Global challenges

• Commercial potential for diagnostic kits worldwide

  There is commercial potential for Q fever diagnostic tools in settings where surveillance, abortion investigation, trade-related testing or control measures create a clear practical demand.

  This potential is strongest for tools that improve operational usefulness rather than simply adding new diagnostic formats: easier sampling, faster turnaround, better interpretability, clearer target specification, improved matrix compatibility, and use in harmonised surveillance or control workflows.

  GAPS

  Market incentives remain heterogeneous across countries, matrices and surveillance objectives. The added value of new tools depends less on basic availability than on improved interpretation, validation, affordability, practical ease of use and surveillance usefulness.

  In some settings, there may be a specific need for affordable, easy-to-perform or field-adapted diagnostic tools, including point-of-care approaches, provided that their performance and interpretation are fit for purpose.

Control Tools

• Diagnostics availability

• Commercial diagnostic kits available worldwide

  Ruminant (main focus)Commercial real-time PCR assays are available for the direct detection of Coxiella burnetii DNA in ruminant samples. Most commercial PCR assays target the multicopy insertion element IS1111, which provides high analytical sensitivity. These assays are routinely used on abortion-related matrices, especially placental samples, foetal fluids or tissues and vaginal swabs. They are also used in practice on milk, including bulk tank milk, for herd- or flock-level monitoring. Use on environmental samples, including dust, exists but remains less standardised and more interpretation-dependent.Commercial ELISAs are available for antibody detection and are mainly used for herd- or flock-level surveillance. Most routine commercial veterinary ELISAs provide broad antibody detection and do not support separate Phase I / Phase II interpretation in ruminants (O’Shannessy et al., 2026).Overall, basic veterinary diagnostic tools are available in many settings, although access, validation status, transparency of molecular targets and fitness-for-purpose remain uneven.

  Other animal species (including ticks)Commercial diagnostic tools for non-ruminant animal species are more limited. Tools for wildlife species, including wild ruminants, camelids, cervids and birds, remain insufficiently established or validated for routine interpretation.In tick- or arthropod-derived samples, molecular detection requires particular caution because some broad molecular targets, including IS1111-based approaches, may detect Coxiella-like organisms rather than specifically indicate C. burnetii (Duron, 2015; Jourdain et al., 2015; Mori et al., 2017). This issue should mainly be considered as a specificity and interpretation concern for tick-derived or other non-standard samples, rather than as a general limitation of routine ruminant diagnosis.Human aspects (brief, contextual)Commercial PCR and serological assays are available for human diagnosis. However, human diagnostic interpretation is not directly transposable to veterinary diagnosis. Phase-specific serology is mainly relevant in the human clinical context.

  GAPS

  Ruminant (main focus)Although PCR-based tools are broadly available, their use remains unevenly supported by matrix-specific validation, transparent reporting of molecular targets, and fit-for-purpose interpretation. Routine serological tools do not reliably distinguish active infection from past exposure in ruminants. Commercial ELISAs remain of limited value for determining individual infection status, and most routine veterinary serological tools do not support phase-specific interpretation in ruminants.The main remaining limitations therefore concern validation, interpretation, fitness-for-purpose and strategic use rather than a complete absence of diagnostic tools.

  Other animal species (including ticks)Routine commercial diagnostic tools for non-ruminant species remain limited or insufficiently validated. For wildlife species, camelids, cervids, birds and tick- or arthropod-derived samples, positive molecular or serological findings may be difficult to interpret because diagnostic performance, target specificity and epidemiological meaning are often insufficiently established.For tick-derived samples, routine workflows able to discriminate C. burnetii from Coxiella-like organisms remain limited. This may lead to overinterpretation of positive molecular results in terms of C. burnetii circulation or vector relevance.Environmental and other non-standard matricesRoutine tools for environmental and other non-standard matrices remain limited in their field interpretation. PCR-positive environmental samples do not necessarily demonstrate viable bacteria, current shedding or direct zoonotic risk.

• Diagnostic kits validated by International, European or National Standards

  Ruminant (main focus)

  No commercial diagnostic kit appears to be validated under a broadly harmonised WOAH- or EU-specific framework dedicated to Q fever diagnosis in ruminants. National standards, licensing, quality-control or inter-laboratory proficiency frameworks apply in some countries, including Belgium, France, Germany and the UK, but their scope and requirements may differ according to country, method, matrix and intended use.

  Commercial PCR and ELISA assays are routinely used in several countries, but their formal validation, licensing or acceptance status depends on the country, the matrix and the intended diagnostic or surveillance objective. This limits comparability across settings and is particularly relevant for matrices used in surveillance, abortion investigation, environmental investigation, or reproductive and breeding-related contexts. Country-specific validation examples also exist for trade- or breeding-related uses, including APHA validation of a C. burnetii PCR for cervine and bovine semen.

  Comparative studies have reassessed the diagnostic performances of some commercial ELISA tests for ruminants in the absence of a gold standard (Lurier et al., 2021; Rivière et al., 2025). In specific contexts, serological assays such as IFA may be used as reference or confirmatory approaches, but this does not remove the need for species-, matrix- and objective-specific validation. Their interpretation is not directly transferable across species, matrices or surveillance objectives. Certain commercial real-time PCR assays are also used within nationally validated workflows for the differential diagnosis of infectious abortive pathogens, and commercial PCR approaches on milk, including bulk tank milk, are used in practice, although their validation status, practical applicability and field interpretation differ according to country, matrix and surveillance objective (Rousset et al., 2012; Rousset and Prigent, 2023; Rousset and Prigent, 2024).

  IS1111-based PCR assays are highly sensitive and widely used for C. burnetii DNA detection. However, genomic and qPCR data show that IS1111 copy number varies substantially across strains and genomic groups, and sometimes even within groups (Klee et al., 2006; Brangsch et al., 2026). Operational thresholds proposed for abortion investigation remain useful within defined contexts (Sidi-Boumedine et al., 2010), but quantitative interpretations based on fixed copy-number assumptions may introduce bias when bacterial-load estimates are compared across strains, matrices or epidemiological contexts.

  At national level, some ELISA and PCR methods or commercial assays have been documented through inter-laboratory proficiency testing reports or external quality assessment schemes, showing satisfactory analytical performance within the scope of these exercises. In some countries, national reference laboratories may also be formally involved in quality control of diagnostic reagents or control procedures. However, such schemes do not necessarily provide broad international harmonisation across matrices, target populations and diagnostic objectives.

  Inter-lot comparability of commercial ELISA kits remains an important issue for long-term consistency of serological interpretation, especially around diagnostic cut-offs. Some laboratories use calibrated materials or defined sample panels for batch control or inter-batch validation, but these approaches are not yet harmonised internationally.

  Other animal species (including ticks)

  Multi-species ELISA formats are available, but their diagnostic sensitivity and specificity across mammalian species remain insufficiently validated. Validation data for non-ruminant species remain limited, including New World camelids, wild ruminants and cervids.

  Validation data also remain limited for tick- or arthropod-derived samples and for complex multi-host contexts, where diagnostic performance and epidemiological interpretation may differ from domestic ruminant settings.

  Human aspects (brief, contextual)

  Human diagnostic methods are supported by more established clinical laboratory frameworks and external quality assessment schemes. However, these frameworks cannot be directly transposed to veterinary validation needs.

  GAPS

  Ruminant (main focus)

  The distinction between kit validation, method validation and matrix-specific validation is not always clear and should be better defined. Diagnostic validation should better reflect the intended objective, such as abortion investigation, herd or flock surveillance, monitoring of shedding, reproductive or breeding-related uses, export or certification purposes.

  Broadly available and internationally harmonised reference materials for validating commercial Q fever diagnostic tools across matrices and target populations are lacking. At European level, the absence of a dedicated EURL limits the coordinated generation and distribution of diagnostic standard materials and the structuring of EU-level inter-laboratory proficiency testing.

  Quantitative interpretation of IS1111-based PCR results remains vulnerable to copy-number variability. Further work is needed to harmonise how multicopy targets are used for sensitive detection and how single-copy or multiplex approaches can support more robust quantification across strains, matrices and surveillance contexts.

  Field performance of commercial tests remains insufficiently documented across target populations, matrices and epidemiological contexts. Validation data remain limited for pooled samples, bulk tank milk in some settings, and matrix-specific applications such as faeces, manure or semen.

  Inter-lot variability of commercial ELISA kits remains insufficiently addressed in validation frameworks. Standardised approaches for inter-lot calibration, reference sera, standard DNA materials and long-term comparability should be further developed and validated.

  For phase-specific serological approaches, standardised production, characterisation and validation of Phase I and Phase II antigens remain critical, particularly where such interpretation is required.

  Other animal species (including ticks)

  Validation remains insufficient for non-ruminant species, including New World camelids, wild ruminants and cervids. Validation data remain limited for complex multi-host contexts and for tick- or arthropod-derived samples.

  Environmental and other non-standard matrices

  Environmental matrices should be mentioned here only from a validation perspective. Validation remains limited for environmental and other non-standard matrices, and the field meaning of results depends strongly on sampling strategy, matrix type, analytical target and intended use.

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

  Ruminant — main focus

  Diagnostic methods described in WOAH and/or national diagnostic frameworks include indirect ELISA for serology in ruminants, as well as direct detection methods for abortion-related investigations.

  Complement fixation test (CFT) is still described or used in some diagnostic frameworks and may be retained in specific contexts, including historical or export-related testing. However, CFT is not currently a preferred routine serological method for ruminant Q fever. Compared with ELISA, it is generally less sensitive, more dependent on laboratory implementation and operator reading, and may be constrained by the limited availability of commercial CFT antigens in some countries. Its interpretation may also be affected by the immunoglobulin profile of tested sera because only some antibody subclasses efficiently activate complement (Rousset et al., 2007; Kittelberger et al., 2009).

  Direct diagnostic methods routinely used on abortion-related matrices include real-time PCR, stained smear examination, histopathology and, in some laboratories, immunohistochemistry. The main abortion-related matrices include placental samples, foetal tissues or fluids such as spleen, liver, lung and abomasal or stomach content, and vaginal swabs collected shortly after abortion.

  Among these matrices, placenta is generally considered one of the most informative samples for direct investigation of Q fever abortion, followed by foetal abomasal or stomach content and vaginal swabs collected rapidly after abortion. Histopathology can identify lesions compatible with C. burnetii infection in placenta and foetal organs. Etiological attribution of abortion is best supported by convergent evidence, including compatible placental lesions, immunohistochemical localisation of the organism, direct detection and epidemiological context. Experimental infection in pregnant goats supports the role of placental infection, trophoblastic localisation and necrotising placentitis in C. burnetii-associated abortion (Sánchez et al., 2006).

  Bacterial culture may be performed in specialised laboratories, but it is not used routinely because of biosafety and technical constraints. Axenic culture media have improved host-cell-free growth of C. burnetii, but these approaches remain specialised and are not part of routine diagnostic workflows (Omsland et al., 2009).

  Other animal species — including ticks

  Methods described in ruminant diagnostic frameworks cannot be directly extrapolated to non-ruminant species, wildlife or tick-derived samples. For these species and sample types, the availability of described methods does not necessarily imply validated diagnostic performance or clear epidemiological interpretation.

  Human aspects (brief, contextual)

  In humans, PCR, serology and, in selected contexts, culture or tissue-based methods are described in clinical laboratory frameworks, but these should not be directly extrapolated to veterinary diagnostic interpretation. Complementary tests such as IFN-γ-based assays or anti-cardiolipin antibody testing may provide useful information in specific human clinical contexts, but they are not first-line diagnostic tools for routine Q fever diagnosis.

  Some clinical microbiology laboratories have developed high-throughput PCR workflows for human Q fever diagnosis and outbreak-related screening. These approaches illustrate clinical diagnostic capacity, but they should not be directly extrapolated to veterinary diagnostic standards or ruminant abortion investigation frameworks (Jaton et al., 2013).

  GAPS

  Ruminant — main focus

  Broadly similar diagnostic methods are used in many countries, but their framing, interpretation and degree of harmonisation remain uneven across countries and intended uses.

  CFT interpretation remains particularly sensitive to laboratory- and operator-dependent variability, limited antigen availability and serum immunoglobulin profiles. Its place should therefore be framed cautiously, especially when compared with ELISA-based routine serology.

  The relative place of histopathology, immunohistochemistry and PCR in abortion case definitions may differ according to national frameworks and laboratory capacity. Attribution of abortion to C. burnetii is relatively well supported when direct detection is combined with compatible placental lesions and epidemiological context, but criteria for attributing non-abortion reproductive disorders, such as infertility, foetal resorption, retained placenta or metritis, are less clearly developed. Detection or seropositivity alone should not be considered sufficient to demonstrate causation for these outcomes (Agerholm, 2013).

  Environmental matrices and pooled samples remain less clearly framed in available standards than abortion-related diagnostic matrices. Their detailed interpretation should remain outside this section.

  Culture and axenic-medium approaches remain insufficiently harmonised across specialised laboratories and are not readily deployable for routine diagnostic use. Harmonisation and experience sharing between reference laboratories may be useful, particularly for culture and axenic-medium approaches.

  Other animal species — including ticks

  For non-ruminant species, wildlife and tick-derived samples, methods described in ruminant frameworks are not sufficient to ensure validated diagnostic interpretation. Standardised approaches remain limited, especially where closely related Coxiella-like organisms may complicate molecular interpretation.

  Human aspects — brief, contextual

  Human clinical diagnostic frameworks are more established for some methods, but they do not resolve veterinary gaps in ruminant abortion attribution, non-ruminant species diagnosis or environmental interpretation.

• DIVA tests required and/or available

  Ruminant — main focus

  No DIVA diagnostic test is currently available for Q fever in animals. Such tests would be particularly relevant for surveillance, interpretation and follow-up in vaccinated populations if vaccination were more widely implemented in control programmes.

  Routine commercial ELISAs do not reliably discriminate between vaccinated animals, naturally exposed animals and animals with past infection. Considering the course of infection and the sensitivity of direct detection, the DIVA need mainly concerns serological interpretation rather than routine molecular detection.

  Routine molecular detection does not currently provide reliable discrimination between vaccinated and naturally infected animals. Molecular results in recently vaccinated animals may also require cautious interpretation, as vaccine-derived C. burnetii DNA has been reported for a short period after vaccination in some settings (Hermans et al., 2011).

  Alternative screening approaches, including cell-mediated immunity assays, may be promising in some field settings where vaccination history is unknown or incomplete, but they do not currently constitute validated DIVA tools (Matthijs et al., 2025).

  Human aspects — brief, contextual

  Human vaccination contexts are distinct and should not be directly transposed to veterinary DIVA needs.

  GAPS

  Ruminant — main focus

  DIVA-compatible serological tests are lacking. This limits the interpretation of serological results in vaccinated populations and complicates evaluation of vaccination programmes, surveillance design and follow-up of control measures.

  True molecular DIVA tools compatible with vaccination strategies are lacking. Routine molecular detection does not currently provide reliable discrimination between vaccinated and naturally infected animals.

  Validated DIVA approaches would require clearly defined surveillance objectives in different epidemiological and economic contexts. The strongest need is not eradication, but improved interpretation for surveillance, control, vaccination follow-up and assessment of vaccination programme success.

• Vaccines availability

• Commercial vaccines availability (globally)

  Ruminant (main focus)

  Commercial animal vaccines for Q fever are currently limited to inactivated whole-cell Phase I vaccines for ruminants. In Europe, the main currently documented commercial veterinary product is Coxevac, authorised for cattle, goats and sheep. Vaccine availability, authorisation and field access remain dependent on national regulatory frameworks, commercial supply, market conditions and programme context.

  This vaccine is used mainly in cattle, sheep and goats in some countries or regions where Q fever is endemic or where control measures are implemented. Vaccination is available and useful in some settings but should not be framed as a uniformly available or sufficient stand-alone control tool.

  In some non-European settings, access to commercial vaccines may be constrained by import restrictions, which can stimulate interest in local herd-specific or autogenous approaches.

  Other animal species

  No commercial Q fever vaccines are currently available for non-ruminant animal species.

  Human aspects (brief, contextual)

  For comparative context only, Q-VAX remains a licensed human Q fever vaccine used in Australia. Its wider deployment is constrained by reactogenicity concerns, the need for pre-vaccination screening, including serology and skin testing, and variable access or cost depending on provider and programme context.

  GAPS

  Ruminant (main focus)

  No commercial next-generation vaccine platforms, such as recombinant, vectored, DNA/RNA or subunit vaccines, are currently available for animal Q fever.

  Commercial availability should be interpreted with caution, as access and relevance depend on species, regulatory context, market incentives, affordability and practical ease of use. In some markets, reliance on a single or very limited selection of commercial vaccine products may affect affordability, supply resilience and suitability for low-resource settings.

  Other animal species

  Information on vaccine use, authorisation and field performance in other ruminant species or non-conventional livestock settings remains limited. This includes deer farms in Europe, camel or dromedary production systems in some African contexts, and New World camelids in countries where these species are increasingly kept.

  Human aspects

  For human vaccination, access is not only determined by licensing status, but also by production capacity, availability, pre-vaccination screening requirements, cost and implementation logistics.

• Marker vaccines available worldwide

  Ruminant — main focusNo marker vaccine or DIVA-compatible vaccine strategy is currently available for animal Q fever worldwide. Current commercial veterinary vaccines do not allow vaccinated animals to be distinguished from naturally infected or previously exposed animals through a compatible routine diagnostic strategy.This limitation is particularly relevant where vaccination is used in control programmes, because interpretation of serological results and follow-up of vaccinated populations remain difficult.

  Other animal speciesNo marker vaccine strategy is currently available for non-ruminant animal species.

  GAPS

  DIVA-compatible vaccines and compatible diagnostic tools are lacking. Any future DIVA strategy would require alignment between vaccine design, surveillance objectives, vaccinated-population follow-up and compatible diagnostic tools.The main need is not only a marker vaccine as a product, but a validated strategy allowing interpretation of infection, exposure and vaccination status in relevant field contexts.

• Effectiveness of vaccines / Main shortcomings of current vaccines

  Ruminant (main focus)Inactivated whole-cell Phase I vaccines, currently represented in Europe by Coxevac, are the only commercial veterinary vaccines with documented protective efficacy against Q fever in ruminants, although the strength and nature of the supporting evidence remain uneven between species and study designs.Vaccination can reduce abortion risk and bacterial shedding, and may help reduce environmental contamination, especially when applied before primary exposure or before the first pregnancy. The clearest causal evidence for vaccine-mediated protection comes from experimental pregnant-ruminant challenge models, in which vaccination reduced abortions and/or shedding, particularly with Phase I formulations. However, comparisons between Phase I and alternative phase- or antigen-based formulations remain dependent on the model, formulation, adjuvant and challenge conditions (Arricau-Bouvery et al., 2005; Williams-Macdonald et al., 2023).Field studies with vaccinated and control groups support a cautious but credible attribution of reduced shedding burden to vaccination, particularly in replacement animals and primiparous females, rather than full prevention of infection under high-exposure conditions . In some programmes, reductions in detectable shedding have been reported, particularly when vaccination is sustained and combined with herd-level monitoring (Hogerwerf et al., 2011; Jansen et al., 2022).Current commercial Phase I vaccines should therefore not be interpreted as providing sterile immunity or complete eradication of infection. Vaccination may reduce shedding without fully preventing infection, especially under high exposure conditions or in already infected herds. Effectiveness may vary according to species, infection status at vaccination, timing before pregnancy, epidemiological context and programme design.Experimental studies suggest that primary vaccination may induce limited cell-mediated responses in naïve animals, while stronger Th1/CD8-type responses after booster vaccination or previous exposure may be associated with improved immune responses. These data are useful for understanding vaccine response but should not be interpreted as a general failure of current vaccines.

  GAPS

  Ruminant (main focus)Important uncertainties remain regarding duration of immunity, optimal revaccination or booster schedules, and the definition of target populations for vaccination, including susceptible animals, naïve animals, replacement animals, already infected herds or flocks, and high-risk areas.Independent longitudinal field data on vaccine effectiveness remain limited.Field effectiveness remains context-dependent and often difficult to interpret because vaccination is frequently implemented together with other control measures and under heterogeneous epidemiological conditions. More data are needed to clarify the relative contribution of vaccination itself, including effects by species, parity, infection status at vaccination, timing before pregnancy and programme design.Natural exposure appears to shape post-vaccination immune responses, and interpretation remains particularly difficult in already infected herds or flocks.Comparative performance across vaccine formulations, antigenic composition, adjuvants and host species remains insufficiently resolved.Correlates of protection remain insufficiently defined, including the respective roles of humoral and cell-mediated immunity. The effectiveness of vaccination in already infected animals, including its effect on persistence or recurrent shedding and environmental contamination, remains insufficiently resolved.Follow-up in vaccinated populations remains an operational weak point. Current commercial vaccines do not resolve DIVA-related follow-up needs.Vaccine tolerability and reported adverse effects, including possible transient milk yield decrease after injection, should be further documented because they may influence farmer acceptance, compliance with booster schedules and long-term implementation.

  Other animal speciesData on vaccine effectiveness are lacking for non-ruminant species and non-conventional livestock settings.

  Human aspects Human vaccine effectiveness and reactogenicity issues are distinct and should not be extrapolated to veterinary vaccine effectiveness.

• Commercial potential for vaccines

  Commercial potential exists mainly in settings where Q fever has a recognised animal-health or zoonotic impact and where vaccination is part of control strategies.Vaccine value may derive both from prevention of reproductive disorders in ruminants and from reduction of shedding and environmental contamination, with possible downstream public-health benefit.Commercial potential should, however, be interpreted in relation to species, regulatory access, programme context and practical field value. For example, the currently authorised duration of immunity differs by target species, with a shorter duration reported for sheep than for cattle and goats, which may affect the perceived usefulness and cost-benefit balance in ovine settings.

  GAPS

  Commercial incentives remain limited by heterogeneous national policies, uneven demand, variable recognition of Q fever as a priority disease, affordability constraints, and uncertainty about cost-benefit balance across species and production systems.Species-specific authorised duration of immunity may also influence perceived commercial usefulness and uptake, particularly where short protection duration makes implementation less attractive in field conditions.Commercial uptake may also be constrained by perceived cost-benefit balance, practical implementation constraints, and tolerability concerns, including reported or perceived adverse effects. Better comparative data are needed to understand how these factors influence vaccine uptake across production systems and countries.

• Regulatory and/or policy challenges to approval

  Approval of Q fever vaccines requires demonstration of quality, safety and efficacy. Practical expectations regarding field effectiveness and vaccination objectives may nevertheless vary according to the epidemiological, regulatory and policy context.The place of vaccination within surveillance, movement control and outbreak management is not uniformly defined across countries or regions. This may affect how vaccination is authorised, recommended, implemented or evaluated in the field.The absence of DIVA-compatible vaccination and diagnostic strategies complicates the integration of vaccination into surveillance and control programmes, especially where vaccinated populations need to be monitored over time.

  GAPS

  The place of vaccination in relation to surveillance, movement control and outbreak management remains insufficiently defined.

  Regulatory expectations for future or improved vaccines should better anticipate their operational role within surveillance and control programmes, including compatibility with herd- or flock-level monitoring and follow-up in vaccinated populations.

  Policy and regulatory frameworks may need to clarify when vaccination is intended for prevention, outbreak control, reduction of shedding, protection of high-risk settings, or long-term management of endemic situations.

• Commercial feasibility (e.g manufacturing)

  Current whole-cell Phase I vaccines require specialised production under high biosafety and quality-control constraints. Manufacturing feasibility therefore depends not only on production capacity, but also on standardised cultivation, antigen preparation, batch validation and quality-control procedures.

  GAPS

  Safer and easier-to-manufacture vaccine platforms are needed. The industrial feasibility of next-generation Q fever vaccines remains to be demonstrated.

  Standardisation of whole-cell vaccine production remains an important issue, including batch-to-batch consistency, validation of primary biological steps, and harmonisation of methods used to quantify or characterise antigen content.

• Opportunity for barrier protection

  Vaccination may be used as part of a barrier protection strategy in infected, endemic or high-risk situations, with the aim of reducing abortion risk, bacterial shedding and environmental contamination (Hogerwerf et al., 2011; Toledo-Perona et al., 2024).Its preventive value is likely to be greatest when applied consistently before first pregnancy or before expected exposure, and when integrated with biosecurity, surveillance and herd-management measures.Vaccination alone is not sufficient to guarantee zoonotic-risk reduction or control of infection, and should not be presented as a stand-alone barrier protection measure (Toledo-Perona et al., 2024; Jansen et al., 2022).This may be relevant in specific public-facing settings, such as open farms, agricultural shows, petting farms or urban grazing schemes, where the public may be exposed to parturient ruminants or contaminated environments but should be framed as a context-dependent complementary measure.

  GAPS

  The role of vaccination as a barrier-protection tool in different epidemiological contexts should be better defined.

  The combined effect of vaccination and other control measures remains difficult to quantify, particularly regarding prevention of shedding, environmental contamination and zoonotic risk (Hogerwerf et al., 2011; Alvarez-Alonso et al., 2018; Jansen et al., 2022).

  More standardised longitudinal studies are needed to assess how vaccination, biosecurity, hygiene, surveillance and herd-management measures interact in naturally infected herds or flocks.

• Pharmaceutical availability

• Current therapy (curative and preventive)

  Ruminant (main focus)No curative or preventive pharmaceutical treatment is currently available to eliminate Coxiella burnetii infection or to reliably control Q fever at herd or flock level.Antibiotic treatment, particularly oxytetracycline, has been investigated in ruminants but is not supported as a reliable routine control tool for reducing abortion or bacterial shedding. Field studies in naturally infected dairy sheep showed that oxytetracycline treatment did not prevent abortion, did not reduce the duration of bacterial excretion, and did not significantly reduce bacterial load or provide residual benefit in the following lambing season (Astobiza et al., 2010; Astobiza et al., 2013).In cattle, antimicrobial treatment has been investigated in combination with other measures, but the specific added value of antibiotics remains difficult to separate from vaccination, herd management and surveillance effects. Overall, veterinary antimicrobials should not be considered a strong control pillar in routine Q fever management.

  Other animal speciesTherapeutic approaches in non-ruminant animal species are not sufficiently documented for routine control purposes.

  Human aspects (brief, contextual)In humans, doxycycline remains the treatment of choice for acute Q fever, while persistent forms require prolonged combination therapy in specialised clinical settings. This human therapeutic framework should not be extrapolated to routine veterinary control of shedding or abortion in ruminants.

  GAPS

  Alternative therapeutic approaches with acceptable efficacy, feasibility and antimicrobial-stewardship profiles are lacking.The potential role of pharmaceuticals for Q fever control remains limited and context-dependent. Any future pharmaceutical approach would need to demonstrate added value beyond vaccination, biosecurity, surveillance and herd-management measures, while addressing antimicrobial-residue and stewardship constraints.

• Future therapy

  No validated future therapeutic strategy is currently available for routine veterinary use in Q fever control, and prevention remains the main practical approach.

  GAPS

  New anti-Coxiella burnetii approaches remain exploratory and require proof of field relevance.

  Their added value would need to be demonstrated in relation to prevention- and control-based strategies, rather than assumed as a routine alternative.

• Commercial potential for pharmaceuticals

  Commercial potential for pharmaceuticals in veterinary Q fever control appears limited at present. Current evidence does not support pharmaceuticals as a major routine control pillar for reducing abortion, shedding or environmental contamination at herd or flock level.

  GAPS

  Any future commercial value would depend on clearly demonstrated field efficacy, practical feasibility, acceptable cost-benefit balance and compatibility with antimicrobial stewardship.

• Regulatory and/or policy challenges to approval

  Any future pharmaceutical approval for veterinary Q fever would depend on clearly defined indications and acceptable evidence of benefit. Given the limited role of antimicrobials in herd- or flock-level control, regulatory expectations would likely require evidence of practical added value beyond existing prevention and management measures.

  GAPS

  Regulatory endpoints remain unclear for future pharmaceutical approaches, particularly for claims related to shedding reduction, reproductive outcomes or transmission control.

  Any antimicrobial-based approach would need careful stewardship justification, including antimicrobial-residue considerations, field feasibility and evidence that benefits exceed risks.

• Commercial feasibility (e.g manufacturing)

  Manufacturing is not the main bottleneck for conventional antimicrobials.

  GAPS

  The main limitation is the lack of demonstrated veterinary utility for Q fever control. No clear industrial pathway is currently identified for innovative veterinary anti-Coxiella products.

• New developments for diagnostic tests

• Requirements for diagnostics development

  Ruminant (main focus)

  Ruminant (main focus)New diagnostic developments are mainly needed to improve interpretation rather than simple detection. Priority needs include approaches able to better distinguish herd/flock infection status, support source investigation, and improve interpretation of environmental contamination.Combining serology, animal PCR and environmental PCR may support a more graded assessment of C. burnetii circulation in small ruminant farms, provided results are interpreted according to matrix, sampling strategy and epidemiological context. A study specifically addresses the combination of serology and PCR analysis of environmental samples to assess C. burnetii infection status in small ruminant farms (García-Pérez et al. 2025). Cell-mediated immunity assays, including ex vivo IFN-γ recall assays, may represent promising complementary diagnostic developments in selected contexts, such as incomplete vaccination history or pre-purchase screening. However, antigen standardisation, timing of sampling, interpretation and validation require further work before routine use (Matthijs et al., 2025).

  Other animal speciesFor non-ruminant species, wildlife and companion animals, diagnostic developments are still needed for validated and interpretable testing. Serological tools require species-specific validation, and commercial assays cannot be assumed to perform equivalently across species

  GAPS

  RuminantValidated approaches distinguishing active infection, major shedding situations, environmental contamination and likely source attribution remain lacking.Diagnostic tools and interpretation frameworks are still insufficient to reliably connect detection results with infection status, shedding relevance, environmental contamination and operational decision-making.Further diagnostic development is also needed to support source investigation.More specific development priorities are addressed in research sections below.

  Other animal speciesDiagnostic tools and matrix-specific sampling strategies remain limited for non-ruminant species, wildlife and companion animals, constraining investigation of their possible epidemiological role in some settings.

  Cross-cutting gapsFurther diagnostic development is needed to support source investigation and attribution, but genotyping, WGS and data integration should be developed mainly in the source-tracing, digital and preparedness sections.

• Time to develop new or improved diagnostics

  Ruminant-main focus

  Development of improved diagnostics is generally faster than vaccine development, but validation across matrices, species, epidemiological contexts and laboratories remains time-consuming.

  In practice, diagnostic development and validation timelines may also be prolonged when Q fever competes with other diagnostic priorities in multi-pathogen laboratory workflows.

  GAPS

  Ruminant- main focus

  Time requirements for development and validation of improved Q fever diagnostics are insufficiently documented.

  Multi-laboratory validation, field evaluation and fit-for-purpose interpretation remain major bottlenecks.

  Other animal species

  Development and validation timelines are likely longer for non-ruminant species and non-standard matrices because reference data, validated protocols and field experience remain limited.

• Cost of developing new or improved diagnostics and their validation

  Ruminant — main focus

  Costs depend strongly on the type of diagnostic test, the need for reference materials, the diversity of matrices and species targeted, and the scale of inter-laboratory validation.

  Development costs may be higher when exploratory approaches are used, for example for identifying or validating new antigens, epitopes or serological targets.

  GAPS

  Ruminant — main focus

  The cost of developing and validating improved Q fever diagnostics remains insufficiently documented.

  Building broadly usable reference materials and harmonised validation panels remains a major bottleneck, especially when tools must be applicable across matrices, species, laboratories and surveillance objectives.

  Other animal species

  Costs are likely higher for non-ruminant species and non-standard matrices because reference data, validation panels and field samples are more limited.

• Research requirements for new or improved diagnostics

  Ruminant

  Priority research needs include improved diagnostic tools and interpretation frameworks for animal-level, herd/flock-level and environmental investigation of Q fever.

  At animal and herd/flock level, research is needed to improve the interpretation of serology, animal PCR and environmental PCR according to the sampled matrix, timing, bacterial load, infection status, shedding status and epidemiological context. Combining environmental PCR, animal excretion PCR and structured serology may support a graded interpretation of C. burnetii circulation at herd level, although broader validation is still needed.

  For environmental and pooled samples, current molecular detection mainly documents the presence of C. burnetii DNA. It does not, on its own, demonstrate viable bacteria, current shedding, infectiousness or direct zoonotic risk. Research should therefore distinguish DNA persistence from bacterial viability and infectious potential.

  Research and validation efforts should further assess multiplex PCR approaches combining highly sensitive multicopy targets, such as IS1111, with single-copy quantification or confirmation targets, such as com1 and htpAB, in order to preserve analytical sensitivity while improving robustness of bacterial-load estimation across strains, matrices and epidemiological contexts.

  A marine mammal-associated C. burnetii genome lacking IS1111 has been reported, suggesting that reliance on a single multicopy target may be insufficient in some non-standard hosts or ecological contexts. This supports the development of complementary molecular targets for confirmatory detection and genomic interpretation (Gardner et al., 2023).

  No validated commercial point-of-care or rapid field test is currently available for routine veterinary Q fever diagnosis.

  Other animal species

  For non-ruminant species, wildlife and companion animals, diagnostic developments are still needed for validated and interpretable testing. Serological tools require species-specific validation, and commercial assays cannot be assumed to perform equivalently across species.

  Environmental, tick-derived and other non-standard matrices

  In environmental or vector-related contexts, molecular interpretation may be complicated by Coxiella-like organisms. Although phylogenetically related to C. burnetii, Coxiella-like organisms are often arthropod-associated endosymbionts and should not be overinterpreted as evidence of C. burnetii circulation or zoonotic relevance.

  Tools able to distinguish C. burnetii from Coxiella-like organisms remain important for tick-derived, arthropod-derived and other non-standard samples.

  GAPS

  Research is needed on:

  • validated animal-level and herd/flock-level diagnostic interpretation according to matrix, timing, infection status, shedding status and epidemiological context;
  • validated sampling and interpretation strategies for animal, pooled and environmental matrices, including dust, air and other farm matrices;
  • viability-and infectivity- oriented methods to complement PCR-based detection:
  • standardised experimental models assessing survival across matrices, strains and physical or chemical stress conditions;
  • field-relevant evaluation of disinfectants and environmental decontamination measures, including the influence of organic matter and matrix effects;
  • harmonised metadata and reporting formats linking laboratory, epidemiological, environmental and animal data;
  • integrated decision-support approaches, linking laboratory, epidemiological; environmental and movement data;

  Routine genotyping or WGS on animal and environmental material may contribute to future source-investigation capacity, but for C. burnetii, source attribution is not yet operational in routine practice.

  Surveillance-compatible tools for vaccinated-population follow-up remain needed.

• Technology to determine virus freedom in animals

  At present, no single diagnostic technology is sufficient to certify Q fever infection freedom in animals or herds/flocks. Existing approaches rely on combinations of herd/flock history, repeated sampling, serology and PCR, but interpretation remains context-dependent and imperfect. The WOAH framework identifies Q fever as a disease for which population or individual freedom from infection is difficult to establish with current tools.

  GAPS

  No harmonised and validated protocol is available to determine animal, herd or flock freedom from infection.

  Technologies and algorithms combining repeated testing, multiple matrices and epidemiological context should be further developed and validated.

  The interpretation of freedom-from-infection remains particularly difficult in the context of silent spread and environmental persistence.

• New developments for vaccines

• Requirements for vaccines development / main characteristics for improved vaccines

  Ruminant — main focus Improved vaccines are needed that are safer to produce, easier to scale up, effective across target ruminant species, and ideally compatible with DIVA strategies.Current protective vaccines are based on inactivated whole-cell Phase I material, but this platform has manufacturing, biosafety and field-use limitations. Future vaccines should also be more compatible with surveillance needs.Experimental work continues on adjuvant optimisation, Phase II bacterins, modified whole-cell vaccines, subunit approaches and antigen discovery for next-generation vaccines.Recent experimental studies suggest that adjuvanted formulation may strengthen Th1/CD8+-type responses and improve protection in goats, while Phase II bacterin formulations may show protective effects in pregnant ewe challenge models. However, these findings remain experimental and should not be directly extrapolated to commercial field use without further validation across species, formulations and challenge conditions (Tomaiuolo et al., 2023; Williams-Macdonald et al., 2023).For comparative human-vaccine context only, less reactogenic vaccine formulations remain a priority, together with clearer evidence on duration of protection and correlates of protection (Long, 2021).Dedicated biosafe production systems would be needed to support safe, scalable production and avoid risks associated with production or distribution of whole-cell C. burnetii material.

  GAPS

  Ruminant — main focus Improved vaccines should ideally combine protective efficacy, clearer duration of immunity, easier manufacturing, DIVA compatibility and practical field usability.Protective antigens and correlates of protection remain insufficiently identified, including the respective contribution of humoral, Th1/CD8+-type and other cell-mediated responses.The ability to monitor infection in vaccinated populations remains a key unmet operational need.

  Human aspects — brief, contextual For comparative human-vaccine context, less reactogenic vaccine remains a priority, together with clearer evidence on duration of protection and correlates of protection (Long, 2021).

• Time to develop new or improved vaccines

  Ruminant — main focus

  A timeframe of at least 10 years may be more realistic for development, experimental evaluation, field validation and licensing of improved veterinary Q fever vaccines. This is especially true if DIVA capability, broader species evidence, safer production platforms or new vaccine technologies are sought.

  GAPS

  Ruminant — main focus

  Long and costly efficacy studies in pregnant ruminants remain a major constraint.

  Field validation across species, epidemiological contexts and vaccination strategies may further extend development timelines.

• Cost of developing new or improved vaccines and their validation

  Ruminant — main focus

  Vaccine development and validation are expected to be expensive because they require controlled challenge studies, safety assessment, reproductive outcome data and field-level evaluation under different epidemiological conditions.

  Manufacturing constraints further increase development costs for current whole-cell approaches. Costs may be higher when DIVA compatibility, safer production platforms, broader target-species coverage or easier field deployment are sought.

  Other animal species

  Development costs for non-ruminant species would likely be difficult to justify unless a clear animal-health, production or zoonotic-risk need is demonstrated.

  GAPS

  Ruminant — main focus

  Robust cost estimates for different vaccine platforms are lacking.

  The economic implications of developing DIVA-compatible or easier-to-manufacture vaccines remain insufficiently documented.

  Cost-benefit assessment should include not only efficacy, but also surveillance compatibility, vaccinated-population follow-up, duration of immunity, practical deployment and field usability.

• Research requirements for new or improved vaccines

  Ruminant main focusResearch priorities include identification and validation of protective antigens, clarification of correlates of protection and protective immunity, better understanding of duration of immunity, evaluation of vaccination in already infected animals, and development of DIVA-compatible strategies.Recent immunology work supports the importance of both B-cell and T-cell responses in protection, with cell-mediated responses, including Th1/CD8+-type responses, appearing particularly relevant for bacterial control. However, operational correlates of protection in ruminants remain to be established (Alam et al., 2024; Bauer et al., 2023; Tomaiuolo et al., 2023). These findings should be interpreted cautiously because some evidence comes from mouse models or controlled experimental settings and may not directly translate into field protection in ruminants.Experimental studies using IFN-γ recall assays after vaccination and challenge suggest that cell-mediated responses may help characterise vaccine-induced immunity and protection dynamics. However, these assays require further standardisation, antigen validation and field interpretation before they can be used as operational correlates of protection (Tomaiuolo et al., 2023).Under experimental conditions, some alternative formulations, including adjuvanted Phase II bacterins, have shown protective effects in a pregnant ewe model, but these findings are not consistent with the earlier pregnant-goat challenge study in which a commercial Phase II vaccine showed no protective effect. Vaccine formulation, adjuvant, host species and experimental design therefore matter (Arricau-Bouvery et al., 2005; Williams-Macdonald et al., 2023).Research is also needed on safer, scalable and field-adapted vaccination strategies, including alternatives to individual injectable vaccination where relevant, such as mucosal or herd-level administration approaches, provided that efficacy, safety and practicality can be demonstrated.

  GAPS

  Ruminant main focus

  Research is needed on:• protective-antigen discovery and validation;• correlates of protection and protective immunity, including humoral and cell-mediated responses; • DIVA-compatible vaccine strategies; • field effectiveness and duration of immunity across species; • vaccination of already infected herds or flocks;• safer and more scalable platforms; • vaccination strategies adapted to different epidemiological contexts

• New developments for pharmaceuticals

• Requirements for pharmaceuticals development

  Ruminant main focus

  No veterinary pharmaceutical strategy currently offers a clear routine control tool for Q fever in ruminants.Any new pharmaceutical approach would need to demonstrate added value beyond vaccination, biosecurity, surveillance and herd-management measures, for example by reducing clinically relevant shedding, persistence or transmission risk under field conditions.At present, pharmaceutical development for veterinary Q fever control should be considered exploratory rather than a near-term operational pillar.

  GAPS

  Ruminant main focus

  The intended role of pharmaceuticals relative to vaccination, biosecurity, surveillance and integrated herd-level control remains insufficiently defined.Any candidate pharmaceutical approach would require evidence of field relevance, acceptable feasibility, and compatibility with antimicrobial-stewardship principles.

• Time to develop new or improved pharmaceuticals

  Ruminant main focus

  A timeframe of 5–10 years remains a reasonable expectation for discovery, validation and licensing of new anti-Coxiella pharmaceuticals, especially if intracellular efficacy, safety and field relevance must all be demonstrated.

  GAPS

  Ruminant main focus

  Intracellular efficacy and field applicability remain key development constraints.

• Cost of developing new or improved pharmaceuticals and their validation

  Ruminant main focus

  Development costs are likely to be high because demonstration of meaningful field efficacy would require difficult and expensive studies.GAPS

  Ruminant main focus

  The economic feasibility of veterinary anti-Coxiella drug development remains unclear.

• Research requirements for new or improved pharmaceuticals

  Ruminant main focus

  Research opportunities include exploration of intracellular anti-Coxiella targets, host-directed approaches and alternatives that could reduce transmission or persistence without excessive antimicrobial use. However, this field remains much less advanced than diagnostics or vaccines.Research in this area should currently be framed as exploratory and longer-term.

  GAPS

  Ruminant main focus

  Research is needed on:• intracellular targets and anti-Coxiella compounds, • alternatives to conventional antimicrobials, • pharmacodynamic relevance in the intracellular niche, • realistic field indications for veterinary use.

Disease details

• Description and characteristics

• Pathogen

  Ruminant main focus Q fever is caused by Coxiella burnetii, a globally distributed obligate intracellular Gram-negative bacterium, with domestic ruminants acting as the main reservoirs. C. burnetii alternates between an intracellular, metabolically active and replicating large cell variant (LCV) and a small cell variant (SCV), generally considered more compatible with extracellular persistence and transmission.Morphologically intermediate transitional cells have been described during SCV–LCV transitions, but they should not be presented as a fully established developmental stage comparable to SCV and LCV. Direct experimental evidence linking specific developmental forms to environmental survival under defined physical, chemical and matrix-specific conditions remains limited.

  GAPS

  The biological significance of developmental forms, especially transitional forms, remains incompletely understood. Their relevance under natural infection and environmental conditions remains unclear.

  The links between developmental forms, extracellular persistence, infectivity, environmental survival and control targets remain insufficiently characterised.

  Standardised experimental frameworks are lacking to assess survival and infectivity of well-characterised C. burnetii preparations across strains, matrices and physical or chemical stress conditions.

• Variability of the disease

  Ruminant main focus

  Coxiella burnetii shows marked genetic diversity, including variation in genomic groups, plasmid content and other genomic features. Some bacterial features are biologically relevant to pathogenicity, host-cell interaction or diagnostic interpretation, including LPS structure, the Dot/Icm type IV secretion system, plasmid-associated features and effector repertoires. Recent genomic analyses suggest that several genomic traits and effector repertoires are more strongly associated with genomic groups than with host species, while disease manifestation probably reflects both bacterial genomic traits and host-related factors (Brangsch et al., 2026).

  This diversity may contribute to temporal, spatial and host-associated variability in disease presentation, shedding patterns and outbreak dynamics. However, links between genotype and phenotype remain only partly understood, and clinical presentation or epidemiological patterns probably reflect combined effects of bacterial diversity, host species, individual host factors, reproductive status, immune status, exposure conditions and environmental context.

  Recent genomic analyses support the need for this cautious framing. Brangsch et al. 2026 found that genome characteristics and type IV effector protein repertoires were more strongly associated with genomic groups than with host species, while host adaptation, species specificity and pathoadaptation remain insufficiently resolved.

  Comparative genomics with Coxiella-like organisms may help contextualise the evolution of C. burnetii within the broader Coxiella lineage, especially regarding host association, genome evolution and virulence-related systems. However, Coxiella-like organisms should not be conflated with C. burnetii, as they differ substantially in biology, host association and pathogenic potential (Duron et al., 2018).

  Phase I / Phase II variation is particularly important for virulence and serological interpretation, especially in humans, but should not be interpreted as a simple proxy for strain-level diversity in natural ruminant infection.

  Clinical presentation and epidemiological patterns appear heterogeneous across regions, host populations and contexts. This heterogeneity probably reflects combined effects of strain diversity, host species, immune status, reproductive status, management practices and environmental exposure.

  GAPS

  Ruminant main focus

  The relationships between genotype, antigenic properties, host range, virulence, shedding patterns and clinical expression remain insufficiently resolved.

  The extent to which strain diversity, genomic group, effector repertoires, LPS structure, plasmid content and host-specific factors contribute to clinical expression, shedding, host range and outbreak dynamics remains insufficiently resolved.

  The functional contribution of LPS structure, Dot/Icm-related effectors, plasmids and other genomic features to field-relevant virulence, shedding, transmission and host adaptation requires further study.

  Host adaptation, species specificity and pathoadaptation require further investigation..

• Stability of the agent/pathogen in the environment

  Ruminant main focus

  Environmental persistence is considered epidemiologically important in Q fever. Coxiella burnetii DNA is frequently detected in a wide range of environmental matrices, including dust, bedding, manure, slurry, birth products and other farm-environment matrices, particularly around parturition and abortion events (Abeykoon et al., 2021).Such environmental detection may support evidence of contamination and may contribute to indirect transmission and airborne spread. However, detection is primarily based on PCR and does not necessarily reflect the presence of viable or infectious bacteria.Field studies have documented prolonged detection of C. burnetii DNA and, in some settings, viable bacteria in environmental dust, including farm and non-farm environments such as animal-contaminated caves (Kersh et al., 2013; Hurtado et al., 2023; Zendoia et al., 2024). These examples support the epidemiological relevance of environmental persistence, while remaining context-specific and not replacing standardised survival studies across matrices, strains and environmental conditions (Abeykoon et al., 2021).SCV-like forms are structurally compatible with extracellular persistence, but SCV-specific resistance to environmental stress or inactivation remains insufficiently demonstrated. Controlled studies have demonstrated heat inactivation of Coxiella burnetii in milk and UVC-induced loss of detectable growth in translucent laboratory suspensions. These studies involved bacterial populations shown or presumed to include SCV, but they do not determine SCV-specific susceptibility or validate inactivation procedures for complex livestock environmental matrices (Wittwer et al., 2022; Mertens-Scholz et al., 2024). Commonly repeated statements on SCV-specific environmental resistance should be interpreted cautiously: although environmental persistence is a core feature of Q fever epidemiology, direct standardised evidence linking developmental form, matrix-specific survival and infectivity remains limited.Environmental contamination may be highly heterogeneous, especially around parturition and abortion events, creating practical challenges for environmental investigation and decontamination.

  GAPS

  Ruminant main focus

  The resistance and persistence of extracellular survival forms in the environment remain insufficiently characterised under standardised experimental conditions.The timing and duration of environmental contamination after parturition or abortion events, as well as the survival and maintenance of infectivity under different environmental conditions, including moisture, desiccation, temperature, UV exposure and organic-matter-rich matrices, remain poorly defined.The relative contribution of different environmental matrices, including dust, bedding, manure, slurry, water and birth products, to persistence, aerosolisation and transmission risk remains insufficiently quantified.Validated methods to assess viability and infectious potential in environmental samples are lacking, limiting interpretation of PCR-based detection.Evidence on the effectiveness of disinfectants and environmental decontamination measures under field-relevant conditions remains scarce and heterogeneous, particularly when organic matter, matrix effects and different C. burnetii strains are considered. In particular, the susceptibility of defined developmental forms, including SCV, has not been established across complex livestock matrices and field-relevant treatment conditions.The relationships between environmental persistence, aerosolisation and zoonotic risk remain insufficiently understood.

• Species involved

• Animal infected/carrier/disease

  Ruminant — main focus

  A wide range of domestic and wild animals can be infected with Coxiella burnetii. Cattle, sheep and goats are the most commonly recognised livestock reservoirs and represent the main domestic sources of human exposure.

  Infection or exposure has also been reported in pets, wildlife, birds, reptiles, zoo animals and captive mammals, although epidemiological importance varies considerably by species and context. Wildlife data support this broad host range, with exposure or infection reported in numerous wild mammal species worldwide (González-Barrio and Ruiz-Fons, 2019) and field detection in wild ungulates and birds in northern Spain (Zendoia et al., 2022).

  In most species, infection is often asymptomatic or subclinical, but reproductive disorders or clinical disease may occur, especially in ruminants and occasionally in some companion, captive or wild mammals. Wildlife findings should be interpreted cautiously, because infection, exposure or molecular detection does not necessarily indicate maintenance, major shedding or zoonotic relevance. More longitudinal and molecular epidemiology studies are needed to clarify when wildlife contributes to maintenance, spillover or spillback at the wildlife–livestock–human interface.

  Other animal species

  For non-ruminant species, including companion animals, zoo animals, wildlife and captive mammals, C. burnetii infection may occasionally be associated with clinical disease or reproductive disorders. For example, placental lesions associated with C. burnetii have been described in a northern fur seal population/rookery in Alaska, although the consequences for reproductive success or population dynamics remain uncertain (Conway et al., 2022). The Conway study is useful here because it shows both high placental PCR positivity and marked limits in lesion interpretation: 89/117 placentas were PCR-positive, while visible bacteria were identified in only 5/117 placentas by histology/IHC, supporting a cautious interpretation of infection versus disease significance.

  In arthropods, especially ticks, detection should be interpreted cautiously. Their epidemiological significance remains uncertain, and some molecular detections may reflect Coxiella-like organisms rather than C. burnetii itself.

  GAPS

  Ruminant — main focus

  The epidemiological role of non-ruminant domestic species, companion animals, zoo animals, birds and wildlife remains insufficiently clarified.

  Wildlife findings should be interpreted cautiously because infection or exposure does not necessarily indicate a maintenance reservoir, major shedding or relevant zoonotic transmission.

  Host species, reproductive status, immune background, management practices and environmental context may influence clinical expression and shedding, but the significance of subclinical carriage requires further study.

  Other animal species

  Validated diagnostic interpretation remains limited for non-ruminant species, making it difficult to distinguish incidental exposure from epidemiologically meaningful infection.

• Human infected/disease

  Human aspects — main focus

  Q fever is a worldwide zoonosis in humans. Most infections are asymptomatic or present as a mild self-limiting flu-like illness, but clinical expression can be highly variable, including pneumonia, hepatitis, meningoencephalitis and other neurological manifestations, cardiac involvement and persistent focalized infections such as endocarditis or vascular infection (Eldin et al., 2017; Melenotte et al., 2018).

  Clinical presentation may vary geographically and according to host factors, exposure context and, potentially, strain-related factors. Human data also suggest that some manifestations remain under-recognised or insufficiently quantified, including adverse pregnancy outcomes, post-infectiousor immune-mediated manifestations, chronic fatigue syndrome, and other context-dependent presentations (Baud & Greub, 2011; Ghanem-Zoubi & Paul, 2020; Melenotte et al., 2018).

  GAPS

  Human aspects — main focus

  The determinants of clinical expression, severity and long-term sequelae remain incompletely understood.

  The relationships between infectious dose, strain diversity, exposure route, host factors and clinical expression require further clarification.

  Important manifestations may remain under-recognised or insufficiently quantified, including adverse pregnancy outcomes, post-infectious forms, persistent focalized infections and other context-dependent clinical presentations.

  The burden of acute, persistent and post-infectious forms remains underestimated in many settings, partly because Q fever is underdiagnosed or inconsistently investigated.

• Vector cyclical/non-cyclical

  Ticks and other arthropods have long been discussed in the ecology of C. burnetii, especially in sylvatic cycles, but their epidemiological role remains debated and context-dependent (Duron et al., 2015; Celina & Černý, 2022). Experimental studies indicate that some tick species can acquire C. burnetii under controlled conditions, may support transstadial persistence, and may excrete viable bacteria in feces (Körner et al., 2020; Buysse et al., 2021). However, in livestock and human epidemiological situations, airborne or environmental transmission from infected ruminant sources remains the dominant route, and maintenance or spread is generally not vector-dependent.

  In tick-associated samples, interpretation requires particular caution because molecular detections may correspond to Coxiella-like organisms rather than C. burnetii. These organisms are phylogenetically related to C. burnetii, but often differ substantially in biology, host association and pathogenic potential, and are mainly associated with ticks or other arthropods rather than being established major vertebrate pathogens.

  The role of ticks in domestic animal epidemiology and human infection therefore remains secondary, context-dependent and insufficiently resolved. Their relative importance may be greater in wildlife or sylvatic settings than in most domestic ruminant–associated outbreaks, but this remains insufficiently documented.

  GAPS

  The epidemiological significance of ticks in the maintenance and transmission of C. burnetii remains incompletely resolved under natural conditions.

  Further field-relevant studies are needed to determine when tick-associated findings are relevant to livestock, wildlife or human Q fever epidemiology.

  The contribution of tick feces, salivary transmission, transstadial or transovarial maintenance, and environmental aerosolisation from tick-associated material requires further clarification under field-relevant conditions.

  Improved molecular discrimination and ecological interpretation are needed when tick-associated detections may reflect true C. burnetii infection, transient contamination or Coxiella-like endosymbionts.

• Reservoir (animal, environment)

  Ruminant — main focus

  Domestic ruminants are the main reservoirs implicated in most documented human Q fever transmission events. In many European outbreak settings, sheep and especially goats have played a prominent role, whereas cattle may be more important in other epidemiological contexts, including settings where occupational exposure to cattle is common (Georgiev et al., 2013; Graves and Islam, 2016).

  In a New South Wales case series, cattle contact was the most frequently reported animal contact among patients with documented animal exposure, but this should be interpreted as reported exposure rather than definitive source attribution (Graves and Islam, 2016).

  The relative contribution of cattle, sheep and goats depends on region, production system, shedding patterns, animal management and human exposure pathways. A narrative review of European outbreak reports suggests that, where a likely animal source was reported, sheep were most frequently implicated, goats less often and cattle only occasionally; however, attribution often relied on epidemiological links rather than fully integrated microbiological confirmation (Hurtado et al., 2026, Supplementary Note S4).

  Environmental contamination can act as an important persistence and exposure interface between infected animals and susceptible humans or animals but should not be conflated with an independent animal reservoir.

  Other domestic and wild species may occasionally contribute to local transmission in specific contexts, but their reservoir role and zoonotic significance remain less clearly established and context-dependent.

  Other animal species / environmental interface

  Non-ruminant or atypical reservoir contexts have been described or suspected in specific regions.

  In Australia, macropods and their ticks have been discussed as possible contributors to Q fever ecology. Aerosolisation of contaminated wildlife faeces or contaminated grass has been proposed as potential sources of human infection, and a particularly high incidence in Proserpine, a region characterised by wildlife, tourism and cane farming. However, the exact transmission mechanism and the relative importance of wildlife versus livestock sources remain insufficiently resolved (Sivabalan et al., 2017).

  Marine mammal contexts, such as northern fur seal rookeries in Alaska, illustrate possible non-ruminant exposure interfaces, but their role as human infection sources remains insufficiently demonstrated (Kersh et al., 2020).

  The French Guiana situation illustrates that reservoir patterns may differ substantially from the usual domestic-ruminant framework, but the reservoir and transmission cycle remain incompletely resolved (Epelboin et al., 2021).

  These examples illustrate that reservoir and exposure patterns may be context-dependent, but they should not be interpreted as replacing domestic ruminants as the main reservoirs in most documented Q fever outbreaks.

  GAPS

  Ruminant — main focus

  The respective roles of cattle, sheep and goats in human epidemiology remain context-dependent and should be interpreted according to region, production system, shedding route, environmental contamination and exposure pathway.

  The relative contribution of different animal reservoirs remains difficult to establish because integrated investigations combining human clinical data, animal sampling, environmental investigation and genotyping remain limited.

  The reservoir role of companion animals, zoo animals, wildlife and other non-ruminant species remains insufficiently defined. Infection or exposure in a species does not necessarily demonstrate maintenance capacity or major zoonotic relevance.

  The role of environmental contamination as a persistence and exposure interface requires clearer conceptual and operational framing.

  The role of animal movements in introducing or redistributing C. burnetii strains, and its interaction with farm management, herd connectivity and trade-related exposure, remains insufficiently documented.

  The zoonotic significance of raw milk exposure remains debated and is better addressed under transmission routes or human risk factors (Koehler et al., 2019).

• Description of infection & disease in natural hosts

• Transmissibility

  Transmission in animals is strongly associated with parturition and abortion, when large quantities of bacteria may be excreted in placentas, birth fluids and vaginal discharges. Airborne spread from contaminated environments is considered central. Milk, faeces and other routes may also contribute depending on species and context. Subclinical infection and heterogeneous excretion may facilitate silent spread and delayed recognition.

  GAPS

  The relative importance of the different transmission routes remains insufficiently quantified

  The roles of vertical transmission, oral exposure and non-pregnant animals in maintenance and spread remain incompletely understood.

  The role of breeding males, animal movements and introduction of untested animals in maintaining or spreading C. burnetii within and between small-ruminant herds remains insufficiently characterised and should be framed as a biosecurity and herd-introduction issue rather than as evidence for a major established venereal transmission route (Matthijs et al., 2025).

  The interpretation of faecal detection requires caution, as it may reflect true shedding in some settings, passive digestive passage, environmental contamination, or oral uptake from contaminated environments (Roest et al., 2013).

  The contribution of exposure dose and route to infection outcome requires further study.

• Pathogenic life cycle stages

  C. burnetii follows a developmental cycle involving intracellular replication and extracellular survival forms. The SCV/LCV transition is central to infection and persistence.

  GAPS

  The in vivo significance of the different developmental stages for pathogenesis, persistence and transmission remains incompletely understood.

  The role of developmental stage transitions in placental infection, fetal involvement, mammary persistence or environmental contamination remains insufficiently characterised.

  Experimental models allowing physiologically relevant study of the ruminant maternal–fetal interface and C. burnetii infection remain limited.

• Signs/Morbidity

  Ruminant (main focus)

  Infection in non-pregnant ruminants is usually asymptomatic or subclinical. In pregnant animals, infection may lead to placentitis, abortion, stillbirth and weak offspring, especially in late gestation. Abortion is the most firmly established clinical manifestation. Other reproductive disorders, including infertility and metritis, have been suggested but remain less clearly demonstrated. Associations with mastitis or mammary disorders are heterogeneous and should not be interpreted as a clear causal link without supporting evidence..Clinical expression may vary according to host species, pregnancy status, immune background, production system, geography and possibly bacterial strain/genotype, but these factors are difficult to disentangle in field conditions.

  Documented clinical expression in domestic ruminants is mainly centred on reproductive and production-related outcomes, especially abortion, stillbirth and weak offspring. This does not necessarily mean that C. burnetii pathogenic effects are biologically limited to these manifestations; it also reflects surveillance priorities, diagnostic triggers and the economic relevance of reproductive disorders in livestock systems.

  Other animal species (including ticks) Clinical disease or reproductive disorders may occur in some non-ruminant, captive or wild mammals, but available evidence is more fragmented and should not be extrapolated to domestic ruminants without caution.

  Human aspects (brief, contextual)The apparent contrast between the broad human clinical spectrum and the more reproduction-centred animal disease profile should be interpreted cautiously, as animal investigations are often triggered by reproductive or production impacts. In humans, pregnancy-related outcomes potentially associated with C. burnetii may be under-recognised, particularly because early pregnancy losses are multifactorial and are not routinely investigated for Q fever outside documented exposure or outbreak contexts.

  GAPS

  Ruminant (main focus)

  The evidence linking C. burnetii to non-abortion reproductive disorders remains limited and heterogeneous. Causal mechanisms for non-abortion reproductive disorders remain poorly understood.Experimental data remain insufficient, especially in cattle and sheep.Species differences in morbidity and reproductive consequences require further clarification.The contribution of strain/genotype, geography, host species, immune status and management practices to clinical variability remains insufficiently characterised.For cattle, clinical attribution remains difficult because C. burnetii may be detected in milk or around calving without a clear clinical syndrome. Herd-level infection dynamics may be better captured by combined serology, PCR and cellular immunity approaches than by isolated clinical signs (Böttcher et al., 2024).

• Incubation period

  The incubation period in animals appears variable and is likely influenced by host species, gestation stage, route of exposure, infectious dose, immune status and possibly co-infections.

  GAPS

  The incubation period remains insufficiently defined in natural host conditions.

  More data are needed to clarify the role of host species, gestation stage, infectious dose, route of exposure, immune status, co-infections and clinical or subclinical infection context.

  Because many infected animals remain asymptomatic or subclinical, it is difficult to determine the incubation period under field conditions.

• Mortality

  Mortality is generally not observed in adult ruminants. Major losses are mainly related to abortion, stillbirth and perinatal weakness. In some goat outbreaks, very high reproductive losses may occur.

  GAPS

  The causes of death in weak-born offspring are not always clearly attributable to C. burnetii.

  The frequency and determinants of severe outcomes in different host species remain insufficiently documented.

• Shedding kinetic patterns

  Shedding patterns are heterogeneous and species-, matrix- and time-dependent.

  The highest bacterial loads are generally associated with placentas, birth products and periparturient vaginal excretion, particularly during abortion or clustered parturition events (Rousset et al., 2009; Alvarez-Alonso et al., 2018).

  Milk shedding may persist for prolonged periods, especially in cattle and goats. Faecal shedding has been reported in ruminants, but its frequency, duration and epidemiological significance remain variable and sometimes debated according to species, herd context and study design (Rousset et al., 2009; Böttcher et al., 2024; O’Shannessy et al., 2026).

  In small ruminants, longitudinal studies during successive kidding or lambing seasons show that active infection, shedding and environmental contamination can persist beyond the initial abortion episode, although patterns may change over time and under control measures (Alvarez-Alonso et al., 2018; Alvarez-Alonso et al., 2020; Zendoia et al., 2024).

  In cattle, persistent and intermittent shedding may occur, including through milk and around calving, and individual persistent animals may complicate identification of herd-level circulation and interpretation (Böttcher et al., 2024; O’Shannessy et al., 2026).

  Heterogeneous shedding, including in apparently asymptomatic situations, contributes to silent spread and complicates surveillance (Rousset et al., 2009; Muleme et al., 2017b; Alvarez-Alonso et al., 2020).

  GAPS

  Shedding kinetics remain insufficiently characterised in cattle, sheep and goats, especially in asymptomatic situations, outside abortion waves and under different management or vaccination contexts.

  The duration, intermittence and epidemiological significance of the different shedding routes require better definition by species and matrix.

  Periparturient dynamics are particularly important in small ruminants, as seroconversion and shedding patterns around kidding or lambing may reveal active transmission periods and help explain environmental contamination during clustered parturition events (Muleme et al., 2017a; Alvarez-Alonso et al., 2018; Alvarez-Alonso et al., 2020).

  Faecal detection has been reported, but its biological origin and epidemiological significance remain difficult to interpret, as it may reflect true shedding, passive digestive passage, environmental contamination, or oral uptake from contaminated environments (Roest et al., 2013).

  The relationship between individual immune responses, serological status and actual shedding remains imperfectly understood, especially in cattle (Böttcher et al., 2024; O’Shannessy et al., 2026).

  Data remain scarce for pets, wildlife and other non-ruminant species.

• Mechanism of pathogenicity

  Ruminant (main focus)

  The main lesion in ruminant abortion is a necrotising placentitis with abundant bacteria in trophoblasts. Experimental infection in pregnant goats supports the role of placental colonisation, trophoblastic localisation and placental lesions in abortion pathogenesis (Sánchez et al., 2006).

  Foetal lesions are less frequent and less specific. The placenta is the key pathological site explaining major excretion at parturition or abortion.

  In cattle, the mammary gland may also be an important site linked to prolonged or intermittent milk shedding, but its role in persistence and transmission is less clearly understood than placental pathogenesis (O’Shannessy et al. 2026; Böttcher et al. 2024). In one naturally infected and vaccinated dairy goat identified as an intermittent milk shedder, C. burnetii DNA was detected in mammary gland tissue and teat cistern, and bacterial antigen/cells were confirmed in mammary epithelial cells by immunohistochemistry and FISH (Bauer et al., 2024).

  Other animal species

  In some non-ruminant wild mammals, C. burnetii infection may also be associated with placental lesions; for example, multifocal placental lesions have been described in northern fur seals from a population with high placental prevalence of C. burnetii, although the consequences for fetal survival or population dynamics remain uncertain (Conway et al., 2022).

  GAPS

  Ruminant (main focus)

  How and where C. burnetii persists in non-pregnant animals remains poorly understood.

  The mechanisms triggering renewed bacterial multiplication in the placenta are still unclear.

  The extent to which fetal infection occurs systematically during C. burnetii-associated abortion remains insufficiently characterised. It is unclear whether fetal involvement is consistent, variable or secondary to placental damage, and how it relates to bacterial load, gestational stage and lesion distribution.

  The dynamics of fetal organ colonisation remain poorly understood, including whether bacterial dissemination follows reproducible tissue tropism or occurs heterogeneously according to gestational stage, placental lesion severity, bacterial load or host factors.

  The mechanisms underlying mammary gland persistence, particularly in dairy cattle and goats, and the contribution of intermittent milk shedding to within-herd and zoonotic transmission remain poorly understood.

  The tissue or biological origin of faecal shedding remains poorly defined, limiting interpretation of its role in pathogenesis, environmental contamination and transmission.

  The contribution of strain/genomic variation, bacterial virulence-related features and host factors to pathogenicity remains insufficiently defined, particularly for placental lesions, fetal involvement and mammary persistence or faecal shedding in ruminants.

  Human aspects (brief, contextual)

  Human genomic studies suggest associations between some genomic or plasmid profiles and clinical presentations, but the extent to which these observations translate to ruminant reproductive pathogenesis remains unclear (Abou Abdallah et al. 2022; Brangsch et al. 2026).

• Zoonotic potential

• Reported incidence in humans

  Q fever occurs worldwide in humans, but reported incidence varies greatly between countries, regions and over time. This variation reflects true epidemiological and outbreak occurrence differences, but also differences in surveillance, disease awareness, diagnostic laboratory methods and interpretation, case definitions, notification procedures and reporting systems. In many settings, most cases are sporadic or occur in small outbreaks, while major outbreaks remain uncommon.

  GAPS

  Human incidence remains underestimated in many settings because of underdiagnosis and underreporting.

  Comparability between countries is limited by heterogeneous surveillance system, case definitions, diagnostic practices and notification pathways.

  Reported incidence should therefore be interpreted cautiously and should not be used alone to infer the true burden of infection or the intensity of zoonotic transmission.

• Risk of occurence in humans, populations at risk, specific risk factors

  Human infection occurs mainly through inhalation of contaminated aerosols or dust originating from infected animal sources or other contaminated environments. Living near infected farms, occupational exposure and contact with parturient or aborting animals are major risk factors.

  Q fever also occurs in people without direct animal contact, likely through indirect environmental exposure, including windborne dispersal of contaminated aerosols or dust. Climatic and environmental conditions may modulate exposure.

  At-risk populations include highly exposed persons, such as livestock farmers, veterinarians, abattoir workers, animal-health workers, laboratory staff and people living near infected farms or contaminated environments. Visitors to animal-associated settings may also be exposed in specific contexts.

  In endemic or wildlife-interface settings, occupational risk may also extend beyond traditional livestock-related occupations. In a North Queensland retrospective review, landscapers represented 15.9% of respondents with Q fever, suggesting that outdoor workers exposed to soil, dust, vegetation, wildlife-contaminated environments or dry organic material may require attention in selected contexts (Sivabalan et al., 2017). This finding should be interpreted cautiously because the study was retrospective, had a small sample size and no control group.

  Groups at increased risk of severe outcomes or persistent focalized Q fever include people with pre-existing valvular or vascular conditions, vascular prostheses or aneurysms, and immunocompromised patients. Pregnant women should be considered separately because of potential adverse pregnancy outcomes.

  The relative contribution of manure, pets and raw milk products and tick exposure to human Q fever occurrence remains context-dependent and debated.

  GAPS

  The contribution of different exposure pathways remains insufficiently quantified.

  In many settings, a proportion of human cases remain without an identified source of infection, and the spatial epidemiology of exposure remains only partially explained, as illustrated by recent seroprevalence data from Israel (Ghanem-Zoubi et al, 2024).

  The relative contribution of manure, pets, raw milk products, tick exposure, contaminated environments and non-occupational exposure settings remains insufficiently quantified.

  Improved source attribution is needed to better link human cases to animal and environmental sources.

• Symptoms described in humans

  Most human infections are asymptomatic. Symptomatic acute Q fever typically presents as a febrile flu-like illness; pneumonia or hepatitis may occur. A minority of patients develop persistent focalized infections, including endocarditis, vascular infection and, less commonly, osteoarticular infection or granulomatous hepatitis. Rare manifestations, including lymphadenitis, pancreatitis and cholecystitis, have been reported. Post-infectious fatigue syndromes have also been described.Clinical presentation may vary geographically. In Spain, a systematic review found pneumonia to be reported more frequently in northern areas, whereas isolated fever and hepatitis were more frequent in central and southern areas (Alende-Castro et al., 2018). These differences may reflect exposure settings, diagnostic practices, host factors or circulating strains, but should not be interpreted as direct evidence for a specific transmission route.Pregnancy-related outcomes and post-infectious or immune-mediated manifestations remain incompletely recognised and insufficiently quantified (Baud & Greub, 2011; Ghanem-Zoubi & Paul, 2020; Melenotte et al., 2018).

  GAPS

  The factors influencing symptom patterns, disease severity and long-term outcome remain incompletely understood.The clinical significance of strain diversity, route of infection, exposure dose and host factors remain to be clarified.

  Important knowledge gaps remain regarding the pathogenesis and burden of post-Q fever fatigue syndrome and the frequency and variability of pregnancy-related outcomes.Sequelae after acute disease, including post-Q fever fatigue syndrome and progression to persistent focalized infection in susceptible patients, remain incompletely understood and insufficiently quantified.

  Recent Spanish data suggest high diversity of C. burnetii genotypes in human clinical cases and a possible geographical pattern between molecular variability and clinical signs, but this association requires further investigation and should not be interpreted as causal at this stage (Gil-Zamorano et al., 2025)

• Estimated level of under-reporting in humans

  Because the disease is underreported, scientists cannot reliably assess how many cases of Q fever have actually occurred worldwide. The current method for the diagnosis of Q fever in humans is largely based on serology (IFA, ELISA). The early diagnosis, before antibodies appear, is performed by PCR on blood or respiratory material. Acute Q fever is on the EU list of notifiable infectious diseases, but not all countries comply with this. For example in France and Denmark, Q fever is not notifiable.

  GAPS: Lack of microbiological testing in patients presenting with community-acquired pneumonia.

• Likelihood of spread in humans

  Human-to-human transmission is considered rare and epidemiologically anecdotal. Most human cases result from exposure to animal or environmental sources.

  In ordinary Q fever settings, humans should not be regarded as an epidemiological amplifier and are better viewed as a dead-end host from a population-transmission perspective.

  Person-to-person or human-source transmission routes have been described or suspected, including obstetric or delivery-related exposure, vertical transmission, transfusion, transplantation, sexual transmission, autopsy-related exposure and other nosocomial situations. However, these routes do not appear to drive sustained human-to-human spread (Koehler et al., 2019).

  GAPS

  Rare transmission routes, including obstetric exposure, transfusion, transplantation or sexual transmission, and other nosocomial contexts, remain only partly characterised.

  Their practical significance for public health appears limited and non-structuring, but may require infection-control awareness in specific clinical or laboratory contexts.

• Impact on animal welfare and biodiversity

• Both disease and prevention/control measures related

  Q fever may affect animal welfare mainly through abortion, reproductive losses and associated management measures.

  Some control measures, including culling, movement restrictions, repeated handling, isolation, vaccination campaigns, chemical disinfection or other environmental interventions, may also affect animal welfare, farm management and the environment.

  These impacts are context-dependent and may vary according to outbreak size, production system, control strategy and the proportionality of the measures implemented.

  Control measures should consider not only target-pathogen reduction, but also possible effects on animal welfare, environmental microbial communities, farm practices and ecosystem balance.

  From a One Health perspective, poorly controlled Q fever may also have indirect human and social consequences.

  GAPS

  The welfare consequences of both disease and control measures remain insufficiently documented.

  The environmental effects of repeated chemical disinfection and related management practices require further evaluation, including whether disinfectant performance under field conditions reflects experimental evidence.

  Beyond target-pathogen reduction, the environmental consequences of repeated disinfection practices, including possible effects on environmental microbial communities, require further evaluation.

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

  Data on the impact of Q fever on endangered wildlife are very limited. Infection has been detected in some wild species, but population-level consequences are poorly documented.

  Occasional reports suggest that C. burnetii may be associated with reproductive disorders in endangered captive ungulates, including North African gazelles, but available evidence remains case-based and insufficient to quantify conservation impact (García et al., 2017). In northern fur seals from St. Paul Island, Alaska, placental C. burnetii infection and associated lesions have also been described in a declining population, but the consequences for fetal survival, recruitment or population dynamics remain uncertain (Conway et al., 2022).

  GAPS

  The occurrence and impact of C. burnetii in endangered wild species remain largely unknown.

  Systematic wildlife surveillance data are lacking, and the consequences of infection for reproductive success, captive breeding programmes and conservation management remain insufficiently characterised.

• Slaughter necessity according to EU rules or other regions

  Slaughter or culling is not generally mandatory for Q fever control.

  However, targeted culling has been used in exceptional outbreak situations, notably during the Dutch epidemic in 2009–2010, where pregnant dairy goats and dairy sheep on infected farms were culled as part of a broader control strategy including vaccination, bulk milk monitoring, movement restrictions and other control measures (Roest et al., 2011).

  This should be interpreted as an exceptional, high-impact public-health and animal-health response, not as a standard or generally recommended Q fever control measure.

  GAPS

  The epidemiological, animal-welfare, social and economic value of culling in different outbreak contexts remains insufficiently documented.

  No harmonised approach exists across countries, and the place of culling within integrated control programmes remains difficult to compare across settings.

  The proportionality of culling compared with other measures — vaccination, movement restrictions, enhanced surveillance, hygiene and environmental management — remains difficult to assess retrospectively, especially when several measures are implemented simultaneously.

• Geographical distribution and spread

• Current occurence/distribution

  Q fever is globally distributed in humans and animals, and C. burnetii infection is considered widespread, although it is apparently absent from New Zealand (Eldin et al., 2017).

  However, documented occurrence remains uneven across regions, reflecting both true epidemiological differences and differences in diagnostic access, surveillance capacity, awareness and reporting pratices (EFSA/ECDC, One Health Zoonoses Report; Hurtado et al., 2026, Supplementary Note S2).

  GAP

  Reliable prevalence data are lacking for many countries and regions.

  Comparability is limited by heterogeneous surveillance and diagnostic strategies, especially where testing is unavailable, unaffordable or rarely performed despite close human–animal interfaces (Hurtado et al., 2026, Supplementary Note S2).

  The historical pathways of introduction and establishment of C. burnetii in different regions remain incompletely documented.

• Epizootic/endemic- if epidemic frequency of outbreaks

  C. burnetii infection in animals is enzootic in many countries, particularly in ruminants. Epizootic events, especially abortion-related or parturition-associated shedding episodes, may occur under favourable epidemiological and environmental conditions.

  Their frequency remains difficult to quantify because systematic animal surveillance is often limited or lacking.

  Human Q fever outbreaks are less common than silent animal circulation. They may appear as sporadic cases, small clusters or, more rarely, large outbreaks. Large human outbreaks are usually linked to substantial shedding from infected ruminants and environmental exposure, whereas smaller clusters are more regularly observed and may have diverse or unidentified sources.

  Recent European outbreak reviews show that human Q fever outbreaks occur in heterogeneous settings, including traditional livestock-related contexts, community settings, public-facing animal settings, and non-traditional occupational environments. Many community outbreaks are linked to indirect exposure through environmental contamination, windborne spread or fomites, whereas direct animal or tissue contact is more typical of traditional occupational exposure (Hurtado et al., 2026).

  GAPS

  The drivers of transition from endemic animal circulation to epizootic or outbreak situations remain insufficiently understood.

  Human Q fever outbreak frequency remains difficult to quantify and compare across settings because surveillance systems, reporting practices and investigation intensity are heterogeneous.

  More comparable data are needed on outbreak frequency in different production and ecological systems.

  The influence of livestock intensification, herd density, animal movements, herd connectivity and trade-related introductions on C. burnetii circulation and epizootic dynamics remains insufficiently documented.

• Seasonality

  Yes due to seasonality of small ruminant kidding. Higher seroprevalence is reported when time spent in stable increases.

• Speed of spatial spread during an outbreak

  Spatial spread may be rapid under some conditions, especially when airborne or dust-mediated dispersal is facilitated by meteorological and environmental factors. However, spread is highly context-dependent.

  Outbreak occurrence depends on local combinations of animal infection pressure, parturition or abortion events, environmental contamination, proximity to exposed populations, weather conditions, landscape features, built environment and human behaviour. Outbreaks may occur when high-shedding ruminant events take place close to exposed human populations, as illustrated by the Jena outbreak linked to sheep farming near residential areas (Gilsdorf et al., 2008; Boden et al., 2014).

  Indirect exposure pathways may also contribute to spatial spread, including contaminated equipment or clothing, fomites, animal transport, animal products or waste, and public-facing animal or farm-like settings (Hurtado et al., 2026).

  Windborne or dust-mediated spread has been implicated in several outbreaks, but its spatial extent depends on local meteorological and topographical conditions (Tissot-Dupont et al., 2004). GIS-based and modelling approaches can help assess likely sources and the plausibility of airborne spread, as shown in Dutch and UK outbreak investigations (Schimmer et al., 2010; Wallensten et al., 2010).

  GAPS

  The influence of host species, herd/flock density, production system, weather, topography, land use, built environment and human behaviour on spatial spread remains insufficiently quantified.

  The relative contribution of animal infection pressure, weather conditions, landscape, farm management, environmental persistence, built environment and human behaviour remains insufficiently characterised across settings.

  Outbreak investigations should avoid applying fixed distance thresholds without considering source strength, environmental conditions, local topography, vegetation, buildings, exposure behaviours and surveillance intensity.

• Transboundary potential of the disease

  Q fever is generally not managed as a classical rapidly spreading transboundary animal disease. Most outbreaks are driven by local or regional combinations of infected animal sources, shedding events, environmental contamination and human exposure.

  Airborne spread may occur over variable distances under favourable meteorological and topographical conditions, but this should not be equated with sustained cross-border spread.

  Transboundary relevance may nevertheless arise through animal movements, trade-related introductions, shared production systems, border-area outbreaks, and possible redistribution of C. burnetii strains. In some contexts, movement of asymptomatically infected animals, including ruminants or captive/zoo animals, may contribute to dissemination if infection status is unknown.

  The role of wildlife, birds, zoo animals and non-ruminant reservoirs in transboundary spread remains less clear and should be framed cautiously.

  GAP

  No harmonised protocols are available to define freedom from infection for trade purposes. Scenario-tree modelling work in Australian dairy goat herds illustrates that evidence of herd freedom from C. burnetii depends on combining surveillance components, assumptions on prior herd status and probability of introduction, but such approaches remain context-specific and are not harmonised internationally (Hou et al., 2023).

  The transboundary significance of wildlife, birds, zoo/captive animals and non-ruminant reservoirs remains insufficiently documented.

  The extent to which C. burnetii strains are introduced, redistributed or maintained through animal movements, herd connectivity, trade or production networks remains poorly characterised.

  Harmonised reporting, metadata standards and cross-sector data exchange are needed to better interpret cross-border relevance and support coordinated One Health responses.

• Route of Transmission

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

  Ruminant — main focus

  The main mode of transmission is through inhalation of contaminated aerosols or dust originating from reproductive fluids, placentas, birth products and contaminated environments.

  Introduction into herds or flocks may occur through movement of infected animals, while local spread is mainly facilitated by environmental contamination, airborne dispersal and contact with contaminated materials.

  Direct animal-to-animal transmission may occur in some contexts, but the relative contribution of contact transmission compared with environmental and airborne spread remains insufficiently defined.

  GAPS

  Ruminant — main focus

  Within-herd dynamics remain insufficiently understood, especially the role of non-pregnant animals.

  The relative contribution of animal movements, local airborne spread, contaminated materials and between-herd transmission remains insufficiently quantified.

  The possible role of reproductive materials, semen or shedding males in transmission within or between farms remains uncertain and should not be interpreted as an established major transmission route.

• Occasional mode of transmission

  Occasional or context-dependent transmission settings may include ticks, ingestion of raw milk or raw dairy products, contaminated pasture or feed, and other indirect exposures. Their epidemiological importance appears much less than airborne or environmental transmission.

  Occasional or contextual transmission settings include indirect exposure through contaminated dust, fomites, clothing or equipment, animal transport, animal products or waste, and contaminated occupational, recreational or public-facing environments. Recent outbreak reviews include examples such as waste-sorting plants, machine-tool factories, cardboard plants, pet courier services, natural caves, schools, prisons, animal facilities and cosmetics factories using ovine placental material. These should be interpreted as context-dependent exposure settings rather than as distinct primary biological transmission routes (Hurtado et al. 2026, Supplementary Note S4 / Table S2).

  Occupational exposure through contaminated animal fibre or dust should also be considered in specific settings. In a Belgian wool/goat-hair processing factory, airborne dust collected during goat hair processing contained C. burnetii DNA and workers showed high Q fever seroprevalence, supporting the relevance of industrial dust exposure in selected non-farm settings (Wattiau et al., 2011).

  Raw dairy products and ingestion may represent possible exposure routes, but their epidemiological significance remains debated. Experimental mouse studies show that oral infection is biologically possible, but less efficient than aerosol or injection routes, supporting cautious interpretation of ingestion as a secondary or context-dependent route rather than a major driver of Q fever epidemiology (Miller et al., 2020; Miller et al., 2021).

  Human-source routes, including obstetric exposure, transfusion, transplantation, sexual transmission and nosocomial contexts, and remain rare.

  GAPS

  The significance of occasional or indirect transmission routes remains insufficiently documented and poorly quantified.

  The epidemiological relevance of raw dairy products, contaminated pasture or feed, fomites, animal transport, waste, natural sites and non-traditional occupational settings requires further clarification.

  Unusual indirect exposure settings, including contaminated workplaces, animal transport environments, public-facing animal settings and natural or recreational sites, require better recognition during outbreak investigations, particularly when no direct animal contact is reported.

  The relative contribution of these occasional or indirect exposure settings remains difficult to quantify, because source attribution often relies on epidemiological links rather than integrated microbiological confirmation.

• Conditions that favour spread

  Spread is favoured by abortion or parturition events, high bacterial shedding, environmental contamination, dry and windy conditions, and certain high-density or high-contact husbandry situations.

  Clustered or synchronised parturition in intensive small-ruminant systems may amplify environmental contamination and transmission risk when multiple infected animals shed around the same period (Muleme et al., 2017).

  Spread may also be favoured by conditions that increase aerosolisation or exposure to contaminated materials, including manure handling, bedding, dust, housing configuration, animal movements, and close or repeated contact with birth products or contaminated environments.

  GAPS

  The relative contribution of climate, animal density, husbandry system, manure handling, transport and landscape factors remains insufficiently characterised.

  More integrated analyses are needed to understand combined risk scenarios.

  The nature of environmental carriers and particle-size fractions involved in the spread of C. burnetii remain insufficiently characterised. The respective roles of dust, aerosolised biological material, contaminated fomites and other environmental materials in local and longer-distance dissemination remain poorly quantified.

  The relative contribution of biological, environmental and management-related amplification factors remains insufficiently characterised across epidemiological settings.

• Detection and Immune response to infection

• Mechanism of host response

  Ruminant (main focus)

  Cell-mediated immunity appears important in the control of C. burnetii infection, but the respective roles of humoral and cellular responses in protection, persistence and shedding remain incompletely defined.

  In dairy cattle, recent longitudinal data suggest that immune-response orientation may contribute to shedding patterns: higher antibody titres were associated with later intermittent milk shedding, while IFN-γ responses appeared lower among milk shedders. These findings support a possible link between humoral/Th2-oriented responses and mammary persistence, but the relationship remains insufficiently confirmed (O’Shannessy et al., 2026).

  In ruminants, C. burnetii may localise in the mammary gland, uterus, placenta and associated lymphoid tissues. Immune responses vary according to infection stage, host species, reproductive status and possibly bacterial strain or genotype.

  GAPS

  Ruminant (main focus)

  The correlates of protective immunity remain insufficiently defined.

  The relationship between humoral responses, cell-mediated immunity, persistence and shedding requires further clarification, particularly for intermittent milk shedding and mammary gland persistence in dairy cattle.

  The significance of different antibody patterns in relation to infection stage, infectiousness and reproductive outcomes remains limited.

• Immunological basis of diagnosis

  Ruminant (main focus)

  Serology mainly informs on exposure and herd/flock-level circulation and may support surveillance. Antibody responses may follow infection or vaccination, and interpretation at individual level remains limited. Longitudinal work in goats shows that serological responses can help describe infection dynamics around kidding, including early seroconversion and subsequent shedding risk, but this does not make serology a direct marker of active shedding in every individual animal (Muleme et al., 2017).

  Phase I / Phase II serological distinctions are well established in humans, but their interpretation in ruminants remains less clear and insufficiently standardised. In cattle, phase-specific serology has been explored for epidemiological interpretation of herd-level infection status and infection dynamics, including in endemically infected dairy herds (Böttcher et al., 2011; Böttcher et al., 2024).

  In ruminants, serology mainly informs on exposure at herd level and does not reliably indicate active shedding, infectiousness or protection at individual level. Phase-specific serology has been explored in cattle to help identify chronic or occasional milk shedders, but its operational value remains insufficiently standardised and requires further validation before routine interpretation (Lucchese et al., 2015).

  Recent work suggests that combined interpretation of humoral and cell-mediated responses may improve understanding of shedding patterns. In dairy cattle, higher antibody titres were associated with later intermittent milk shedding, while IFN-γ responses appeared lower among milk shedders, supporting a possible link between humoral/Th2-oriented responses and mammary persistence; however, this relationship remains insufficiently confirmed (O’Shannessy et al., 2026).

  Current vaccines are non-DIVA, so serology cannot distinguish vaccinated from naturally exposed animals.GAPS

  Ruminant (main focus)

  The relationship between individual seropositivity and active shedding is variable, matrix-dependent and insufficiently predictive when used alone.

  The diagnostic and epidemiological value of Phase I / Phase II serology in ruminants remains insufficiently defined and standardised. Validated commercial assays allowing reliable separate phase-specific interpretation are lacking.

  The informative value of milk-based serology, including bulk tank milk serology, remains insufficiently characterised, particularly because milk matrices are more heterogeneous than serum and analytical performance data remain limited.

  Further work is needed to assess whether phase-specific humoral responses, alone or combined with cell-mediated immune markers, can support herd-level risk stratification and interpretation of persistent or intermittent shedding profiles (Böttcher et al., 2024; O’Shannessy et al., 2026).

  Cell-mediated immunity assays, such as ex-vivo IFN-γ recall assays, may complement serology for interpreting exposure or infection status in some ruminant contexts, including pre-purchase screening or situations with incomplete vaccination history, but they are not yet validated as routine diagnostic tools and require further standardisation and field evaluation (Matthijs et al., 2025).

  Better tools are needed to distinguish between vaccinated, previous exposure, current infection and active shedding status.

• Main means of prevention, detection and control

• Sanitary measures

  Sanitary measures mainly rely on management practices such as isolation of aborting or parturient animals, control of animal introductions, and hygiene measures around kidding, together with practical measures to reduce human exposure during high-shedding events, including restricted access, protective equipment and handling precautions.

  During high-shedding events or high-exposure interventions, respiratory protection (preferably a fit-tested FFP2/FFP3 or equivalent respirator), restricted access and careful handling of animals, birth products and contaminated materials should be prioritised for human protection. The Dutch culling experience showed that culling workers may remain at substantial risk of infection despite personal protective equipment, highlighting the need for clear procedures, training, compliance monitoring and consideration of vaccination where available for highly exposed workers (Whelan et al., 2011).

  GAPS

  The efficacy of individual sanitary measures and their respective contributions to disease control remain insufficiently documented.

  The effectiveness of measures intended to reduce human exposure during high-shedding events or high-exposure interventions remains poorly quantified. This includes personal protective measures, restricted access, animal and material handling procedures, and respiratory protection.

  Further evaluation is needed on implementation factors, including compliance, duration of exposure, work location, feasibility under field conditions, and husbandry conditions around kidding/lambing.

• Mechanical and biological control

  Mechanical and environmental control measures include safe disposal of placentas, aborted materials and birth products, cleaning and disinfection of washable, non-porous contaminated surfaces and equipment where feasible, and careful management of manure, litter, bedding and dust-generating practices.

  In farm environments, the practical scope of disinfection is limited because many contaminated matrices or surfaces — litter, bedding, manure, soil, dust, porous materials and rough surfaces — are not reliably amenable to standard cleaning and disinfection.

  Manure, litter and bedding may become contaminated when parturition or abortion occurs in housing areas, especially through birth products, vaginal fluids and contaminated bedding material.

  Practical manure-management recommendations may include forming a manure heap and delaying land application before spreading, in some contexts for several weeks or months, and preferably under conditions limiting aerosolisation. Covering manure heaps has also been proposed in some management contexts. However, these measures should be interpreted as precautionary management practices rather than as validated universal inactivation protocols for Coxiella burnetii.

  Composting, passive heating and other livestock-effluent management processes may contribute to reducing microbial loads, particularly when sufficient time–temperature conditions are achieved. However, their specific efficacy against viable and infectious C. burnetii remains insufficiently documented under field-relevant conditions. PCR detection after treatment or storage indicates DNA persistence and does not necessarily demonstrate bacterial viability or infectivity.

  Limited direct evidence nevertheless exists in a livestock matrix. In an experimental caprine infection model, calcium cyanamide treatment of slurry resulted in no detectable infectivity following mouse inoculation under defined conditions, providing proof of principle for chemical slurry decontamination, but not a validated routine field procedure (Arricau-Bouvery et al., 2001).

  Evidence from the Dutch outbreak suggests that land-applied goat manure probably played a minor role in human transmission compared with exposure near infected dairy goat farms, although manure may contain C. burnetii DNA (van den Brom et al., 2015). The relevance of manure, litter and bedding therefore depends on contamination level, handling practices, dust generation, storage conditions, composting dynamics, and exposure scenarios.

  GAPS

  The efficacy of mechanical and environmental control measures under field conditions remains insufficiently quantified.

  Clear evidence-based protocols for manure, litter, bedding, dust reduction, washable-surface decontamination and contaminated material management are still lacking.

  The effectiveness of recommended manure-management practices, including heaping, possible covering and delayed land application before spreading, remains insufficiently quantified for viable and infectious C. burnetii under field-relevant conditions.

  The effect of composting, passive heating and other effluent-management processes on viable and infectious C. burnetii in manure, digestates, litter, bedding and related natural matrices remains insufficiently documented.

  Practical methods to verify residual viability or infectivity of C. burnetii in manure, bedding or digestates before land application are lacking. Available evidence relies mainly on indirect epidemiological observations, experimental or extrapolated time–temperature data, culture attempts and PCR-based detection, which does not demonstrate infectivity.

  Practical methods to verify residual viability or infectivity of Coxiella burnetii in manure, bedding or digestates before land application are lacking. Although proof-of-principle evidence exists for calcium cyanamide treatment of slurry, operationally validated and contemporary field procedures for chemical, thermal or biological management of contaminated livestock matrices remain unavailable. Further studies should assess viable or infectious C. burnetii in slurry, manure, bedding, birth products, dust and digestates under realistic treatment conditions.

  The contribution of time–temperature conditions, moisture, pH, organic matter, pile size, aeration, covering, turning and matrix composition to C. burnetii inactivation remains poorly characterised.

• Diagnostic tools

  Ruminant — main focus

  For abortion investigations, matrix selection should be fit-for-purpose and balance diagnostic value, sample quality, biosafety, logistical feasibility and compatibility with multi-pathogen testing schemes.

  Fresh placental samples remain among the most informative matrices for supporting attribution of ruminant abortion to C. burnetii, especially when PCR detection is interpreted together with compatible pathological findings. Where available, histopathology and immunohistochemistry (IHC) can strengthen causal attribution by demonstrating C. burnetii antigen in compatible placental lesions (Van den Brom et al. 2025).

  However, placental colonisation may be heterogeneous. When available, sampling should preferably include several macroscopically affected or necrotic cotyledons from a fresh or nearly fresh placenta. Operationally, collecting several cotyledons, with three often used as a practical example, may reduce the risk of missing focal lesions or heterogeneous bacterial distribution.

  Vaginal swabs are often a practical and safer alternative when placenta or fetal tissues are unavailable, degraded or difficult to handle.

  They are particularly useful for documenting post-abortion or periparturient shedding, but their interpretation is time-dependent because bacterial load may decrease after abortion or parturition. Vaginal swabs should therefore not be regarded as universally equivalent to placental examination for attributing abortion to C. burnetii.

  Quantitative PCR interpretation may support abortion attribution when applied to relevant pathological matrices, including fresh placental cotyledons and early post-abortion vaginal swabs. The underlying principle is to assess whether C. burnetii is present at a bacterial load compatible with marked colonisation of the pathological site, rather than relying on qualitative detection alone. Such thresholds should be interpreted as operational, method-dependent decision criteria designed to improve diagnostic specificity, not as universally validated biological cut-offs for attributing abortion to C. burnetii (Gache et al., 2017; Sidi-Boumedine et al., 2010).

  Harmonised schemes or decision-making templates exist in some countries to define which tests to perform according to the clinical context. Surveillance objectives include identifying the etiological cause of abortion, detecting sources of shedding and monitoring environmental contamination.

  Environmental samples, including dust, may provide useful complementary information for herd/flock-level investigation, especially when interpreted together with animal sampling, reproductive history, serology and PCR on relevant matrices. However, environmental PCR should not be interpreted in isolation, as detection of C. burnetii DNA does not demonstrate viable bacteria, current shedding or direct zoonotic risk.

  Human aspects — brief, contextual

  In humans, PCR is most useful early in illness, ideally on blood collected before antibiotic treatment, whereas serology generally requires paired acute and convalescent samples for more reliable interpretation.

  For persistent focalized infection diagnosis requires integrated interpretation of serology, PCR when relevant, alongside clinical and imaging findings, rather than reliance on a single laboratory result.

  GAPS

  Ruminant — main focus

  Evidence remains insufficient to define harmonised matrix selection strategies according to diagnostic objective, sampling constraints and epidemiological context.

  The level of evidence required to attribute abortion to C. burnetii still varies between countries and laboratories.

  Further work is needed to harmonise how quantitative PCR results should be interpreted for abortion attribution, taking into account matrix type, sampling delay, analytical performance, lesion distribution, pathological findings and epidemiological context.

  More evidence is needed on placental sub-sampling strategies, including the number and type of cotyledons to sample, and on the kinetics of vaginal shedding after abortion or parturition.

  Diagnostic algorithms combining matrix choice, PCR quantification, histopathology, immunohistochemistry, lesion distribution and epidemiological context remain insufficiently harmonised across countries and laboratories.

  The diagnostic value of environmental matrices, including dust, remains insufficiently standardised. More evidence is needed to define when, where and how environmental samples should be collected, and how their PCR results should be interpreted in relation to animal shedding, abortion investigations and source attribution.

• Vaccines

  Ruminant — main focus

  Current veterinary vaccines for Q fever are limited to inactivated whole-cell Phase I vaccines.

  Vaccination may reduce abortion risk and shedding when used preventively, especially before first pregnancy or before known exposure. It should be framed as a useful component of integrated control rather than as a stand-alone control solution.

  Human aspects — brief, contextual

  Human vaccination is effective for prevention of human cases, but is currently available only in Australia.

  Integrated control should aim for sustainable risk reduction, balancing animal health, human exposure reduction, environmental integrity and feasibility for farmers.

  GAPS

  Ruminant — main focus

  The optimal vaccination protocols, duration of immunity, target populations and added value of vaccination in different epidemiological settings remain insufficiently defined.

  The comparative advantages and limitations of different vaccination strategies — including preventive vaccination before first pregnancy, vaccination of replacement animals, vaccination in already infected herds, and integration with monitoring programmes — require further evaluation across epidemiological settings.

  DIVA-compatible vaccination strategies are lacking.

  Sustained multi-year vaccination may be needed in some contexts, adding costs for farmers. The benefit–risk balance of vaccinating infected herds with substantial pre-existing natural immunity requires further evaluation.

• Therapeutics

  Ruminant — main focus

  No curative veterinary therapeutic strategy is currently available as a reliable routine control tool for Q fever at herd or flock level.

  Antimicrobial treatment is not considered a reliable control strategy for preventing abortion outbreaks or reducing shedding in small ruminants (Astobiza et al., 2010).

  Antimicrobial use should therefore remain restrictive when evidence of benefit for Q fever control is lacking.

  GAPS

  Ruminant — main focus

  The role of therapeutics in integrated control remains very limited.

  Validated alternatives to antimicrobials are lacking.

• Biosecurity measures effective as a preventive measure

  Ruminant — main focus

  Effective biosecurity includes safe handling of parturition products and aborted materials, personal protective equipment during high-risk tasks, control of animal introductions, separation of risky activities, visitor access management, and reduction of environmental contamination.

  Particular attention is needed for public-facing herds, open farms, zoos and lambing/kidding visitor contexts, where non-occupational exposure may occur.

  Biosecurity should also include control of animal introductions and breeding practices, including attention to purchased, borrowed or returning breeding males where farm health status or vaccination history is unknown (Matthijs et al., 2025).

  Human aspects — brief, contextual

  Vaccination of humans where available may contribute to protection of highly exposed occupational groups, but this remains a comparative One Health point rather than a routine veterinary control measure.

  GAPS

  Ruminant — main focus

  The relative importance of the different biosecurity measures remains insufficiently quantified.

  The reasons for poor implementation or limited compliance require further study.

  Farm-type-specific protocols tailored to different production systems, herd/flock sizes and management contexts are needed, taking into account herd size, production type, housing, manure management, visitor access and public-facing activities.

  The role of pre-introduction screening and management of breeding males in reducing C. burnetii introduction or spread remains insufficiently evaluated.

• Border/trade/movement control sufficient for control

  Ruminant — main focus

  Movement control may have some value for reducing the introduction or redistribution of C. burnetii, particularly when infected or potentially infected animals are introduced into naïve or low-prevalence herds.

  However, its effectiveness is limited by asymptomatic infection, environmental and airborne spread, intermittent shedding, incomplete knowledge of herd/flock status, and the absence of standardised freedom-from-infection protocols.

  Movement control should therefore be considered a complementary biosecurity and surveillance measure rather than a dominant control pillar.

  GAPS

  Ruminant — main focus

  Testing strategies for animal introduction, movement or certification remain insufficiently defined.

  The real value of movement control in different epidemiological, production and trade contexts remains insufficiently documented.

  Genotyping and genomic approaches may help clarify broad patterns of C. burnetii dissemination, including possible links with animal movements, but their current resolution is mainly macro-epidemiological. Further technical development, comparative genomic datasets and integration with movement and epidemiological data are needed before these tools can support fine-scale tracing or routine movement-control decisions.

• Prevention tools

  Ruminant — main focus

  Other preventive tools may include education, awareness raising, advisory support, and practical guidance for farmers, veterinarians and other exposed actors.

  In some contexts, additional prevention may also involve husbandry adjustments, farm organisation, housing or activity separation, and landscape-aware approaches aimed at reducing exposure to contaminated dust, aerosols or high-risk animal environments. These approaches should be considered exploratory and complementary.

  Vegetation barriers, farm architecture and landscape configuration are insufficiently documented for Q fever, but may deserve further investigation as potential ways to influence airflow, dust movement, exposure pathways and the interface between animal, human and environmental health.

  GAPS

  Ruminant — main focus

  The effectiveness and feasibility of these additional preventive tools remain insufficiently documented, including their contribution to risk reduction in different epidemiological and production settings.

  The potential role of farm architecture, vegetation, landscape configuration, dust control and airflow management in reducing exposure pathways remains poorly characterised.

  Further work is needed to assess whether such approaches can support sustainable risk reduction without being overinterpreted as validated control measures.

• Surveillance

  Ruminant — main focus

  Surveillance is crucial for prevention and control of Q fever. Passive surveillance based on abortion events remains central in many settings, but active or targeted surveillance may also be used depending on the objective.

  Surveillance objectives differ according to whether the aim is outbreak investigation, detection of shedding sources, monitoring of circulation, follow-up of control measures or reduction of zoonotic risk.

  Herd- or flock-level surveillance may rely on serology, PCR on bulk tank milk, pooled vaginal swabs, environmental or dust sampling, or repeated targeted sampling. Surveillance design should be adapted to the objective pursued. A single sample type or a single sampling time point may be insufficient because shedding can be intermittent, matrix-dependent and time-dependent after abortion or parturition. Multi-matrix and, where relevant, repeated sampling approaches may therefore be more informative than isolated testing for assessing herd/flock-level circulation.

  Bulk tank milk and environmental or dust sampling may contribute to herd/flock-level surveillance when used within a defined sampling design and interpreted alongside animal-level, herd-level and epidemiological data. Their value lies mainly in supporting broader assessment of C. burnetii circulation or environmental contamination, rather than in providing stand-alone evidence of viable infection, current shedding or zoonotic risk.

  Bulk tank milk can support cost-effective herd/flock-level surveillance in dairy systems, but its interpretation depends on species, production system, seroprevalence, shedding patterns and surveillance objective. BTM results may indicate exposure or circulation at population level, but are insufficient alone to determine active infection or current shedding at herd level; additional targeted animal or environmental sampling may be needed (Ruiz-Fons et al., 2011; Piñero et al., 2014).

  In vaccinated populations, interpretation of PCR-positive milk results shortly after vaccination may require caution. Vaccine-derived C. burnetii DNA has been detected transiently in milk after Coxevac® vaccination in a small experimental study, but this should be interpreted as a short-term PCR interpretation issue rather than evidence of vaccine shedding or active infection (Hermans et al., 2011).

  GAPS

  Ruminant — main focus

  Integrated vaccine-diagnostic strategies for future surveillance and control programmes are lacking.

  Method harmonisation, sensitivity and specificity evaluation, and interpretation at herd level remain insufficient.

  The relationships between sampling design, surveillance objective and epidemiological meaning remain insufficiently standardised.

  Scenario-tree modelling may support surveillance design for confidence in herd/flock freedom from infection but remains context-specific and not harmonised for routine use (Hou et al., 2023).

  The role of bulk tank milk screening in surveillance should be better defined, particularly regarding its applicability, interpretative value and comparability across settings.

  Further work is needed to define how BTM ELISA and PCR results should be interpreted according to species, herd/flock seroprevalence, shedding patterns, age structure, production system and surveillance objective.

  Environmental and dust-based surveillance strategies remain insufficiently harmonised. More evidence is needed to define sampling frequency, sampling location, interpretation of positive PCR results, and the relationship with current shedding, residual DNA and environmental persistence.

  A single matrix or a single sampling time point may miss intermittent shedding or, conversely, detect residual DNA after the main shedding event. Longitudinal and multi-matrix approaches are needed to improve interpretation of circulation, persistence and response to control measures.

  Follow-up in vaccinated populations remains a recurrent surveillance challenge.

  Silent spread, delayed recognition and under-detection remain major operational limitations.

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

  Ruminant — main focus

  Vaccination and combined control measures have reduced C. burnetii prevalence, shedding indicators or clinical problems in some settings, but eradication has not been consistently demonstrated and the specific contribution of each measure is often difficult to disentangle (Hogerwerf et al., 2011; van den Brom et al., 2015).

  Past experiences, such as the Netherlands epidemic, illustrate that large-scale integrated control may be possible, but can be costly, operationally demanding and associated with substantial economic and social costs. In the Dutch context, control included several combined measures, including vaccination, bulk tank milk monitoring, movement restrictions and exceptional culling of pregnant animals on infected farms (Hogerwerf et al., 2011).

  Vaccination appeared to contribute to reduced C. burnetii prevalence and shedding-related indicators, but its effect was assessed in a context that also included intensive surveillance and other control measures. Reported success or failure of control strategies may also depend on how infection is defined, detected and monitored in each country (van den Brom et al., 2015).

  GAPS

  Ruminant — main focus

  Comparative evidence on the success or failure of different integrated control strategies remains limited.

  Long-term documentation is needed on which integrated strategies are effective, proportionate and feasible under field conditions.

  The relative contribution of individual measures within combined control programmes remains difficult to quantify, especially when vaccination, movement restrictions, surveillance, hygiene measures and culling are implemented together.

  Criteria for adapting, maintaining or lifting control measures remain insufficiently harmonised.

• Costs of above measures

  Ruminant — main focus

  Control measures may generate substantial costs, including vaccination, surveillance, culling where implemented, movement restrictions, hygiene and environmental management, additional labour, communication burden and indirect costs related to implementation constraints, trade disruption or adverse effects of interventions.

  Economic modelling in Dutch dairy goat herds suggests that control-strategy costs vary strongly by measure and context, and that conclusions depend heavily on assumptions about infection dynamics, herd management and human cases averted (van Asseldonk et al., 2015).

  These costs may affect farmers, veterinary services, public authorities and, indirectly, exposed communities. The economic impact depends strongly on production system, outbreak size, control strategy, duration of measures and compensation mechanisms.

  GAPS

  Ruminant — main focus

  The costs of different control options remain insufficiently documented.

  Comparative cost-effectiveness analyses of integrated control strategies remain limited across species, production systems and control contexts.

  The distribution of costs and benefits between farmers, veterinary services, public authorities and public-health systems remains insufficiently characterised.

• Disease information from the WOAH

• Disease notifiable to the WOAH

  Infection with Coxiella burnetii is included in the WOAH Terrestrial Animal Health Code as Chapter 8.22.

• WOAH disease card available

  Direct links to the WOAH.

• WOAH Terrestrial Animal Health Code

  Direct links to the WOAH.

  Chapter 8.22 — Infection with Coxiella burnetii (Q fever), first adopted in 2024.

  Chapter 8.22.

• WOAH Terrestrial Manual

  Direct links to the WOAH.

  Chapter 3.1.18 (2018)

• Socio-economic impact

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

  Human / One Health main focus

  Q fever is a worldwide zoonosis. In Europe, most human cases are sporadic or occur in small outbreaks, but large outbreaks may occur under favourable epidemiological and environmental conditions. The 2007–2010 epidemic in the Netherlands remains the main European benchmark in terms of public-health impact.

  The incidence and burden of Q fever remain underestimated in many countries because of underdiagnosis, underreporting, non-specific symptoms and heterogeneous surveillance systems.

  The burden of Q fever can be expressed in disability-adjusted life years (DALYs), years of healthy life lost, healthcare use, absenteeism, persistent focalized infections and post-infectious fatigue. Using the BCoDE approach, Q fever was identified as a disease with a non-negligible burden in the Netherlands, notably because of long-term sequelae such as persistent Q fever and post-infectious fatigue.

  Important clinical outcomes may still be insufficiently quantified, including adverse pregnancy outcomes, persistent focalized infections, post-infectious fatigue and other incompletely recognised manifestations. This may contribute to underestimation of Q fever burden, especially in endemic settings.

  EU-level monitoring is available through the annual EU One Health Zoonoses Reports, but these surveillance outputs should be interpreted cautiously because reporting systems and diagnostic practices differ between countries. EU-level human Q fever data were included in previous EU One Health Zoonoses Reports up to 2023, whereas recent reports mainly provide animal and environmental data on Coxiella burnetii. Human burden estimates therefore remain dependent on national surveillance systems, diagnostic practices, notification pathways and reporting coverage.

  GAPS

  Human / One Health main focus

  Comparable and up-to-date burden estimates, including DALYs and long-term sequelae, are lacking for most countries.

  The frequency, long-term impact and public-health significance of post-infectious fatigue, persistent focalized infection and pregnancy-related outcomes remain insufficiently documented (Ghanem-Zoubi et al, 2020).

  The frequency and public health significance of small clusters outside major outbreaks should be better documented.

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

  Human / One Health main focus

  The Dutch Q fever epidemic remains the main benchmark for documented human health costs in Europe. Published estimates included substantial healthcare-related costs and additional productivity losses, particularly when persistent focalized infections, chronic Q fever, post-infectious fatigue and other long-term outcomes are considered.

  Human costs are not limited to acute Q fever treatment. They may include delayed diagnosis, medical consultations, laboratory testing, hospitalisation, long-term antibiotic treatment, imaging, follow-up of at-risk patients, management of persistent focalized infections, post-infectious fatigue, absenteeism and reduced productivity.

  Hospital-based data from Spain illustrate that severe or hospitalised Q fever cases can generate substantial healthcare costs: among 4,214 hospitalised patients recorded between 1998 and 2015, the mean hospital stay was 13.8 days and the total mean cost was estimated at approximately €154 million, although such data capture only hospitalised cases and therefore do not reflect the full burden of infection (Rodríguez-Alonso et al., 2020).

  In the Netherlands, targeted screening for chronic Q fever after the 2007–2010 epidemic has been evaluated economically. Model-based work suggested that cost-effectiveness varied strongly by risk group and geographical exposure, with screening of cardiovascular-risk patients in high-incidence areas ranging from cost-saving to moderate cost per QALY gained depending on assumptions (de Boer et al., 2020).

  A later targeted screening programme in Dutch general-practitioner practices detected chronic Q fever patients ten years after the outbreak and was still estimated to be cost-effective in certain high-risk groups, showing that long-term follow-up costs and benefits may persist long after the acute outbreak phase (Reukers et al., 2022).

  GAPS

  Human / One Health main focus

  Comparable and up-to-date cost estimates for human Q fever are lacking for most countries.

  The long-term economic impact of persistent focalized infections, chronic Q fever, post-infectious fatigue, pregnancy-related outcomes and other sequelae remains insufficiently documented.

  Human cost estimates are likely underestimated where Q fever is underdiagnosed, underreported or inconsistently notified, and where analyses capture only hospitalised or laboratory-confirmed cases.

  More evidence is needed on the cost-effectiveness of targeted follow-up and screening strategies for high-risk groups after outbreaks or in endemic areas.

• Direct impact (a) on production

  Ruminant — main focus

  The direct impact on production is variable and is mainly related to abortion losses, stillbirths, weak offspring, neonatal losses and other reproductive consequences, with possible additional difficulties in rearing kids or lambs in some settings.

  The magnitude of production losses depends on species, herd/flock status, production system, abortion rate, fertility effects, timing of detection and control, and the management measures implemented. Farm-level economic tools may help assess context-specific production impacts, especially in dairy cattle, but their outputs should not be generalised across ruminant species or production systems (Raboisson et al., 2024).

  Milk production effects may occur in some contexts but should not be overgeneralised, as available evidence remains heterogeneous and species- or system-dependent.

  GAPS

  Ruminant — main focus

  The real economic impact of Q fever on animal production remains insufficiently quantified across species and production systems.

  The contribution of fertility-related disorders, neonatal losses, reduced offspring viability, rearing difficulties and other non-abortion outcomes remains uncertain.

  More comparable data are needed to assess production losses according to species, herd/flock status, production type, infection dynamics and control strategy.

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

  Ruminant / One Health main focus

  Control measures may generate substantial private and public costs, including vaccination, surveillance, culling where implemented, hygiene and environmental management, movement restrictions, administrative coordination, communication, and compensation mechanisms.

  The Dutch epidemic remains the best documented example of large-scale Q fever control costs. Economic modelling in Dutch dairy goat herds suggests that control-strategy costs vary strongly by measure and context, and that conclusions depend heavily on assumptions about infection dynamics, herd management and human cases averted (van Asseldonk et al., 2015).

  Control costs are not distributed equally across actors. Farmers may bear immediate and visible costs, while public-health benefits, avoided human disease burden and societal benefits may occur later and be more difficult to quantify.

  GAPS

  Ruminant / One Health main focus

  The costs of containment, culling where implemented, and integrated control measures remain insufficiently documented in most settings.

  Comparative cost-effectiveness data for different control strategies are limited.

  The respective contribution of individual measures to overall cost and effectiveness is difficult to disentangle when vaccination, surveillance, movement restrictions, culling, hygiene and environmental measures are implemented together.

  The distribution of costs and benefits between farmers, veterinary services, public authorities and public-health systems remains insufficiently characterised.

• Indirect impact

  One Health / socio-economic focus

  Indirect impacts may include movement restrictions, manure and bedding management constraints, disruption of farm organisation, farm access restrictions, public access limitations to farms or recreational sites, and potential effects on trade or market confidence.

  Their magnitude appears highly context-dependent and may vary according to production system, outbreak size, control measures, public perception, compensation mechanisms and the economic role of livestock in the affected community (van Asseldonk et al. 2015).

  In smallholder or low-resource farming systems, indirect impacts may extend beyond production losses, because goats and other ruminants can contribute to household income, food supply and rural livelihoods. In such settings, limited access to veterinary services, diagnostics, vaccines, compensation or markets may increase the social and economic consequences of control measures (Burns et al. 2023).

  GAPS

  One Health / socio-economic focus

  Indirect costs related to manure management, movement restrictions, farm access restrictions and potential trade effects remain poorly quantified.

  The broader socio-economic impact beyond direct herd losses and formal control costs should be better documented.

  More evidence is needed on how indirect impacts are distributed between farmers, public authorities, downstream sectors, local communities and public-health systems.

  The feasibility and acceptability of control measures in smallholder, low-resource or market-fragile systems remain insufficiently characterised.

• Trade implications

• Impact on international trade/exports from the EU

  Q fever is generally not considered a major trade-driven transboundary disease.

  Direct impact on international trade appears limited in most contexts. A specific WOAH Terrestrial Animal Health Code chapter on infection with Coxiella burnetii was adopted in 2024. This chapter defines the occurrence of infection in susceptible animals, but does not provide a detailed operational protocol for trade certification, surveillance or control.

  In the WOAH Terrestrial Manual, diagnostic methods are listed according to different intended purposes. For Q fever in domestic ruminants, however, available methods are generally more informative at herd/flock or population level than at individual-animal level. They are therefore not well suited to certifying individual animal freedom from infection prior to movement.

  Some importing countries may nevertheless request Q fever-related guarantees for live animals or reproductive materials. Such requirements appear heterogeneous and are not supported by universally harmonised sampling and testing protocols for demonstrating freedom from infection.

  GAPS

  The practical impact of Q fever on international trade and export requirements remains poorly documented.

  The extent to which importing countries apply specific guarantees or additional requirements should be better characterised.

  No universally harmonised, operationally applicable sampling and testing strategy appears to be established for demonstrating Q fever-free status in trade contexts, especially at individual animal level.

  Further work is needed to clarify how herd/flock-level surveillance, matrix choice and test interpretation could support trade-related guarantees without overinterpreting individual test results.

• Impact on EU intra-community trade

  Direct impact on intra-EU trade appears limited in most situations.

  Coxiella burnetii infection is listed under the EU Animal Health Law framework as a category E disease for listed ruminant species, meaning that surveillance is required within the Union. This supports EU-level reporting and comparability, but does not in itself establish harmonised movement restrictions or a trade-certification pathway for Q fever-free status.

  EU-level surveillance may support comparability and awareness of animal infection, but it does not currently provide a harmonised operational framework for demonstrating freedom from infection for trade purposes.

  GAPS

  The practical implications of EU surveillance obligations for animal movements and intra-EU trade remain insufficiently documented.

  Greater clarity is needed on how category-E surveillance data may influence movement management, certification practices or risk-based decisions in different Member States.

  The extent to which national authorities or trading partners use Q fever data in movement-related decisions remains poorly characterised.

• Impact on national trade

  Impact on national trade is generally limited, although movement restrictions or precautionary measures may apply in some situations involving infected herds/flocks or outbreak investigations.

  Their practical and economic significance is likely to vary according to production sector, outbreak context and national policy context.

  GAPS

  The economic and operational consequences of national movement restrictions or precautionary measures remain poorly documented.

  Their impact may differ according to production sector, outbreak context and national policy framework.

• Links to climate

  Seasonal cycle linked to climate

  Wind and dry environmental conditions may favour aerosolisation and spread of Coxiella burnetii from contaminated animal sources.

  Seasonal patterns are therefore likely to depend on the interaction between meteorological conditions, animal reproduction periods, housing practices, land use and environmental contamination. In southern France, an unusual winter increase in human Q fever cases was associated with increased mistral frequency after the main lambing season, illustrating how wind, rainfall and lambing periods may combine in specific settings (Tissot-Dupont et al., 2004).

  However, seasonal patterns should not be reduced to dry, dusty and windy conditions alone. In an endemic region of North Queensland, a retrospective study reported a non-significant trend towards more Q fever diagnoses during seasons with higher rainfall, and discussed a possible pathway whereby rainfall may increase vegetation and wildlife presence, followed by conditions favouring environmental exposure or aerosolisation (Sivabalan et al., 2017). This supports a context-dependent interpretation of meteorological drivers rather than a single climatic model.

  GAPS

  The combined influence of wind, humidity, temperature, rainfall, dry periods, surface conditions, animal reproduction periods and housing practices on transmission remains insufficiently characterised across settings.

  The role of seasonal climatic conditions should be better studied in relation to specific epidemiological settings and husbandry systems.

  The interaction between kidding/lambing periods, housing conditions, pasture/outdoor management and aerosolisation risk remains insufficiently documented.

• Distribution of disease or vector linked to climate

  Environmental and climatic factors, especially wind, dry conditions, temperature and landscape features, may influence the spatial distribution of observed Q fever risk (Clark & Soares Magalhães, 2018; De Rooij et al., 2019). Their effects are likely to interact with animal density, husbandry systems, wildlife ecology, land use and landscape characteristics.

  Airborne dispersal from livestock holdings to human communities is influenced by urbanisation level, ruminant species, stocking density, wind speed and other landscape or environmental features (Clark & Soares Magalhães, 2018).

  Spatial analyses and quantitative microbial risk assessment approaches developed after the Dutch epidemic have improved understanding of source identification, exposure assessment and risk characterisation, but their operational value depends on accurate, structured and rapidly shared data (De Rooij et al., 2019).

  Recent spatiotemporal analyses in French Guiana illustrate how remote-sensing and georeferenced data can help identify local risk configurations, including forest interfaces, wildlife observations, slaughterhouse proximity, housing conditions and spatial clustering of human cases. These findings should be interpreted as context-specific and hypothesis-generating rather than as a general model of Q fever distribution (Desmoulin et al., 2026).

  Risk-mapping approaches in other ecological contexts, such as a national cattle serosurvey in Kenya, also suggest that environmental variables including wind speed, vegetation cover and soil characteristics may be associated with C. burnetii exposure. Such findings are useful for hypothesis generation and targeted surveillance but should not be interpreted as causal evidence or directly transferable risk rules across settings (Wambua et al., 2025).

  In Australia, macropods, especially kangaroos, have been considered context-specific wildlife reservoirs and potential sources of human infection. Aerosolisation of contaminated macropod faeces or contaminated grass during dry or dust-generating activities has been proposed as a possible exposure pathway (Graves & Islam, 2016). However, attribution to wildlife remains less robust than attribution to domestic ruminant sources.

  GAPS

  The relative contribution of climatic versus non-climatic determinants of spatial risk remains insufficiently quantified.

  Climate-based suitability models may suggest possible future shifts in the potential distribution of C. burnetii, but these projections need to be interpreted with livestock density, wildlife ecology, land use, husbandry systems, animal movements, surveillance intensity and human exposure pathways before being translated into operational risk maps (Aldwekat et al., 2025).

  The influence of climate on disease distribution should be better documented across different ecological and production systems.

• Outbreaks linked to extreme weather

  Meteorological conditions may favour environmental persistence, dust generation and airborne dispersal of C. burnetii, and may therefore contribute to Q fever outbreak occurrence.

  However, outbreaks are multifactorial and cannot be attributed to weather conditions alone. Their occurrence depends on the interaction between animal infection pressure, shedding events, environmental contamination, landscape features, husbandry practices, human exposure and surveillance intensity.

  Several human Q fever outbreak investigations suggest that wind and dry conditions can facilitate airborne or dust-mediated spread, but these observations remain context-dependent.

  GAPS

  The specific role of extreme weather events in triggering or amplifying Q fever outbreaks remains insufficiently documented.

  More studies are needed to distinguish the effect of weather from that of concurrent epidemiological, environmental and management factors.

  Fine-scale data linking meteorological conditions, animal shedding, environmental contamination, land use, farming practices and human cases remain limited.

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

  Climate change, environmental change and land use may influence the future distribution and transmission patterns of Q fever. These effects are likely to act through complex interactions involving host populations, livestock density, husbandry systems, wildlife–livestock–human interfaces, environmental persistence and airborne dispersal.

  Recent climate-suitability modelling suggests that the potential distribution of C. burnetii may shift under future climate-change scenarios, including possible northward expansion under some scenarios. However, these projections should be interpreted as climatic suitability outputs rather than direct predictions of disease incidence or outbreak risk, because non-climatic determinants such as livestock density, land use, farming practices, animal movements, human mobility and surveillance intensity also shape observed risk (Aldwekat et al., 2025).

  Climate change may also alter tick distributions and therefore the ecological context of tick-associated detections, but the role of ticks in Q fever epidemiology remains uncertain and should not be overinterpreted (Körner et al., 2021).

  GAPS

  The impact of climate change on Q fever remains insufficiently characterised.

  Climate-based suitability models need to be integrated with livestock density, wildlife ecology, land use, husbandry practices, animal movements, environmental contamination, surveillance intensity and human exposure pathways before being translated into operational risk maps.

  The role of climate and land-use changes in modifying wildlife–livestock–human interfaces remains insufficiently understood.

  The contribution of climate-related changes in tick distribution to Q fever epidemiology remains uncertain and should not be overinterpreted without evidence of field-relevant transmission.

• Main perceived obstacles for effective prevention and control

  Technical obstacles.

  Effective prevention and control of Q fever remain limited by difficulties in interpreting diagnostic and surveillance signals. PCR, serology, bulk tank milk, environmental dust and other matrix-based results are useful, but their meaning depends on sampling objective, matrix quality, timing, bacterial load, viability, epidemiological context and herd/flock history. Diagnostic tools exist, but the main obstacle is often their interpretation and integration into actionable risk assessment rather than their mere availability. Environmental PCR remains particularly difficult to interpret because detection of C. burnetii DNA does not demonstrate viable bacteria, current shedding or direct zoonotic risk.

  Harmonised diagnostic and interpretative algorithms combining matrix choice, PCR quantification, histopathology, immunohistochemistry, environmental data and epidemiological context remain insufficiently developed (Sidi-Boumedine et al., 2010; Gache et al., 2017; van den Brom et al., 2025).

  Scientific obstacles.

  Major knowledge gaps remain on C. burnetii biology and epidemiology. The bacterium is a strictly intracellular BSL-3 pathogen, difficult to isolate from field samples and therefore difficult to study at the scale required for robust comparative genomics, virulence assessment and experimental validation. Few well-contextualised strains are available for WGS compared with many other zoonotic bacteria. Consequently, the links between genotype, host adaptation, virulence, shedding, environmental persistence and zoonotic potential remain incompletely resolved. Environmental persistence is recognised as epidemiologically important, but matrix-specific viability, infectivity, resistance to physical or chemical conditions, and duration of survival under field conditions remain insufficiently quantified.

  Organisational and One Health obstacles.

  Prevention and control are further constrained by heterogeneous surveillance and reporting systems, delayed diagnosis and sampling, fragmented data flows, and insufficiently harmonised One Health coordination. These limitations reduce the ability to connect human cases, animal infection, shedding patterns, environmental contamination and genomic information in a timely and actionable way. Source investigation remains difficult because molecular, environmental, spatial and epidemiological evidence often provides converging hypotheses rather than definitive source attribution. Preparedness is also weakened by limited peacetime coordination, unclear roles and responsibilities, and insufficient stakeholder engagement (Hurtado et al., 2026). Knowledge gaps among human and veterinary professionals may further delay early recognition, reporting and coordinated response (Winter & Campe, 2022). The Dutch epidemic highlighted the need for coordinated diagnostic, public-health, veterinary and long-term follow-up strategies during and after major Q fever outbreaks (Schneeberger et al., 2014).

  Structural obstacles.

  Q fever remains structurally under-prioritised compared with other human and animal diseases, despite being recognised for decades and despite its zoonotic, environmental and One Health relevance. This low prioritisation limits dedicated funding, sustained surveillance, field investigations, strain isolation, experimental work, data integration and long-term interdisciplinary research. It also contributes to delayed recognition during routine periods and to reactive, sometimes difficult-to-calibrate responses when animal or human signals intensify.

  GAPS

  Technical gaps.

  More harmonised surveillance, diagnostic and reporting systems are needed. Rapid source investigation tools, validated environmental approaches and viability tests remain lacking. Diagnostic algorithms combining matrix choice, PCR quantification, pathology, immunohistochemistry, environmental data and epidemiological context require further development and harmonisation.

  Scientific gaps.

  Improved isolation capacity, genomic resources, standardised strain collections and field-linked metadata are needed to understand the genetic basis of host adaptation, virulence, persistence and zoonotic risk. Research on environmental persistence, viability, infectivity and the effects of physical or chemical conditions in natural matrices remains insufficiently developed. Wildlife reservoirs, environmental interfaces and non-classical exposure settings require better characterisation without overinterpreting isolated detections.

  Organisational and One Health gaps.

  Preparedness is limited by weak peacetime One Health coordination, fragmented data sharing, unclear responsibilities and insufficient stakeholder engagement. More operational frameworks are needed to support early cross-sector mobilisation, integrated source investigation, proportionate decision-making, communication, and post-crisis learning.

  Structural gaps.

  Sustained funding and coordinated research programmes are needed to address the structural under-prioritisation of Q fever as a neglected zoonosis. Long-term support is required for surveillance, strain collections, comparative genomics, environmental viability studies, field investigations, and integration of animal, human, environmental and social data.

• Main perceived facilitators for effective prevention and control

  Technical facilitators.

  Several diagnostic, surveillance and control tools already exist and can support Q fever prevention and control when they are used in a fit-for-purpose and context-aware manner. PCR, ELISA, bulk tank milk testing, abortion investigation protocols, environmental sampling, histopathology, immunohistochemistry and molecular typing can all contribute to different parts of the risk assessment and control process. Their value increases when results are interpreted together rather than in isolation, and when sampling design, matrix choice, timing, quantitative results and epidemiological context are clearly documented.

  Scientific facilitators.

  Important scientific foundations are already available. The main transmission pathway, the role of domestic ruminants, the importance of parturition and abortion events, and the relevance of environmental contamination are well established. Field studies, experimental work and outbreak investigations provide useful evidence for targeted prevention, including vaccination where relevant, biosecurity, safe management of birth products, surveillance of infected herds/flocks and protection of exposed workers. Emerging genomic and molecular resources also create opportunities to better understand strain diversity, host adaptation and possible zoonotic patterns, provided that isolates, metadata and comparative datasets become more available.

  Organisational and One Health facilitators.

  Existing surveillance systems, national reference laboratories, veterinary diagnostic networks, public-health authorities, local veterinarians, farmers and One Health initiatives provide an important foundation for integrated prevention and response. Past outbreak investigations and European collaborative work have generated practical knowledge on case detection, source investigation, communication, control measures and post-crisis learning.

  Initiatives such as Q-Net-Assess may support European collaboration on Coxiella burnetii sample collection, isolation, WGS, functional genomics and One Health surveillance harmonisation. Complementary expert networks such as QFIG may support international knowledge exchange, complex case discussion, training, surveillance reflection and collaborative research.

  Structural facilitators.

  The increasing recognition of Q fever as a neglected but important One Health zoonosis can support renewed prioritisation, improved funding, harmonised data collection and more integrated research programmes. The existence of WOAH references, EU surveillance obligations, national surveillance schemes, and previous large outbreak experiences, and EU-level One Health initiatives provides a basis for more coherent preparedness and control strategies.

  The main opportunity is to build on these existing structures to move from reactive, case-by-case management toward proactive, proportionate and monitorable risk reduction.

  EU One Health governance and surveillance-prioritisation initiatives provide a useful framework for coordinated surveillance, data sharing, cross-sector integration and risk assessment (European Commission, 2024; EFSA et al., 2023). Q fever is included among EU-level priorities for coordinated One Health surveillance (EFSA et al., 2023), although this facilitation remains incomplete, particularly because recent EU-level reporting no longer provides detailed comparable human data, leaving human burden assessment largely dependent on national surveillance systems and reporting practices.

  GAPS

  Technical gaps.

  The effectiveness of existing tools depends on harmonised interpretation frameworks, validated sampling strategies, and integration of diagnostic, environmental, epidemiological and genomic data. More work is needed to translate available tools into operationally comparable and decision-supportive systems.

  Scientific gaps.

  Further integration of field studies, strain collections, comparative genomics, environmental viability studies and host-response research is needed to transform existing scientific knowledge into robust risk assessment and control strategies.

  Organisational and One Health gaps.

  More evidence is needed on how to sustain peacetime One Health coordination, stakeholder engagement, data sharing, and operational readiness. Existing networks and projects can act as facilitators, but their long-term impact will depend on continuity, funding, interoperability and uptake by field actors and authorities.

  Structural gaps.

  Facilitators remain unevenly distributed across countries and production systems. Long-term support is needed to maintain expertise, update guidance, harmonise protocols, and ensure that tools developed through research projects can become usable in routine surveillance, preparedness and control.

Global challenges

• Antimicrobial resistance (AMR)

• Mechanism of action

  Human / One Health main focus

  Antimicrobial activity against Coxiella burnetii is constrained by the obligate intracellular lifestyle of the bacterium and its replication in acidic phagolysosome-like compartments.

  In humans, doxycycline is the reference treatment for acute Q fever, while prolonged doxycycline–hydroxychloroquine combinations are commonly used for persistent focalized infections. The rationale is linked to intracellular localisation and pH-dependent antimicrobial activity, although the evidence base for prolonged regimens remains limited and largely observational (Delahaye et al., 2024).

  In animals, these pharmacological considerations have not translated into a reliable routine antimicrobial strategy for herd/flock-level control. Antimicrobial treatment should not be considered a reliable control strategy for preventing abortion outbreaks, reducing shedding, or lowering environmental contamination at population level.

  Antimicrobial use should therefore remain restrictive when evidence of benefit for Q fever control is lacking, in line with antimicrobial stewardship principles.

  GAPS

  Human / One Health main focus

  The relationship between intracellular localisation, vacuolar pH and antimicrobial efficacy remains insufficiently characterised.

  The practical relevance of in vitro antimicrobial susceptibility data for veterinary field control remains limited.

  Validated antimicrobial alternatives for herd/flock-level control are lacking.

  The risk is not primarily antimicrobial resistance in C. burnetii as a dominant operational problem, but inappropriate or unnecessary antimicrobial use if Q fever is misinterpreted as controllable through routine herd/flock treatment.

• Conditions that reduce need for antimicrobials

  Animal / One Health main focus

  In animal Q fever, reducing the perceived need for antimicrobial use relies primarily on vaccination where relevant, biosecurity, surveillance, early detection and herd/flock management, rather than on therapeutic control.

  Antimicrobial treatment is not considered a reliable routine control tool for abortion outbreaks or shedding reduction in ruminants (Astobiza et al., 2013).

  GAPS

  Animal / One Health main focus

  More evidence is needed on which integrated control strategies most effectively reduce the perceived need for antimicrobial use under field conditions.

  The role of early detection, targeted herd/flock management, vaccination where appropriate, and clear farmer/veterinary guidance in reducing unnecessary antimicrobial treatments should be better documented.

• Alternatives to antimicrobials

  Animal / One Health main focus

  No validated non-antibiotic therapeutic alternative is currently available for routine veterinary use against Q fever in ruminants.

  Current control relies mainly on vaccination where relevant and on non-pharmaceutical preventive measures, including biosecurity, surveillance, early detection and management practices.

  GAPS

  Animal / One Health main focus

  Alternative anti-Coxiella approaches remain insufficiently explored.

  Validated non-antibiotic therapeutic strategies reducing shedding or transmission without antimicrobial use are lacking, apart from preventive and management-based approaches.

• Impact of AMR on disease control

  Animal / One Health main focus

  At present, antimicrobial resistance is not the main operational challenge for Q fever control in animals.

  The main challenge is the limited usefulness of antimicrobial treatment for controlling abortion, shedding or environmental contamination in ruminants. Antimicrobial use should therefore not be framed as a major control pillar for animal Q fever.

  GAPS

  Animal / One Health main focus

  Structured data on antimicrobial susceptibility and resistance in C. burnetii remain limited.

  The possible impact of antimicrobial use on future treatment efficacy, especially in human medicine, should be monitored.

  Current evidence does not support framing Q fever as a major animal AMR-control problem.

• Established links with AMR in humans

  Human / One Health main focus

  Human Q fever treatment still relies on antibiotics, mainly doxycycline for acute Q fever and prolonged doxycycline-based combinations for persistent focalized infections.

  However, well-established population-level links between Q fever control in animals and antimicrobial resistance or reduced antimicrobial susceptibility in humans are not clearly documented.

  GAPS

  Human / One Health main focus

  The One Health links between antimicrobial use in animals, C. burnetii susceptibility patterns and human therapeutic implications remain insufficiently characterised.

  Any potential antimicrobial-resistance or reduced-susceptibility concern should be monitored and documented if robust evidence emerges.

• Digital health

• Precision technologies available/needed

  One Health / digital-molecular interface

  Existing digital resources already support molecular epidemiology of C. burnetii, including the historical MST database and more recent genomic platforms such as CoxBase using MLVA, SNP or WGS-based approaches (Fasemore et al., 2021).

  These tools can support molecular comparison and, in selected cases, contribute to source-investigation hypotheses. However, routine genomic source attribution for C. burnetii is not yet operational, mainly because available strain datasets remain limited, unevenly contextualised and insufficiently linked across animal, human and environmental data.

  Digital tools should therefore be framed as support for interpretation, not as stand-alone solutions. Their practical value depends on the quality of epidemiological metadata, sampling context, typing-method comparability, and links between animal, human and environmental data.

  Multi spacers typing – IHU

  MST Coxiella Burnetii

  CoxBase: an Online Platform for Epidemiological Surveillance, Visualization, Analysis, and Typing of Coxiella burnetii Genomic Sequences - PMC

  GAPS

  One Health / digital-molecular interface

  More integrated tools and datasets are needed to combine animal, human, environmental and genomic information in a decision-support perspective.

  The current gap is not only the availability of typing or WGS tools, but the lack of sufficiently large, standardised and contextualised strain datasets to support more robust source-investigation and, eventually, source-attribution approaches.

  The practical usefulness of digital and precision approaches for routine Q fever surveillance remains insufficiently demonstrated. Links between historical typing schemes, such

  as MST, and whole-genome-based classifications remain insufficiently operationalised for routine source tracing.

  Recent initiatives such as Q-Net-Assess may further support integration, harmonisation and pan-European molecular surveillance (https://q-net-assess.com/).

• Data requirements

  One Health / data-integration focus

  Digital approaches for Q fever require structured epidemiological, laboratory, geographic and genomic data, together with consistent metadata on species, animal category, matrix, sampling date, sampling location, sampling strategy, diagnostic method, quantitative result, surveillance objective and epidemiological context.

  For environmental or pooled samples, additional metadata are needed, including sampling surface or matrix, sampling location within the premises, relationship to parturition or abortion events, cleaning/disinfection history, and whether the sample is intended for outbreak investigation, routine surveillance or source investigation.

  GAPS

  One Health / data-integration focus

  Data requirements are not yet sufficiently standardised across surveillance systems and countries.

  The minimum metadata needed to support integrated interpretation, including environmental samples, dust, bulk tank milk and pooled samples, should be better defined.

  Data structures should clearly distinguish between individual-animal diagnosis, herd/flock-level surveillance, environmental-contamination assessment and source-investigation objectives.

  Harmonised vocabularies, common reporting formats and interoperable databases are needed to improve comparability across animal, human, environmental and genomic datasets.

• Data availability

  One Health / data-integration focus

  Some molecular and surveillance data are already available through online resources and project platforms, including typing databases and genomic repositories dedicated to C. burnetii.

  However, data availability remains heterogeneous across countries, sectors and surveillance objectives.

  Data linking animal, human, environmental and genomic information remain limited, which constrains integrated source investigation, cross-sector interpretation and cross-country comparability.

  GAPS

  One Health / data-integration focus

  Comparable multi-country datasets remain limited.

  Data linking animal, human and environmental information are still insufficiently available for integrated analyses.

  Access rules, confidentiality constraints and differences in reporting systems may further limit cross-sector and cross-border data use.

  Sustainable data-sharing mechanisms are needed to support integrated interpretation while respecting data protection, ownership and confidentiality constraints.

• Data standardisation

  One Health / data-integration focus

  Data standardisation is a major prerequisite for improving Q fever surveillance, comparability and interpretation.

  Existing resources are complementary, but typing schemes, genomic databases and surveillance systems are not yet fully harmonised.

  Standardised data collection tools would improve comparability across animal, human and environmental surveillance datasets.

  Interoperability between typing resources, genomic databases and surveillance systems is needed to support future source-attribution capacity, cross-sector interpretation and longitudinal monitoring. At present, limited availability of contextualised and harmonised metadata remains a major bottleneck.

  GAPS

  One Health / data-integration focus

  Interoperability between existing typing resources, genomic databases and surveillance systems remains insufficient.

  Standardised metadata, common reporting formats and links between historical typing schemes and genomic groupings are still needed.

  Harmonised metadata and vocabularies are needed for sample type, matrix, sampling objective, epidemiological context, diagnostic method, quantitative result, genomic data and result interpretation. Without these, molecular comparisons cannot reliably be translated into source-attribution conclusions.

• Climate change

• Role of disease control for climate adaptation

  Climate change, environmental change and land use may influence Q fever transmission through multiple interacting pathways, including environmental persistence, aerosolisation, animal management, wildlife–livestock interfaces and human exposure.

  In this context, Q fever control may contribute to climate adaptation when it is integrated into broader resilient surveillance, biosecurity, herd/flock management and sustainable environmental risk-reduction strategies.

  GAPS

  The role of Q fever control in climate adaptation remains insufficiently characterised.

  More work is needed to distinguish the effects of climate-related factors from those of concurrent changes in husbandry, animal density, land use, wildlife ecology and environmental management.

  Scenario-based approaches are needed to better understand combined risk configurations, including climate, landscape, animal management, shedding, environmental contamination and human exposure.

• Effect of disease (control) on resource use

  Q fever control measures may influence resource use through surveillance, vaccination, hygiene, manure and bedding management, animal housing, movement-related measures and environmental management.

  Preventive and integrated strategies may reduce the need for repeated emergency interventions, but their net effect on water, energy, labour and material use remains poorly documented.

  GAPS

  The effect of Q fever and its control measures on water, energy, labour and other resource use is poorly documented.

  Comparative assessments of different control strategies from a resource-use perspective are lacking.

  More evidence is needed to determine whether preventive strategies reduce overall resource use compared with repeated crisis-driven interventions.

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

  Some Q fever control measures may have environmental consequences, for example through manure and bedding handling, animal confinement, transport, culling where implemented, cleaning and disinfection practices, and changes in environmental management.

  Their overall effect on greenhouse gas emissions, nutrient losses, chemical pollution and other environmental impacts remains unclear and likely depends on the control strategy, production system and implementation context.

  GAPS

  Some Q fever control measures may have environmental consequences, for example through manure and bedding handling, animal confinement, transport, culling where implemented, cleaning and disinfection practices, and changes in environmental management.

  Their overall effect on greenhouse gas emissions, nutrient losses, chemical pollution and other environmental impacts remains unclear and likely depends on the control strategy, production system and implementation context.

• Preparedness

• Syndromic surveillance

  Preparedness for Q fever should cover both grouped human cases and animal or environmental signals with zoonotic significance.

  In practice, this includes early detection of human clusters, but also rapid recognition of serial abortions, high-shedding events or substantial environmental contamination in ruminant herds/flocks, which may indicate increased risk of human exposure.

  Human outbreak management requires rapid identification of related cases, tracing of infection source(s), and proportionate control measures, while Q fever in ruminants may lead to serial abortions and environmental contamination before human cases are recognised.

  Preparedness should also address stakeholder awareness and cross-sector knowledge gaps, as these may delay early detection, reporting and coordinated One Health response (Hurtado et al., 2026; Winter & Campe 2022).

  GAPS

  Baseline syndromic and event-based surveillance remains insufficiently implemented or harmonised for linking human clusters with animal and environmental signals.

  Alert thresholds and trigger criteria for activating One Health response should better integrate grouped human cases, serial abortions and other high-risk shedding situations.

• Diagnostic platforms

  Preparedness depends on coordinated diagnostic capacities across human, veterinary and environmental sectors.

  In outbreak settings, animal-source investigation relies on epidemiological data, rapid and appropriate sampling of suspected herds/flocks, PCR on vaginal fluids and birth products, and, where relevant, bulk tank milk and environmental screening.

  Environmental PCR may help prioritise farms or sites for detailed animal investigation but should not be interpreted alone as evidence of viable bacteria, current shedding or source attribution.

  When source investigation is needed, diagnostic platforms should anticipate the preservation of suitable animal, environmental and, where available, human samples for genotyping or WGS.

  Diagnostic platforms for source investigation should account for the diversity of outbreak settings, including community, occupational, recreational, educational and non-traditional exposure contexts. Source investigation often requires rapid integration of human clinical data, animal sampling, environmental investigation, spatial information and, where possible, molecular typing. Recent outbreak reviews show that fully integrated One Health investigations remain limited to a subset of documented episodes (Hurtado et al. 2026, Supplementary Note S4 / Table S2; Bellini et al., 2014).

  GAPS

  Preparedness remains limited by delayed sampling, lack of suitable human samples for genotyping in acute cases, and insufficiently standardised veterinary and environmental sampling strategies.

  The availability of comparable isolates or high-load samples suitable for robust molecular comparison remains a practical bottleneck.

  Validated interpretative criteria for environmental samples and rapid viability tools are also lacking.

• Mathematical modelling

  Preparedness may be strengthened by integrating human, animal, environmental and meteorological data for source investigation and risk analysis.

  GIS-based analyses, atmospheric dispersion models, wind-informed analyses and multicriteria approaches may be particularly relevant when outbreaks occur without obvious direct animal contact. Mathematical and spatial modelling may help structure source-investigation hypotheses, prioritise field investigations and visualise potential exposure areas (De Rooij et al. 2019). However, models should not be interpreted as stand-alone predictors of infection source (van Leuken et al., 2015).

  Genotyping or WGS may strengthen source-investigation hypotheses when comparable bacterial material is available from human, animal or environmental sources. However, for C. burnetii, molecular source attribution is not yet routine, and molecular similarity should be interpreted cautiously together with epidemiological, spatial, temporal, environmental and exposure data.

  In outbreaks without obvious direct animal contact, source investigation may require combining exposure histories, GIS, wind or meteorological data, environmental sampling, animal data and molecular information. However, source attribution for C. burnetii often remains based on converging evidence rather than definitive microbiological confirmation (Hurtado et al. 2026, Supplementary Note S4 / Table S2).

  GAPS

  Advanced modelling and multicriteria risk-analysis tools remain insufficient for routine operational use.

  Models integrating cross-sectoral data should be further developed and tested in real outbreak settings.

  Genomic source attribution requires larger and better contextualised strain datasets.

  Research and preparedness work should clarify how molecular evidence, GIS, meteorological data, exposure history and field investigation can be combined to support proportionate decisions.

• Intervention platforms

  Preparedness requires predefined One Health intervention frameworks able to activate cross-sector coordination when grouped human cases are detected or when animal, environmental, spatial and epidemiological signals converge toward a plausible zoonotic source.

  Early mobilisation may also be warranted when high-risk animal or environmental situations could expose humans, even before a source is formally attributed, for example serial abortions, clustered parturition, high-shedding events, contaminated animal environments or public-facing animal settings.

  Timely mobilisation, clear roles, shared information pathways, and integrated investigation of nearby animal reservoirs or potentially contaminated environmental interfaces are central to effective response.

  The diversity of outbreak contexts supports the need for predefined One Health frameworks, clear roles, rapid cross-sector mobilisation and data-sharing procedures before crises occur (Hurtado et al. 2026, Supplementary Note S4 / Table S2).

  GAPS

  Preparedness is limited by slow coordination, unclear responsibilities, fragmented information exchange and insufficient peacetime preparation.

  Operational frameworks for early cross-sector mobilisation remain insufficiently structured in many settings.

  Few frameworks explicitly support both adaptive risk management and risk mitigation, including contextual interpretation of signals, adjustment of response levels, and identification of proportionate measures to reduce human exposure, animal amplification and environmental dissemination.

• Communication strategies

  Preparedness and response rely on timely, targeted and two-way communication with clinicians, veterinarians, farmers, public health authorities, decision-makers and exposed populations.

  Communication should support early recognition, shared interpretation of uncertain evidence, proportionate action and trust-building.

  Communication strategies should be transparent and timely, but carefully framed to avoid unnecessary alarm, stigma or disproportionate economic damage to farmers, farms or territories. Poorly framed communication may reduce trust, discourage cooperation, damage reputations and create severe economic consequences for implicated farmers before source attribution is sufficiently established.

  Participatory approaches may improve preparedness by giving farmers and other field stakeholders a more explicit role in discussing feasible management strategies.

  Communication strategies should not target only traditional occupational groups. Residents, visitors, workers in non-traditional exposure settings, farm-like public venues, waste-management workers, transport workers and exposed communities may also require tailored information depending on the outbreak context (Hurtado et al. 2026, Supplementary Note S4 / Table S2).

  GAPS

  Preparedness remains limited by delayed or fragmented messaging, weak feedback loops and insufficient evaluation of communication impact.

  More work is needed on peacetime stakeholder engagement, communication channels, trust and participatory approaches adapted to Q fever.

  The unintended consequences of outbreak communication, including stigma, loss of trust, reduced cooperation and economic damage to farmers or territories, remain insufficiently considered in preparedness planning.

  Awareness-raising in high-risk communities and among medical practitioners remains an important preparedness and early-recognition need.

Risk

• Q fever is a potential biological warfare agent being very infectious and very durable in the environment as well as capable of windborne spread.Risks are at least linked to the different sources and routes involved for the transmission which are not well known. Assessment of infectious dose in natural conditions needs to be further studied. Some reports suggested that a great quantity of bacteria in the ambient vicinity is required to be infective and induce pathological lesions (see Section “Zoonotic potential - Risk of occurrence in humans, populations at risk, specific risk factors”). Moreover, the distances of windborne spread has to be better defined.

  GAP: No knowledge on “background”-levels of Coxiella in the environment in the different regions/countries.

Main critical gaps

• The main critical gaps for Q fever do not concern a single missing tool, but rather the lack of integrated, harmonised and operationally interpretable systems across diagnostics, surveillance, source investigation, vaccination follow-up and control.

  Existing tools and knowledge already support partial prevention and control, but persistent weaknesses remain in diagnostic harmonisation, environmental investigation, source investigation, vaccinated-population monitoring, cross-sector coordination, data integration and field implementation.

  Critical technical gaps.

  Critical technical gaps include the lack of harmonised diagnostic interpretation across matrices, species, surveillance objectives and epidemiological contexts. Environmental and dust-based surveillance still lack validated sampling strategies, interpretative criteria, and rapid viability or infectivity approaches. More robust criteria are also needed to combine PCR, serology, bulk tank milk, environmental results, pathology and epidemiological context into cautious but operational conclusions.

  DIVA-compatible tools and strategies for monitoring vaccinated populations remain insufficient. Follow-up in vaccinated herds/flocks remains limited by non-DIVA vaccines, uncertainty around long-term vaccination strategies, and insufficient integration between diagnostics, vaccination and surveillance.

  Critical scientific gaps.

  Critical scientific gaps remain on the biology, persistence and diversity of Coxiella burnetii. The limited availability of well-contextualised strains, the difficulty of isolating C. burnetii from field samples, and the constraints linked to working with a strictly intracellular BSL-3 pathogen limit comparative genomics, virulence studies and experimental validation.

  Improved strain collections, WGS datasets, metadata quality and, where feasible, direct-from-matrix genomic approaches are needed to better understand host adaptation, virulence, shedding patterns, environmental persistence and zoonotic potential. The contribution of landscape, airflow, soil, dust, microbial biodiversity and farming practices to Q fever risk-reduction strategies also remains insufficiently explored.

  Critical surveillance / data gaps.

  Integrated One Health source-investigation capacity remains limited, especially across heterogeneous and non-traditional outbreak settings. Better integration is needed between human clinical data, animal sampling, environmental investigation, meteorological data, spatial analysis and molecular typing.

  Source investigation remains constrained by limited access to comparable human, animal and environmental samples, insufficiently contextualised strain/genome datasets, and the absence of standardised criteria for combining molecular similarity, epidemiological context, environmental evidence and exposure data into cautious source-investigation conclusions without overclaiming source attribution.

  Critical One Health / preparedness gaps.

  Evidence remains limited on the effectiveness, duration, cost-benefit and optimal integration of combined control measures, including vaccination, biosecurity, environmental management, surveillance and communication. The respective contribution of individual measures is difficult to disentangle when they are implemented as packages.

  Preparedness gaps include weak peacetime One Health coordination, insufficiently defined alert thresholds and data flows, limited integration of farmers and other field stakeholders, and weak post-crisis knowledge transfer. Comparative evaluation of outbreak investigations, control experiences and after-action learning remains insufficient.

  Critical pharmaceutical and AMR-related gaps.

  Pharmaceutical gaps are context-dependent. In animals, antimicrobials remain of limited usefulness for herd/flock-level control of abortion, shedding or environmental contamination. The main gap is therefore not the lack of antimicrobial options, but the need to clarify where treatment has a clinical role and where prevention, vaccination, surveillance and management are more appropriate.

  Critical structural gaps.

  Q fever remains structurally under-prioritised compared with other human and animal diseases, despite its zoonotic, environmental and One Health relevance. This limits sustained funding, long-term surveillance, strain isolation capacity,experimental work, field investigations, training, institutional support and continuity of international expert networks. This under-prioritisation contributes to delayed recognition in routine periods and to reactive, sometimes poorly calibrated responses when animal or human signals intensify.

Conclusion

• Q fever remains a neglected but important One Health zoonosis. Existing diagnostic, surveillance, vaccination and control tools already provide a basis for action, but their value is limited by interpretation difficulties, insufficient harmonisation and weak integration across animal, human and environmental sectors.

  The main challenge is not the absence of a single tool, but the need to combine animal, environmental, human and genomic signals into proportionate and timely decisions. Zoonotic risk should be understood as a graded, contextual assessment rather than a binary laboratory result. Diagnostic detection, environmental positivity, seropositivity, shedding or genetic similarity between C. burnetii strains should support interpretation but should not be treated as stand-alone proof of risk, source attribution or control success.

  Environmental persistence should therefore not be translated mechanically into transmission risk. For Q fever, the environment is not only a contaminated matrix to be detected or decontaminated, but a set of conditions — dust, airflow, soil, vegetation, topography, husbandry practices and human activities — that may modulate exposure and risk.

  Key recurring challenges include environmental persistence, silent or delayed detection, efficient animal-to-human transmission under favourable exposure conditions, insufficient understanding of both favourable and unfavourable conditions for transmission, DIVA-related limitations, imperfect follow-up in vaccinated populations, and difficulties in linking diagnostic or environmental signals to actionable epidemiological interpretation.

  Vaccination is an important preventive tool, but primary prevention cannot be reduced to vaccination alone. Future priorities should include harmonised diagnostic interpretation, environmental viability and persistence, DIVA-compatible and vaccine-monitoring tools, comparative genomics, source investigation, integrated surveillance, preparedness and sustainable risk-reduction strategies.

  For Q fever, One Health preparedness means not waiting for human cases to reveal late a problem that is already animal, environmental and organisational; it requires structuring methods, data flows, expertise networks and after-action learning during peacetime. Strengthening Q fever control will require sustained funding, maintained expertise, interoperable data systems, peacetime One Health coordination, and meaningful engagement with farmers, veterinarians, public-health actors and exposed communities. The objective should be to support practical, proportionate and monitorable control strategies that reduce zoonotic risk while preserving animal health, human health, environmental integrity and farming-system feasibility.

Sources of information

• Expert group composition

  Agnieszka Jodełko, PIWET, Poland

  Ana Hurtado, NEIKER, Spain

  Ana Santos, INSA, Portugal

  Aurélie Couesnon, Anses, France

  Ben Bauer, Faculty of Veterinary Medicine, University of Calgary, Canada

  Chantal Rovers, Radboud UMC, The Netherlands

  Élodie Rousset, Anses Sophia Antipolis, National Reference Laboratory for Animal Q Fever, France

  Gilbert Greub, CHUV Lausanne, Switzerland

  Katja Mertens-Scholz, Friedrich-Loeffler-Institut, Germany

  Katrina Bosward, University of Sydney, Australia

  Marcella Mori, Sciensano, National Reference Laboratory for Animal Q Fever and National Reference Centre for Human Q Fever, Belgium

  Marleen Kannekens-Jager, Wageningen Bioveterinary Research, WUR, National Reference Laboratory for Notifiable Bacterial Diseases and Zoonoses, The Netherlands

  Mateus de Souza Ribeiro Mioni, São Paulo State University (UNESP), Brazil

  Matteo Bonazzi, IRIM UMR9004, CNRS, Université de Montpellier, France

  Nesrin Ghanem-Zoubi, Rambam Health Care Campus, Israel

  Olivier Duron, MIVEGEC, CNRS, IRD, Université de Montpellier, France

  Penny Hutchinson, West Moreton Health, Australia

  Pierre-Edouard Fournier, IHU Méditerranée Infection, Centre National de Référence des Rickettsies, Coxiella et Bartonella, France

  René van den Brom, Royal GD / GD Animal Health, The Netherlands

  Robert Horvath, Queensland Health, Australia

  Rudolf Reichel, APHA, United Kingdom

  Sue Neale, APHA, United Kingdom

  Tarka Bhatta, Australian Rickettsial Reference Laboratory, Australia

  Tatiana Proboste Iberti, University of Sydney, Australia

  Tom McNeilly, Moredun Research Institute, United Kingdom

• Reviewed by

  Project Management Board.

• Date of submission by expert group

  25th May 2026

• References

  1. Scientific articles

  Abeykoon, A. M. H., N. J. Clark, R. J. Soares Magalhães, G. A. Vincent, M. A. Stevenson, S. M. Firestone, and A. K. Wiethoelter. 2021. “Coxiella burnetii in the Environment: A Systematic Review and Critical Appraisal of Sampling Methods.” Zoonoses and Public Health 68 (3): 165–181. https://doi.org/10.1111/zph.12791.

  Abou Abdallah, Rita, Matthieu Million, Jérémy Delerce, Hicham Anani, Alioune Diop, Aurélia Caputo, et al. 2022. “Pangenomic Analysis of Coxiella burnetii Unveils New Traits in Genome Architecture.” Frontiers in Microbiology 13: 1022356. https://doi.org/10.3389/fmicb.2022.1022356.

  Agerholm, Jørgen S. 2013. “Coxiella burnetii Associated Reproductive Disorders in Domestic Animals—A Critical Review.” Acta Veterinaria Scandinavica 55: 13. https://doi.org/10.1186/1751-0147-55-13.

  Alam, Shawkat, Venkatesh Kumaresan, Rajesh Palanisamy, Yan Zhang, Janakiram Seshu, Na Xiong, and Guoquan Zhang. 2024. “Coxiella burnetii Nine Mile Phase I Primary Infection Derived Protective Immunity against Coxiella burnetii Reinfection in Mice Depends on Both B and T Cells, but T Cells Play a Critical Role.” Frontiers in Immunology 15: 1427822. https://doi.org/10.3389/fimmu.2024.1427822.

  Aldwekat, Abdallah Falah Mohammad, Niloufar Lorestani, and Farzin Shabani. 2025. “Impacts of Climate Change on the Global Spread and Habitat Suitability of Coxiella burnetii: Future Projections and Public Health Implications.” The Journal of Climate Change and Health 22: 100442. https://doi.org/10.1016/j.joclim.2025.100442.

  Alende-Castro, V., C. Macía-Rodríguez, I. Novo-Veleiro, X. García-Fernández, M. Treviño-Castellano, S. Rodríguez-Fernández, et al. 2018. “Q Fever in Spain: Description of a New Series, and Systematic Review.” PLoS Neglected Tropical Diseases 12: e0006338. https://doi.org/10.1371/journal.pntd.0006338.

  Álvarez-Alonso, Raquel, Ion I. Zendoia, Jesús F. Barandika, Isabel Jado, Ana Hurtado, Ceferino M. López, and Ana L. García-Pérez. 2020. “Monitoring Coxiella burnetii Infection in Naturally Infected Dairy Sheep Flocks Throughout Four Lambing Seasons and Investigation of Viable Bacteria.” Frontiers in Veterinary Science 7: 352. https://doi.org/10.3389/fvets.2020.00352.

  Álvarez-Alonso, Raquel, Mikel Basterretxea, Jesús F. Barandika, Ana Hurtado, Jasone Idiazabal, Isabel Jado, Xabier Beraza, Milagros Montes, Paloma Liendo, and Ana L. García-Pérez. 2018. “A Q Fever Outbreak with a High Rate of Abortions at a Dairy Goat Farm: Coxiella burnetii Shedding, Environmental Contamination, and Viability.” Applied and Environmental Microbiology 84 (20): e01650-18. https://doi.org/10.1128/AEM.01650-18.

  Arricau-Bouvery, Nathalie, Armel Souriau, A. Moutoussamy, K. Ladenise, and Annie Rodolakis. 2001. “Étude de l’excrétion de Coxiella burnetii dans un modèle expérimental caprin et décontamination des lisiers par la cyanamide calcique.” Rencontres Recherches Ruminants 8: 153–156.

  Arricau-Bouvery, Nathalie, Armel Souriau, Christelle Bodier, Philippe Dufour, Elodie Rousset, and Annie Rodolakis. 2005. “Effect of Vaccination with Phase I and Phase II Coxiella burnetii Vaccines in Pregnant Goats.” Vaccine 23 (35): 4392–4402. https://doi.org/10.1016/j.vaccine.2005.04.010.

  Astobiza, Ianire, Jesús F. Barandika, Ana Hurtado, Ramón A. Juste, and Ana L. García-Pérez. 2010. “Kinetics of Coxiella burnetii Excretion in a Commercial Dairy Sheep Flock after Treatment with Oxytetracycline.” The Veterinary Journal 184 (2): 172–175. https://doi.org/10.1016/j.tvjl.2009.01.017.

  Astobiza, Ianire, Jesús F. Barandika, Ramón A. Juste, Ana Hurtado, and Ana L. García-Pérez. 2013. “Evaluation of the Efficacy of Oxytetracycline Treatment Followed by Vaccination against Q Fever in a Highly Infected Sheep Flock.” The Veterinary Journal 196 (1): 81–85. https://doi.org/10.1016/j.tvjl.2012.07.028.

  Baud, David, and Gilbert Greub. 2011. “Intracellular Bacteria and Adverse Pregnancy Outcomes.” Clinical Microbiology and Infection 17 (9): 1312–1322. https://doi.org/10.1111/j.1469-0691.2011.03604.x.

  Bauer, Benjamin U., Kay M. Schwecht, Rico Jahnke, Svea Matthiesen, Martin Ganter, and Michael R. Knittler. 2023. “Humoral and Cellular Immune Responses in Sheep Following Administration of Different Doses of an Inactivated Phase I Vaccine against Coxiella burnetii.” Vaccine 41 (33): 4798–4807. https://doi.org/10.1016/j.vaccine.2023.06.061.

  Bauer, Benjamin U., Matthias Peters, Tobias L. Herms, Martin Runge, Peter Wohlsein, Tim K. Jensen, and Martin Ganter. 2024. “Detection of Coxiella burnetii in the Mammary Gland of a Dairy Goat.” Veterinary Research Communications 48 (3): 1341–1352. https://doi.org/10.1007/s11259-023-10233-8.

  Bellini, Chiara, Ioannis Magouras, Catherine Chapuis-Taillard, Olivier Clerc, Eric Masserey, Gennaro Peduto, Olivier Peter, Saskia Schaerrer, G. Schuepbach, and Gilbert Greub. 2014. “Q Fever Outbreak in the Terraced Vineyards of Lavaux, Switzerland.” New Microbes and New Infections 2 (4): 93–99. https://doi.org/10.1002/nmi2.37.

  Boden, Kerstin, Stefanie Brasche, Elisabeth Straube, and Wolfgang Bischof. 2014. “Specific Risk Factors for Contracting Q Fever: Lessons from the Outbreak Jena.” International Journal of Hygiene and Environmental Health 217 (1): 110–115. https://doi.org/10.1016/j.ijheh.2013.04.004.

  Brangsch, Hanna, Christian Berens, Stefanie Fuchs, Stephen Fitzgerald, Tom N. McNeilly, Antje Lührmann, and Katja Mertens-Scholz. 2026. “Genome Characteristics and Type IV Effector Protein Repertoire of Coxiella burnetii Depend Rather on Genomic Groups than on Host Species.” BMC Microbiology 26 (1): 393. https://doi.org/10.1186/s12866-026-04897-w.

  Burns, Rebekah J. L., Kim Khanh Le, Jarunee Siengsanun-Lamont, and Stuart D. Blacksell. 2023. “A Review of Coxiellosis (Q Fever) and Brucellosis in Goats and Humans: Implications for Disease Control in Smallholder Farming Systems in Southeast Asia.” One Health 16: 100568. https://doi.org/10.1016/j.onehlt.2023.100568.

  Buysse, Marjolaine, Marie Duhayon, Fabienne Cantet, Matteo Bonazzi, and Olivier Duron. 2021. “Vector Competence of the African Argasid Tick Ornithodoros moubata for the Q Fever Agent Coxiella burnetii.” PLoS Neglected Tropical Diseases 15 (1): e0009008. https://doi.org/10.1371/journal.pntd.0009008.

  Böttcher, Jens, Annette Vossen, Britta Janowetz, Michaela Alex, Armin Gangl, Andreas Randt, and Norbert Meier. 2011. “Insights into the Dynamics of Endemic Coxiella burnetii Infection in Cattle by Application of Phase-Specific ELISAs in an Infected Dairy Herd.” Veterinary Microbiology 151 (3–4): 291–300. https://doi.org/10.1016/j.vetmic.2011.03.007.

  Böttcher, Jens, Michaela Alex, Sven Dänicke, Jörn Gethmann, Katja Mertens-Scholz, and Britta Janowetz. 2024. “Susceptibility, Immunity, and Persistent Infection Drive Endemic Cycles of Coxiellosis on Dairy Farms.” Animals 14 (7): 1056. https://doi.org/10.3390/ani14071056.

  Celina, Seyma S., and Jiří Černý. 2022. “Coxiella burnetii in Ticks, Livestock, Pets and Wildlife: A Mini-Review.” Frontiers in Veterinary Science 9: 1068129. https://doi.org/10.3389/fvets.2022.1068129.

  Clark, Nicholas J., and Ricardo J. Soares Magalhães. 2018. “Airborne Geographical Dispersal of Q Fever from Livestock Holdings to Human Communities: A Systematic Review and Critical Appraisal of Evidence.” BMC Infectious Diseases 18: 218. https://doi.org/10.1186/s12879-018-3135-4.

  Conway, Robert, Colleen Duncan, R. A. Foster, Gregory J. Kersh, Stephen Raverty, Thomas Gelatt, and Colleen Frank. 2022. “Histologic Lesions in Placentas of Northern Fur Seals (Callorhinus ursinus) from a Population with High Placental Prevalence of Coxiella burnetii.” Journal of Wildlife Diseases 58 (2): 333–340. https://doi.org/10.7589/JWD-D-21-00037.

  de Boer, Pieter T., Marit M. A. de Lange, Cornelia C. H. Wielders, Frederika Dijkstra, Sonja E. van Roeden, Chantal P. Bleeker-Rovers, Jan Jelrik Oosterheert, Peter M. Schneeberger, and Wim van der Hoek. 2020. “Cost-Effectiveness of Screening Program for Chronic Q Fever, the Netherlands.” Emerging Infectious Diseases 26 (2): 238–246. https://doi.org/10.3201/eid2602.181772.

  de Rooij, Myrna M. T., Jeroen P. G. van Leuken, Arno Swart, Mirjam E. E. Kretzschmar, Mirjam Nielen, Aline A. de Koeijer, Ingmar Janse, Inge M. Wouters, and Dick J. J. Heederik. 2019. “A Systematic Knowledge Synthesis on the Spatial Dimensions of Q Fever Epidemics.” Zoonoses and Public Health 66 (1): 14–25. https://doi.org/10.1111/zph.12534.

  Delahaye, A., Carole Eldin, A. Bleibtreu, F. Djossou, T. J. Marrie, N. Ghanem-Zoubi, S. van Roeden, and L. Epelboin. 2024. “Treatment of Persistent Focalized Q Fever: Time Has Come for an International Randomized Controlled Trial.” Journal of Antimicrobial Chemotherapy 79 (8): 1725–1747. https://doi.org/10.1093/jac/dkae145.

  Desmoulin, A., A. Esparon, F. Quet, C. Teillet, P. Thill, M. Nacher, E. Roux, T. Catry, and L. Epelboin. 2026. “Querying Q Fever: Spatiotemporal Patterns and Environmental Drivers in French Guiana.” BMJ Global Health 11 (3): e020069. https://doi.org/10.1136/bmjgh-2025-020069.

  Duron, Olivier, Karim Sidi-Boumedine, Elodie Rousset, Sara Moutailler, and Elsa Jourdain. 2015. “The Importance of Ticks in Q Fever Transmission: What Has (and Has Not) Been Demonstrated?” Trends in Parasitology 31 (11): 536–552. https://doi.org/10.1016/j.pt.2015.06.014.

  Duron, Olivier, Patricia Doublet, Fabrice Vavre, and Didier Bouchon. 2018. “The Importance of Revisiting Legionellales Diversity.” Trends in Parasitology 34 (12): 1027–1037. https://doi.org/10.1016/j.pt.2018.09.008.

  Duron, Olivier. 2015. “The IS1111 Insertion Sequence Used for Detection of Coxiella burnetii Is Widespread in Coxiella-like Endosymbionts of Ticks.” FEMS Microbiology Letters 362 (17): fnv132. https://doi.org/10.1093/femsle/fnv132.

  Eldin, Carole, Cléa Mélenotte, Oleg Mediannikov, Eric Ghigo, Matthieu Million, Sophie Edouard, Jean-Louis Mege, Max Maurin, and Didier Raoult. 2017. “From Q Fever to Coxiella burnetii Infection: A Paradigm Change.” Clinical Microbiology Reviews 30 (1): 115–190. https://doi.org/10.1128/CMR.00045-16.

  Epelboin, Loïc, Carole Eldin, Pierre Thill, Valérie Pommier de Santi, Philippe Abboud, Géraldine Walter, Aurélie Melzani, et al. 2021. “Human Q Fever on the Guiana Shield and Brazil: Recent Findings and Remaining Questions.” Current Tropical Medicine Reports 8: 173–182. https://doi.org/10.1007/s40475-021-00243-4.

  Fasemore, Adekunle M., Andrea Helbich, Mathias C. Walter, Thomas Dandekar, Gilles Vergnaud, Konrad U. Förstner, and Dimitrios Frangoulidis. 2021. “CoxBase: An Online Platform for Epidemiological Surveillance, Visualization, Analysis, and Typing of Coxiella burnetii Genomic Sequences.” mSystems 6 (6): e00403-21. https://doi.org/10.1128/mSystems.00403-21.

  Gache, Kristel, Elodie Rousset, Jean-Baptiste Perrin, Renée de Crémoux, Stéphane Hosteing, Elsa Jourdain, Raphaël Guatteo, Philippe Nicollet, Anne Touratier, Didier Calavas, and Caroline Sala. 2017. “Estimation of the Frequency of Q Fever in Sheep, Goat and Cattle Herds in France: Results of a 3-Year Study of the Seroprevalence of Q Fever and Excretion Level of Coxiella burnetii in Abortive Episodes.” Epidemiology and Infection 145 (15): 3131–3142. https://doi.org/10.1017/S0950268817002308.

  García, Elena, Gerardo Espeso, Rocío Fernández, Ángel Gómez-Martín, José María Rodríguez-Linde, and Christian De la Fe. 2017. “Coxiella burnetii Detected in Three Species of Endangered North African Gazelles That Recently Aborted.” Theriogenology 88: 131–133. https://doi.org/10.1016/j.theriogenology.2016.09.019.

  García-Pérez, Ana L., Ion I. Zendoia, Daniel Ferrer, Jesús F. Barandika, Carlos Ramos, Raquel Vera, Teresa Martí, Aina Pujol, Aitor Cevidanes, and Ana Hurtado. 2025. “Combination of Serology and PCR Analysis of Environmental Samples to Assess Coxiella burnetii Infection Status in Small Ruminant Farms.” Applied and Environmental Microbiology 91: e00931-25. https://doi.org/10.1128/aem.00931-25.

  Gardner, Bradley R., Julia C. Laidlaw, Jessica K. H. Tan, Aidan F. A. D. Emery, Karrie Rose, Mathew C. Mahony, et al. 2023. “A Novel Marine Mammal Coxiella burnetii—Genome Sequencing Identifies a New Genotype with Potential Virulence.” Pathogens 12 (7): 893. https://doi.org/10.3390/pathogens12070893.

  Georgiev, M., A. Afonso, H. Neubauer, H. Needham, R. Thiéry, A. Rodolakis, H. Roest, et al. 2013. “Q Fever in Humans and Farm Animals in Four European Countries, 1982 to 2010.” Eurosurveillance 18 (8): 20407.

  Ghanem-Zoubi, Noor, and Mical Paul. 2020. “Q Fever during Pregnancy: A Narrative Review.” Clinical Microbiology and Infection 26 (7): 864–870. https://doi.org/10.1016/j.cmi.2019.10.024.

  Ghanem-Zoubi, Noor, Y. Atiya-Nasagi, E. Stoyanov, M. Szwarcwort, B. Darawsha, M. Paul, and E. Shinar. 2024. “Cross-Sectional Study of Q Fever Seroprevalence among Blood Donors, Israel, 2021.” Emerging Infectious Diseases 30 (5): 941–946. https://doi.org/10.3201/eid3005.230645.

  Gil-Zamorano, J., D. Cifo, M. T. Llorente, M. Rodríguez-Vargas, R. Estévez-Reboredo, D. Gómez-Barroso, et al. 2025. “High Diversity of Coxiella burnetii Genotypes in Q Fever Human Cases from Spain, 2012–2024.” International Journal of Infectious Diseases 158: 107948. https://doi.org/10.1016/j.ijid.2025.107948.

  Gilsdorf, Andreas, Christian Kroh, Sonja Grimm, Elisabeth Jensen, Christine Wagner-Wiening, and Katharina Alpers. 2008. “Large Q Fever Outbreak due to Sheep Farming near Residential Areas, Germany, 2005.” Epidemiology and Infection 136 (8): 1084–1087.

  González-Barrio, David, and Francisco Ruiz-Fons. 2019. “Coxiella burnetii in Wild Mammals: A Systematic Review.” Transboundary and Emerging Diseases 66 (2): 662–671. https://doi.org/10.1111/tbed.13085.

  Graves, Stephen R., and Aminul Islam. 2016. “Endemic Q Fever in New South Wales, Australia: A Case Series (2005–2013).” American Journal of Tropical Medicine and Hygiene 95 (1): 55–59. https://doi.org/10.4269/ajtmh.15-0828.

  Hermans, M. H. A., C. J. J. Huijsmans, J. J. A. Schellekens, P. H. M. Savelkoul, and P. C. Wever. 2011. “Coxiella burnetii DNA in Goat Milk after Vaccination with Coxevac®.” Vaccine 29 (15): 2653–2656. https://doi.org/10.1016/j.vaccine.2011.01.111.

  Hogerwerf, L., R. van den Brom, H. I. J. Roest, A. Bouma, P. Vellema, M. Pieterse, D. Dercksen, and M. Nielen. 2011. “Reduction of Coxiella burnetii Prevalence by Vaccination of Goats and Sheep, the Netherlands.” Emerging Infectious Diseases 17 (3): 379–386. https://doi.org/10.3201/eid1703.101157.

  Hou, K. W., Simon M. Firestone, and Mark A. Stevenson. 2023. “Scenario Tree Modelling to Inform Surveillance Design for Maintaining Freedom from Coxiella burnetii Infection in Australian Commercial Dairy Goat Herds.” Preventive Veterinary Medicine 219: 106024. https://doi.org/10.1016/j.prevetmed.2023.106024.

  Hurtado, Ana, Elodie Rousset, Aurélie Couesnon, Tara de Haan, Frederika Dijkstra, Silke F. Fischer, Pierre-Edouard Fournier, Ana L. García-Pérez, Isabel Jado, Elsa Jourdain, Katja Mertens-Scholz, Tom N. McNeilly, Susan Neale, Jane C. Osborne, Marjan Van Esbroeck, Marcella Mori, and René van den Brom. 2026. “Human Q Fever Outbreak Investigation and Management in Six European Countries: A One Health Compendium of Practices and Recommendations.” CMI Communications. https://doi.org/10.1016/j.cmicom.2026.105195.

  Hurtado, Ana, Ion I. Zendoia, Eva Alonso, Xabier Beraza, Joseba Bidaurrazaga, Blanca Ocabo, Iñaki Arrazola, Aitor Cevidanes, Jesús F. Barandika, and Ana L. García-Pérez. 2023. “A Q Fever Outbreak among Visitors to a Natural Cave, Bizkaia, Spain, December 2020 to October 2021.” Eurosurveillance 28 (28): 2200824. https://doi.org/10.2807/1560-7917.ES.2023.28.28.2200824.

  Jansen, Wiebke, Martina Cargnel, Souad Boarbi, Ilse Mertens, Marjan Van Esbroeck, Daisy Fretin, and Marcella Mori. 2022. “Belgian Bulk Tank Milk Surveillance Program Reveals the Impact of a Continuous Vaccination Protocol for Small Ruminants against Coxiella burnetii.” Transboundary and Emerging Diseases 69 (4): e141–e152. https://doi.org/10.1111/tbed.14273.

  Jaton, Katia, Olivier Peter, Didier Raoult, Jean-Daniel Tissot, and Gilbert Greub. 2013. “Development of a High Throughput PCR to Detect Coxiella burnetii and Its Application in a Diagnostic Laboratory over a 7-Year Period.” New Microbes and New Infections 1 (1): 6–12. https://doi.org/10.1002/2052-2975.8.

  Jourdain, Elsa, Olivier Duron, Séverine Barry, Daniel González-Acuña, and Karim Sidi-Boumedine. 2015. “Molecular Methods Routinely Used to Detect Coxiella burnetii in Ticks Cross-React with Coxiella-like Bacteria.” Infection Ecology & Epidemiology 5: 29230. https://doi.org/10.3402/iee.v5.29230.

  Kersh, Gregory J., K. A. Fitzpatrick, J. S. Self, et al. 2013. “Presence and Persistence of Coxiella burnetii in the Environments of Goat Farms Associated with a Q Fever Outbreak.” Applied and Environmental Microbiology 79 (5): 1697–1703. https://doi.org/10.1128/AEM.03472-12.

  Kersh, Gregory J., K. Fitzpatrick, K. Pletnikoff, M. Brubaker, M. Bruce, and A. Parkinson. 2020. “Prevalence of Serum Antibodies to Coxiella burnetii in Alaska Native Persons from the Pribilof Islands.” Zoonoses and Public Health 67 (1): 89–92. https://doi.org/10.1111/zph.12661.

  Kittelberger, R., J. Mars, G. Wibberley, R. Sting, K. Henning, G. W. Horner, K. M. Garnett, M. J. Hannah, J. A. Jenner, C. J. Pigott, and J. S. O’Keefe. 2009. “Comparison of the Q-Fever Complement Fixation Test and Two Commercial Enzyme-Linked Immunosorbent Assays for the Detection of Serum Antibodies against Coxiella burnetii (Q Fever) in Ruminants.” New Zealand Veterinary Journal 57 (5): 262–268. https://doi.org/10.1080/00480169.2009.58619.

  Klee, S. R., J. Tyczka, H. Ellerbrok, T. Franz, S. Linke, G. Baljer, and B. Appel. 2006. “Highly Sensitive Real-Time PCR for Specific Detection and Quantification of Coxiella burnetii.” BMC Microbiology 6: 2. https://doi.org/10.1186/1471-2180-6-2.

  Koehler, Lisa Marie, Bärbel Kloppert, Hans-Peter Hamann, Amr El-Sayed, and Michael Zschöck. 2019. “Comprehensive Literature Review of the Sources of Infection and Transmission Routes of Coxiella burnetii, with Particular Regard to the Criteria of ‘Evidence-Based Medicine.’” Comparative Immunology, Microbiology and Infectious Diseases 64: 67–72. https://doi.org/10.1016/j.cimid.2019.02.004.

  Körner, Sophia, G. R. Makert, K. Mertens-Scholz, K. Henning, M. Pfeffer, A. M. Nijhof, and S. Ulbert. 2020. “Uptake and Faecal Excretion of Coxiella burnetii by Ixodes ricinus and Dermacentor marginatus Ticks.” Parasites & Vectors 13: 75. https://doi.org/10.1186/s13071-020-3956-z.

  Körner, Sophia, Gustavo R. Makert, Sebastian Ulbert, Martin Pfeffer, and Katja Mertens-Scholz. 2021. “The Prevalence of Coxiella burnetii in Hard Ticks in Europe and Their Role in Q Fever Transmission Revisited—A Systematic Review.” Frontiers in Veterinary Science 8: 655715. https://doi.org/10.3389/fvets.2021.655715.

  Long, Carrie Mae. 2021. “Q Fever Vaccine Development: Current Strategies and Future Considerations.” Pathogens 10 (10): 1223. https://doi.org/10.3390/pathogens10101223.

  Lucchese, Laura, Katia Capello, Antonio Barberio, Federica Zuliani, Arjan Stegeman, Letizia Ceglie, Eulalia Guerrini, Stefano Marangon, and Alda Natale. 2015. “IFAT and ELISA Phase I/Phase II as Tools for the Identification of Q Fever Chronic Milk Shedders in Cattle.” Veterinary Microbiology 179 (1–2): 102–108. https://doi.org/10.1016/j.vetmic.2015.02.010.

  Lurier, Thibaut, Elodie Rousset, Pascal Gasqui, Caroline Sala, Caroline Claustre, Didier Abrial, Philippe Dufour, Renée de Crémoux, Kristel Gache, Marie-Laure Delignette-Muller, and Elsa Jourdain. 2021. “Evaluation Using Latent Class Models of the Diagnostic Performances of Three ELISA Tests Commercialized for the Serological Diagnosis of Coxiella burnetii Infection in Domestic Ruminants.” Veterinary Research 52: 56. https://doi.org/10.1186/s13567-021-00926-w.

  Matthijs, Anneleen, François Claine, Xavier Simons, Ana Soares, Damien Desqueper, Eva Van Mael, and Marcella Mori. 2025. “Pre-Purchase Screening for Coxiella burnetii in Small Ruminants: Farm Acceptance and Field Evaluation Identify the Ex-Vivo Interferon-γ Assay as a Promising Tool.” Frontiers in Veterinary Science 12: 1708200. https://doi.org/10.3389/fvets.2025.1708200.

  Mertens-Scholz, Katja, Amira A. Moawad, Elisabeth M. Liebler-Tenorio, Andrea Helming, Jennifer Andrack, Peter Miethe, Heinrich Neubauer, Mathias W. Pletz, and Ina-Gabriele Richter. 2024. “Ultraviolet C Inactivation of Coxiella burnetii for Production of a Structurally Preserved Whole Cell Vaccine Antigen.” BMC Microbiology 24: 118. https://doi.org/10.1186/s12866-024-03246-z.

  Miller, H. K., R. A. Priestley, and G. J. Kersh. 2020. “Transmission of Coxiella burnetii by Ingestion in Mice.” Epidemiology and Infection 148: e21. https://doi.org/10.1017/S0950268820000059.

  Miller, H. K., R. A. Priestley, and G. J. Kersh. 2021. “Comparison of Three Coxiella burnetii Infectious Routes in Mice.” Virulence 12 (1): 2562–2570. https://doi.org/10.1080/21505594.2021.1980179.

  Mori, Marcella, Katja Mertens, Sally J. Cutler, and Ana Sofia Santos. 2017. “Critical Aspects for Detection of Coxiella burnetii.” Vector-Borne and Zoonotic Diseases 17 (1): 33–41. https://doi.org/10.1089/vbz.2016.1958.

  Muleme, Michael, John Stenos, Gemma Vincent, Colin R. Wilks, Joanne M. Devlin, Angus Campbell, Alexander Cameron, Mark A. Stevenson, Stephen Graves, and Simon M. Firestone. 2017a. “Peripartum Dynamics of Coxiella burnetii Infections in Intensively Managed Dairy Goats Associated with a Q Fever Outbreak in Australia.” Preventive Veterinary Medicine 139: 58–66. https://doi.org/10.1016/j.prevetmed.2017.02.006.

  Muleme, Michael, Angus Campbell, John Stenos, Joanne M. Devlin, Gemma Vincent, Alexander Cameron, Stephen Graves, Colin R. Wilks, and Simon M. Firestone. 2017b. “A Longitudinal Study of Serological Responses to Coxiella burnetii and Shedding at Kidding among Intensively Managed Goats Supports Early Use of Vaccines.” Veterinary Research 48: 50. https://doi.org/10.1186/s13567-017-0452-3.

  Mélenotte, Cléa, C. Protopopescu, Matthieu Million, Sophie Edouard, Marie-Pierre Carrieri, Carole Eldin, E. Angelakis, et al. 2018. “Clinical Features and Complications of Coxiella burnetii Infections from the French National Reference Center for Q Fever.” JAMA Network Open 1 (4): e181580. https://doi.org/10.1001/jamanetworkopen.2018.1580.

  Omsland, Anders, Derek C. Cockrell, Daniel Howe, Elizabeth R. Fischer, Kimmo Virtaneva, David E. Sturdevant, Stephen F. Porcella, and Robert A. Heinzen. 2009. “Host Cell-Free Growth of the Q Fever Bacterium Coxiella burnetii.” Proceedings of the National Academy of Sciences of the United States of America 106 (11): 4430–4434. https://doi.org/10.1073/pnas.0812074106.

  O’Shannessy, Lucy, John K. House, Bridgette G. Logan, John M. Morton, Sam Rowe, Paul A. Sheehy, Benjamin U. Bauer, and Katrina L. Bosward. 2026. “Coxiella burnetii Shedding in Dairy Cattle and Its Correlation with Humoral and Cell-Mediated Immune Responses.” Veterinary Microbiology 317: 111011. https://doi.org/10.1016/j.vetmic.2026.111011.

  Piñero, A., Jesús F. Barandika, Ana Hurtado, and Ana L. García-Pérez. 2014. “Evaluation of Coxiella burnetii Status in Dairy Cattle Herds with Bulk-Tank Milk Positive by ELISA and PCR.” Transboundary and Emerging Diseases 61 (2): 163–168. https://doi.org/10.1111/tbed.12013.

  Raboisson, Didier, Guillaume Lhermie, and Raphaël Guatteo. 2024. “A New Tool to Assess the Economic Impact of Q Fever on Dairy Cattle Farms.” Animals 14 (8): 1166. https://doi.org/10.3390/ani14081166.

  Reukers, Daphne F. M., Pieter T. de Boer, Alfons O. Loohuis, Peter C. Wever, Chantal P. Bleeker-Rovers, Arianne B. van Gageldonk-Lafeber, Wim van der Hoek, and Aura Timen. 2022. “Targeted Screening for Chronic Q Fever, the Netherlands.” Emerging Infectious Diseases 28 (7): 1403–1409. https://doi.org/10.3201/eid2807.212273.

  Rivière, Laureline, Elodie Rousset, Elsa Jourdain, Marie-Laure Delignette-Muller, and Thibaut Lurier. 2025. “Harmonisation of the Diagnostic Performances of Serological ELISA Tests for Coxiella burnetii in Ruminants in the Absence of a Gold Standard: Optimal Cut-Offs and Performances Reassessment.” Preventive Veterinary Medicine 239: 106509. https://doi.org/10.1016/j.prevetmed.2025.106509.

  Rodríguez-Alonso, B., et al. 2020. “Epidemiological Scenario of Q Fever Hospitalized Patients in the Spanish Health System: What’s New.” International Journal of Infectious Diseases 90: 226–233. https://doi.org/10.1016/j.ijid.2019.10.043.

  Roest, Hein I. J., Annet Bossers, Frans G. van Zijderveld, and Jan M. L. Rebel. 2013. “Clinical Microbiology of Coxiella burnetii and Relevant Aspects for the Diagnosis and Control of the Zoonotic Disease Q Fever.” Veterinary Quarterly 33 (3): 148–160. https://doi.org/10.1080/01652176.2013.843809.

  Roest, Hein I. J., J. J. H. C. Tilburg, W. van der Hoek, P. Vellema, F. G. van Zijderveld, C. H. W. Klaassen, and D. Raoult. 2011. “The Q Fever Epidemic in the Netherlands: History, Onset, Response and Reflection.” Epidemiology and Infection 139: 1–12. https://doi.org/10.1017/S0950268810002268.

  Rousset, Elodie, Benoit Durand, Mustapha Berri, Philippe Dufour, Myriam Prigent, Pierre Russo, Thibault Delcroix, Anne Touratier, Annie Rodolakis, and Michel Aubert. 2007. “Comparative Diagnostic Potential of Three Serological Tests for Abortive Q Fever in Goat Herds.” Veterinary Microbiology 124 (3–4): 286–297. https://doi.org/10.1016/j.vetmic.2007.04.033.

  Rousset, Elodie, Mustapha Berri, Benoit Durand, Philippe Dufour, Myriam Prigent, Thibault Delcroix, Anne Touratier, and Annie Rodolakis. 2009. “Coxiella burnetii Shedding Routes and Antibody Response after Outbreaks of Q Fever-Induced Abortion in Dairy Goat Herds.” Applied and Environmental Microbiology 75 (2): 428–433. https://doi.org/10.1128/AEM.00690-08.

  Rousset, Elodie, Myriam Prigent, R. Brugidou, I. Martel, A. Grob, G. Le Gall, S. Kerninon, J. Delaval, A. Chassin, B. Vassiloglou, et al. 2012. “Adoption by a Network’s Laboratories of a Validated Quantitative Real-Time PCR Method for Monitoring Q Fever Abortions in Ruminant Livestock.” Euroreference 8: 21–28.

  Ruiz-Fons, Francisco, Ianire Astobiza, Jesús F. Barandika, Ramón A. Juste, Ana Hurtado, and Ana L. García-Pérez. 2011. “Measuring Antibody Levels in Bulk-Tank Milk as an Epidemiological Tool to Search for the Status of Coxiella burnetii in Dairy Sheep.” Epidemiology and Infection 139 (10): 1631–1636. https://doi.org/10.1017/S0950268810003134.

  Schimmer, B., R. ter Schegget, M. Wegdam, L. Züchner, A. de Bruin, P. M. Schneeberger, P. Veenstra, et al. 2010. “The Use of a Geographic Information System to Identify a Dairy Goat Farm as the Most Likely Source of an Urban Q-Fever Outbreak.” BMC Infectious Diseases 10: 69. https://doi.org/10.1186/1471-2334-10-69.

  Schneeberger, Peter M., C. Wintenberger, Wim van der Hoek, and J. P. Stahl. 2014. “Q Fever in the Netherlands—2007–2010: What We Learned from the Largest Outbreak Ever.” Médecine et Maladies Infectieuses 44 (8): 339–353.

  Sánchez, J., A. Souriau, A. J. Buendía, N. Arricau-Bouvery, C. M. Martínez, J. Salinas, A. Rodolakis, and J. A. Navarro. 2006. “Experimental Coxiella burnetii Infection in Pregnant Goats: A Histopathological and Immunohistochemical Study.” Journal of Comparative Pathology 135 (2–3): 108–115. https://doi.org/10.1016/j.jcpa.2006.06.003.

  Sivabalan, Pirathaban, Apoorva Saboo, James Yew, and Robert Norton. 2017. “Q Fever in an Endemic Region of North Queensland, Australia: A 10 Year Review.” One Health 3: 51–55. https://doi.org/10.1016/j.onehlt.2017.03.002.

  Tissot-Dupont, H., M. A. Amadei, M. Nezri, and D. Raoult. 2004. “Wind in November, Q Fever in December.” Emerging Infectious Diseases 10 (7): 1264–1269. https://doi.org/10.3201/eid1007.030724.

  Toledo-Perona, Raquel, Antonio Contreras, Jesús Gomis, Juan José Quereda, Ana García-Galán, Antonio Sánchez, and Ángel Gómez-Martín. 2024. “Controlling Coxiella burnetii in Naturally Infected Sheep, Goats and Cows, and Public Health Implications: A Scoping Review.” Frontiers in Veterinary Science 11: 1321553. https://doi.org/10.3389/fvets.2024.1321553.

  Tomaiuolo, Sara, Wiebke Jansen, Susana Soares Martins, Bert Devriendt, Eric Cox, and Marcella Mori. 2023. “QuilA® Adjuvanted Coxevac® Sustains Th1-CD8+-Type Immunity and Increases Protection in Coxiella burnetii-Challenged Goats.” npj Vaccines 8: 17. https://doi.org/10.1038/s41541-023-00607-z.

  van Asseldonk, M. A. P. M., D. M. Bontje, J. A. Backer, H. J. W. van Roermund, and R. H. M. Bergevoet. 2015. “Economic Aspects of Q Fever Control in Dairy Goats.” Preventive Veterinary Medicine 121 (1–2): 115–122. https://doi.org/10.1016/j.prevetmed.2015.06.010.

  van den Brom, René, E. van Engelen, H. I. J. Roest, W. van der Hoek, and P. Vellema. 2015. “Coxiella burnetii Infections in Sheep or Goats: An Opinionated Review.” Veterinary Microbiology 181 (1–2): 119–129. https://doi.org/10.1016/j.vetmic.2015.07.011.

  van den Brom, René, Susan Neale, Elsa Jourdain, Anneleen Matthijs, Marcella Mori, Elodie Rousset, Katja Mertens-Scholz, Tom N. McNeilly, and Ana Hurtado. 2025. “Detection of Abortifacient Agents in Domestic Ruminants, with a Specific Focus on Coxiella burnetii.” Open Research Europe 5: 94. https://doi.org/10.12688/openreseurope.19270.2.

  van Leuken, Jeroen P. G., Jan van de Kassteele, Ferd J. Sauter, Wim van der Hoek, Dick Heederik, Arie H. Havelaar, and Arno N. Swart. 2015. “Improved Correlation of Human Q Fever Incidence to Modelled Coxiella burnetii Concentrations by Means of an Atmospheric Dispersion Model.” International Journal of Health Geographics 14: 14. https://doi.org/10.1186/s12942-015-0003-y.

  Wallensten, A., P. Moore, H. Webster, C. Johnson, G. van der Burgt, G. Pritchard, et al. 2010. “Q Fever Outbreak in Cheltenham, United Kingdom, in 2007 and the Use of Dispersion Modelling to Investigate the Possibility of Airborne Spread.” Eurosurveillance 15 (12): 19521. https://doi.org/10.2807/ese.15.12.19521-en.

  Wambua, Lillian, Bernard Bett, Hussein M. Abkallo, Mathew Muturi, Daniel Nthiwa, Richard Nyamota, Enock Kiprono, et al. 2025. “National Serosurvey and Risk Mapping Reveal Widespread Distribution of Coxiella burnetii in Kenya.” Scientific Reports 15: 9706. https://doi.org/10.1038/s41598-025-94154-3.

  Wattiau, Pierre, Erika Boldisova, Rudolf Toman, Marjan Van Esbroeck, Sophie Quoilin, Sonia Hammadi, H. Tissot-Dupont, Didier Raoult, J.-M. Henkinbrant, M. Van Hessche, and D. Fretin. 2011. “Q Fever in Woolsorters, Belgium.” Emerging Infectious Diseases 17 (12): 2368–2369. https://doi.org/10.3201/eid1712.101786.

  Whelan, J., B. Schimmer, P. Schneeberger, J. Meekelenkamp, A. Ijff, W. van der Hoek, and M. Robert-Du Ry van Beest Holle. 2011. “Q Fever among Culling Workers, the Netherlands, 2009–2010.” Emerging Infectious Diseases 17 (9): 1719–1723. https://doi.org/10.3201/eid1709.110051.

  Williams-Macdonald, Sarah E., Mairi Mitchell, David Frew, Javier Palarea-Albaladejo, David Ewing, William T. Golde, David Longbottom, Alasdair J. Nisbet, Morag Livingstone, Clare M. Hamilton, and Tom N. McNeilly. 2023. “Efficacy of Phase I and Phase II Coxiella burnetii Bacterin Vaccines in a Pregnant Ewe Challenge Model.” Vaccines 11 (3): 511. https://doi.org/10.3390/vaccines11030511.

  Winter, Friederike, and Alexander Campe. 2022. “Q Fever Expertise among Human and Veterinary Health Professionals in Germany—A Stakeholder Analysis of Knowledge Gaps.” PLoS ONE 17 (3): e0264629. https://doi.org/10.1371/journal.pone.0264629.

  Wittwer, Marcel, Philipp Hammer, Martin Runge, Peter Valentin-Weigand, Heinrich Neubauer, Klaus Henning, and Katja Mertens-Scholz. 2022. “Inactivation Kinetics of Coxiella burnetii During High-Temperature Short-Time Pasteurization of Milk.” Frontiers in Microbiology 12: 753871. https://doi.org/10.3389/fmicb.2021.753871.

  Zendoia, Ion I., Aitor Cevidanes, Ana Hurtado, Patricia Vázquez, Marta Barral, Jesús F. Barandika, and Ana L. García-Pérez. 2022. “Stable Prevalence of Coxiella burnetii in Wildlife after a Decade of Surveillance in Northern Spain.” Veterinary Microbiology 268: 109422. https://doi.org/10.1016/j.vetmic.2022.109422.

  Zendoia, Ion I., Jesús F. Barandika, Aitor Cevidanes, Ana Hurtado, and Ana L. García-Pérez. 2024. “Coxiella burnetii Infection Persistence in a Goat Herd during Seven Kidding Seasons after an Outbreak of Abortions: The Effect of Vaccination.” Applied and Environmental Microbiology 90: e02201-23. https://doi.org/10.1128/aem.02201-23.

  2. Reports, standards and regulatory documents

  EFSA and ECDC. 2025. “The European Union One Health 2024 Zoonoses Report.” EFSA Journal 23 (12): e9759. https://doi.org/10.2903/j.efsa.2025.9759.

  EFSA Panel on Animal Health and Welfare. 2010. “Scientific Opinion on Q Fever.” EFSA Journal 8 (5): 1595. https://doi.org/10.2903/j.efsa.2010.1595.

  EFSA, ECDC, EMA, EEA, and ECHA. 2024. “The Framework for Action of the Cross-Agency One Health Task Force.” One Health 19: 100768. https://doi.org/10.1016/j.onehlt.2024.100768.

  EFSA. 2023. “Prioritisation of Zoonotic Diseases for Coordinated Surveillance Systems under the One Health Approach for Cross-Border Pathogens that Threaten the Union.” EFSA Journal 21 (3): e7853. https://doi.org/10.2903/j.efsa.2023.7853.

  European Commission: Directorate-General for Research and Innovation, Group of Chief Scientific Advisors. 2024. One Health Governance in the European Union. Scientific Opinion No. 16. Luxembourg: Publications Office of the European Union. https://doi.org/10.2777/8697309.

  Rousset, Elodie, and Myriam Prigent. 2023. Final Inter-Laboratory Proficiency Testing Program Report (FQELSE23): Q Fever Serology on Serum by ELISA. Sophia Antipolis: ANSES, Sophia Antipolis Laboratory, Animal Q Fever Unit.

  Rousset, Elodie, and Myriam Prigent. 2024. Final Inter-Laboratory Proficiency Testing Program Report (FQPCRMV24): PCR Detection and/or Quantification of Coxiella burnetii for the Diagnosis of Abortion in Ruminants. Sophia Antipolis: ANSES, Sophia Antipolis Laboratory, Animal Q Fever Unit.

  Sidi-Boumedine, Karim, Elodie Rousset, Kerstin Henning, Michael Ziller, Krzysztof Niemczuk, Hein I. J. Roest, and Richard Thiéry. 2010. “Development of Harmonised Schemes for the Monitoring and Reporting of Q-Fever in Animals in the European Union.” EFSA Supporting Publications 7 (5): EN-48. https://doi.org/10.2903/sp.efsa.2010.EN-48.

  World Organisation for Animal Health. 2018. “Q Fever.” In Manual of Diagnostic Tests and Vaccines for Terrestrial Animals, Chapter 3.1.18. Paris: WOAH.

  World Organisation for Animal Health. 2024. “Chapter 8.22. Infection with Coxiella burnetii (Q Fever).” In Terrestrial Animal Health Code. Paris: WOAH.

  3. Web resources / project pages

  CoxBase. n.d. “CoxBase: Online Platform for Epidemiological Surveillance, Visualization, Analysis, and Typing of Coxiella burnetii Genomic Sequences.” Accessed May 21, 2026. https://coxbase.q-gaps.de/.

  European Medicines Agency. n.d. “Coxevac.” EMA Medicines: Veterinary EPAR. Accessed May 21, 2026. https://www.ema.europa.eu/en/medicines/veterinary/EPAR/coxevac.

  MST Coxiella burnetii Database. n.d. “MST Database for Coxiella burnetii.” IHU Méditerranée Infection. Accessed May 21, 2026. https://ifr48.timone.univ-mrs.fr/mst/coxiella_burnetii/.

  Q Fever Interest Group. n.d. “QFIG — Q Fever Interest Group.” Accessed May 21, 2026. https://qfig.au/.

  Q-Net-Assess. n.d. “Improved Molecular Surveillance and Assessment of Host Adaptation and Virulence of Coxiella burnetii in Europe.” Accessed May 21, 2026. https://q-net-assess.com/.