Control Tools

• Diagnostics availability

• Commercial diagnostic kits available worldwide

  Commercial kits for serological diagnosis:

  • Competitive enzyme-linked immunosorbent assay (cELISA) based on a monoclonal antibody developed at CIRAD, France (Thiaucourt et al., 1994). The kit commercialised by IDEXX, France, ceased its production in 2023. A cELISA kit based on the same technology is being developed by Innovative Diagnostics – IDvet, France.
  • Complement fixation test BORATEST® CCPP CFT Test Kit. The kit is commercialised by Bora Biotech Ltd. and used to detect antibodies against Mccp as described by the World Organisation for Animal Health (WOAH). It is available in Kenya.
  • Contagious Caprine Pleuropneumonia Antibody (Anti-CCPP) ELISA Kit (Abbexa, UK). This qualitative indirect sandwich ELISA kit for CCPP antibody detection is for research only. Its performances (specificity and sensitivity) are not known. It is therefore not recommended for diagnostic purposes.
  • Indirect ELISA for Mycoplasma capricolum capripneumoniae (Mccp) and M. ovipneumoniae antibodies developed by LVRI, China, and commercialised for use in China.
  • Latex Agglutination Assay (CapriLAT, UK): used for rapid screening in the field. Polysaccharide-based, resulting in cross-reactions with Mycoplasma capricolum capricolum (Mcc), M. leachii, and probably other bacteria. The production of this kit ceased due to its high market price.
  • Indirect Haemagglutination Test (IHT): developed by Lanzhou Veterinary Research Institute (LVRI), registered and commercialised for use in China. Polysaccharide-based, so subject to the same cross-reactions as LAT, but inexpensive and easy to operate at the pen-side (Yuefeng Chu, LVRI, personal communication; no generally accessible references available).

  Commercial culture media for Mccp isolation:

  • CCPP diagnostic medium from Mycoplasma Experience, UK: sterile liquid base to be stored at room temperature and frozen supplement at -20°C.

  Commercial kits for antigen detection:

  • Contagious Caprine Pleuropneumonia (CCPP) ELISA Kit (Abbexa, UK). CCPP antigen detection. No validation data available. This qualitative sandwich ELISA kit is for research only.
  • Goat contagious pleuropneumonia (GCP) Elisa Kit from AFG Scientific (USA). CCPP antigen detection. No validation data available.This qualitative sandwich ELISA kit is for research only.

  Commercial kits for molecular detection:

  • AICON-BIO Mycoplasma Capricolum subsp. Capripneumoniae (MCCP) Real-time PCR Kit (Aicon-Bio, Oregon, USA). For the specific detection of Mccp DNA. For research use only, not for use in diagnostic procedures.
  • OneqPCR-realtime Mycoplasma capricolum subsp. capripneumoniae q PCR KIT (kitpcr.com), BioinGentech (Santiago, Chile). We are uncertain about its availability.
  • Real Time PCR Detection Kit Mycoplasma capricolum, GPS, Biopremier, Portugal (com). For the detection of M. capricolum (both Mccp and Mcc).

  List of commercially available diagnostics (Diagnostics for Animals)

  GAPS :

  None of the serological tests commercially available worldwide is validated, since the IDEXX cELISA and CapriLAT kits have been discontinued and no alternative kits have been validated by international standards yet, though an alternative cELISA kit is currently under development. An indirect ELISA and IHT are available in China, but their validation status is unknown.

  There is only one ready-to-use commercial medium allowing the isolation of Mccp. This medium is extremely expensive and difficult to obtain and preserve (frozen supplement).

  A few commercial PCR assays are available, though they have not been validated and are intended for research use only.

  No commercial pen-side tests, whether direct or indirect, are available for CCPP diagnosis other than the IHT, which is licensed only in China.

• Diagnostic kits validated by International, European or National Standards

  No diagnostic kits have been validated by European standards but two serological kits have been validated under ISO/IEC 17025 standards:

  • The CCPP cELISA was validated by the WOAH/FAO Reference Laboratory/Centre at CIRAD, France (WOAH 2021, Peyraud et al., 2014) and was implemented under ISO 17025 accreditation delivered by COFRAC. However, the new cELISA kit produced by IDvet based on the same monoclonal antibody will need to be fully validated.
  • The IHT has been validated by LVRI, China, and is implemented under ISO 17025 accreditation delivered by CNAS in China.

  GAPS :

  Neither serological nor PCR-based diagnostic kits have been validated by European standards and only two serological assays by international standards. The IHT is commercialised exclusively in China and the cELISA has been discontinued, making the validation of accessible kits, both for serology and direct detection, necessary.

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

  Several diagnostic methods are either described or listed in the CCPP chapter of the WOAH Manual of Diagnostic Tests and Vaccines (WOAH, 2021):

  Serological methods (only “a” described; “b” and “c” are just listed):

  (a) Complement fixation test (MacOwan, 1976; MacOwan and Minette, 1976)

  (b) Latex agglutination test (Rurangirwa et al., 1987a; March et al., 2000)

  (c) Competitive enzyme-linked immunosorbent assay, cELISA (Thiaucort et al., 1994; Peyraud et al., 2014).

  Direct detection and identification methods:

  -In-vitro culture: The composition of culture media, along with the protocols for sampling and Mccp isolation, are provided in the WOAH manual. Mccp is a highly fastidious organism, making isolation particularly challenging. Nevertheless, this growth characteristic represents a distinctive feature, enabling cultures to be distinguished from other related mycoplasma species (see section 7.1).

  -Biochemical and immunological identification: The biochemical tests most commonly used for the identification of mycoplasma cultures are: sensitivity to digitonin, glucose fermentation, reduction of tetrazolium salts, arginine and urea hydrolysis, casein and serum digestion. The main biochemical features of Mccp are presented in section 7.1. However, biochemical tests alone do not provide sufficient resolution for accurate identification, making immunological assays necessary. The most commonly used assay is the growth inhibition test (GIT), which is described in the manual.

  -Molecular detection: direct molecular detection is the prescribed test for laboratory confirmation. (“a” described; “b” and “c” only listed):

  (a) Conventional PCR: PCR followed by restriction enzyme analysis (Bascunana et al., 1994), and direct, specific PCR (Woubit et al., 2004)

  (b) Real-time PCR: either SYBRGreen (Lorenzon et al., 2008) or TaqMan, used as multiplex assay in combination with detection of “peste des petits ruminants” (PPR) virus, Capripoxvirus and Pasteurella multocida (Settypalli et al., 2020).

  (c) Field-applicable isothermal Recombinase Polymerase Amplification (RPA; Liljander et al., 2015).

  GAPS :

  In the CCPP Chapter of the WOAH terrestrial code (WOAH, 2008) only CFT is mentioned as a prescribed test for importation of domestic goats from CCPP infected countries. However, CFT is highly unreliable due to a severe lack of specificity, and its commercial availability is limited to a few African countries. As stated in the CCPP manual (WOAH, 2021), c-ELISA should be the preferred serological test, considering its higher specificity and its potential for commercialization.

  Classical biochemical and immunological identification tests are used only rarely, since molecular methods offer greater specificity, sensitivity, reproducibility, and ease of standardisation.

  A specificity issue with the real-time PCR by Settypally et al. (2020) was identified following the publication of the genome sequence of a Mycoplasma mycoides subsp. capri (Mmc) strain isolated from a goat in Germany (Mmc Wi8079, Accession NZ CP065574; Hill et al., 2021), which contains the target sequence of this PCR assay, previously believed specific for Mccp. Thus, new Mccp-specific target sequences must be identified from an extended range of “Mycoplasma mycoides” cluster strains, followed by the development of multi-target real-time PCR assays with enhanced specificity and sensitivity.

• Commercial potential for diagnostic kits worldwide

  The market is limited, particularly since CCPP affects goats, which have lower monetary value than cattle, and is present in many Low- & Middle-Income Countries (LMIC), where affordability is an issue. In those countries the conditions for delivery, thermostability, and robustness are critical. On the other hand, the disease is widely spread in the Middle East, where it has been shown to affect wildlife, including endangered species, which may represent a significant market.

  CCPP is a neglected disease, but the situation is slowly changing. It has been listed in many countries/regions including Europe and China, which has increased awareness and boosted surveillance and diagnostic capacity. Also, the Global Eradication Strategy launched by the FAO and the WOAH aiming at global eradication of PPR can be an opportunity to increase CCPP surveillance.

  GAPS :

  More research is needed to develop highly effective tests. Market research is necessary to assess demand and affordability of new diagnostics, particularly pen-side tests.

• DIVA tests required and/or available

  No DIVA test exists since there are no DIVA vaccines available for the control of CCPP.

  In China, a subunit vaccine is currently under development, which may boost interest in a DIVA test.

  GAPS :

  Companion DIVA tests are required, in line with DIVA vaccine developments (see section 2.2).

• Vaccines availability

• Commercial vaccines availability (globally)

  It should be noted that the previously marketed “Pulmovac live” attenuated Mccp vaccine from VETAL (Turkey), as well as its inactivated counterpart “Pulmovac-In”, are no longer available. On the other hand, the inactivated “Pulmovac M. capri (BQT)”, which is still commercialised by VETAL, is based on Mmc rather than Mccp, and its efficacy against CCPP has not been demonstrated. To our knowledge, there are currently no live Mccp vaccines available in the market.

  The duration of protection claimed by commercial CCPP vaccines is 6 months to 1 year after a single injection. For example, the vaccination protocol of Chinese vaccines, as well as that of KEVEVAPI and IBRIZE is twice per year, whereas that of TVLA, NVI-E, Jovac and Dollvet is once a year.

  Veterinary vaccine batches to be used in Africa are controlled by the African Union Pan African Veterinary Vaccine Centre (AU-PANVAC, Ethiopia) but to date this requirement is not mandatory for vaccine batch release and commercialisation.

  Methods for the quality control (QC) of current inactivated CCPP vaccines (WOAH, 2021): Sterility, identity, protein content, purity (level of extraneous proteins, notably growth medium contaminants), safety (innocuity in target and non-target animals) and efficacy (protection to live pathogen challenge in goats) must be assessed by vaccine producers for regulatory approval.

  Several different methods are available for the QC of CCPP vaccine batches:

  -Total protein quantification (e.g., bicinchoninic acid technique): This assay does not guarantee the identity of the protein as Mccp antigen (whereas the level of protein contaminants from the culture medium can be extremely high).

  -Sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE): This technique is used to assess the presence of medium contaminants in the final concentrated antigen.

  -Mass spectrometry: allows quantification of Mccp-specific peptides in relation to those originating from culture medium components (Thiaucourt et al., 2018).

  -Serology: Seroconversion by cELISA is induced 2-4 weeks post-vaccination when using WOAH standard vaccines, but not when lower antigen / adjuvant concentrations are used (Peyraud et al., 2014). This seroconversion may also be evaluated by Western blot analysis (WOAH, 2021).

  -Immuno-capture ELISA (ICE): This assay allows specific detection and quantification of the Mccp antigen in the CCPP vaccine (Baziki et al., 2020).

  -In China, a transtracheal challenge in goats 4 weeks post-vaccination is required to validate vaccine efficacy before the release of CCPP vaccine batches (Y Chu, personal communication).

  GAPS :

  There are few vaccine producers and insufficient vaccines available in the market to satisfy the demand in Africa (Wambura et al., 2014). This may also be true in Asian countries such as Pakistan and India.

  Production of inactivated Mccp antigen according to WOAH guidelines is very cumbersome and expensive, so some vaccine producers (with the exception of certain Chinese manufacturers) have deviated from these standards (Thiaucourt et al., 2018).

  Data supporting potency, thermostability and shelf life of commercial CCPP vaccines is unavailable, whereas there is evidence that at least some of them do not induce the expected seroconversion and protection (Peyraud et al., 2014; Lignereux et al, 2018) and are not produced according to WOAH guidelines (Thiaucourt et al., 2018).

  However, assessing the potency of CCPP vaccines is complicated by the need to implement infectious challenge experiments in goats, since there are no small animal models or biomarkers of vaccine efficacy that may serve as correlates of protection. These in vivo challenge trials are not conducted in practice, with the exception of Chinese manufacturers (Y Chu, personal communication).

  Independent QC on vaccine batches (at least those commercialised in Africa) is not performed systematically and the number of vaccine batches undergoing QC by AU-PANVAC is very limited.

  Furthermore, the methods used for the QC of current inactivated CCPP vaccines (with the exception of China) are insufficient to ensure their efficacy. ICE and mass spectrometry analyses have been described but are not routinely applied by AU-PANVAC. Furthermore, when antigens are treated with inactivating agents such as formalin (formaldehyde), commonly used in the production of CCPP vaccines, the antigenic conformation is altered and the ICE test fails to perform reliably.

  New tools to control the stability of Mccp antigens are required in order to assess the thermostability and shelf life of current inactivated vaccines. The use of ICE (Baziki et al., 2020) and other methods must be assessed and correlated with potency assays in goats.

• Marker vaccines available worldwide

  No marker vaccines allowing for immunological differentiation of infected from vaccinated animals (DIVA) are available for the control of CCPP. However, a subunit vaccine is under development in China, which would enable a DIVA strategy (see section 5.1).

  A DIVA vaccine would allow vaccination campaigns in endemic areas while maintaining reliable serological surveillance, facilitating zoning, safe trade, and early detection of residual or re‑introduced infection.

  GAPS :

  Market studies are needed to assess the demand and requirements for DIVA vaccines and their companion tests.

• Effectiveness of vaccines / Main shortcomings of current vaccines

  Effectiveness:

  When produced according to WOAH guidelines (WOAH, 2021), CCPP vaccines consisting in killed whole-cell Mccp antigens inactivated and adjuvanted with saponin (i.e., 0.15 and 3 mg per dose, respectively) can protect goats (100% protection against mortality and clinical disease; Rurangirwa et al., 1987b) for up to 1 year. Considering the very limited intraspecies diversity of Mccp, any strain may be used as seed for vaccine production. The alternative Mccp vaccine in oil adjuvant used in China has been validated by goat challenge (80% protection against clinical disease for up to 1 year), though revaccination is recommended every 6 months (Y. Chu, personal communication).

  Shortcomings:

  The CCPP bacterins currently recommended by the WOAH present serious limitations. The fastidious nature of Mccp, makes antigen production very costly, while the high dose of crude saponin required to induce protection is incompatible with current safety standards., that is recommended by the WOAH. This reconstitution may compromise the stability of the Mccp antigen.

  Most commercial CCPP vaccines currently available consist of a ready-to-use liquid suspension of Mccp antigen in saponin, rather than the lyophilized formulation to be reconstituted immediately before use, validated in the 1980s and recommended by the WOAH (Thiaucourt et al., 2018). The thermostability of the Mccp antigen may be compromised in such preparations.

  The QC of inactivated vaccines is difficult, and has been mainly based on quantification of total protein content. However, a recent study using mass spectrometry to analyse the antigen content of several commercially available vaccines revealed that they were composed of very small quantities of specific Mccp antigen and high amounts of residual proteins from the production medium (Thiaucourt et al, 2018). These results showed that commercial CCPP vaccines did not meet the WOAH standards, casting serious doubts on their quality and highlighting the urgent need for improvement.

  GAPS :

  There is little data available regarding the protection conferred by current commercial CCPP vaccines: the level and duration of immunity and protection must be assessed by infectious challenge in goats.

  Similarly, no data are available regarding vaccine thermostability and efficacy at the end of the shelf life, which should be evaluated by infectious challenge in goats.

  With the exception of China, current quality control procedures applied are basically limited to contamination and total protein quantification but do not assess vaccine efficacy.

  The need for CCPP challenge in goats is limiting the evaluation of vaccine efficacy (validation of new vaccines, formulations, combinations, batches, etc.) but there is currently no alternative to in vivo experiments allowing this assessment (see section 2.1).

• Commercial potential for vaccines

  The commercial potential for safe and effective CCPP vaccines is considerable, given the wide geographic distribution of the disease and the substantial economic losses it causes in Africa and Asia. Uptake would likely be high, as currently available commercial vaccines are limited in number, and present several drawbacks, including safety issues, short immunity and high cost (Salt et al., 2019). Nevertheless, affordability remains a significant limitation in many LMIC where CCPP is endemic. The commercial viability of any new vaccine will therefore depend strongly on its cost.

  GAPS :

  Very few studies have examined farmers’ willingness to pay or the cost-benefit ratio of CCPP vaccination programmes (Salt et al., 2019. Market assessments for improved vaccine formulations and for next-generation vaccines (including subunit vaccines and live, genetically modified strains) should incorporate evaluations of product acceptability (particularly for GMO-derived vaccines), willingness to pay at both farmer and governmental levels, and cost-benefit analyses under diverse production systems. Such studies are essential to guide investment, regulatory planning and technology adoption.

• Regulatory and/or policy challenges to approval

  Regulatory and policy challenges to CCPP vaccine approval include the lack of harmonised guidelines for evaluating vaccine quality, safety and efficacy, particularly in LMIC. Limited national regulatory capacity will further delay approval. In some countries, policies regarding genetically modified vaccines are unclear or restrictive, hindering the adoption of next-generation products.

  GAPS :

  Clear regulatory pathways, harmonised quality standards and strengthened national regulatory authorities are needed to guarantee the quality of commercial vaccines.

  Guidance on the evaluation and licensing of GMO-based vaccines, as well as validated assays for potency and batch control, should be prioritised.

• Commercial feasibility (e.g manufacturing)

  Manufacturing CCPP vaccines presents significant challenges, greater than those encountered with other mycoplasma vaccines such as CBPP. Current CCPP vaccines are inactivated, and the causative agent grows slowly, requires richer and more expensive media, and yields low biomass, making large-scale production less efficient and more costly. Furthermore, CCPP vaccines are produced under variable manufacturing conditions in LMIC, and some facilities do not fully comply with international standards

  GAPS :

  Clear manufacturing guidelines and performance standards must be established to ensure reliable large-scale production and facilitate regulatory approval.

  Production of CCPP vaccines under full Good Manufacturing Practice (GMP) conditions remains limited, with many manufacturers still operating with outdated processes and a lack of validated QC assays specific to CCPP vaccines.

  Regional production capacity in endemic LMIC remains insufficient, contributing to higher costs and restricted vaccine availability.

• Opportunity for barrier protection

  Barrier (“ring”) vaccination may be a good tool for CCPP control where rapid containment around infected foci is needed, provided an effective, quality-assured vaccine and logistics are available. The saponin inactivated and adjuvanted bacterin vaccines produced according to WOAH guidelines can reduce morbidity and mortality but present safety issues owing to their high saponin content. On the other hand, the efficacy of commercial vaccines needs to be fully assessed (Thiaucourt et al., 2018).

  For example, during the CCPP outbreaks in the Thrace region of Turkey (Özdemir et al., 2005), barrier vaccination and movement-control measures could have complemented antimicrobial treatments, provided that quality-controlled vaccines were available and authorised for emergency use. Such measures are consistent with WOAH recommendations for the control of CCPP (WOAH, 2021).

  GAPS :

  Any barrier-vaccination plan for CCPP should: (i) define clear protection zones around confirmed outbreaks, (ii) pair vaccination with immediate movement restrictions and active surveillance, and (iii) ensure independent batch QC and post-vaccination monitoring to verify coverage and effectiveness.

• Pharmaceutical availability

• Current therapy (curative and preventive)

  Antibiotic treatments with tetracyclines, macrolides and fluoroquinolones reduce symptoms, lesions and excretion levels, and oxytetracycline, enrofloxacin and tylosin are commonly used in treatment of CCPP in the field (Yatoo et al., 2019; Kumar et al., 2015; Kimeli et al., 2025). However, they must be administered at the earliest stage of the disease (Thiaucourt et al 1996, WOAH, 2009, Abd-Elrahman et al., 2020) and there are concerns that treated animals may become carriers, though their role in the epidemiology of the disease is not clear.

  Although reports on the use of antibiotics by farmers for the control of CCPP in Africa and Asia are rare, it is well known that several antibiotics are freely available and widely used in the field with little or no antibiotic stewardship (Caudell et al., 2017 and 2022; George, 2017). The quality of the antimicrobials, as well as use of the optimal dose and duration of treatments is not guaranteed, while withdrawal periods are not respected to ensure safety and limit the development of antimicrobial resistance (AMR).

  In clinical trials, treatment with streptomycin (alone or combined with penicillin) resulted in cured animals (Rurangirwa 1981a) . Tylosin and oxytetracycline were tested in vivo and resulted in improved clinical signs, but 20% of treated animals still remained infected (El Hassan et al.,1984). In one study, marbofloxacin and spiramycin were found to be more effective in reducing clinical signs than oxytetracycline (Abd-Elrahman et al., 2020). Danofloxacin treated goats had fewer lung lesions and lower combined clinical scores than saline treated goats, however the authors noted that Mccp could still be isolated from the lungs of treated goats (Özdemir et al., 2006).

  In attempts to increase treatment efficacy, Cheng et al. compared two administration routes for tiamulin fumarate: nebulisation and intramuscular injection. The animals receiving nebulised tiamulin fumarate became symptom-free earlier than those treated intramuscularly (Cheng et al., 2024). Yatoo et al. combined tylosin, oxytetracycline and enrofloxacin respectively, with a nonsteroidal anti-inflammatory drug, meloxicam, and an antihistamine, pheneramine maleate. CCPP-affected goats that were treated with these combinations recovered more rapidly than those in the control group, which received oxytetracycline alone (Yatoo et al., 2019).

  In China, neoarsphenamine was widely used for many years, particularly in the 1950s and 1960s, but its use has declined considerably due to its high toxicity, which poses risks to the quality and safety of animal products, public health and ecological safety. Intramuscular and intravenous injections can be applied but inhalation is the most effective in reducing clinical CCPP. Intramuscular injection of acetyl isovaleryl tylosin, oxytetracycline, doxycycline, lincomycin, tilmicosin, and gamithromycin, respectively for 5 days has also shown to have good clinical efficacy. Some traditional Chinese medicines are also used.

  In a recent outbreak of CCPP in Iran, the animals were treated with florfenicol and tylosin, yet the disease relapsed after 2 weeks (Abdollahi et al., 2023). Similarly, tylosin failed to improve the condition of CCPP affected animals in an outbreak in a sand gazelle herd (Lignereux et al., 2018). The reason for the failures of the antibiotics to stop the disease outbreaks are not known.

  GAPS :

  There is an urgent need to provide guidelines describing the optimal dose and duration of treatment for CCPP to promote judicious antibiotic stewardship in order to minimise side effects as well as the development of AMR.

  Effective protocols of combination therapies including antibiotics, non-steroidal anti-inflammatory drugs and (NSAIDs), and anti-allergic drugs must be validated and promoted for therapeutic management of CCPP-affected animals.

• Future therapy

  A better understanding of host-pathogen interactions may facilitate the discovery of new treatments. For example, immune responses associated with inflammation were characterized in goats both in vivo and in vitro (Ma et al., 2020, Yang et al., 2025). Since short-chain fatty acids (SCFAs) are known to inhibit these responses when added to food (Trompette et al., 2014; Cait et al., 2018; Lewis et al., 2019) they were tested as a preventive treatment in a mouse model of CCPP. SCFAs mixed with water and administered for 7 days prior to infection significantly reduced body weight loss, the number of bacteria in the lungs, and lung inflammation (Yang et al., 2025).

  Investigations into non-conventional treatments against several mycoplasma species including the goat pathogen Mmc, have primarily focused on in vitro testing (Arjoon et al., 2012; Sleha et al., 2014; Furneri et al., 2012; Kama-Kama et al., 2016). Extracts derived from medicinal plants have shown some degree of inhibitory activity under laboratory conditions; however, their safety profiles and pharmacokinetic or pharmacodynamic characteristics remain uncharacterised, and no in vivo evidence of therapeutic benefit has yet been produced.

  For what concerns conventional antibiotic treatments, it is unlikely that efforts will be made to develop or validate new molecules specifically for the treatment of CCPP, as antibiotherapy is its control. Moreover, novel antimicrobial agents are generally prioritised for human medicine and are therefore unlikely to be applied to livestock diseases such as CCPP. On the contrary, global efforts are made to limit antibiotic use in order to reduce AMR, which is recognised as a major contemporary public-health challenge (Murray et al., 2022).

  GAPS :

  Host-pathogen interaction studies must be continued as a means of discovering new therapies. The therapeutic efficacy of short-chain fatty acids must be validated in goats.

  The mouse model of CCPP described by Yang et al (2025) needs to be better characterized to ensure that it accurately reproduces the disease observed in goats. Indeed, although an inflammatory response and neutrophil infiltration is observed in lungs, Mccp multiplication peaks at 24 hours and then drops after 48 hours, suggesting an abortive infection in mice.

  To date, there appear to be no published studies assessing the suitability of alternative antimicrobial treatments for CCPP such as antimicrobial peptides, bacteriophage therapy, or phage-derived enzymes for treating CCPP or other mycoplasma infections. Reviews of phage therapy in livestock note its potential for treating bacterial infections in animals, but do not report trials targeting mycoplasmas (Ferriol-González & Domingo-Calap, 2021). The effectiveness of such alternative therapies against Mccp, should be explored.

• Commercial potential for pharmaceuticals

  Very high in affected countries. Conventional antibiotherapy is extensively used in the field, with limited control in many countries of Africa and Asia.

  The use of antimicrobials is not envisaged in Europe and other CCPP-free regions, where any outbreak must be managed through the implementation of immediate eradication measures (see sections 11.3 & 16.1).

• Regulatory and/or policy challenges to approval

  The same challenges noted for the assessment of vaccine efficacy and safety apply to therapeutics, notably concerning the need for validated goat challenge models and harmonised guidelines.

  A major concern arises from the widespread use of illegal drugs, particularly in affected LMIC of Africa and Asia, where counterfeit, falsified and unregistered products are commonly used.

• Commercial feasibility (e.g manufacturing)

  The commercialisation of new antimicrobials should be feasible but limited mainly by cost.

• New developments for diagnostic tests

• Requirements for diagnostics development

  Serological tools are generally useful for surveillance, confirmation of clinical cases, confirmation of freedom from infection, and monitoring vaccination campaigns (particularly cELISA for the latter). The CFT is cheap, but difficult to perform and not specific. Thus, most laboratories do no longer apply this method. The cELISA is expensive and not available at the moment. However, it is much more specific than CFT and detects antibodies for a longer time during the infection process (also in the chronic phase). It is a wide-spread and standardized technique and equipment is available in most laboratories. Both tests need to be conducted in a laboratory and must be interpreted at herd level.

  The Latex Agglutination Test (LAT) and Indirect Haemagglutination Test (IHT), both based on Mccp exopolysaccharide, though not specific, are most suited for confirmation of clinical cases at the pen-side. The LAT can be directly performed using a drop of whole blood (Rurangirwa et al., 1987a). The commercial IHT currently used in China is cheap and very simple to implement in a basic laboratory setting or at the pen-side (Yuefeng Chu, LVRI communication; no generally accessible references available).

  Although isolation of Mccp remains the gold standard confirmatory test for the WOAH, molecular biological methods are best suited for clarifying a suspected diagnosis based on clinical and pathological signs or positive serological results, and to identify isolates. They are useful both at herd and individual animal levels and characterised by their potential for high specificity, allowing differentiation of Mccp from the closely related mycoplasmas of the M. mycoides cluster.

  In addition to the methods listed in the WOAH Manual of diagnostic tests and vaccines, further protocols with different validation statuses have been suggested in the scientific literature:

  Serological assays:

  A blocking ELISA has been developed by AU-PANVAV for use in African laboratories (Jean de Dieu et al., 2019). Less specific than cELISA, it may be particularly useful for use as a diagnostic tool in endemic regions. Zhu et al. (2022) presented a colloidal gold-based immunochromatographic assay strip (lateral flow test) for rapid pen-side detection of antibodies against Mccp in serum samples. Recombinant P20 membrane protein was used as the binding antigen in the test.

  Conventional PCR assays: A nested PCR test has been described (Hotzel et al., 1996). However, nested assays are subject to contamination problems and are thus not recommended for routine diagnosis. A new Mccp-specific target for conventional PCR has been proposed and tested by Wu et al., (2020).

  Real-time PCR assays: SYBR Green (Fitzmaurice et al., 2008; Lin et al., 2018); Taqman (Zhu et al., 2018); High Resolution Melting (HRM; Zhang et al., 2021).

  Loop-mediated isothermal amplification (LAMP) assays have been developed in China (Song et al., 2022), with limited validation and application in the field.

  GAPS :

  Development of pen-side tests could facilitate diagnostics for CCPP outside main laboratories but cost effectiveness will need to be addressed.

  Isothermal amplification methods (RPA and LAMP) intended for CCPP detection at the pen-side are costly due to expensive enzymes. Furthermore, they are prone to contamination, resulting in false-positive results.

  Lateral flow tests are promising field-applicable diagnostic tools, but they are also expensive, so cost-effectiveness must be improved.

  An interesting option may also be optimising the LAT, notably to make it cheaper.

  Genomic and antigenic heterogeneity within Mmc and, most particularly, Mcc species, which overlap with Mccp, cause cross reactivity and hamper unambiguous identification. Therefore, the design of PCR assays needs to be improved by including a higher number of field strains of the M. mycoides cluster in sequence alignments, which requires greater whole genome sequencing efforts. Further, more extensive field validation and inter-laboratory testing is required to assess the performances of available and novel molecular diagnostic assays.

  Proteomic approaches for the identification of immunogenic proteins as potential diagnostic antigens should be pursued.

• Time to develop new or improved diagnostics

  The development timeline for new CCPP diagnostics is influenced by several constraints, including: i) the limited growth efficiency of Mccp, ii) the scarcity of high-quality reference materials, and iii) the need for robust validation in multiple field settings. These factors typically extend development cycles. Regulatory requirements for assay validation, standardisation and registration further add to these timelines.

• Cost of developing new or improved diagnostics and their validation

  The cost of developing new or improved CCPP diagnostics is comparatively high due to the factors exposed above (section 4.2), which increase production and validation costs. Overall, these factors make validation costs proportionally higher than for many other livestock diagnostics, especially when aiming for assays acceptable to international regulatory bodies.

• Research requirements for new or improved diagnostics

  Serological tests could be improved by the use of recombinant proteins or peptides: defining and implementing relevant targets (antigens) and test schemes for a highly specific test with good exclusivity (avoiding cross-reactions) while maintaining a good sensitivity, is crucial. Prior studies are therefore needed before test development.

  For molecular diagnostics, large genomic datasets are needed to allow intra- and inter-specific comparisons. More and more data are available for Mccp and other members of the M. mycoides cluster, which should allow the identification of alternative targets for the design of specific molecular diagnostic tests. These data should however be enlarged, particularly for what concerns other cluster members, which are under-represented.

  Extensive validation of diagnostic assays in the field is an important requirement for both serological and molecular diagnostics.

  GAPS :

  Only a few studies exist on the identification of promising antigenic peptides for CCPP diagnosis and even fewer have been tested in serological assays.

  Comparative genomic analyses conducted on a large panel of strains representing the temporal and spatial diversity of Mccp and the other members of the “M. mycoides” cluster are needed to determine representative pan and core genomes for developing appropriate diagnostic tools.

  The necessary exchange of Mccp-positive samples and isolates between laboratories, regions or countries is restricted by biosecurity measures and Nagoya protocol compliance.

• Technology to determine virus freedom in animals

  The cELISA is the only recommended serological test for the determination of mycoplasma freedom at herd level and with limitations also for individual animals prior to movements.

  However, due to its limited sensitivity, serology should be applied at herd, not at individual level, and, whenever possible, paired serum samples collected 3–8 weeks apart, should be examined (WOAH, 2021).

  CFT and LAT are not recommended for proving disease-free status since they often lead to false-positive results due to cross-reactivity with other mycoplasma species that affect goats (EFSA AHAW Panel, 2022; WOAH, 2021). Conversely, false-negative results may occur, particularly in the early stages of the disease before specific antibodies are produced and in the late or chronic stages when antibody titres drop.

  Positive serological results require confirmation by PCR testing of samples from life animals (e.g., swabs, BAL, pleural fluid puncture) post-mortem samples (e.g., lung tissue, pleural fluid).

  GAPS :

  Specific and sensitive tools for individual diagnosis as opposed to today’s available tools for diagnosis at herd level are needed for reliable import clearance.

  A major problem is the detection of symptomless, low- or non-shedding individuals that may act as carriers.

  Goats are often infected with other mycoplasmas of the M. mycoides cluster which can cause cross-reactions by CFT. Additionally, the CFT detects mainly IgM, which drops earlier in the course of infection compared to IgG. Therefore, the CFT is not recommended to determine freedom of Mccp (WOAH Terrestrial Manual, Chapter 3.8.4, Section 2).

  Specific and sensitive tools for individual diagnosis as opposed to today’s available tools for diagnosis at herd level are needed for reliable import clearance.

  A major problem is the detection of symptomless, low- or non-shedding individuals that may act as carriers.

  Goats are often infected with other mycoplasmas of the M. mycoides cluster which can cause cross-reactions by CFT. Additionally, the CFT detects mainly IgM, which drops earlier in the course of infection compared to IgG. Therefore, the CFT is not recommended to determine freedom of Mccp (WOAH Terrestrial Manual, Chapter 3.8.4, Section 2).

• New developments for vaccines

• Requirements for vaccines development / main characteristics for improved vaccines

  The first experimental CCPP vaccines were successfully implemented in the 1880s for the control of CCPP following its introduction in South Africa (Hutcheon, 1889), well before the first isolation of the CCPP agent (F38 strain) in 1976 (MacOwan and Minette 1976). The traditional prophylactic procedure applied consisted in the subcutaneous inoculation of goats with infected lung extracts and pleural fluids. A century later, an experimental vaccine based on a high passage culture of F38 inoculated intratracheally to goats significantly reduced their susceptibility to CCPP infection, although it did not prevent clinical infection (MacOwan and Minette 1978).

  A major milestone was the development of inactivated, saponin-adjuvanted vaccines. Early experimental vaccines using inactivated F38 mycoplasma antigens with various adjuvants induced robust immunity in goats and they proved efficacious in the field (Rurangirwa et al., 1981b; Rurangirwa et al., 1984; Rurangirwa et al., 1987b; Litamoi et al., 1989). Subsequent studies defined 0.15 mg of F38 antigens inactivated and adjuvanted with 3 mg of saponin per 1 mL as the optimal dose, providing about one year of protection and remaining stable for over 14 months (Rurangirwa et al., 1991). Although limited by high antigen requirement, production complexity and cost, as well as saponin‑related side-effects, these remain the WOAH-endorsed vaccines (WOAH, 2021).

  Improved vaccine formulations have been proposed, notably by using Montanide oil adjuvants, which confer improved safety and stability. Water in oil (W/O) emulsions of Mccp whole cell antigens from strain M1601 inactivated in formalin induced good protection (Zhao et al., 2014) and are currently used in China.

  The Mccp strain ILRI-181, which shows a faster growth rate than the F38 strain, was evaluated both as a live vaccine and as a saponin-inactivated formulation, resulting in 87.5% and 100% survival of goats, respectively, following a CCPP challenge 1 month post vaccination (E. Schieck, personal communication).

  Furthermore, since Mcc shares extremely close genetic and antigenic similarity with Mccp, which results in cross-serological responses, the potential for cross-protection between the two subspecies was recently investigated. Semmate et al. (2024) evaluated binary ethylenimine (BEI)-inactivated vaccines prepared from either Mccp strain F38 (0.15 mg per dose) or the virulent Moroccan Mcc strain MOR20 (0.3 mg per dose), formulated in Montanide W/O emulsions. A two-dose vaccination protocol administered 4 weeks apart induced a strong humoral immune response for both vaccines and provided protection against challenge with the virulent Mcc strain 2 weeks after the booster vaccination. Although challenge with a virulent Mccp strain was not performed, these preliminary results suggest that cross-protection between the two M. capricolum subspecies may occur and that Mcc-based vaccines could potentially be used to protect small ruminants, not only against contagious agalactia caused by Mcc, but also against CCPP. Indeed, good short-term protection against Mccp challenge in goats, performed according to Liljander et al. (2019), was recently achieved using an Mcc-based W/O emulsion vaccine (L. Manso-Silván, personal communication). Considering that the yield of the Mcc strain, under research laboratory conditions, was at least three times higher than that of a “fast growing” Mccp strain, replacing the classical F38 seed by an Mcc strain shall dramatically reduce vaccine production costs.

  Molecules such as capsular polysaccharides (CPS) and recombinant proteins have also been proposed as candidate antigens for novel vaccine formulations (Chen et al., 2017; March et al., 2000; Zhao et al., 2012; Zhao et al., 2013). Some of these molecules have demonstrated good immunogenicity and have shown promising potential to induce protective immune responses. In China, reverse vaccinology and immunoproteomics approaches were used to identify candidate immunogenic proteins. Thirteen proteins were initially selected for evaluation and tested in animal trials, leading to the identification of four novel proteins as potential components of a recombinant subunit vaccine against CCPP. Subsequent evaluation indicated that one of these proteins alone was capable of inducing full protection (Yuefeng Chu, LVRI, personal communication; no generally accessible references available).

  Multi-valent and co-administered vaccines, which target multiple diseases in a single dose or administration, have been proposed as practical and cost-effective alternatives for small-scale farmers (https://www.galvmed.org/why-combination-vaccines-are-better-for-small-scale-livestock-producers/); among other combined formulations, a trivalent PPR-sheep and goat pox-CCPP vaccine is under development by GALVmed .

  Other preliminary studies assessing the immune response and safety of either multivalent or co-administered vaccines that include a CCPP component have provided promising results. These include a gel-based vaccine combining CCPP, PPR and foot-and-mouth disease (Khalil et al., 2019), as well as several combinations of co-administered vaccines against CCPP, PPR, sheep and goat pox, and pasteurellosis in goats (Hurisa et al., 2024). These studies indicate that the immunogens do not interfere with each other’s immunogenicity when administered within the same vaccination programme.

  Synthetic biology tools are available and may be used for the development of improved vaccine strains (improved growth / yield and reduced requirements in vitro, as well as stability).

  Opportunities:

  Synthetic biology tools have been recently developed for the genetic engineering of Mccp genomes, allowing the production of mark-less, targeted Mccp mutants for pathogenicity studies, as well as development of rationally-designed vaccines (Gourgues et al., 2024).

  A robust and reliable in vivo infection model is available and allows live animal trials for the evaluation of virulence and protection (efficacy assays) (Liljander et al., 2019). A scoring system designed for CBPP (Hudson and Turner, 1963) was modified for CCPP in an antibiotic efficacy trial in Turkey (Özdemir et al., 2006).

  The global plan for PPR eradication by 2030 may increase CCPP surveillance and provide opportunities for combined vaccination campaigns.

  GAPS :

  Safe, thermostable and cost-effective vaccines inducing good and long-lasting protection (at least one year) against mortality, clinical disease and shedding are urgently needed to improve CCPP control.

  The safety, potency, and duration of immunity of current killed vaccines must be urgently improved, for example through the use of alternative adjuvants such as oil emulsions, which have been shown to enhance protective immunity. In the longer term, a better understanding of the protective immune responses required would be highly valuable for optimising vaccine design.

  The main limitation to the production of cost-effective CCPP vaccines is the low yield of Mccp strains. Bacterins based on the much faster growing Mcc strains, which have provided promising results in initial trials, must be fully validated, including demonstration of long-term protection under industrial production conditions and in the field. The use of oil adjuvants, compatible with foot and mouth disease and other ruminant vaccines, opens the way for the production of multi-valent vaccines. Strategies based on the use of multi-valent and/or co-administered vaccines should be considered to dramatically reduce the cost of vaccination against major small-ruminant diseases prevalent in affected countries in Africa and Asia. Market studies are needed to develop this strategy.

  DIVA vaccines would also be useful in countries implementing eradication plans or in the event of emergence in Europe or other disease-free regions.

  Synthetic biology tools are available and may be used to develop improved vaccine strains with increased yield, reduced growth time and in vitro growth requirements, as well as enhanced stability. They may also enable the development of negatively and/or positively marked strains suitable for DIVA vaccines.

  Improved infrastructures and capacity building in vaccine production facilities may be needed to move on from the current live vaccine towards the production of new generation (ex. recombinant and subunit vaccines).

  Adapted tools will need to be developed for the quality control of new CCPP vaccines (e.g., adapted to new antigens, new nature such as live strains or recombinant proteins, new formulations, etc.).

  Although a robust challenge model using ILRI 181 strain is available (Liljander et al., 2019) and a scoring system has been proposed (Özdemir et al., 2006), a robust standard clinical/pathological scoring system has not yet been established for use in efficacy trials. Limitations imposed by the application of the Nagoya protocol and other national “access and benefit sharing” requirements in Kenya, make both the procurement of ILRI-181 strain and the implementation of live animal experiments in Kenya challenging. The use of alternative virulent Mccp strains available in different regions of Africa and Asia remains to be assessed.

• Time to develop new or improved vaccines

  The same limitations applying to the development of diagnostics apply to vaccines (see sections 4.2 & 4.3), to which are added difficulties for vaccine efficacy and safety studies requiring challenge experiments (refer to sections 2.1 and 5.1).

• Cost of developing new or improved vaccines and their validation

  The same limitations exposed above (section 5.2) have an impact on vaccine development and validation costs.

• Research requirements for new or improved vaccines

  Characterisation of the virulence determinants of Mccp and, more importantly, of the components that elicit a protective host immune response is required to enable the rational design of improved vaccines, whether inactivated or live. Little is known at present, as reviewed in sections 9.7 and 15.1, respectively.

  GAPS :

  Research towards the characterisation of the virulence determinants of the pathogen and of the protective host immune response are needed to allow the rational design of improved vaccines (refer to sections 9.7 and 15.1 for research gaps).

• New developments for pharmaceuticals

• Requirements for pharmaceuticals development

  Novel antimicrobial development is unlikely to be prioritised for livestock diseases such as CCPP.

  There is however still room to study the role of antimicrobial peptides, bacteriophage therapy, or phage-derived enzymes, as well as validation of combination therapy including antibiotics, non-steroidal anti-inflammatory drugs and (NSAIDs), and anti-allergic drugs for therapeutic management of CCPP-affected animals.

• Time to develop new or improved pharmaceuticals

  The same limitations applying to the development of diagnostics apply to vaccines (see sections 4.2 & 4.3), to which are added difficulties for vaccine efficacy and safety studies requiring challenge experiments (refer to sections 2.1 and 5.1).

• Cost of developing new or improved pharmaceuticals and their validation

  The same limitations exposed above (sections 4.2 and 5.2) have an impact on pharmaceuticals development and validation costs.

• Research requirements for new or improved pharmaceuticals

  Refer to sections 9.7 and 15.1 regarding research on characterisation of mechanisms of pathogenicity and host immune response, respectively.

Disease details

• Description and characteristics

• Pathogen

  Mycoplasma capricolum subsp. capripneumoniae (Mccp), is a bacterium belonging to the class Mollicutes, order Mycoplasmatales, family Mycoplasmataceae, and genus Mycoplasma (Leach et al., 1993).

  The Mollicutes, trivially referred to as “mycoplasmas”, are distinguished from other eubacteria by their small size and lack of a cell wall, which makes them intrinsically resistant to antimicrobials targeting the cell wall, such as beta-lactam antibiotics. They are phenotypically Gram-negative but mycoplasmas evolved from Gram-positive bacteria by a process of massive genome reduction involving the loss of many metabolic pathways and adaptation to a commensal or parasitic mode of life (Thiaucourt & Manso-Silván, 2018). This explains their strict host and tissue tropism, as well as their fastidious nature in vitro, which is particularly relevant to Mccp.

  Mccp belongs to the “Mycoplasma mycoides” cluster, a group of five very closely related ruminant pathogens sharing many genetic and phenotypic traits (Manso-Silván & Thiaucourt, 2019; Manso-Silván et al., 2009). With the exception of Mycoplasma leachii, which induces mainly mastitis and arthritis in cattle, all the members of this cluster are responsible for WOAH-listed diseases. M. mycoides subsp. mycoides (Mmm) is the agent of contagious bovine pleuropneumonia (CBPP), a disease of cattle presenting many similarities with CCPP; M. mycoides subsp. capri (Mmc) and M. capricolum subsp. capricolum (Mcc) are involved in the contagious agalactia or “MAKePS” syndrome of small ruminants, characterised by mastitis, arthritis, keratoconjunctivitis, pneumonia, and septicaemia (Thiaucourt & Bölske, 1996). To complicate matters, other mycoplasma species are also implicated in this syndrome: Mycoplasma putrefaciens, closely related to the “M. mycoides” cluster, and Mycoplasma agalactiae, a distant species more closely related to Mycoplasma bovis.

  More precisely, according to phylogenetic relationships, Mccp belongs to the “Capricolum” sub-cluster, together with Mcc, and M. leachii, while the “Mycoides” sub-cluster comprises Mmm and Mmc (Manso-Silván et al., 2007; Manso-Silván et al., 2009).

  Mccp cells are pleomorphic, non-spiral, and non-motile. They secrete an exo-polysaccharide (glucan) that can be found either as a free extracellular form (extracellular polysaccharide, EPS) or around the cells forming a pseudo-capsule (capsular polysaccharide, CPS) (Bertin et al., 2015).

  Mccp is a facultative anaerobe that grows very slowly in culture. It produces minute colonies on solid medium, with the typical fried-egg appearance characteristic of mycoplasmas. No “film and spot” formation is observed. In broth, Mccp produces a small sediment at the bottom of the tube, sometimes forming characteristic “comets” from trailing growth through the medium. Gentle agitation disperses the sediment into typical “silky swirls”, while full agitation results in slight turbidity. It ferments glucose and digests casein and coagulated serum, but does not metabolize arginine or urea and can be distinguished from other members of the “M. mycoides” cluster by its total inability to oxidise maltose, trehalose, mannose and glucosamine (Manso-Silván et al., 2009).

  Mccp is the sole causative agent of CCPP, though for many years there has been confusion regarding the aetiology of this disease, attributed to other mycoplasmas of the M. mycoides cluster, particularly Mmc. The CCPP agent was isolated in Kenya in 1976 (MacOwan and Minette 1976), and this first isolate, named “F38” became the Type strain. The name “F38 type” was retained for the taxon until 1993, when sufficient evidence was gathered to support a subspecies relationship with M. capricolum (Leach et al., 1993).

  GAPS :

  Persistent confusion regarding the aetiology of CCPP continues to hinder accurate disease recognition, particularly in parts of Asia. This confusion often arises from the misidentification of pneumonic infections caused by other mycoplasmas of the M. mycoides cluster (especially Mmc) as cases of CCPP.

  This taxonomic and diagnostic confusion has significant practical consequences. It has led to the dissemination of misleading information in the literature regarding CCPP’s epidemiology, including its host specificity, geographical distribution and prevalence. Misclassification and lack of awareness contribute to a systemic underestimation of the true distribution and impact of CCPP, particularly in regions where diagnostic capacity is limited. This, in turn, presents a major gap in global surveillance and response, ultimately affecting the formulation of evidence-based policy, resource allocation, and international reporting standards (EFSA, 2017). Furthermore, it has led to the distribution of vaccines targeting Mmc instead of Mccp, which may offer little to no protection against CCPP, compromising disease control efforts.

  Limited awareness combined with insufficient training of veterinary personnel and farmers (especially in Central-West and North Africa and various regions of Asia) significantly hampers disease recognition and reporting. This lack of capacity contributes to the scarcity of targeted investigations and limits our understanding of the true diversity and geographical distribution of Mccp strains.

  Strengthening veterinary services through targeted training and capacity building is therefore essential. In parallel, participatory epidemiology offers a powerful complement to conventional surveillance by increasing the sensitivity and contextual relevance of data collection. These approaches not only support community-level engagement but also help raise disease awareness and provide critical insights into the relative incidence and perceived impact of CCPP, particularly in settings where laboratory confirmation is limited or unavailable.

• Variability of the disease

  Mccp is an extremely monomorphic pathogen (i.e., presenting very limited intra-species diversity). Molecular typing tools have been developed for the molecular epidemiology of CCPP, from single locus techniques (Lorenzon et al., 2002; Pettersson et al, 1998). to whole genome analyses. Molecular typing schemes based on the analysis of eight genetic markers, known as Multi-Locus Sequence Analysis (MLSA, Akhtar et al., 2022, Manso-Silván et al., 2011) discriminated Mccp strains in several groups showing a good correlation with phylogenetic relationship and geographic origin. These groups were also correlated to more sophisticated genotyping methods; from a multi-gene or extended Multi-Locus Sequence Typing scheme (eMLST, Dupuy et al., 2015) to a whole-genome sequence analysis pipeline, attaining optimum strain typing for molecular epidemiology studies and outbreak investigations (Loire et al., 2020).

  Evolutionary history analysis indicated that Mccp originated from its Mcc ancestor approximately 300 years ago (Dupuy et al., 2015). This relatively recent divergence explains the low genetic diversity observed in Mccp despite its high mutation rate (estimated at around 1.3x10^-6 substitutions per site per year). It is therefore presumed that Mccp emerged through the specialisation of Mcc, a goat pathogen with a broad tissue tropism, into the restricted ecological niche of the lung (Dupuy et al., 2015).

  As opposed to other members of the “M. mycoides” cluster, Mccp exhibits few insertion sequences and long duplications are limited to the rRNA operons. Whole genome assembly is relatively easy to obtain and 20 whole genome sequences were available in GenBank in 2022 (Akhtar et al., 2022), whereas very few are available from other cluster members. These genomes provide valuable resources for comparative analyses and understanding of Mccp's genetic diversity.

  Variability in strain virulence has been described. The Kenyan isolate ILRI 181 is a highly virulent strain inducing acute disease and extremely high morbidity and mortality rates upon experimental goat infection (Liljander et al., 2019). On the other hand, a high passage of the type strain F38 induced neither symptoms nor lesions upon intratracheal inoculation of goats, demonstrating its complete attenuation (MacOwan & Minette, 1978).

  GAPS :

  Both virulent and avirulent strains are critical for research workflows involving experimental infection setups, pathogenicity exploration, and protective vaccine trials. However, very few Mccp strains of documented virulence are available.

  Furthermore, access to strains of interest is restricted due to Nagoya Protocol compliance, making it difficult for laboratories outside the source countries to lawfully obtain and use isolates for variability or virulence studies, or to implement infectious challenge experiments. A centralised strain bank containing genetically and phenotypically verified virulent and avirulent isolates would be highly valuable.

  More complete genomes of Mccp strains from diverse geographic regions, dates and hosts are needed to capture the full genetic diversity and unravel the evolutionary history of CCPP in Asia and Africa.

  Broader multi-omics investigations must be undertaken across the members of the “M. mycoides” cluster. All associated scripts, workflows, and data repositories should be made publicly accessible. Such a platform would facilitate the identification of the genetic determinants governing virulence/attenuation, host and tissue tropism, as well as the acquisition and spread of AMR.

• Stability of the agent/pathogen in the environment

  Due to the lack of a cell wall, mycoplasmas are quite fragile outside their ecological niche. Mccp’s resistance to physical and chemical action is described in the WOAH technical card, based on determinations made for the CBPP agent, Mmm, (WOAH 2009, Thiaucourt, 2018): very sensitive to physical, chemical, and biological factors; does not persist in the environment for more than 3 days in tropical areas and up to 2 weeks in temperate zones. Cultures are inactivated within 60 minutes at 56°C and 2 minutes at 60°C and within a few minutes by ultraviolet radiation or routinely used disinfectants. Conversely, it can survive for extended periods under freezing conditions, with reports of viability in frozen pleural fluid for up to 10 years. In any case, Mccp is known to be more fastidious and sensitive than Mmm, so its stability and persistence in the environment are expected to be lower than those described in the WOAH technical card.

  GAPS :

  Data on Mccp resistance to physical and chemical factors is not available but is based on Mmm. Specific studies assessing Mccp's susceptibility to a range of chemical agents are needed to inform effective sanitation protocols.

  Precise measurements of Mccp viability across various environmental matrices (e.g., water, soil, fomites) under different conditions are lacking.

  The potential for Mccp to form biofilms, which may enhance environmental survival, has not been explored.

• Species involved

• Animal infected/carrier/disease

  CCPP mainly affects domestic goats (Capra aegagrus hircus), and there are no notable differences in susceptibility according to breed, sex, or age (Manso-Silván & Thiaucourt, 2019).

  For a long time, domestic goats were considered to be the only susceptible host of CCPP, whereas domestic sheep (Ovis aries) were regarded as refractory to natural and experimental infection (Harbi et al., 1983; Hutcheon, 1889; Manso-Silván & Thiaucourt, 2019; Nicholas & Churchward 2011). However, in mixed small ruminant herds with CCPP, it has been demonstrated that sheep can be infected, seroconvert, and occasionally develop pleuropneumonia (Bölske et al, 1995; Houshaymi et al., 2002) Furthremore, Mccp has been isolated from the nose of healthy sheep (Litamoi et al., 1990) and from the lungs of clinically affected sheep (Bölske et al, 1995).

  Since 2004, CCPP has been reported in a growing number of wild ungulate species, showing that they are also susceptible and suffer substantial morbidity and mortality, at least in captivity (Manso-Silván & Thiaucourt, 2019). Susceptible species identified in the Middle East include wild goat (Capra aegagrus), Nubian ibex (Capra ibex nubiana), Laristan mouflon (Ovis orientalis laristanica), gerenuk (Litocranius walleri), Arabian and scimitar-horned oryx (Oryx leucoryx; Oryx dammah), and gazelle species (Gazella marica, Gazella subgutturosa; Arif et al., 2007; Chaber et al., 2014; Lignereux et al., 2018; Ali et al., 2024). In China, a fatal CCPP outbreak was reported in Tibetan antelope (Pantholops hodgsonii; Yu et al., 2013).

  However, wildlife does not seem to act as a CCPP reservoir for the domestic goat. On the contrary, reported cases suggest that wild ungulates were most likely contaminated from domestic goats, though Mccp could be transmitted directly across wild ruminant species, at least in captivity (Lignereux et al., 2018). CCPP seems to have appeared in wildlife only recently due to increased opportunity for contacts between wild and domestic animals driven by land-use changes and human encroachment into wild habitats (Manso-Silván & Thiaucourt, 2019).

  The existence of latent and chronic carriers (animals who appear healthy but harbour infection) is still debated. Goats in the chronic stage of the disease may present neither symptoms and sequestered lesions, nor detectable antibody titres. And yet a long-term carrier status has long been suspected. For example, when CCPP was introduced in South Africa by a shipment of Angora goats from Turkey, no symptoms were observed during the entire journey, which took 11 weeks from Angora, current Ankara, (Hutcheon, 1881). However, in the absence of infectious “sequestra”, it is not known where the CCPP agent may persist. Mccp may be harboured in the ear canal of recovered animals, as demonstrated for Mmc (Da Massa & Brooks, 1991), or may persist in other animal species such as sheep, acting as silent carriers (Thiaucourt, 2018).

  GAPS :

  Most sources indicate that breed and sex do not significantly affect epidemiology, but this has not been rigorously studied across diverse breeds and age groups. Increased susceptibility in young animals has been mentioned in reviews but this is not well documented.

  Although CCPP is known to affect a relatively large number of wild ruminant species, the full range of susceptible wild species has not been systematically studied or documented.

  It is not clear whether sheep and wild ungulates may act as reservoirs and play a role in transmission to domestic goats or they just become occasionally infected. Their role in the epidemiology of CCPP should be investigated

  The existence of latent or chronic carriers, harbouring the pathogen without symptoms, and their epidemiological importance in the transmission of CCPP need to be characterised.

  The mechanisms of Mccp persistence (localisation, duration) in the host and possible reservoirs need to be elucidated (particularly considering the absence of long-lasting sequestra). The possible carriage of Mccp in the ears of goats and other ruminant species merits investigation.

• Human infected/disease

  None. CCPP is not a zoonosis.

• Vector cyclical/non-cyclical

  No vectors have been described. However, goat fleas have been identified as vectors for the transmission of Mmc with reproduction of disease in goat kids, and ticks sampled on sheep and goats have been found to carry viable M. agalactiae strains, suggesting a potential role of these ticks as either reservoirs or vectors of ruminant mycoplasmoses (Galluzzo et al., 2021).

  GAPS :

  The potential carriage of Mccp by ectoparasites such as ticks, and their possible role in the transmission of CCPP, warrant further investigation, although this is not considered a priority.

• Reservoir (animal, environment)

  No reservoir has been described and persistence in the environment can be practically ruled out given the extreme sensitivity of Mccp to physical and chemical stress, according to the WHOA technical card (WOAH 2009).

  Mccp has been isolated from healthy sheep and wild ungulates. It is not clear whether they may play a role as CCPP reservoirs. Ectoparasite carriage may also be considered.

  GAPS :

  The role of sheep as potential CCPP reservoirs must be analysed. The possible role of wild ungulates may also be investigated, including the possible carriage and transmission via ectoparasites, although this is not considered a priority.

• Description of infection & disease in natural hosts

• Transmissibility

  Mccp is transmitted by direct contact between infected and susceptible animals, mainly by the airborne route. This contact does not need to be very long to allow transmission; 24 hours suffice (Thiaucourt, 2018). Mccp is easily inactivated (WOAH, 2009) and its low persistence outside the host (see section 7.3) practically excludes the possibility of indirect transmission through fomites or animal products. However, airborne transmission can result in distant spread and transmission at a distance of up to 80 m has been reported (Lignereux et al., 2018). Low temperature and humidity may affect this distance but not in a dramatic way. The usual and occasional routes of transmission are described in section 14.

  Transplacental or gamete-associated transmission of CCPP has neither been investigated experimentally nor reported in the field and if it exists, is considered negligible.

  As for CBPP and other airborne infections, the main factors influencing the transmission of CCPP are the level of excretion from infected animals, the intimacy and duration of contact, and the size and vulnerability of the susceptible population (Thiaucourt, 2018).

  Stress induced by extreme weather, transport and concurrent diseases, can both predispose animals to infection and increase the severity of the disease, thus increasing shedding. Animal density, herd size and management system (i.e., intensive vs. extensive, mixed vs. single species, and host and breed species involved) may also influence transmission.

  Transmission models and estimates of the basic reproductive number (R0) of CCPP are discussed in section 23.3, “Mathematical modelling”.

  GAPS :

  The factors influencing transmissibility in different hosts need to be better documented. Stressors or predisposing factors should be addressed, including the role of co-infections in triggering CCPP outbreaks.

  A systematic review on reported field outbreaks is needed and should take into account:

  -Mccp strain involved: strains of diverse virulence have been described (see section 7.2).

  -Host species and breeds involved: age and genetic factors to be characterised.

  -Epidemiological situation: enzootic vs. epizootic

  -Vaccination status: efficacious vaccines will reduce host susceptibility.

  -Concurrent infections: parasites, Contagious Ecthyma or Orf virus, sheep and goat pox virus, Peste de Petits Ruminants (PPR) virus, Mycoplasma ovipneumoniae, other mycoplasma and bacteria, which may trigger outbreaks by increasing host susceptibility. NOTE: parasitic worm infection has been shown to increase morbidity upon experimental Mccp infection (Maritim et al, 2018), and mixed Mccp infections with Orf and sheep and goat pox virus, have been reported in goats (Chu et al, 2011) and are believed to increase CCPP vulnerability.

  -Type of herd management system: mixed vs. single species, intensive vs. extensive: sheep may be involved in “silent” transmission; factors such as overcrowding, especially during confinement at night enclosures, will increase transmission.

  -Geographical location, period of the year: colder seasons can help transmission and may increase persistence of the pathogens (for seasonal patterns see section 13.1).

  -Stress due to extreme weather or sudden weather change.

• Pathogenic life cycle stages

  None.

• Signs/Morbidity

  CCPP is a strictly respiratory disease that can present itself in hyperacute, acute and chronic forms (WOAH, 2009). Hyperacute and acute presentations are observed when fully susceptible animals are exposed to the pathogen for the first time and are thus common during epizootics (epidemics), when the disease enters a new territory, whereas chronic forms occur in enzootically-affected areas.

  CCPP clinical signs and lesions were described in detail by Hutcheon (1881) and have been extensively reviewed by (Nicholas & Churchward 2011; Thiaucourt, 2018). In the hyperacute form, death occurs within a couple of days due to respiratory distress. The acute form/phase is characterised by high fever (41°), lethargy, anorexia, and violent coughing evolving to dyspnoea. In the terminal stage, animals are unable to move and typically stand with abducted forelegs and extended neck, blocked nose with nasal discharge and open mouth with saliva drooling. Death may occur after a few days. Pregnant goats may abort due to the high fever and disease severity.

  Animals surviving the acute phase may develop a chronic infection. The chronic form/phase is characterised by milder signs, limited to intermittent cough, nasal discharge, and weight loss. Respiratory signs only become evident upon exercise. Without treatment, chronic infection may progress to death after several weeks but some animals recover.

  Post mortem lesions of acute cases are characterised by unilateral (occasionally bilateral) fibrinous pleuropneumonia, with large amounts of yellow sero-fibrinous pleural exudate in the thoracic cavity and caseous-fibrinous deposits in the pleura. The mediastinal lymph-nodes are enlarged. The affected lung is also enlarged and presents extensive consolidation and a granular texture with a degree of colours varying from red to purple and grey. However, the enlargement of interlobular septa that gives a characteristic marbled appearance to the lungs in cases of pleuropneumonia due to Mmc and Mmm (in CBPP), is not observed in CCPP (Hutcheon, 1889; Thomas, 1873).

  In the chronic stages/forms there is no plural fluid but fibrotic pleural adhesions are observed. Some authors describe the presence of lung “sequestra”, i.e., lesions consisting of necrotic tissue surrounded by a white fibrotic capsule. These have been observed upon experimental infection or following antibiotherapy (Liljander et al, 2019; Özdemir et al, 2006), and for as long as 18 weeks after the onset of clinical signs (Wesonga et al, 1998). Although, in most cases these chronic lesions appeared to be sterile, Mccp could be isolated from some of them (Özdemir et al, 2006). The persistent “sequestra” harbouring live mycoplasmas up to two years post infection that have been described in chronic CBPP cases are not observed here (Manso-Silván & Thiaucourt, 2019).

  A distinctive feature of the CCPP agent is that, unlike the CBPP agent in cattle and other mycoplasmas in goats, which induce local reactions following subcutaneous injection that may spread and lead to disseminated disease and septicaemia, Mccp does not induce any local inflammatory reaction in goats when injected subcutaneously (Hutcheon 1889; Harbi 1983).

  Morbidity up to 100% is observed in susceptible naive animals, in both domestic goats and wild ungulates (WOAH, 2009), and 100% morbidity has been reported under experimental conditions (Harbi et al., 1983; Liljander et al., 2019). However, it tends to be lower in endemically affected areas. Morbidity rates are influenced by the virulence of the Mccp strain, host species / breed susceptibility, and individual susceptibility (animal immune/health status). The latter is dependent on naiveness, health status, and stress due to climatic conditions and management practices.

  GAPS :

  Although a few accurate historical descriptions exist (Hutcheon, 1881; Thomas, 1873), there is a lack of detailed, systematic data from natural outbreaks, which is essential for understanding disease manifestations under field conditions.

  On the other hand, experimental data on CCPP incubation, morbidity and mortality are derived from different infection models (in-contact, endobronchial, and intratracheal), which yield variable results, making it difficult to compare results across studies and to establish reliable benchmarks (Liljander et al., 2019). There is a clear need for improved, standardised, and reproducible challenge models, such as the one developed by Liljander et al. (2019), to be made more widely available. However, as noted in section 7.2, access to well characterised virulent strains is restricted by the Nagoya Protocol, which limits the international sharing of biological materials. Overcoming these barriers is essential for advancing research and consistency in CCPP experimental studies.

  A more thorough description of chronic lesions is needed, in particular to determine whether sequestra are formed upon natural infection and their evolution over time post infection, including whether they are sterile or contain viable Mccp. This is important to determine whether chronically infected animals can act as silent carriers.

• Incubation period

  In natural conditions and epizootic settings, the reported incubation period is usually around 6-10 days (Hutcheon, 1881, WHOA, 2009), though in some cases it may be prolonged up to 4 weeks (Nicholas & Churchward 2011, WOAH, 2009). In experimental conditions the incubation period observed varies from 3 days to 2 weeks (WOAH, 2009, Liljander et al., 2019) but some experimentally infected goats developed clinical signs 6 weeks after exposure (WOAH, 2009). An incubation period ranging between 12 and 27 days was reported following experimental infection in Sudan, both for intubated and in-contact infected animals (Harbi et al., 1983)

  GAPS :

  The reported duration of the incubation period is very variable but the reasons for this variability are unclear. Most sources agree on a 6 to 10-day incubation range for CCPP as the norm in acute infections but some, less common cases of much longer incubation (up to 6 weeks) have been documented (WOAH, 2009). There is insufficient detailed mechanistic explanation as to why such prolonged incubation occurs in a minority of cases. The factors contributing to delayed onset of clinical disease must be fully investigated.

  Most information regarding these prolonged incubation periods comes from retrospective outbreak data or historical accounts rather than controlled experimental work.

  The role of latent or chronic carriers in influencing the length of the incubation period remains poorly understood and is considered an important gap.

  Breed and individual genetic susceptibility, along with various health and stress factors, may affect both the incubation period and progression of the disease. However, there is a lack of quantitative studies that specifically evaluate the impact of these variables on the duration of incubation.

• Mortality

  Mortality rates ranging from 50 to more than 90% have been observed in both domestic and wild ruminants upon natural infection. The WHOA technical card (WHOA, 2009) indicates a mortality induced in naïve herds that can reach 80%. However, these estimates may vary depending on several factors listed above in relation to morbidity (cf. section 9.3). Under experimental settings mortality rates of 60-70% (Liljander et al, 2019, Hutcheon 1881) and up to 100% (Rurangirwa et al, 1981b) have been reported.

  GAPS :

  See section 9.3

• Shedding kinetic patterns

  The level of shedding varies greatly depending on the form and phase of the disease (acute vs. chronic). It is maximal in the acute form, during the acute clinical phase, when animals cough and sneeze excreting infected droplets facilitating high transmission rates within herds.

  Diagnostic methods such as PCR on nasopharyngeal swabs confirm shedding during symptomatic phases (Liljander et al., 2019; El-Deeb et al., 2017).

  GAPS :

  Although it is established that shedding corresponds with symptomatic phases marked by respiratory distress and lung pathology, quantitative data on the precise timing and duration of shedding in relation to incubation and disease progression remain limited.

  Carriage and shedding during the chronic phase are suspected but have not been demonstrated.

• Mechanism of pathogenicity

  CCPP is the result of an uncontrolled inflammatory response leading to tissue consolidation and respiratory distress that may be induced directly by toxic mycoplasma components or indirectly, through the release of pro-inflammatory cytokines by the host's cells. No classical virulence factors such as adhesins or toxins have been identified in Mccp genomes, apart from one adhesin- and one hemolysinA-related gene (Chen et al., 2017), and virulence has been attributed to surface or secreted components and intrinsic metabolic functions.

  Several components of Mccp are potential triggers of inflammation, although knowledge about their action is scarce and is often derived from studies on Mmm, the causative agent of CBPP. Those components are: i) capsular and free extracellular forms of a polysaccharide characterized as glucan (Bertin et al., 2015); ii) the l‑α‑glycerophosphate oxidase (glpO), an enzyme responsible for the production of hydrogen peroxide as a by‑product of glycerol metabolism, as reported both in vitro and in vivo (Liljander et al.,, 2019); iii) lipoproteins, which are potent stimulators of inflammatory responses by macrophages (Mühlradt et al., 1998); iv) secreted exoproteases including the S41 peptidase family (Ganter et al., 2019); v) a two-protein system (MIB-MIP) capable of capturing and cleaving the VH domain of immunoglobulins (Arfi et al., 2016). The resulting cryptic epitopes may potentiate neutrophil recruitment and oxidative burst. However, the MIB-MIP system is widely present in many distant Mycoplasma spp. including non-pathogenic strains.

  As opposed to CBPP, sequestra harbouring live bacteria are not observed in CCPP and the sub-cutaneous inoculation of Mccp does not induce the invasive oedema (i.e., Willems’ reaction) observed with Mmm. Also, there are no notable differences in susceptibility according to age. Tissue tropism is strictly pulmonary, and more specifically in the lower respiratory tract, as observed in experimental infections by contact (Wesonga et al., 2004)

  Attenuation by in vitro passage has been demonstrated experimentally: The Mccp Type strain, F38^T, was totally attenuated through high-passage cultivation, resulting in no symptoms following intratracheal inoculation in goats (MacOwan & Minette, 1978). However, no other attenuated strains have been described and it is not clear whether the deposited type strain F38^T (NCTC 10192) and available whole genome sequence (Falquet et al, 2014) corresponds to the original virulent isolate from 1976 (MacOwan & Minette, 1976) or to an attenuated passage.

  GAPS :

  A clear picture of the molecular basis of Mccp’s virulence and attenuation is lacking and research is needed to understand how the host environment affects the regulation of Mccp’s virulence genes.

  The impact of the transition between capsular and free extracellular forms of the glucan polysaccharide on the immunomodulatory properties of Mccp remains unknown. Unlike the galactan described in Mmm, the mechanisms underlying this phenotypic variation have not yet been elucidated

  Very little is known about the role of Mccp’s exo-secretome in pathogenicity.

  The mechanisms of Mccp persistence in the host have not been elucidated. It is not clear how and where Mccp survives in the host in the absence of sequestra.

  Overcoming additional technical barriers is essential for advancing research and achieving greater consistency in CCPP experimental studies:

  Well characterised and widely available virulent and avirulent Mccp strains are needed for host-pathogen interaction studies. Verifying the attenuation of the Type strain F38^T is a priority.

  There is much room for improvement of experimental infection models, particularly in vitro. Comprehensive in vitro models, such as respiratory explants and multicellular co-cultures including immune cells may be very useful.

  The goat challenge model developed by Liljander et al. (2019) results in 100% morbidity and very high mortality, which is valuable for reducing the number of animals needed in experimental trials to achieve statistical significance but may not reflect natural infection. Improved, standardised and reproducible in vivo challenge models need to be made widely available.

• Zoonotic potential

• Reported incidence in humans

  None

• 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

  The disease has a substantial negative impact on animal welfare due to its high morbidity and potential to induce severe respiratory distress and high mortality. In addition, as a Category A disease in the EU, compulsory eradication measures including the slaughter of infected and exposed animals (see section 11.3), can further affect animal welfare and could result in the loss of valuable genetic resources if an outbreak is detected.

  Both the disease itself and the measures required to control it could impact locally adapted indigenous breeds with important production or resilience traits (e.g., pashmina goats in Ladakh plateau; Parray et al., 2019), as well as endangered or vulnerable wild ungulate species (Lignereux et al., 2018; see section 11.2), thereby posing risks to biodiversity conservation.

  The disease has a substantial negative impact on animal welfare due to its high morbidity and potential to induce severe respiratory distress and high mortality. In addition, as a Category A disease in the EU, compulsory eradication measures including the slaughter of infected and exposed animals (see section 11.3), can further affect animal welfare and could result in the loss of valuable genetic resources if an outbreak is detected.

  Both the disease itself and the measures required to control it could impact locally adapted indigenous breeds with important production or resilience traits (e.g., pashmina goats in Ladakh plateau; Parray et al., 2019), as well as endangered or vulnerable wild ungulate species (Lignereux et al., 2018; see section 11.2), thereby posing risks to biodiversity conservation.

  GAPS :

  There are no specific analyses in the literature regarding the impact of CCPP on animal welfare and biodiversity per se.

• Endangered wild species affected or not (estimation for Europe / worldwide)

  As stated in section 8.1, CCPP affects a number of wild ungulate species that can suffer substantial morbidity and mortality (Manso-Silván & Thiaucourt, 2019). Among them, the scimitar-horned oryx (Oryx dammah) and Tibetan antelope (Pantholops hodgsonii) are considered endangered based on International Union for Conservation of Nature (IUCN) definitions.

  Following an outbreak of CCPP in the Naqu area of Tibet, in 2012, approximately 2,400 Tibetan antelopes were found dead, representing around 16% of the estimated 15,000 individuals inhabiting the region. This mortality event poses a substantial threat to the survival of the species (Yu et al., 2013).

  Several other species, including the Arabian oryx (Oryx leucoryx), Nubian ibex (Capra ibex nubiana), gerenuk (Litocranius walleri), and sand and goitered gazelles (Gazella marica, and Gazella subgutturosa) are considered vulnerable. The wild goat (Capra aegagrus) is considered near threatened, while the Laristan mouflon (Ovis orientalis laristanica) is regarded as locally endangered due to its highly restricted distribution in southern Iran.

  GAPS :

  The list of endangered and vulnerable species affected by CCPP may be larger, since the full range of susceptible wild species has not been systematically documented.

• Slaughter necessity according to EU rules or other regions

  At the European level, CCPP is classified as Category “A + D + E” according to Regulation (EU) 2018/1882 http://data.europa.eu/eli/reg_impl/2018/1882

  Category A diseases are diseases not normally present in the EU that require immediate compulsory eradication measures if a case is detected, and rapid notification to national and EU authorities; Category D diseases require strict movement control and specific conditions for the entry of animals/products into the EU; and category E diseases require constant surveillance and preparedness.

  The EFSA (European Food Safety Authority) panel assessment of control measures for CCPP notes that strict control measures, including the slaughter of infected (and where appropriate in-contact) animals, is an effective direct way to interrupt transmission in incursion / eradication contexts (EFSA, 2022). Movement bans and import restrictions from infected zones are additional key measures supporting the eradication strategy (WOAH Terrestrial Animal Health Code, 2008).

  In endemic areas, stamping out strategies are difficult to implement due to the lack of resources for disease surveillance, diagnosis, and to compensate farmers. Alternatives such as vaccination and movement control are considered in these scenarios (EFSA, 2022).

  GAPS :

  Applying strict sanitary measures for the immediate eradication of Category A diseases under EU Animal Health Law is extremely challenging in practice. The destruction of entire herds following individual cases may be mandatory, which has provoked strong opposition from the livestock sector during PPR outbreaks in East Europe in 2024, and LSD outbreaks in France in 2025.

  There is a need for rigorous studies that assess the cost-benefit of such eradication policies and investigate the best way to inform and engage farmers and the wider public to improve the acceptance of drastic strategies with significant social and economic consequences.

• Geographical distribution and spread

• Current occurence/distribution

  CCPP is present in Africa, the Middle East, and Asia, although its precise distribution remains uncertain.

  By the end of the 20th century, CCPP had been reported in more than 30 countries in Africa and Asia, mainly based on clinical descriptions (Thiaucourt & Bölske, 1996). However, some of these reports (particularly from Southeast Europe, West Africa and South Asia), may have been misdiagnosed, mainly due to confusion with Mmc infections, which can also produce severe pleuropneumonia in goats (Nicholas & Churchward, 2011; Thiaucourt & Bölske, 1996). With the exception of very clear descriptions in Algeria and India, the presence of CCPP in several of these countries cannot be confirmed due to absence of isolation and identification of the causative agent.

  Isolation of Mccp remains the gold standard for confirming the presence of the disease in a country or region. Mccp was first isolated in Kenya (MacMartin et al., 1980; MacOwan & Minette, 1976), and subsequently in Sudan, Tunisia, Chad, Oman, Yemen, Turkey, Uganda, Ethiopia, Niger, Tanzania, Eritrea, and the United Arab Emirates (WOAH, 2009; Thiaucourt & Bölske, 1996). Additional isolations have been documented over the past two decades, including Qatar (Arif et al., 2007), Tajikistan (Amirbekov et al., 2010), Mauritius (Srivastava et al., 2010), China (Chu et al., 2011), Pakistan (Ahmad et al., 2021, Shah et al, 2017), Saudi Arabia (El Deeb et al., 2017), India (Parray et al., 2019), Iran (Khodakaram-Tafti et al., 2023), and Egypt (Abd-Elrahman et al., 2020). Taken together, these reports bring a total number of 22 countries in which CCPP has been confirmed by isolation.

  Over the past two decades, however, the increasing use of specific molecular and serological diagnostic tools has significantly improved our understanding of the distribution and impact of the disease. These methods enabled confirmation of CCPP in countries where it had most likely been present for many years, before or despite the absence of isolation of Mccp. This applies to countries such as Pakistan (Awan et al., 2010), India (Gupta et al., 2016), Nepal (Regmi et al., 2023), Bangladesh (Rahman et al., 2024) and Iraq (Al-lahibi et al., 2025). On the other hand, these analyses also showed that the disease was spreading to new territories. For example, CCPP was introduced into mainland Europe in 2002, with outbreaks in the Thrace region of Turkey confirmed by serology and PCR in 2003, and Mccp subsequently isolated in 2004 (Özdemir et al., 2005). The disease subsequently reached the Indian Ocean, with cases reported on the island of Mauritius in 2009 (Srivastava et al., 2010). More recent scientific publications and official notifications to the WOAH indicate that CCPP continues to expand its geographical range, with new introductions or reintroductions recorded in Egypt (Abd-Elrahman et al., 2020), Mauritania (Beyit et al., 2024), and Mongolia (reported to the WOAH in 2024). Finally, fatal CCPP outbreaks in wild ungulate species were reported for the first time in Qatar (Arif et al., 2007), highlighting the broader host range and potential ecological impact of CCPP.

  CCPP has never been reported in America or Oceania, and the risk of introduction is minimal, as these continents are protected by their geographical isolation and strict bans on the importation of live animals. Conversely, Europe must be considered at risk, since following the introduction of CCPP in Turkish Thrace (Özdemir et al., 2005), the initial outbreaks were controlled by the use of antibiotics, but the disease subsequently spread throughout the region, becoming endemic and posing a potential risk to neighbouring Greece and Bulgaria (Özdemir et al., 2018).

  GAPS :

  The current distribution of CCPP is not well defined and the disease is likely far more widespread than suggested by the few countries where Mccp has been isolated and officially reported. One major reason is that the pathogen is difficult to isolate from clinical material, so cases go undetected despite active disease circulation (WOAH 2021). In many goat-rearing areas of Africa and Asia, the disease is not well known, seldom suspected, and thus rarely investigated (Akhtar et al., 2022). In addition, attention is often diverted towards better recognised and more heavily targeted diseases such as PPR, which benefits from stronger awareness and established surveillance programmes.

  Conversely, there is considerable uncertainty around many historical accounts and clinical descriptions of CCPP, as other respiratory diseases were frequently mistaken for it. Pasteurellosis, other mycoplasmoses, and especially pleuropneumonia caused by Mmc have long been confused with CCPP, particularly in Asia.

  Together, these factors (under-recognition and diagnostic difficulty on the one hand, and misidentification or misattribution on the other) create a substantial knowledge gap regarding the current occurrence and true geographic distribution of CCPP.

• Epizootic/endemic- if epidemic frequency of outbreaks

  A systematic review conducted by Ahaduzzaman (2021) analysed the worldwide prevalence of CCPP between 1979 and 2018. This review identified 41 articles reporting the disease in 12 countries across sub-Saharan Africa, Asia, and the Thrace region of Turkey, with pooled prevalence estimations in goats and sheep ranging from 8.00% (95% CI 6.91–9.00) in Southeast Europe (Thrace) to 23.21% (95% CI 17.57–28.84) in Africa and 28.70% (95% CI 22.02–35.38) in Asia.

  A supplementary literature review was conducted here to include articles that appeared later on or that were missing from the previous review. A total of 99 articles from Scopus, Google Scholar and SciSpace were retrieved. Among them, 42 countries were identified where CCPP was reported: 22 in Africa, 6 in Asia, 12 in the Middle East and 2 in Europe. In most of the cases (23), CCPP circulation was detected through clinical disease reports or serological investigations: 10 in Africa (Cameroun, Chad, Egypt, Ethiopia, Kenya, Mauritius, Somalia, Sudan, Tanzania, Uganda); 5 in Asia (China, India, Nepal, Pakistan, Tajikistan); and 8 in the Middle East (Bahrain, Iran, Kuwait, Oman, Saudi Arabia, Turkey, United Arab Emirates, Yemen). In the other cases (19) the disease was only suspected or there were just sporadic events reported: 12 in Africa (Angola, Benin, Democratic Republic of the Congo, Djibouti, Guinea-Bissau, Libya, Mali, Mauritania, Niger, Nigeria, Senegal, Tunisia) and 7 in Asia, the Middle East and Europe (Bangladesh, Greece, Malta, Iraq, Jordan, Lebanon, Qatar).

  Data from scientific literature were compared to declarations of CCPP to the WOAH platform WAHIS (https://wahis.woah.org/). Between 1973 and 2015, 27 countries declaring CCPP were recorded: 13 in Africa (Angola, Cameroun, Chad, Eritrea, Ethiopia, Kenya, Libya, Mauritius, Niger, Sierra Leone, Somalia, Sudan, Tanzania), 5 in Asia (China, India, Malaysia, Pakistan, Tajikistan), 7 in the Middle East (Afghanistan, Bahrain, Iran, Kuwait, Oman, Qatar, Yemen), and 2 in Europe (Greece and Serbia, though no further declarations were made from these countries) (https://wahis.woah.org/). In this period, big outbreaks were recorded in Oman (151 thousand cases), Iran (83 thousand cases), Ethiopia (44 thousand cases), China (18 thousand cases), and Tanzania (15 thousand cases).

  Between 2015 and 2025, 26 countries declared CCPP outbreaks, with 6 new countries appearing in Africa (Nigeria, Djibouti, Ivory Coast, Uganda, and the two Congos), 2 in Asia (Mongolia and Bangladesh) and 1 in the Middle East (Saudi Arabia). Almost the same set of countries reported the biggest outbreaks in this period: Tanzania (around 96 thousand cases), Ethiopia (83 thousand cases), Oman (70 thousand cases), China (64 thousand cases), Democratic Republic of Congo (14 thousand cases). A shift from the Middle East to Africa was observed in terms of case recordings: while before 2015 around 80 thousand cases were recorded in Africa and 242 thousand in the Middle East, the figures in 2025 were reversed with 81 thousand in the Middle East and 210 thousand in Africa. In Asia, the number of cases recorded almost doubled between the two periods.

  To summarise the frequency of occurrence, we based our analysis on outbreak declarations, classifying countries as endemic/high occurrence if the disease was declared on average more than once per year, and sporadic otherwise. According to WAHIS records (https://wahis.woah.org/) and literature review, 16 countries were identified where the disease had been reported throughout the study period (1973–2025). In particular, 5 countries in Africa (Tanzania, Ethiopia, Somalia, Kenya and Chad), 3 in Asia (China, India and Pakistan) and 4 in the Middle East (Oman, Iran, Afghanistan and Kuwait) reported frequent CCPP outbreaks (an average of more than one outbreak per year) and may be considered endemic. For Eritrea, Cameroon and Bahrain, CCPP occurrence was considered sporadic (although the impact of the disease may have been tremendous, as in Eritrea and Bahrain). Finally, in Tajikistan, the frequency of CCPP outbreaks reported has drastically reduced to 2 in the last ten years. Before 2015, the disease made sporadic appearances in 6 African countries (Mauritius, Libya, Sierra Leone, Angola, South Sudan), 1 Asian country (Malaysia) and 2 European countries (Serbia and Greece), as well as 3 Middle Eastern countries (Turkey, Qatar and Yemen), although the number of cases recorded and outbreaks were highest in Yemen. In the last 10 years, it has appeared sporadically in new countries: 5 in Africa (the Democratic Republic of the Congo, Djibouti, Ivory Coast, South Sudan and Uganda) and 2 in Asia (Bangladesh and Mongolia). However, in new territories like the Republic of Congo, Nigeria and Saudi Arabia, the disease has occurred with high frequency (Shaheen et al., 2024).

  Except for a few countries (Cameroun, Djibouti, and Eritrea) and those where the disease occurred sporadically, outbreaks were recorded in both semesters of the year. In Asia, independently of the year, the severity of the outbreaks (in terms of number of cases) did not change significantly between semesters, and the same applied to reported deaths, although the number increased suddenly in 2017. In Africa and the Middle East, a similar change in tendency could be observed in the same periods: before 2015, most cases (and deaths) were recorded in the Middle East during the first semester of the year, whereas after 2015, the opposite occurred (most of the outbreaks occurred during the second semester). In Africa, most cases were recorded throughout the year before 2010; nowadays, they are occurring more frequently in the first semester.

  However, semesters do not always coincide with seasonal dynamics related to environmental factors and husbandry practices, and more contextual information is needed to elucidate the relation between frequency of outbreaks and seasonality. CCPP transmission does not involve vectors, but animal movements and husbandry practices, which are influenced by climatic conditions and exhibit seasonal patterns, can impact the frequency of outbreaks.

  Environmental and climatic factors such as cold winters and abrupt changes in temperature and rainfall have been linked to disease outbreaks and increased severity (Manso-Silván et al.,2019). In the pastoral regions of Kenya, Ethiopia, Tanzania and Uganda, seasonal pastoral movements (transhumance) have been identified as a potential factor in the recurrence of outbreaks (Atim et al., 2016; Bett et al., 2009; Kusiluka, 2004; Mekuria et al., 2008; Muhanguzi et al., 2024). The movement of animals and grazing practices can result in infected herds from abroad mixing with local herds (Bett et al., 2009; Mekuria et al., 2008). For additional information about seasonality and outbreak patterns linked to climate in different regions, please refer to Section 13.1.

  GAPS :

  The analysis of the WAHIS data must be regarded with caution. The majority of conclusions are drawn from aggregated data collected via the WAHIS platform. In most of the cases, the areas identified in WAHIS correspond with those described in the scientific literature. However, in some cases, such as the outbreaks in Thrace in 2002, no corresponding reports are recorded in WAHIS. On the other hand, it remains unclear whether the reported cases in Greece and Serbia were in fact attributable to CCPP. Nicholas & Churchward (2012) raised doubts as to whether the declared cases in Greece may instead have represented infections caused by Mmc, endemic in the area, rather than CCPP.

  These data, although valuable, cannot provide detailed information about the precise localisation and time of the outbreak and its evolution in time. Furthermore, since WAHIS relies on passive national reporting, requires laboratory confirmation, and suffers from chronic under-notification (especially in pastoral regions where CCPP is endemic), the database greatly underestimates the true occurrence of CCPP. Consequently, WAHIS records cannot be used to infer outbreak frequency, compare enzootic versus epizootic patterns, or quantify disease burden. They indicate only that the disease has been detected at least once, not how often it occurs in reality.

  Moreover, other information regarding the characteristics of the infected animals, husbandry practices in the areas, and environmental conditions could help characterise the outbreaks. Further analysis should aim to analyse disaggregated data, to identify if outbreaks are related to introduction of the pathogen or due to silent-circulation.

• Speed of spatial spread during an outbreak

  Mccp is transmitted through emission of infected droplets between animals.

  The main way of spatial diffusion depends on livestock mobility. Disease may be diffused through commercial and transhumance routes either by infected goats (active and or latent) or by apparently healthy sheep. In addition, the disease could spread by wild animals during their migration movements, though this has not yet been reported.

  GAPS :

  No studies have been found that may be used to estimate the speed of spatial spread. To estimate the spatial spread, future studies should collect information about:

  - Local, national and transboundary animal movements that may identify possible trajectory of diffusion and the possibility of transmission among herds. Data should contain information about origin estimation of the movements, species involved, and transportation means, as well as the number of heads.

  - Outbreak declarations with timestamp and geographical position

  - A statistical approach similar to the one introduced by Mercier et al. (2018) could be used to estimate the speed rate of the disease.

  Nevertheless, this approach could underestimate the speed rate due to the fact that sheep are most often asymptomatic and could travel undetected.

• Transboundary potential of the disease

  CCPP has a very high transboundary potential. In most areas where it circulates, most herds are raised extensively and transhumance is a common practice involving the movement of animals looking for resources. Moreover, in most of Africa and the Middle East, animals are traded alive, and goats in particular are perceived as less valuable and sold more often. In most cases, movements both internationally and nationally aren’t recorded, and the absence of centralised, harmonised surveillance systems makes it difficult to control diseases such as CCPP.

  GAPS :

  The main scientific gap here is the near absence of mobility data in the regions where the disease is present.

  Trade data collected by the Comtrade platform (https://comtradeplus.un.org/) could be explored to provide a coarse representation of exchanges between countries and variations in flux (Lezaar et al., 2023). However, to improve zoning and control measures, more detailed datasets that consider both time and space are needed.

  Furthermore, no information is available regarding illegal animal movements, which require ad hoc activities to estimate the importance of illegal movement ex post facto.

  Europe is still naïve with respect to CCPP. Movements from Africa to Europe are rare and, in most cases, highly controlled. However, there are exchanges between Africa and the Middle East, and the recent introduction of PPR in Europe should incentivise studying possible pathways of disease introduction that take into account mobility patterns, as well as control and biosecurity measures put in place.

  Furthermore, Lignereux's work (Lignereux et al., 2018) has shown that wild ungulates could transmit the disease. Studying cross-species transmission and including wildlife movements in risk analyses is another area to explore.

• Route of Transmission

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

  CCPP is a respiratory infection and disease transmission occurs by inhalation of infected aerosols during direct contact with infected animals that represent the main source of infection.

  CCPP is a transboundary disease; it spreads into new regions by the introduction of infected animals in susceptible populations.

  GAPS :

  It is suspected that latent /chronically infected animals act as CCPP carriers (EFSA AHAW Panel, 2017; WOAH, 2021) but the mechanisms of persistence and transmission are not known.

• Occasional mode of transmission

  Short distance airborne transmission (up to 80 m) has been reported (Lignereux et al., 2018), but no indirect transmission routes (fomites, vectors) have been described.

  GAPS :

  Wind-assisted transmission has been suggested, but controlled or observational studies confirming the distance, frequency and conditions under which aerosol spread may occur are lacking.

• Conditions that favour spread

  Traditional transhumant and nomadic herding systems, as well as gathering in markets, communal pastures or water holes contribute to CCPP disease transmission and spread.

  Climatic conditions (see sections 13.1 & 13.4), as well as socio-economic and political factors that promote animal movements, interactions and crowding are also predisposing factors. The stress induced through animal movements and other sudden changes in management practices or climatic conditions may exacerbate the spread of the disease. In general, all conditions that increase vulnerability and transmission, may also facilitate the spread of the disease (see section 9.1).

• Detection and Immune response to infection

• Mechanism of host response

  As expected, given the local inflammatory response, phagocytes containing Mccp antigens and lymphocytes are observed in infected goat lungs (Wesonga, 2004). Increased levels of indicators of neutrophil activation such as nitric oxide and malondialdehyde, as well as pro-inflammatory cytokines such as IL-1 and IL-6 are detected in lungs (Ma et al., 2020). Neutrophil chemoattractants such as Cxcl1, Cxcl6, Il-8, Ccl4 and Ccl20 are also detected. Finally, interleukin-17 (IL-17), a key factor in neutrophil-dependent exacerbated pulmonary inflammation (Mize et al., 2018), is produced in lungs of Mccp-infected goats by CD4+ and gdTCR+ T lymphocytes (Ma et al., 2020; Yang et al., 2025). IL-17 induces the production of neutrophil chemoattractants by caprine lung epithelial cells in vitro (Ma et al., 2020).

  In CCPP, antibody responses directed to Mccp protein and polysaccharide antigens are detected but do not correlate with either protection or pathology (March, 2002). A mouse monoclonal immunoglobulin M directed against a polysaccharide antigen of Mccp inhibits its growth in vitro (Rurangirwa, 1995). Convalescent sera reduce hydrogen peroxide production by Mccp in vitro (Liljander et al., 2019).

  As expected, given the local inflammatory response, phagocytes containing Mccp antigens and lymphocytes are observed in infected goat lungs (Wesonga, 2004). Increased levels of indicators of neutrophil activation such as nitric oxide and malondialdehyde, as well as pro-inflammatory cytokines such as IL-1 and IL-6 are detected in lungs (Ma et al., 2020). Neutrophil chemoattractants such as Cxcl1, Cxcl6, Il-8, Ccl4 and Ccl20 are also detected. Finally, interleukin-17 (IL-17), a key factor in neutrophil-dependent exacerbated pulmonary inflammation (Mize et al., 2018), is produced in lungs of Mccp-infected goats by CD4+ and gdTCR+ T lymphocytes (Ma et al., 2020; Yang et al., 2025). IL-17 induces the production of neutrophil chemoattractants by caprine lung epithelial cells in vitro (Ma et al., 2020).

  In CCPP, antibody responses directed to Mccp protein and polysaccharide antigens are detected but do not correlate with either protection or pathology (March, 2002). A mouse monoclonal immunoglobulin M directed against a polysaccharide antigen of Mccp inhibits its growth in vitro (Rurangirwa, 1995). Convalescent sera reduce hydrogen peroxide production by Mccp in vitro (Liljander et al., 2019).

  GAPS :

  The fate of Mccp upon encounter with phagocytes and the potential existence of mechanisms of resistance to phagocytosis and of intracellular survival has not been studied.

  In vivo experiments involving the transfer of immunoglobulin isotypes must be conducted in order to assess their ultimate role in protective immunity or immunopathology.

  The components of Mccp extracts shown to induce the production of IL-17 by lymphocytes in vitro (Ma et al., 2020) have not been characterised.

  Basic knowledge about specific protective and memory cell-mediated immune responses against Mccp are lacking.

  Longitudinal transcriptomic analysis of caprine genes in blood samples conducted until full recovery are needed in order to identify bio-signatures of protective or pathological immune responses.

• Immunological basis of diagnosis

  Before the advent of molecular diagnostic techniques, antibodies against Mccp were used for diagnosis by applying specific antisera (primarily in growth inhibition test, immunofluorescence test and dot immunoblotting) for the identification of the CCPP agent in culture. These methods were prone to cross-reactivity and have largely been replaced by molecular approaches.

  Analysing the humoral immune response with cELISA, CFT, IHT or LAT (see sections 1.1, 1.3 and 4.1) is crucial for CCPP detection and surveillance. Detection by cELISA is delayed compared to CFT, but remains positive for a longer period (for several months) after infection. This is a consequence of the different immunoglobulin classes covered by each method. While the IgG antibodies, produced later in the infection, have a greater affinity in the cELISA, they are unable to fix complement. In contrast, the IgM antibodies produced early in the infection are complement-fixing and can therefore be readily detected by CFT. Similarly, antibodies of the IgM class are agglutinating and thus rapid tests based on serum agglutination such as the LAT are most suited for early detection at the pen-side.

• Main means of prevention, detection and control

• Sanitary measures

  The effectiveness of sanitary measures (for the control of CCPP was demonstrated when the disease was eradicated from South Africa, already in the 19th century, using a strategy based in the slaughter of infected animals coupled to the inoculation of in-contact goats.

  As stated in section 11.3, in Europe CCPP is classified as cat. A + D + E disease, for which it is required immediate eradication, prevention of disease spreading within and across countries, and constant surveillance. In case of an outbreak in Europe and other CCPP-free countries stamping out of the animals in the affected establishments, application of protection and surveillance zones, and restrictions of animal movements need to be implemented, with backward and forward traceability and surveillance activities within and outside the restricted zones (EFSA AHAW Panel, 2022).

  Disease transmission mainly occurs due to direct and repeated exposure to infected animals, releasing infected aerosol, therefore animal movement restrictions represent a cornerstone for disease control. These include implementation of strict regulations on livestock trade from CCPP-affected regions or avoiding communal grazing or shared watering points during outbreaks.

  GAPS :

  Rigorous socioeconomic studies are needed to improve the acceptance of such drastic strategies.

• Mechanical and biological control

  None (no relevant environmental persistence and mechanical or vector-borne transmission demonstrated)

• Prevention through breeding

  There is currently no robust evidence that particular breeds are inherently more susceptible or resistant to CCPP and apparent differences in disease frequency between animals or flocks are more likely linked to individual, management and environmental factors than to breed‑specific genetics.

  In the absence of convincing data for heritable resistance, selective breeding for resistance to CCPP is not currently considered a practical or effective strategy for the control of CCPP.

• Diagnostic tools

  A reliable laboratory diagnosis that can confirm or exclude CCPP is fundamental for the implementation of effective control measures, such as slaughter, movement restrictions, biosecurity measures and antibiotic therapy.

  In endemic countries, diagnosis often relies on pathomorphological observations from slaughterhouses or clinical signs from live animals. Direct detection of Mccp by cultivation or PCR testing plays a minor role, and serological tools are used only occasionally for surveillance and prevalence studies.

  Serological methods such as CFT, cELISA and IHT are used for different purposes with varying suitability (WOAH, 2021). The cELISA is the most recommended test for surveillance studies, export/import clearance, and for assessing immune status following vaccination (Peyraud et al., 2014). Although IHT and CFT have limited specificity, they are cheaper, and IHT can be performed at the pen-side. All serological tests are useful at herd level but not for individual animal diagnosis.

  Molecular diagnostic methods are best suited for confirming disease in suspected cases based on clinical and pathological findings or positive serology, and for identifying isolates. Isolation and culture of Mccp, the gold standard for definitive confirmation, is hindered by the fastidious nature of the agent and reserved to specialised laboratories.

  GAPS :

  Development of an effective pen-side test capable of detecting both acute and chronic infections is a critical gap in diagnostic tools for live animals.

• Vaccines

  Vaccination is considered the main practical tool to control CCPP in smallholder‑dominated systems in endemic areas, but it needs to be integrated with movement control and surveillance to be fully effective.

  Live and inactivated commercial CCPP vaccines are available and a few reports have been published showing divergent results in terms of efficacy (Lignereux et al 2018). Even when effective in preventing clinical disease, the limited availability and the requirement (for many commercial products) of bi-annual vaccinations results in a discontinued application of vaccination.

  In China, big farms vaccinate massively and slaughter sick animals. The Mccp-M. ovipneumoniae combined inactivated vaccine emulsion is most frequently used, but single inactivated vaccines are used in areas where only the prevalence of CCPP has been confirmed.

  GAPS :

  -Limited availability of commercial inactivated vaccines. Current CCPP vaccine production may be sufficient to satisfy local demand but it does not cover the requirements of entire regions (involving more than one infected country)

  -Challenges for scaling up vaccine production. Commercial vaccines consist mostly of inactivated bacterins, which require large amounts of mycoplasma cultures to obtain the minimum dose of immunising antigen required after inactivation, thus limiting the production capacity compared to live vaccines.

  -Vaccine quality is variable and in many cases it does not fulfill the standards required by WOAH. Lack of implementation of appropriate control methods to guarantee vaccine quality.

  -None of the marketed vaccines is suitable for the DIVA strategy.

  -Prolonged immunity is required. Immunity conferred by inactivated vaccines provides up to 1 year protection and annual revaccination is required. Improvement of adjuvant formulations using the current bacterin vaccine may provide longer immunity.

  -Current saponin inactivated vaccines cannot be included in a co-formulation with live vaccines for other prioritised diseases such as PPR and sheep and goat pox. Multiple vaccination with a single dose would have a greater cost-effective impact on control of targeted diseases.

• Therapeutics

  Due to the previously mentioned limitations of current vaccines, antimicrobial treatments (e.g., tetracyclines, macrolides or quinolones) are frequently applied to reduce animal losses in infected flocks. When applied early, antibiotic treatments may reduce mortality, clinical symptoms and pathology, but they do not ensure complete clearance of the infection (El Hassan et al., 1984; Özdemir et al., 2006), so animals may act as asymptomatic carriers.

  In affected countries of Africa and Asia antibiotic treatments are often carried out. This is also true in China, despite regulations regarding antimicrobials for use in animals and particularly by small farmers, who do not generally implement vaccinations.

  GAPS :

  There are few studies addressing the use of antibiotics in Africa and Asia for the control of CCPP. Data on antibiotic classes used, protocols, and efficacy of treatments are extremely limited. Furthermore, there are no reports of treatment failure and there is no data available regarding acquired AMR by Mccp strains in the field.

  There is an urgent need to provide guidelines to optimise antibiotic use and promote antibiotic stewardship (molecules, dose and duration of treatment, as well as withdrawal periods) in order to minimise both the side effects and the development of AMR. Combined therapies including anti-inflammatory drugs should be explored to further reduce mortality, clinical signs and lesions.

  The controlled, targeted use of antibiotic therapy in integrated programmes for the eradication of CCPP deserves further investigation. The efficacy of control strategies including targeted antibiotic treatments combined with mass vaccination and / or slaughter must be evaluated under controlled conditions.

• Biosecurity measures effective as a preventive measure

  Since CCPP is transmitted by direct contact between infected and susceptible animals, biosecurity measures aiming at segregating the two populations are most effective.

  Other hygiene and disinfection procedures have less impact in preventing CCPP, since the agent does not survive for long in the environment.

• Border/trade/movement control sufficient for control

  Current international guidelines promote strict biosecurity and regulatory control measures to prevent and limit the spread of CCPP, including early detection, rapid reporting, movement control and establishment of protection and surveillance zones around outbreaks (WOAH, 2008, (EFSA AHAW Panel, 2022).

  In CCPP-free countries and regions a ban on the importation of live animals from countries where CCPP is present is the most effective measure to maintain the disease-free status.

  GAPS :

  Official trade is relatively easy to control but illegal animal movements constitute the main risk of introduction. Porous international borders in affected regions of Asia and Africa make animal movement control difficult to implement. Furthermore, in many affected countries of Asia and Africa there are no identification systems for small ruminants.

  International cooperation is key to managing the transboundary spread of CCPP through animal movement control.

• Prevention tools

  None.

• Surveillance

  Active serological surveillance is rarely applied. Instead, seroprevalence investigations are applied either to estimate the local and regional burden of disease or to assess post-vaccinal immunity (Peyraud et al., 2014).

  Passive surveillance based on clinical or post mortem lesions is commonly performed in endemic regions. It requires laboratory support for disease confirmation, whereas laboratory diagnostic capacity in most affected areas is not available.

  GAPS :

  In most CCPP-affected countries, effective surveillance is not in place due to limited resources and a lack of diagnostic capacities. China may be exceptional in this regard.

• Past experiences on success (and failures) of prevention, control, eradication in regions outside Europe

  When CCPP was introduced in South Africa, through the import of Angora goats from Turkey (Hutcheon, 1881), control measures consisting in the prompt slaughter of all affected goats in a flock and the “vaccination” of the remaining in-contact goats were implemented (Hutcheon, 1889). The traditional vaccination procedure applied consisted in the subcutaneous inoculation of infectious material to induce protection. Implementation of this strategy resulted in the eradication of the disease from South Africa in less than one and a half years, well before the identification of its etiologic agent (Manso-Silván & Thiaucourt, 2019).

  On the other hand, following the introduction of CCPP in Thrace (Özdemir et al., 2005), the outbreaks were controlled exclusively with antibiotics and the disease became endemic, posing a continuing risk to neighbouring Greece and Bulgaria (Özdemir et al., 2018).

• Costs of above measures

  Renault et al. (2019), provide the following cost estimates for a single vaccination campaign of 4,000 goats:

  Human resources (1 vet, 3 animal health support staff, 1 driver): 162 Euro; fuel costs: 9 Euro; vaccine (4,000 doses): 309 Euro. Total costs: 480 Euro, or 0.12 Euro per animal. See 18.4 below for bi-annual vaccination costs in Kenya.

  The literature makes mention of vaccine access varying by gender, with female farmers having more difficulties in access (Kyotos et al., 2022).

  GAPS :

  No added information at global or other national contexts.

• Disease information from the WOAH

• Disease notifiable to the WOAH

  Yes

• WOAH disease card available

  WOAH Technical Disease Card Contagious Caprine Pleuropneumonia. Last update 2009.

  CONTAGIOUS CAPRINE PLEUROPNEUMONIA

  GAPS :

  Not applicable

• WOAH Terrestrial Animal Health Code

  WOAH Terrestrial Animal Health Code, Chapter 14.3. Contagious Caprine Pleuropneumonia. Last update 2008. Chapter 14.3. - Contagious Caprine Pleuropneumonia

  GAPS :

  Not applicable

• WOAH Terrestrial Manual

  WOAH Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Chapter 3.8.4. Contagious Caprine Pleuropneumonia. Last update 2021. Chapter 3.8.4. – Contagious caprine pleuropneumonia

  GAPS :

  Not applicable

• Socio-economic impact

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

  None.

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

  None.

• Direct impact (a) on production

  Limited information available. WOAH (2009) note morbidity and mortality impacts in naive herds of up to 80% and 100%, respectively. A frequently cited estimate of annual global losses of 507 million USD per year in endemic settings could not be traced to an original empirical source and should therefore be treated with caution.

  Renault et al. (2019) estimated mean annual economic losses of 1,713 Euros per 100-head flock in Kenya. Singh & Prasad (2008) reported CCPP losses in India from 1991-2005 averaging 1.7 Rupees per year, ranging from 0.24 million Rupees in 2004 to 5.96 million Rupees in 1991. Over this period, CCPP ranked fourth among goat diseases in terms of average losses in India, behind PPR, other causes, and sheep and goat pox.

  George (2017) estimated average household-level CCPP losses in Tanzania at 2.27 million Tanzanian Shillings annually, with mortality accounting for 62% of losses, abortions 17%, reduced weight 6%, treatment costs 5%, and reduced milk production 3%.

  GAPS :

  No added information found at global or other national contexts.

  Available data lacks robust, traceable global economic loss estimates and standardised, recent empirical studies across endemic regions to reliably quantify CCPP's impact.

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

  Average costs of CCPP vaccination in Kenya from Renault et al. (2019) range from 24.5 Euro/100 head (95% vaccine efficacy) to 20.1 Euro/100 head (20% efficacy); this is for bi-annual vaccination. Average benefit-cost ratios for Kenya from Renault et al (2019) range from a high of nearly 62 (95% vaccine efficacy) to a low of 5.7 (20% vaccine efficacy).

  GAPS :

  No added information found at global or other national contexts.

  Available data lacks robust, traceable global economic loss estimates and standardised, recent empirical studies across endemic regions to reliably quantify CCPP's impact.

• Indirect impact

  No indirect impacts have been cited in the literature. National-level downstream effects (e.g., trade and market disruptions) are probably comparable to those of PPR for outbreaks of similar severity. Indirect impacts are higher in more developed markets given greater scope of downstream rural activities (tourism, services, etc.).

  GAPS :

  No added information found at global or other national contexts.

  Available data lacks robust, traceable global economic loss estimates and standardised, recent empirical studies across endemic regions to reliably quantify CCPP's impact.

• Trade implications

• Impact on international trade/exports from the EU

  As a notifiable disease to WOAH, CCPP would impact international trade movements and allow countries to ban imports from affected countries. See also Nicholas & Churchward (2011).

  GAPS :

  Specific studies have not computed prospective or estimated trade impacts.

• Impact on EU intra-community trade

  As a notifiable disease to WOAH, CCPP would impact intra-EU trade movements if an outbreak occurred and allow EU countries to ban imports from affected countries. This is not relevant at present. See also Nicholas & Churchward (2011) regarding possible threats to EU from Turkey or North Africa.

  GAPS :

  Specific studies have not computed prospective intra-EU trade impacts

• Impact on national trade

  National (within-country) trade flows could be impacted by movement controls as regulated by national legislation.

  GAPS :

  Specific studies have not computed national-level impacts.

• Links to climate

• Seasonal cycle linked to climate

  As first reported by Thomas (1873) and reviewed by Ali et al. (2023) and Thiaucourt & Bölske (1996), climatic conditions play an important role in triggering CCPP outbreaks. In several regions, outbreaks occur more frequently during periods of climatic stress. In North Africa and in high-altitude areas of India, CCPP is most common during the winter months, particularly during prolonged cold periods. In Oman, outbreaks have been associated both with the cold, rainy season and with peak summer heat, indicating that extreme temperatures in either direction increase susceptibility.

  Sudden weather changes, such as heavy rainfall, post-monsoon transitions or sharp day-to-night temperature fluctuations, can also precipitate outbreaks by inducing stress, lowering immunity, compromising respiratory defences, and increasing pathogen shedding from carrier animals (Ali et al., 2023; Thiaucourt & Bölske, 1996; WOAH, 2021). The same applies to drought-related environmental stress, including feed and water shortages and long-distance movements in search of resources, which force animals to congregate at limited sites, facilitating close contact and transmission, and may also cause spread to disease-free regions.

  Finally, seasonal conditions influence the survival of Mccp: the organism is rapidly inactivated at high temperatures, whereas low temperatures and moisture enhance its viability and can thereby increase the risk of transmission. Wind can further facilitate the spread of infectious aerosols over considerable distances. The most plausible explanation in a sand gazelle outbreak was that transmission occurred over a distance of at least 80 metres (Lignereux et al., 2018).

  GAPS :

  Most evidence linking specific meteorological parameters to outbreak risk is descriptive but there is insufficient quantitative data. Similarly, there is a lack of consistent documentation of environmental and management stressors during outbreaks.

  There are no integrated models combining climate variability, animal movement and management factors to estimate CCPP risk. Such models may support preparedness and targeted surveillance.

  Finally, as stated in section 7.3, there is limited knowledge of Mccp survival under real-world environmental conditions (temperature, humidity, wind exposure, UV light). Targeted, laboratory and field studies assessing Mccp viability under different temperatures and humidity levels would provide essential information for risk assessment.

• Distribution of disease or vector linked to climate

  No vectors identified and distribution of the disease linked to climate not described.

• Outbreaks linked to extreme weather

  Extreme weather conditions can trigger outbreaks.

• Sensitivity of disease or vectors to the effects of global climate change (climate/environment/land use)

  Extreme climatic conditions (including drought, flooding and sudden weather changes), that promote animal movements, mixing of infected and susceptible animals, and congregation at limited sites, can increase CCPP transmission and spread (see section 13.1). The sensitivity of the disease to climate change should therefore be taken into consideration.

• Main perceived obstacles for effective prevention and control

  Diagnostic tests:

  Isolation and culture of Mccp, the gold standard for definitive disease confirmation, is hindered by the fastidious nature of the agent, requiring special media and prolonged incubation, as well as trained personnel in well-equipped specialised laboratories.

  Direct molecular detection by PCR on necropsy or swab samples from acutely infected animals is possible; however commercial availability of test kits is limited and assays on the market are not validated under ISO 17025 accreditation to guide diagnostic laboratories in selecting routine tests.

  There are currently also severe shortages in the production and supply of ELISA kits and reagents for CCPP serology. The commercial assays are either unavailable (cELISA, LAT), exhibit poor specificity (CFT), or have not been validated by international standards (indirect ELISA). In general, the diagnostic performance of Mccp antibody tests, in terms of sensitivity and specificity, is considered suboptimal, which is why they should only be used for assessment at herd level.

  Another major obstacle is the lack of rapid and robust pen-side tests allowing laboratory-independent confirmation of suspect cases, particularly in endemic areas.

  As a consequence, surveillance data is poor and infected animals and herds may remain undetected and continue to spread the disease. Control strategies such as slaughter, movement restrictions, antibiotic therapy or vaccination programs cannot be targeted efficiently.

  Pharmaceuticals:

  The prudent and effective therapeutic management of CCPP remains constrained by important knowledge gaps. To date, no evidence-based recommendations have been established regarding the optimal antibiotic choice, dosage, or duration of treatment for CCPP.

  Despite this lack of standardised guidance, antimicrobials are widely accessible to livestock owners and are frequently used without veterinary oversight. Such unregulated use, combined with limited antibiotic stewardship, creates conditions conducive to inappropriate administration and may accelerate the emergence and spread of antimicrobial resistance (AMR).

  Vaccines:

  There are very few producers of CCPP vaccines, and current supply does not meet demand. This is in contrast with the wide availability of antimicrobials.

  Furthermore, many commercial vaccines do not comply with WOAH guidelines, and do not induce the expected seroconversion and protection.

  Production of current inactivated antigen is cumbersome, expensive, and technically demanding, which limits scalability and results in poor quality products available in the market. Inactivated vaccines cannot be combined in a single formulation with live vaccines such as PPR, which would be strategically advantageous. However, the use of live Mccp vaccines is constrained by the organism’s extreme thermosensitivity.

  Independent quality control (e.g., by AU-PANVAC in Africa) is infrequent, and the methods currently applied are insufficient to ensure vaccine efficacy. Potency, thermostability, and shelf-life data are largely missing.

  GAPS :

  Diagnostic tests:

  More scientific efforts are needed to identify novel antigens as reliable infection markers to be applied for sero-diagnostic purposes. Further, PCR assays need to be improved by including a higher number of whole genome sequences from field strains of the M. mycoides cluster in alignments for a more specific primer/probe design.

  Validation of existing and novel diagnostic tests according to international standards is required. Reference standards and qualified sample panels are needed for these validations.

  Market research is necessary to assess demand and affordability of new diagnostics. The involvement of manufacturing companies is required to target and optimise the development of diagnostic inventions into successful commercial products, particularly pen-side tests for confirmation or screening in the field.

  Pharmaceuticals:

  Robust data from controlled in vitro and in vivo studies evaluating the efficacy of antimicrobial agents against CCPP are needed. These investigations should be complemented by field data collected during natural outbreaks. Generating such evidence is essential to support informed decision-making regarding the role of antibiotic therapy in CCPP control strategies, and to allow the development of guidelines that promote responsible antibiotic stewardship while minimising adverse effects and the emergence of AMR.

  Standardised protocols and reference strains for determining the in vitro minimum inhibitory concentration (MIC) values of Mccp isolates to commonly used antimicrobials are also required. These protocols are needed to establish tentative epidemiological cut-off values and clinical breakpoints to improve clinical interpretation of MICs, facilitate the assessment of AMR acquisition in the field, and assist veterinarians in the rational use of antibiotics. However, determining ECOFFs under EUCAST/VetCAST guidelines will be extremely challenging considering the scarcity of Mccp isolates worldwide.

  Vaccines:

  Quality control requirements need to be reviewed in order to guarantee vaccine compliance. The use of new tools such as mass spectrometry and immuno-capture ELISA is required in order to assess the identity and stability of Mccp antigens in current inactivated CCPP vaccines.

  Affordable, safe and stable vaccines providing good and long-lasting protection (at least one year) against CCPP are needed. The full validation of new formulations based on fast growing strains inactivated and adjuvanted in oil emulsions must be achieved.

  Developing multivalent or co-formulated vaccines for major caprine diseases could greatly improve affordability and adoption. Market studies are needed to develop this strategy.

  Live CCPP vaccines may be combined with PPR vaccines; however, thermostability may be a limiting factor.

• Main perceived facilitators for effective prevention and control

  Diagnostic tests:

  Accurate, rapid and affordable diagnostic tests are important facilitators in applying effective prevention and control of CCPP. Their useful implementation requires regional and national veterinary services that dispose of well-equipped diagnostic laboratories with competent staff and working under quality assurance.

  At field level, awareness of CCPP is a prerequisite for disease recognition, confirmatory diagnosis and reporting.

  Pharmaceuticals:

  CCPP is frequently treated informally with antibiotics that are readily available on the market. Consequently, a revised CCPP control strategy that incorporates regulated antibiotic use is likely to encounter relatively low resistance to adoption. Goat owners in endemic and neighbouring areas are generally well aware of the disease and are willing to invest in effective measures to protect their livestock.

  A better understanding of the pathogenesis of CCPP may lead to the discovery of alternative therapies. A notable example may be the use of short-chain fatty acids (SCFAs) as food additives for the prevention of Mccp, which provided promising results in a mouse model (Yang et al., 2025). The pertinence of this model and the efficacy of SCFAs treatment in goats must be assessed.

  Vaccines:

  Synthetic biology and genome editing tools are available for the genetic engineering of Mccp genomes, allowing the production of mark-less, targeted Mccp mutants for pathogenicity studies, as well as for development of rationally-designed vaccines.

  A robust challenge model has been proposed, but a robust standard clinical/pathological scoring system for efficacy trials has not yet been established and validated reference challenge strains are not readily accessible.

  In the longer term, a better understanding of the protective immune response would be highly valuable for optimising vaccine design and validating vaccine efficacy without the need to resort to animal trials.

  DIVA vaccines would be useful in countries implementing eradication plans or in the event of emergence in Europe or other disease-free regions.

  Improved infrastructures and capacity building in vaccine production facilities would facilitate the transition towards the production of new generation recombinant and subunit vaccines.

  GAPS :

  Diagnostic tests:

  Although a variety of serological and molecular diagnostic tools, both laboratory-based and pen-side were developed in the past (see Sections 1.1-1.3, 4.1), their diagnostic performance, validation status, implementation and acceptance for disease control, are often insufficient.

  Low awareness of CCPP should be increased by education and training for farmers, abattoir workers and veterinarians.

  The main limitations on the application of diagnostic facilitators are financial and organisational constraints.

  Pharmaceuticals:

  Transitioning from informal antibiotic use to targeted, controlled therapeutic regimens will require supportive policy frameworks and effective stakeholder engagement.

  A policy shift toward targeted and controlled antibiotic use could improve adherence to effective treatment regimens compared with the current informal practices. To support such a transition, Knowledge, Attitude, and Practice (KAP) studies should be conducted in endemic communities prior to and during the implementation of new antibiotic-related policies. These studies would help ensure that communication strategies are effective and identify potential barriers that could lead to suboptimal antibiotic use.

  Host-pathogen interaction studies must be continued as a means of discovering new therapies. Validating the therapeutic efficacy of short-chain fatty acids in goats is a priority.

  Vaccines:

  Synthetic biology tools may be used to develop improved vaccine strains with increased yield, reduced growth time and in vitro growth requirements, as well as enhanced stability. They may also enable the development of negatively and/or positively marked strains suitable for DIVA screening.

  Upgrading production facilities will be required to support the production of novel vaccines (e.g., subunit and recombinant vaccines). In parallel, tools specifically adapted for the quality control of these new vaccines will need to be developed, taking into consideration novel antigens, different vaccine types (such as live strains or recombinant proteins), and new formulations. Regulatory frameworks and policies may also need to be updated to enable the commercialisation of vaccines based on genetically modified organisms. Finally, socio-economic studies will be necessary to promote acceptance and uptake of these new vaccines.

  Identify biomarkers correlating with successful vaccination and protection to assess the potency of vaccines, vaccine combinations and vaccine batches without the need to infect animals.

Global challenges

• Antimicrobial resistance (AMR)

• Mechanism of action

  Very little is known about AMR in CCPP. Mutations in the 16S rDNA associated with streptomycin resistance have been described (Manso-Silván et al., 2011). Rahman and colleagues established the minimum inhibitory concentrations (MICs) of four commercially available quinolones in an Mccp isolate from Pakistan (Rahman et al., 2021) and Cheng et al. determined the MICs of nine antimicrobial agents from different classes in 34 recent Chinese isolates. Using MIC cut-off values established for other bacterial species, they concluded that the isolates generally showed low levels of resistance, although a few displayed reduced susceptibility to florfenicol and lincomycin. However, without recognized epidemiological cut-off values for the MIC it is not possible to draw conclusions in regards to possible AMR from MIC values alone.

  Although information on AMR in Mccp remains limited, important insights can be drawn from research on other mycoplasmas. Comprehensive reviews of antimicrobial resistance in both human and animal mycoplasmas are available (Pereyre and Tardy, 2021; Sulyok et al., 2025).

  In 2023, the MyMIC network (a consortium of 22 laboratories specialised in livestock mycoplasmas) was established. The consortium aims to develop standardised antimicrobial susceptibility testing procedures and establish epidemiological cut-off values (ECOFFs) and clinical breakpoints for veterinary mycoplasma species, enabling the classification of isolates as susceptible, resistant, or intermediate to antimicrobials used in livestock (Jaÿ et al., 2025).

  The consortium has recently published a review summarizing current knowledge on the genetic mechanisms underlying AMR in clinically important Mycoplasma species affecting ruminants, swine, and poultry. The review highlights the role of molecular assays in detecting resistance-associated mutations and discusses the potential of genome-wide association studies to link genetic determinants with phenotypic resistance patterns, providing new insights for improving resistance prediction in veterinary medicine (Sulyok et al., 2025).

  GAPS :

  The prevalence and impact of in vivo acquired resistance to different antimicrobials by Mccp strains is not known. No AMR has been described for CCPP, and no studies have looked for AMR in CCPP.

  No mechanisms of action of any possible AMR have been described for Mccp.

  Studies are needed that investigate the possible existence of AMR in the field.

  Standardised protocols for culturing, identification and determination of MICs to antimicrobials commonly used to treat CCPP are needed. Similarly, epidemiological cut-off values (ECOFFs), which represent the MICs above which bacterial isolates have phenotypically detectable acquired resistance mechanisms, are not available for animal mycoplasmas. These cut-offs would help clinical interpretation of MICs and guide veterinarians towards a more reasonable use of antibiotics. However, determination of ECOFFs under Eucast guidelines will be extremely challenging due to the scarcity of wild type strains available world-wide.

• Conditions that reduce need for antimicrobials

  Implementation of mass-vaccination campaigns (targeting as much as possible the entire susceptible population) repeated at least once a year, can reduce the need for antimicrobials.

• Alternatives to antimicrobials

  None, though prophylactic control by vaccination is recommended to reduce the prevalence of the disease.

• Impact of AMR on disease control

  No studies have so far linked AMR of Mccp strains and its impact on disease control.

  GAPS :

  More studies needed to evaluate impact. The studies should focus on mechanisms of AMR and the prevalence of AMR

  Surveillance of AMR in Mccp is required, especially where repeated or prolonged antibiotic treatments are applied, to guide prudent use and inform alternative therapy prioritisation.

• Established links with AMR in humans

  Not studied.

  GAPS :

  The impact on human health of antibiotic treatments implemented during CCPP outbreaks needs to be evaluated, particularly in regards to the development of AMR due to poor antibiotic stewardship.

• Digital health

• Precision technologies available/needed

  Precision technologies (e.g. digital surveillance, advanced on‑farm monitoring) are virtually absent for CCPP in endemic regions, and existing diagnostics are largely limited to basic laboratory serology and PCR in a few reference centres.

  GAPS :

  Affordable, field‑adapted precision tools, harmonised protocols and integrated data systems are needed, as current data collection is limited, fragmented, non‑standardised and not publicly accessible.

  Although smartphone-based applications integrating telediagnosis and artificial intelligence tools have proven beneficial for diagnostic imaging, livestock disease detection, remote decision-making and reporting, there is currently no evidence of their application to CCPP. These technologies would be particularly valuable for CCPP management in regions with limited veterinary infrastructure.

• Data requirements

  Animal‑health and related data needed to build useful digital tools may be:

  -Clinical and diagnostic data: case records, lab test results, pathogen typing, vaccination status ;

  -Herd/production data: animal IDs, movements, performance indicators, mortality, treatments ;

  -Environmental/epidemiological data: location, herd density, wildlife interface, trade and movement patterns, climate or management factors

  GAPS :

  Clinical, diagnostic, production, and epidemiological data are largely unavailable in endemic regions.

• Data availability

  CCPP data availability is very limited. Some Mccp genome sequences are available in open databases but they do not represent the geographic distribution of CCPP and no open genotyping database is available.

• Data standardisation

  No standardised databases are available.

• Climate change

• Role of disease control for climate adaptation

  Climate change is expected to limit animal movements and, thus, disease spread (see section 22.2).

• Effect of disease (control) on resource use

  As exposed in section 13.1, extreme weather associated with climate change, such as droughts, flooding and abrupt weather fluctuations, can restrict access to grazing land and water, forcing animals to move and congregate more closely, thereby increasing the risk of CCPP transmission and spread. In addition, stress linked to harsh environmental conditions and animal movements may increase susceptibility to infection, further facilitating disease transmission.

• Effect of disease (control) on emissions and pollution (greenhouse gases, phosphate, nitrate, …)

  This has not been studied, although infectious diseases are generally expected to exacerbate greenhouse gas emissions from livestock.

• Preparedness

• Syndromic surveillance

  In endemic areas, farmers, animal health-care and slaughterhouse personnel are usually familiar with the typical clinical and pathomorphological signs associated with CCPP (see Section 9.3) and syndromic surveillance plays a key role in detecting the disease. However, misdiagnosis due to pasteurellosis, peste des petits ruminants or infections with other mycoplasmas are common because differential diagnosis in the field and at necropsy may be inadequate (see Section 12.1).

  In CCPP-free regions passive surveillance should also be in place based on abattoir surveillance and post-mortem investigations of animals with respiratory diseases. However, lack of experience and awareness could result in inadequate syndromic surveillance.

  GAPS :

  Constant training on disease recognition, reporting and application of early sanitary measures to all actors involved in disease control will make syndromic surveillance more effective.

• Diagnostic platforms

  Although in CCPP-free countries, molecular diagnostics are available for the rapid confirmation of CCPP suspicions, and serological tools are used for animal testing before trade, general awareness and preparedness for exotic diseases such as CCPP, in terms of diagnostic lab capacity, is generally low. This is also reflected in the current lack of any validated and commercialized molecular or serological testing kits.

  In endemic regions, diagnosis is often limited to clinical and pathomorphological observations with laboratory confirmation rarely achieved.

  GAPS :

  There is an urgent need for validated, commercial, cost-effective laboratory test kits for the serological and direct detection of Mccp in ruminant samples.

  Effective and affordable pen-side tests are needed, particularly in low-income countries.

  The laboratory capacity in endemic regions of Africa, the Middle East and Asia must be strengthened.

• Mathematical modelling

  CCPP affects both domestic goats and wild ruminants, with sheep potentially acting as a reservoir species. CCPP is transmitted directly between infected and susceptible hosts through close contact. Following the acute clinical phase, animals are likely to die, although some may survive. The possibility of silent carriers has been inferred from field observations (Hutcheon, 1881) but this needs to be formally demonstrated.

  Preliminary search on Google Scholar and PubMed using the keywords “contagious caprine pleuropneumonia” and “model” was conducted since 2000. A total of 7 relevant articles were retained (Lignereux et al., 2018; Molla et al., 2023; Renault et al., 2019; Selim et al., 2021; Asmare et al., 2016; Rahman et al., 2024; Ahaduzzaman, 2021).

  Most of the results (5) concerned statistical models for determining CCPP risk factors. Only 2 references were found in peer-reviewed journals and conference communications regarding non-statistical models for CCPP.

  -A compartmental model was developed to study the transmission of Mccp among an isolated and enclosed population of gazelles in Saudi Arabia (Lignereux et al., 2018). In this context, the first dynamic model was developed and calibrated using outbreak data. From the calibration of the model on the data, the authors were able to estimate the basic reproductive ratio R₀, used to assess the probability of large outbreaks, and the case fatality rate. The case fatality rate, p, was estimated at around 59% (95% CI: 54–70) and R₀ was estimated to have an average value of 2.32 (95% CI: 1.86–2.79).

  -A stochastic demographic model was developed to evaluate the annual economic losses due to CCPP in a standard flock of 100 heads, and to evaluate the cost-benefit ratio of vaccination programmes based on different vaccine quantity and schedule scenarios (annual or biannual). The cost-benefit ratio of vaccination supports the current biannual vaccination campaigns implemented in Kenya, even with vaccine efficacy limited to 20% (average cost-benefit ratio of 5.72, SD 3.91; Renault et al., 2019).

  GAPS :

  The application of the two models presented here is restricted to the conditions under which they were developed. The first study by Lignereux et al. (2018) focused on an isolated outbreak and only considered wild animals (sand gazelles), which are not usually considered to be the main hosts of the disease. Moreover, since the animals were restrained in an enclosed area and used the same water and feed sources, the spatial constraints could have modified the contact patterns among the animals. Furthermore, the data used for calibration were based exclusively on mortality records, whereas the serological status of live animals would provide a better estimate of the disease-induced mortality rate.

  On the other hand, the second model by Renault et al. (2019) did not focus on disease dynamics, but only on mortality. Including more information about transmission and vaccination could have improved the cost-benefit ratio estimates.

  In general, more precise information about latency, recovery and mortality rates, and how these relate to scenarios and environmental conditions, should be collected to improve the accuracy of models.

  Since the possibility of carriage after infection cannot be ruled out a priori, the models should be used to test whether and under what conditions the carrier compartment should account for the possibility of carriage after infection and demographic dynamics. To capture the effects of carriage, models should incorporate demographic dynamics, as well as the duration of maternal antibodies and the potential transmission through maternal colostrum.

  The role of sheep is unclear and they may act as asymptomatic spreaders; for this reason, models should consider goats and sheep separately.

  Similarly, in endemic areas, longitudinal studies and serological data by species and age class should be used to calibrate models and estimate the disease-induced mortality rate.

  Finally, depending on the context and husbandry practices (intensive/industrial or extensive/agropastoral), models should include interactions with domestic wildlife where appropriate.

• Intervention platforms

  High‑throughput laboratory or digital surveillance platforms, described for other livestock diseases in non‑endemic, high‑income settings, are currently unrealistic for many CCPP‑affected regions because of limited budgets, laboratory capacity, cold chains, and data systems.

  GAPS :

  Intervention platforms for CCPP must be adapted to poor veterinary infrastructures, long distances, insecurity in some pastoral zones, and high livestock mobility.

  Priority characteristics of intervention platforms for CCPP:

  -Robust, low‑cost pen-side tests suitable for remote areas, integrated with basic sample transport.

  -Cheap, thermostable vaccines that can be combined with other small‑ruminant vaccination programmes, such as PPR vaccination campaigns.

  -Local, community‑based delivery of diagnostics, treatments and vaccines by paravets, trained herders, or NGOs rather than relying only on central government services.

  -Simple mobile‑phone alerts to improve disease reporting and mapping, since sophisticated real‑time mobility or trade‑network data are rarely available.

  Additionally, increased awareness and training for farmers, traders, and veterinary services are needed, as well as improved movement control, for example by applying quarantine before mixing animals and progressively strengthening basic laboratory capacity.

  Finally, linking CCPP-diagnostics and vaccination to PPR or parasite schemes would be highly strategic to cut costs and increase efficiency, particularly considering the Global Eradication Strategy for PPR.

• Communication strategies

  In CCPP-free regions, communication focuses on preventing introduction and maintaining surveillance. Simple CCPP suspicion cards highlight clinical signs and lesions for rapid reporting and movement bans.

  GAPS :

  To our knowledge there are no standard preparedness materials (guides or suspicion cards) and no wildlife-inclusive preparedness for CCPP-free areas.

  In most endemic regions there is virtually no communication. Clear, consistent messages may be sent using radio, community meetings and mobile phones, particularly in communities with low literacy.

  Communication should be integrated with PPR and other small‑ruminant campaigns to save costs and avoid confusion, using shared materials and joint training where possible.

  Two‑way communication is essential: the authorities must also listen to community feedback on suspected cases, constraints to reporting, and acceptability of control measures.

  Special attention should be given to nomadic and cross‑border herders, with harmonised messages across neighbouring countries and languages.

  Awareness is low, even in endemic zones. Trade-focused communication on live goat imports lacks coordination.

  Cross-border messaging remains uncoordinated despite high livestock mobility.

Main critical gaps

• List of the most important research gaps

  Epidemiology and impact:

  A mathematical model for domestic species that provides reliable information about the impact of the disease and can be used to improve control measures is still missing. Including mobility, husbandry and other dynamics data may help identify periods and areas to monitor for improved surveillance and control.

  There are insufficient data on latency, the infectious period, recovery and mortality rates under different conditions, and how these vary with environment, production systems and management practices. Furthermore, the presence of an active carrier state and its role in maintaining disease circulation should be addressed. This information is particularly relevant to develop accurate models of the disease.

  Since CCPP could co-circulate with other diseases like PPR, comparing the impact of CCPP in areas with or without other co-circulating diseases could improve the estimation of the parameters. Additionally, the absence of information regarding animal movements hinders the application of statistical and dynamical models to comprehend CCPP diffusion and estimate the propagation speed and the seasonality or maintenance conditions for the disease. A meta population model is required to assess the role of “silent carriers” and the efficacy of control measures. Information on movements could be collected first using participatory approaches to identify possible hotspots and guide the protocol and in a second stage conduct surveys to collect more quantitative data. These activities could be combined with others on priority small ruminant diseases like PPR.

  Finally, under-notification and passive reporting to WOAH lead to a significant underestimation of the true occurrence of the disease. Moreover, this type of record is insufficient to distinguish between endemic and epizootic patterns.

  When reported, outbreak data lack precise locations, dates and time evolution, which prevents detailed spatio-temporal analysis. In addition to improving data collection on animal movements, we suggest that improving outbreak reporting together with geo-stamped data and metadata about the outbreak conditions (e.g., herd size, species, age and husbandry practices) could help to shed light on the epidemiology of the disease and its impact.

  There are extremely limited studies on economic impact, whether at global or national level. The sophistication of methods currently used to measure impact is relatively modest and could be informed by more in-depth studies and more rigorous tools as used in other disease contexts (e.g., foot-and-mouth disease, avian influenza).

  Data on the costs of controlling CCPP are generally unavailable, and information on secondary effects such as prices, marketing, and trade is also lacking. This scarcity of data further limits the ability of conducting more integrated analyses of disease epidemiology and economic impact, unlike for diseases such as foot‑and‑mouth disease, where such assessments have been conducted (Rich and Winter-Nelson 2007).

  Pathogenicity and host immune response:

  Increased knowledge of the cellular and molecular basis of host-pathogen interactions is needed in order to support the development of more effective control tools. More complex in vitro infection models involving multicellular co-cultures and organoids will be very useful. Given the significant impact of a recently described murine model of CCPP (Yang et al., 2025) in advancing these objectives, it is essential to verify whether this mouse model reproduces the acute form of the disease or instead represents an abortive infection.

  Control strategies:

  Targeted pilot studies on integrated strategies combining mass vaccination, test and slaughter or stamping-out, movement restrictions, and regulated antibiotic treatment should be conducted to assess feasibility and efficacy.

  Robust evidence is required to develop a comprehensive policy framework specifying the recommended antibiotic(s), dosage, duration of treatment, and the epidemiological and management contexts in which treatment should be applied, including how antibiotic use could be integrated with other control measures. Antibiotic treatments must be accompanied by standardised surveillance systems and associated standard antimicrobial susceptibility testing (AST) protocols to monitor the possible emergence and spread of AMR. Standard AST protocols for Mccp or other ruminant mycoplasmas are not currently available.

Conclusion

• A coordinated, multidisciplinary approach is essential to improve the diagnosis, treatment, prevention and control of CCPP. Achieving this will require stronger scientific research and collaboration to develop and validate reliable diagnostic tools, produce safer and more effective vaccines, and generate robust evidence to support responsible and evidence-based antimicrobial use, all of this supported by robust policies and updated regulatory and quality control frameworks. In parallel, improved surveillance and reporting systems, enhanced data collection, epidemiological modelling, and integrated socio-economic and policy approaches will be necessary to support the implementation and acceptance of effective control strategies.

Sources of information

• Expert group composition

  Lucía Manso-Silván, Centre de Coopération Internationale en Recherche Agronomique pour le Développement (CIRAD), France - [Leader]

  Andrea Apolloni, Centre de Coopération Internationale en Recherche Agronomique pour le Développement (CIRAD), France

  Yuefeng Chu, LVRI, China

  Karl M. Rich, Virginia Tech, USA

  Flavio Sacchini, Istituto Zooprofilattico Sperimentale dell’Abruzzo e del Molise (IZSAM), Italy

  Elise Schieck, International Livestock Research Institute (ILRI), Kenya

  Christiane Schnee, Friedrich-Loeffler-Institut (FLI), Germany

• Date of submission by expert group

  20 March 2026

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