as EU regulations do not allow treatment of PPR-infected animals.

  • Commercial feasibility (e.g manufacturing)

    Not applicable

  • New developments for diagnostic tests

  • Requirements for diagnostics development

    Tests need to be sensitive and specific to PPR. Careful choice of target molecule, and high-quality reagents and production are necessary. Validation of new tests must be undertaken both in the laboratory and also under field conditions in countries where the disease exists. Ideally, reference laboratories should be involved in this validation.

    GAPS

    New diagnostic tests are being commercialized without proper validation. Laboratories have to be aware of this issue. Quality management systems are likely required to ensure confidence in testing. Proficiency tests organized by reference laboratories can be used to compare the performance of new methods with validated protocols.
  • Time to develop new or improved diagnostics

    Time and costs depend on the type and nature of the test. Proof of concept and the development of a new test will take time as will the validation necessary before the new tests are accepted as a diagnostic tool by international organisations. Further time will elapse before the tests are commercially available, which is a constraint in view of the 2030 target for global PPR eradication.

    GAPS

    New diagnostic tests are being commercialized without proper independent validation (example: Ingenasa ELISA kit identified as lacking sensitivity from proficiency test results). Laboratories and stakeholders need to be aware of this issue.
  • Cost of developing new or improved diagnostics and their validation

    This is time and labour consuming. Cooperation between all parties involved from discovery to commercial availability will be crucial.

    GAPS

    New diagnostic tests are being commercialized without proper validation. Laboratories have to be aware of this issue.
  • Research requirements for new or improved diagnostics

    Fit-for-purpose diagnostic tests available for surveillance and control activities, but the following improvement may increase efficiency of efforts: Penside tests (antigen and molecular); non-invasive tests for wildlife and environment, DIVA vaccine and appropriate companion tests (ELISA + pen-side). An antigen penside test is already available but its sensitivity is lower than PCR. Penside tests with improved sensitivity (and high specificity) may be of interest as less tests would be needed to ensure status, lowering the cost of use.

    GAPS

    Tests to evaluate PPR virulence and host susceptibility, notably to evaluate risk when emerging in a new area Detection in environmental RNA to explore indirect transmission through water or fomites and apply non-invasive surveillance efforts at the wildlife-livestock interface. Better understanding needed of how/what kind of penside tests would be used in countries with different resource levels.
  • Technology to determine virus freedom in animals

    Tests are available to determine virus freedom: immunocapture test and gene amplification assays for antigen and nucleic acid detection; competitive ELISA for antibody detection.

  • New developments for vaccines

  • Requirements for vaccines development / main characteristics for improved vaccines

    Any new vaccine has to show at least the same efficacy and safety as existing vaccines. Improvements would target: - increased stability of existing vaccines in lyophilised form; - increased stability of existing vaccines in reconstituted form; - New DIVA vaccine. Several multivalent vaccines (i.e. PPR in combination with other pathogens) were recently developed, but WOAH validation guidelines are missing concerning such vaccines

    GAPS

    All these avenues of development are being researched, and some multivalent vaccines have market authorisation, but information on their success in the field and about WOAH validation requirements are still limited. Common standards protocols for thermostable vaccines do not exist although a recent publication from AU-PANVAC proposes a protocol to define and test thermostable vaccines Validation of existing vaccines with improved stability would take place much faster than validation of new vaccines. Vaccination with combined vaccines would be cost effective, given the major cost is usually putting the vaccinators in the field.
  • Time to develop new or improved vaccines

    10 years for development, clinical trials and licensing is realistic.

  • Cost of developing new or improved vaccines and their validation

    Very expensive (rough estimate: 10 million EUR).

    GAP

    Cost-benefit analysis needed to make the case.
  • Research requirements for new or improved vaccines

    - Increased stability in lyophilised form: highly thermostable vaccines are now available from multiple producers. Such stability should be targeted by all producers to increase efficacy of vaccine delivery in remote areas. - Increased stability in reconstituted form. - Multivalent vaccines (e.g. PPR/SGP) which are now available: demonstration of their benefits in the field. - DIVA vaccine: prototypes available without companion test or in development/validation.

    GAPS

    Efficacy of multivalent vaccines tested with sufficiently large-scale animal tests to show that all antigens in a mix are still immunogenic, and there are no long-term sequelae in the animals (including testing of pregnant dams). Clear WOAH guidelines concerning PPR thermostable vaccines (thermostable in lyophilised form) to clarify to countries how and when to use them. Difficulty of working in field conditions means that it is hard to use all of the large (most economic) vials within the recommended 1 hour at tropical temperatures. Improvements in diluents (without increased cost) would be a very helpful development.
  • New developments for pharmaceuticals

  • Requirements for pharmaceuticals development

    There is limited interest as EU regulations do not allow treatment of PPR-infected animals.

  • Time to develop new or improved pharmaceuticals

    Not known

  • Cost of developing new or improved pharmaceuticals and their validation

    Not known

  • Research requirements for new or improved pharmaceuticals

    None at present

Disease details

  • Description and characteristics

  • Pathogen

    Virus name: peste des petits ruminants virus family Paramyxoviridae, genus Morbillivirus, Species: Morbillivirus caprinae. Antigenically close to canine distemper virus. Other members of the genus include measles virus, porcine morbillivirus, dolphin morbillivirus and phocine distemper virus.

    GAPS

    Poor knowledge among scientific community of the correct naming conventions for PPRV leads to articles referring to the virus with different names, leading to confusion.
  • Variability of the disease

    Four genetic lineages (lineages 1-4) of PPRV have been identified, but there is only one serotype. Lineages I and II are restricted to West and Central Africa. Lineage III is found in East Africa. Lineage IV is found in Asia, Middle East, and Africa. This lineage is spreading in Africa, replacing other lineages, and is at the origin of emergence in new areas, notably Europe and Asia. High variability in virulence is reported among strains across all four lineages. Host susceptibility also varies among species and breeds, and appears to be strain-dependent.

    GAPS

    Variability in virulence and host susceptibility poorly understood. The dominance of new Lineage IV strains over other strains is not understood. Genetic determinants of PPR virus host range expansion are not understood. Underlying reason for specificity of disease to SRs not understood. How high is the barrier for another morbillivirus to jump to become pathogenic in SRs? Drivers for emergence not well understood (climate change, migration, animal movements, trade, etc..).
  • Stability of the agent/pathogen in the environment

    The virus is enveloped and susceptible to most disinfectants, e.g. phenol, sodium hydroxide, but can survive for long periods in chilled and frozen tissues. There is little information on the virus survival in the environment. According to one study, PPRV would have a half-life of approximately 2 h at 37°C. It may survive more than a week at 4°C. It can survive over 15 days in water at room temperature and over 30 days in water at 4°C. The virus is stable between pH 5.8 and 9.9.

    GAPS

    Lab and field studies required, especially in cooler climates, and in matrices likely to be implicated in transmission (water, mud, fodder, fecal matter). Thorough testing of survival of the virus in meat and dairy products, especially the inactivation of the virus in milk etc. Thorough testing of thermal inactivation of the virus in different matrices, whether food or environmental. In vivo experiments to evaluate likeliness of indirect transmission via different matrices and depending on distance between animals.
  • Species involved

  • Animal infected/carrier/disease

    Main hosts are goats and sheep, but a large number of species of the order Artiodactyla, both wild and captive, have been reported with clinical signs or antibodies against PPR. Notably it has been shown that pigs can shed and transmit PPRV. Cattle are considered dead-end hosts and not thought to play an epidemiological role. Several studies have found no transmission of the virus from infected cattle. The role of camelids is still not clear with experimental infection showing no viral shedding but cases of mortality observed in the field. No carrier state has been identified, but sub-clinical infections can be common in wild and domestic populations, representing a risk of disease transmission. Notably, subclinical transmissions were reported during the emergence in Europe.

    GAPS

    More work is needed to understand the role of Artiodactyla other than sheep and goats in the epidemiology of PPR. In particular the role of wildlife, notably in Asia, as well as any role of suids and camelids, in the epidemiology of the disease requires clarification. Critical information is missing on the complete range of susceptible wildlife species, necessary to evaluate if it represents a risk for biodiversity in different areas. More work is needed to adapt surveillance strategies to take into account risk of emergence through subclinical transmissions. Clear definition from WOAH as to what is meant by “susceptible”: Onward transmission? Clinical signs? Seroconversion?
  • Human infected/disease

    None

  • Vector cyclical/non-cyclical

    None

  • Reservoir (animal, environment)

    Unknown

    GAP

    Work is underway to determine the role of wild Artiodactyla and water holes in virus transmission. Survival in the environment is of importance to consider (fomites etc.).
  • Description of infection & disease in natural hosts

  • Transmissibility

    Infected goats and sheep generate aerosols containing infectious droplets and may shed the virus in ocular, nasal and oral secretions as well as in faeces. Viral shedding may occur before the onset of clinical signs or in subclinical infections (i.e. no signs). Successful transmission usually requires relatively close contact between sick and healthy animals. The risk of indirect transmission is not yet well understood, but it seems that it may happen at least during a short time frame. There are recorded instances during the outbreak in Romania and Hungary where fomite transfer by humans is the only possible transmission route.

    GAPS

    Lab and field studies required, especially at wildlife-livestock interface, and in matrices likely to be implicated in transmission (water, mud, faecal matter).
  • Pathogenic life cycle stages

    Not applicable

  • Signs/Morbidity

    PPR infection can be characterised by some of the following clinical signs: severe pyrexia, nasal discharge, lacrimation, erosive lesions on different mucous membranes and particularly in the mouth, diarrhoea and pneumonia. Animals become very dull, with sneezing and lip-licking, followed by salivation due to mouth lesions and severe diarrhoea. Number of animals to die and condition of survivors will depend on the breed infected and viral strain. Animals become more susceptible to other diseases. Sub-acute and asymptomatic cases may be frequent in some areas, depending on host susceptibility and virus strains. Such cases have been frequently observed during emergence in Europe (Romania, Kosovo). Asymptomatic PPR or circulation of mild disease complicates the epidemiology of PPR and the capacity of field veterinarians to suspect PPR infections. Morbidity is expected to be very high in a naïve population or in an immunodeficient population (up to 100%). Mortality can be lower than 15% in local breeds in regions where PPR is endemic or if animals are in good condition as usually observed in Europe.

    GAPS

    Better understanding of possible co-infections or of possible other aetiologies with the same clinical signs. More widespread knowledge of the variable nature of PPR disease, notably that subclinical infection is possible. Better understanding of the mechanisms affecting host susceptibility and virulence of PPRV strains is needed Subclinical infections, notably those observed in Europe, need to be studied and better understood.
  • Incubation period

    The incubation period is on average 4–6 days, but may range between 3 and 10 days.

  • Mortality

    Mortality rate can be as high as 100% in naïve population or in an immunodeficient population (e.g. stressful living condition), but lower than 15% in local breeds in regions where PPR is endemic or if animals are in good condition.

  • Shedding kinetic patterns

    Shedding via nasal and lachrymal discharges, saliva, faecal matter, and milk. Viral material can be detected in excretions as early as 4 days post infection, and in some cases as long as 21 days post infection.

    GAPS

    Assessment of conditions for successful transmission of the disease (minimum exposure time required). Potential role of faecal matter important to define as agricultural practices may inadvertently increase transmission risk. We need much better understanding of the shedding of infectious virus, as distinct from the shedding of viral RNA or antigen.
  • Mechanism of pathogenicity

    The initial site for virus replication is the tonsillar tissue and lymph nodes draining the site of inoculation. It has been proposed that the virus-infected immune cells within the respiratory mucosa migrate to the local lymphoid tissue, where primary virus replication occurs, with the virus then entering the general circulation. PPRV is highly lymphotropic and infection often leads to a profound immunosuppression that includes a transient leucopoenia (4-14 days) and longer term (thought to be months) reduced antibody responses.

    GAPS

    More studies on the longer term immune suppressive effect of PPRV needed, particularly the systems affected longer term and the duration of the effects. Currently our assumptions are largely based on work with measles virus in primates.
  • Zoonotic potential

  • Reported incidence in humans

    There are no reports of PPRV infecting humans.
  • Risk of occurence in humans, populations at risk, specific risk factors

    None

  • Symptoms described in humans

    None

  • Likelihood of spread in humans

    None

  • Impact on animal welfare and biodiversity

  • Both disease and prevention/control measures related

    Acute PPR is a severe welfare problem in terms of the disease syndromes it causes.

    GAP

    Need proper quantification of the impacts on animals, humans (socio-economic including stigma and fear) and environment.
  • Endangered wild species affected or not (estimation for Europe / worldwide)

    Spill-over from livestock to critically endangered Saïga antelope (Saiga tatarica mongolica) resulted in mass mortality (several thousands) in Mongolia, and also led to mortalities of goitered gazelle (Gazella subgutturosa), Siberian ibex (Capra ibex sibirica) and Argali (Ovis ammon). PPR has also caused mass mortality of wild mountain caprines in Iran and Iraq classified as vulnerable by the IUCN. Wild species in disease-free countries should be considered at risk in case of PPR emergence.

    GAPS

    Further understanding of the difference in susceptibility among wild species, and the highest risk livestock-wildlife interfaces is needed to evaluate the risks for each species and ecosystem.
  • Slaughter necessity according to EU rules or other regions

    Yes, in free countries and free zones

  • Geographical distribution and spread

  • Current occurence/distribution

    PPRV is currently distributed in most of Africa, except Southern Africa, in the Arabian Peninsula, throughout most of the Near East and Middle East, and in countries located from Central Asia to China. It is endemic in Turkey, close to the European Union. There have been first outbreaks in Georgia and Mongolia in 2016/2017, in Bulgaria in 2018, in Romania and Greece in 2024 and in Hungary, Albania and Kosovo in 2025.

    GAPS

    There is limited information on possible presence of PPRV in some regions (e.g. Central Asia) due to lack of surveillance and reporting. Comprehensive serological studies in the countries currently affected are necessary to determine the extent and spread of PPRV infection in the country. More sequencing of currently circulating strains and timely release of the information would contribute to understanding the transmission pathways of the virus as well as its evolutionary dynamics.
  • Epizootic/endemic- if epidemic frequency of outbreaks

    In sub-Saharan Africa, PPR cycles endemically in the extensive small ruminant production systems. Intense transhumance, commercial and informal movements maintain the circulation of the virus south of the Sahel with disastrous results. Each year, females give birth to 1.5-2 offspring which means that every year over 50% of the SR flocks are naïve and fully susceptible, even in endemic countries.

    GAPS

    More precise data on the age of sheep and goats and the proportion of offspring in individual countries would be desirable. This is the only way to more accurately define the proportion of newly susceptible animals in a vaccinated or naturally infected population. Identification of sources responsible for virus maintenance during inter-epidemics.
  • Speed of spatial spread during an outbreak

    Reproduction rate (Ro; the mean number of cases infected by one infectious case) of PRRSV differs depending on the species and the strain itself. Ro values for PRRSV-1 range from 2 to 5. There is not so much info for PRRSV-2 or subtypes 2 to 4 of PRRSV-1. Compared to other diseases, PRRS spread is not so rapid. Nevertheless, the constant movement of animals, the high density areas and the aerosol spread suggests that PRRSV spread can be moderately rapid.

    GAPS:

    • Identification of temporo-spatial patterns of dissemination tracing the circulation of PRRSV strains in an area.
    • Reproduction rate of PRRSV-2 and subtypes 2 to 4 of PRRSV-1.
  • Transboundary potential of the disease

    The increase of animal movement for commercial and trade purposes (e.g. the massive imports of small ruminants to the Middle East), transhumance and nomadic customs along with extensive farming practices have all contributed to the global spread of PPR. Emergence in EU may occur via illegal importation of animals, notably from North Africa or Turkey. Recent genomic study of PPR emergence in Europe points towards a link with PPRV strains circulating in Northern Africa, although genetic data on currently circulating strains are missing to point the origin of this emergence. Movement of wildlife (e.g. wild deer) throughout Europe may also play a role in disease emergence and spread, but control of PPR in small ruminant will be sufficient to stop the spread of the disease. The fact that both PPRV lineage IV, lineage of Asian PPRV strains, and lineage III, East African PPRV lineage, have been found in the Middle East indicates that many sources of infection in this region are probably infected sheep and goats imported from both Asia and East Africa. Likewise, outbreaks in Georgia and Mongolia have been linked to East Africa and China, respectively. Phylogenetic data show that PPRV transboundary movement is frequent.

    GAPS

    -Improved knowledge of the sources of new outbreaks, especially first occurrence in a country or zone. We often have no knowledge of the source of the virus in a new outbreak. -Combined analysis of phylogenetic data and data on animal trade to better understand transboundary transmission dynamics. -More surveys in the field needed to estimate importance of transboundary movement, especially transhumance. -Further understanding in difference in susceptibility among wild species is needed to evaluate the risk for biodiversity and reduce the risk that countries put responsibility of PPR circulation on wildlife when their control efforts are inadequate. -Regionally coordinated approaches are necessary to control and eradicate the disease.
  • Route of Transmission

  • Usual mode of transmission (introduction, means of spread)

    Direct contact through aerosol spread or contact with infected respiratory secretions or faeces.

    GAP

    Transmission via milk has to be studied. Infectivity of feed/pasture has to be studied.
  • Occasional mode of transmission

    None known. Indirect transmission through water, mud and faecal matter is possible, at least over short term (in communal water holes for example).

    GAPS

    Lab and field studies required to determine the risk of indirect transmission.
  • Conditions that favour spread

    - Transhumance and trade movement of infected animals. - Important social gatherings (e.g. Islamic celebrations). - Sharing sources of water and grazing (livestock and wildlife).

    GAP

    Need to understand the dynamics of these activities per region or episystem to inform prevention and control strategies.
  • Detection and Immune response to infection

  • Mechanism of host response

    Maternal antibodies against the virus can be detected in young animals and remain able to neutralise virus for three to four months providing a level of protection in newborn animals. Cellular and humoral immune responses are induced upon infection. Sheep and goats that recover from PPR develop an active immunity against the disease. Seroconversion appears typically 7-10 days after infection. Antibodies have been demonstrated 4 years after infection suggesting that immunity is probably life-long.

    GAPS

    It must be clarified whether and what influence maternal antibodies have on active vaccination with attenuated PPRV vaccines. Precise data on the level and duration of maternal antibodies in different animal species should be collected. The influence of health, breed, concomitant diseases, or malnutrition on the formation of maternal antibodies should also be investigated.

  • Immunological basis of diagnosis

    Goats and sheep infected with PPRV develop antibodies that may be demonstrated to support a diagnosis by the antibody detection tests. The WOAH recommends cELISA and virus neutralisation tests to confirm immunological status of animals.

  • Main means of prevention, detection and control

  • Sanitary measures

    In Europe affected animals have to be slaughtered, and a 3km protection zone and 10 km surveillance zone set up around the infected premises. Stamping-out is recommended when PPR appears in new areas. It should include quarantine, movement control, slaughter, and proper disposal of carcasses and contact fomites, decontamination of premises and vehicles, and restrictions on importation of sheep and goats from affected areas. Disease control measures would be put in place including ring vaccination or mass prophylactic vaccination depending on the situation in individual countries, and on risks to endangered captive and wild species.

    GAPS

    For control/eradication/quarantine it is of outmost importance that they are accompanied by proper communication and compensation to animal owners to avoid negative impact for animal owners (destruction of livelihoods) and ensuing low compliance. There is a need to study acceptance of different control measures in case of PPR emergence with low mortality and/or subclinical infection. Acceptance is much lower when disease is not observed notably for ethical reasons, leading to political decisions driving ineffective control actions.
  • Mechanical and biological control

    In free zones, slaughter of affected flocks. Disposal of carcasses. Detailed epidemiology to identify origin and potential spread.

    GAPS

    Governments need to know the WOAH protocols in this regard.
  • Diagnostic tools

    Quantitative nucleic acid amplification (RT-qPCR) is the most currently used and most sensitive diagnostic test for PPRV detection. Serological tests can also be used, including the competitive ELISA and virus neutralisation, however these only indicate where the virus has been.

    GAPS

    Access to the tools often limited in some governmental labs. Ways to increase access at critical times should be identified (diagnostic bank similar to vaccine bank through FAO and EU?). No validated serological tests for atypical hosts except one kit validated for suids and camelids. More frequent virus isolation, or collaboration with reference labs for virus isolation. Training on sampling techniques and storage Ensuring that the field vet and the animal owner gets a report from the lab.
  • Vaccines

    There are homologous live attenuated PPR virus vaccines. The attenuated PPR Nigeria 75/1 vaccine strain is most widely produced and is commercially available from over 20 producers. DIVA vaccines are being developed /tested. Vaccines highly stable in lyophilized form (with some thermotolerance in this lyophilized form) and combined PPR/capripox vaccines are available.

    GAPS

    There is a need to develop a robust tool to assess the whole socio-technical system related to vaccination and the immunity coverage gained with vaccination, in order to maximize the vaccination efficacy, identify gaps, and reorient future vaccination strategies.
  • Therapeutics

    None

  • Biosecurity measures effective as a preventive measure

    Avoiding inter-flock contacts can help control the disease, which is possible in sedentary systems but difficult in mobile systems.

    GAP

    Protocols for biosecurity should be made available and attractive to (prioritised by) users.
  • Border/trade/movement control sufficient for control

    Import controls on live sheep and goats and other animal products (meat, dairy). In the event of an outbreak in a free country or region movement controls would be imposed on the infected, protection and surveillance zones.

    GAPS

    Better knowledge of the survival of the live PPR virus in meat and other animal products. Protocols for border control and vaccination should be made available to users.
  • Prevention tools

    Rules on imports of live animals.

  • Surveillance

    Surveillance in infected zones and surrounding areas is paramount for early detection. Effective surveillance requires veterinary awareness, outbreak reporting, investigation and active clinical surveillance with diagnostic confirmation. This is rarely the case even in countries where PPR is endemic, and recent experience shows that PPR is not suspected in countries that have not previously seen the disease. Reports of subclinical infections in Europe show that surveillance based on clinical signs is not enough. Risked-base surveillance can be efficient if well implemented using relevant, knowledge-based risk factors.

    GAPS

    There is a need for educating EU vets / farmers on the clinical expression of PPR as it was shown that there were delays in identifying PPR suspicions in the first infected EU countries (Greece, Romania). Surveillance strategies should include random sampling and testing of animals with strong suspicion of epidemiological link to infected PPR animals to rule out subclinical infections. Incentives/dis-incentives for reporting including trust in governments and compensation in case of confirmed cases and enforced slaughter. Important to give follow up from reports and testing.
  • Past experiences on success (and failures) of prevention, control, eradication in regions outside Europe

    The lessons learnt from the PPR epidemics in Morocco are that PPR can be controlled in areas, such as Northern Africa, through mass vaccination campaigns implemented at the national level, provided that adequate means are available and correctly implemented. However, in endemic areas, assiduous vigilance is needed because there is a risk of PPR reoccurrence, especially with risk factors of continuous introduction such as the illegal cross-border movements of livestock. In general, early detection of (re)occurrence is a necessary condition for rapid response and the effective management of possible outbreaks of PPR. Control strategies based on knowledge of connectivity between populations (including transboundary connectivity) maintaining virus circulation (episystem approach) is now recommended by WOAH and FAO.

    GAPS

    Modelling and cost-benefit analyses of vaccination strategies adapted to each system, notably in multi-species systems, is needed to identify best strategies in each context.
  • Costs of above measures

    A new tool, VacciCost – has been developed to estimate the resource requirements for implementing livestock vaccination campaigns. For PPR, it was estimated that the average resource requirements for undertaking 7.9 million vaccines against PPR ranged between USD 1.5 million and 2.7 million, depending on the scenario applied. It has also been calculated that the total estimated undiscounted cost of the global eradication programme would be USD 3.08 billion. Results of a benefit-cost analysis suggest strong economic returns from PPR eradication. Based on a 15-year programme with total discounted costs of USD 2.26 billion, we estimate discounted benefits of USD 76.5 billion, yielding a net benefit of USD 74.2 billion.

    GAP

    Need for more of such studies to influence decision making in investment in vaccination/PPR control.

  • Disease information from the WOAH

  • Disease notifiable to the WOAH

    Yes

  • WOAH disease card available

    Link

    GAP

    Not applicable

  • WOAH Terrestrial Animal Health Code

    Link

    GAP

    Not applicable

  • WOAH Terrestrial Manual

    Link

    GAP

    Not applicable

  • Socio-economic impact

  • Zoonosis: impact on affected individuals and/or aggregated DALY figures

    Not applicable

  • Zoonosis: cost of treatment and control of the disease in humans

    Not applicable.

  • Direct impact (a) on production

    This disease is the most important endemic pig disease causing continuously negative impact on health and welfare of piglets and sows and production losses. During outbreaks of high virulent PRRSV, large losses are reported (30-50% of mortality). When high virulent strains remain on a farm (endemic situation), mortality remains high in the nursery unit.A small-scale study performed in The Netherlands estimated that in an acute reproductive outbreak, cost of PRRS reaches € 59-379 per sow. In endemic situation, the cost varies from € 3 to 160 per sow. In growing animals, the cost is very variable, moving from € 1.6 to 7 per piglet.The total impact on production is not known. It was estimated for US $ 664 million annually in USA.

    GAP:

    Knowledge on financial impact of PRRS is limited.

  • Direct impact (b) cost of private and public control measures

    It has been estimated that there are 37.4 million PPR-associated sheep and goat deaths each year (minimum 20.2 million, maximum 67.7 million), with a most likely total value of USD 1,475 million, although it could be as low as USD 794 million or as high as USD 2.7 billion.

    GAP

    More socio-economic studies needed, context specific.

  • Indirect impact

    The large number of small ruminants reared in PPR-endemic areas, makes PPR a serious disease threatening the livelihoods of poor farmers. The presence of disease can limit trade, export, import of new breeds and the development of sustainable productive small ruminant livestock rearing. PPR is a major constraint on the availability of protein for human consumption as well, and represents a threat to food security. It has an important impact on livelihood and economic stability for low-income farmers as small ruminants provide the day-to-day cash flow for expenses in education and health amongst other sectors. PPR virus infection has for many years been one of the most important constraints to the increased production of small ruminants in sub-Saharan Africa.

    GAP

    More socio-economic studies needed, context specific.

  • Trade implications

  • Impact on international trade/exports from the EU

    In the case of free countries, movement controls imposed on the country or region. In endemic countries, restrictions on exports of live sheep and goats. Standards for the control of movements are contained in the WOAH Terrestrial Animal Health Code.

  • Impact on EU intra-community trade

    Movement controls and trade restrictions within the EU.

  • Impact on national trade

    Local movement controls imposed on movement from the protection and surveillance zones.

  • Links to climate

    Seasonal cycle linked to climate

    Seasonal variations: more frequent outbreaks during the rainy season or the dry cold season in sub-Saharan Africa. Transmission cycles will vary with area/production system (shared water points and grazing areas; transhumance; seasonality of breeding).

    GAPS

    Need to understand the determinants of transmission in regard to seasonality and production practices. - Identifying new animal movement patterns due to climate change and insecurity. Remote sensing can be used to develop regional risk maps considering landscape change. - Need to establish the impact of vaccination on greenhouse gas emissions.
  • Distribution of disease or vector linked to climate

    No

  • Outbreaks linked to extreme weather

    Drought and animal movement to seek for food increase the likelihood of outbreaks. At the end of the dry season, animals are weakened and more susceptible to viral infections (and this is exacerbated in a context of climate change).

    GAP

    Need to understand the links between animal level physiological state in relation to nutrition/feeding and immune response to vaccination.
  • Sensitivity of disease or vectors to the effects of global climate change (climate/environment/land use)

    At the end of the dry season, animals are weakened and more susceptible to viral infections (and this is exacerbated in a context of climate change).

    GAP

    Need to understand how land use and change affect PPR outbreaks.
  • Main perceived obstacles for effective prevention and control

    - Difficulties in the control of movements of affected and more importantly incubating animals across regions and borders. Controlling animal movements can lead to livelihood impacts for e.g. pastoralists. -Problems of differentiating infected from vaccinated animals. -Quality of vaccines varies a lot because of lack of standard quality control measures. -Issues with vaccine delivery and equitable access to farmers, vaccine application in some environments and proper storage over long period of time. - Differential diagnosis of PPR-like diseases. -Lack of regionally coordinated approach and of investment in disease control in LMICs -Issues with poorly planned and monitored vaccination campaigns that limit effectiveness - Persistence of disease in remote communities which receive poor animal health service delivery - Limited testing availability and/or efficacy combined with limited or incorrect clinical criteria, leading to failure to diagnose PPR
  • Main perceived facilitators for effective prevention and control

    Strong international advocacy - Awareness, involvement of livestock keepers/community leaders as stakeholders in the planning and implementing of prevention and control. - Adequate veterinary services and animal health service delivery system at field level. -Availability of diagnostic kits and vaccines for use in endemic countries -Training and integration of auxiliary animal health workers from communities in control and prevention activities to reach remote communities - Support system including infrastructure in place Financing of e.g. compensation for euthanized animals -Fast and robust diagnosis, easy methods for surveillance in remote areas. - Development of DIVA vaccine, vaccine stable for long periods at relevant temperatures in lyophilized form, diluent that keep vaccine stable for >2h at relevant temperature once reconstituted. -Effective use of the PPR Global Research and Expertise Network to address the main knowledge gaps and apply these to the GEP

    GAPS

    Explore easier use of vaccine in Europe in case of outbreak with low mortality Explore ways to avoid immediate slaughter of vaccinated animals in countries seeking disease free-status Use sentinel animals to monitor PPR circulation after vaccination Explore the use of penside tests to rule out quickly PPR suspicions in naïve areas

Risk

  • Rapid mutation may result in a high virulent PRRSV, that destroys pig population in a very short time (similar scenario took place in China after the emergence of the High Pathogenic PRRSV).

    GAPS:

    • Monitoring of the population.
    • Determination of the basis of virulence.
    • Adaptable vaccines.

Main critical gaps

  • main critical gaps

    Diagnostic and vaccines - Diagnostic kits and methods should be validated using appropriate field samples (including penside/field tests); serological tests must be validated for use with samples from atypical and wildlife hosts). - Development of DIVA vaccines and DIVA tests should be completed. - Clear WOAH guidelines are needed concerning PPR thermotolerant vaccines (increased thermostability in lyophilised form) to clarify to countries how and when to use them. Disease control -Awareness of the existence of effective and safe vaccines, and communication with remote communities and women livestock keepers should be increased. - Factors affecting vaccine access and acceptance by farmers needs to be studied and strong communication campaigns need to be implemented to improve vaccine coverage and avoid vaccine rejection. - Surveillance and control strategies need to be adapted to take into account the risks of disease transmission/emergence through subclinical and indirect transmissions. - We need greater understanding of the dynamics of animal movement (through trade, transhumance etc…) to identify episystems (i.e. connected host populations capable of PPR virus maintenance) and inform prevention and control strategies. -Cost-benefit and cost-effectiveness analyses of interventions are needed to make the case for PPR control and eradication. Epidemiology and pathogenesis - Improved data and sample collection is required in affected countries to determine the extent and spread of PPRV infection and increase PPRV sequence data availability. - Data is required to inform assessment of the risks of indirect PPR transmission from different materials (meat, waterholes, fomites, etc.). - PPR virulence and host susceptibility need to be studied, notably to evaluate risk when emerging in a new area.

Conclusion

  • PRRSV is one of the most important infectious pig pathogens nowadays. A high mutation rate is problematic for diagnosis and future control of PRRS. High virulent strains may emerge and PRRSV mutants may be difficult to control by the registered vaccines. Farmers should be informed about the impact of PRRSV infections in their herds and should be helped to control PRRSV circulation.

    GAP:

    Many knowledge gaps exist.

  • Conclusion summary (s)

    1. The PPR situation in the EU countries and in countries bordering the EU emphasises the importance of implementing and maintaining appropriate control measures with regard to illegal imports and animal movements to mitigate risks. Equally the tools necessary to control and eradicate the incursions into the EU must be available. 2. PPR is one of the most economically important diseases in developing countries. There is now a global effort to eradicate PPR. Filling the gaps in our knowledge of the disease and development of new diagnostic tools and new vaccines will increase our chances to reach this goal. Importantly, regional coordination and involvement of all stakeholders will be paramount to success. Cooperation of EU member states and European commission should be encouraged.

Sources of information

  • Expert group composition

    1. Corina Ancuceanu, IDAH, Romania
    2. Michael D Baron, Pirbright Institute, UK
    3. Arnaud Bataille, CIRAD, France – [Leader]
    4. Camilla Benfield, GALVmed, UK
    5. Marion Bordier, CIRAD, France
    6. Michel Dione, ILRI, Senegal
    7. Erika Chenais, SVA, Sweden
    8. Bernd Hoffmann, FLI, Germany
    9. Konstantia Tasioudi, Veterinary Centre of Athens, Greece
  • Reviewed by

    Project Management Board

  • Date of submission by expert group

    November 2025

  • References

    1. World Organization for Animal Health WOAH Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 2021
    2. https://www.woah.org/en/what-we-do/standards/codes-and-manuals/terrestrial-manual-online-access/
    3. World Organization for Animal Health WOAH Terrestrial Animal Health Code 2021
    4. https://www.woah.org/en/what-we-do/standards/codes-and-manuals/terrestrial-manual-online-access/
    5. EFSA AHAW Panel (EFSA Panel on Animal Health and Welfare). Scientific Opinion on peste des petits ruminants. EFSA Journal 13:3985.
    6. EFSA AHAW Panel (EFSA Panel on Animal Health and Welfare), Nielsen SS, Alvarez J, Bicout DJ, Calistri P, Canali E, Depner K, Drewe JA, Garin-Bastuji B, Gonzales Rojas JL, Gort_azar C, Herskin M, Michel V, Miranda Chueca M_A, Padalino B, Pasquali P, Roberts HC, Sihvonen LH, Spoolder H, St_ahl K, Velarde A, Viltrop A, Winckler C, Gubbins S, Libeau G, Broglia A, Aznar I and Van der Stede Y, 2021. Scientific Opinion on the assessment of the control measures of the category A diseases of Animal Health Law: peste des petits ruminants. EFSA Journal 2021;19 (7):6708, 94 pp. https://doi.org/10.2903/j.efsa.2021.6708.
    7. Baron MD, Diallo A, Lancelot R, Libeau G. 2016. Chapter One - Peste des Petits Ruminants Virus. In: Margaret Kielian KM, Thomas CM, editors. Advances in Virus Research: Academic Press. p. 1-42.
    8. Baron MD, Diop B, Njeumi F, Willett BJ, Bailey D. 2017. Future research to underpin successful peste des petits ruminants virus (PPRV) eradication. Journal of General Virology.
    9. Bataille, A., & Baron, M. D. (2024). Rinderpest and peste des petits ruminants: state of play in disease eradication efforts. Rev Sci Tech, Special Edition, 43-52.
    10. Bodjo, C. S., Gelaw, H. B., Luhanga, Z. D., Tessema, Y. D., Baziki, J.-D.-D., Boukary, C. R. M., Melesse, G. A., Chitsungo, E., Nwankpa, N., Kihu, S., Njeumi, F., Parida, S., & Diallo, A. (2025). Peste des Petits Ruminants Vaccine: Criteria for Assessing Its Thermotolerance. Viruses, 17(9), 1151.
    11. Chenais, E., Wennström, P., Kartskhia, N., Fischer, K., Risatti, G., Chaligava, T., Enukidze, T., Ståhl, K., & Vepkhvadze, N. G. (2021). Perceptions of pastoralist problems: A participatory study on animal management, disease spectrum and animal health priorities of small ruminant pastoralists in Georgia. Preventive Veterinary Medicine, 193, 105412.
    12. Dione, M. M., Traoré, I., Kassambara, H., Sow, A. N., Touré, C. O., Sidibé, C. A. K., Séry, A., Yena, A. S., Wieland, B., Dakouo, M., Diall, O., Niang, M., Fomba, C. O., Traoré, M., & Fall, A. (2019). Integrated Approach to Facilitate Stakeholder Participation in the Control of Endemic Diseases of Livestock: The Case of Peste Des Petits Ruminants in Mali. Frontiers in Veterinary Science, 6(392).
    13. FAO, & WOAH. (2021). Guidelines for the Control and Prevention of Peste des Petits Ruminants (PPR) in Wildlife Populations https://www.fao.org/documents/card/en/c/cb5148en.
    14. Guendouz, S., Kwiatek, O., Kirtzalidou, A., Katsifa, A., Gianniou, M., Ancuceanu, C., Ghiță, M., Mortasivu, C. L., Zdravkova, A., Kostov, I., Ivanova, E., Bărbuceanu, F., Tasioudi, K. E., & Bataille, A. (2025). Genomic analysis of peste des petits ruminants virus in Europe: Common origin for emergence in Greece, Romania, and Bulgaria. Infection, Genetics and Evolution, 132, 105774.
    15. Jahel, C., Lenormand, M., Seck, I., Apolloni, A., Toure, I., Faye, C., Sall, B., Lo, M., Diaw, C. S., Lancelot, R., & Coste, C. (2020). Mapping livestock movements in Sahelian Africa. Scientific Reports, 10(1), 8339.
    16. Jones BA, Rich KM, Mariner JC, Anderson J, Jeggo M, Thevasagayam S, Cai Y, Peters AR, Roeder P. 2016. The Economic Impact of Eradicating Peste des Petits Ruminants: A Benefit-Cost Analysis. PLoS ONE 11:e0149982.
    17. Kwiatek, O., Libeau, G., Guendouz, S., Corbanini, C., Gogin, A., Lunitsin, A., Sindryakova, I., Koblasov, D., & Bataille, A. (2022). Genomic characterization of peste des petits ruminants vaccine seed “45G37/35-k”, Russia. Veterinary Research, 53(1), 79.
    18. Libeau G, Diallo A, Parida S. 2014. Evolutionary genetics underlying the spread of peste des petits ruminants virus. Animal Frontiers 4:14-20.
    19. Mesdour, A., Ijoma, S., Bolajoko, M.-B., Arsevska, E., Ciss, M., Cardinale, E., Andraud, M., & Apolloni, A. (2024). Assessing the impact of structural modifications in the construction of surveillance network for Peste des petits ruminants disease in Nigeria: The role of backbone and sentinel nodes. PLoS ONE, 19(11), e0303237.
    20. Parida S, Muniraju M, Altan E, Baazizi R, Raj GD, Mahapatra M. 2016. Emergence of PPR and its threat to Europe. Small Ruminant Research 142:16-21.
    21. Parida S, Muniraju M, Mahapatra M, Muthuchelvan D, Buczkowski H, Banyard AC. 2015. Peste des petits ruminants. Veterinary Microbiology 181:90-106.
    22. Tago D, Sall B, Lancelot R, Pradel J. 2017. VacciCost – A tool to estimate the resource requirements for implementing livestock vaccination campaigns. Application to peste des petits ruminants (PPR) vaccination in Senegal. Preventive Veterinary Medicine 144:13-19.

STAR-IDAZ Research Road Maps