Foot-and-Mouth Disease Pathogenesis and Control

Foot‐and‐mouth disease (FMD) is an acute, highly contagious viral illness of cloven‐hoofed animals, caused by foot‐and‐mouth disease virus (FMDV), a member of the Picornaviridae family. Seven serotypes (O, A, C, Asia-1, SAT1–3) circulate globally, with limited cross-protection among them. Infection typically follows inhalation or ingestion of contaminated material, leading to primary replication in the oropharyngeal and nasopharyngeal epithelium. A brief viraemic phase disseminates virus to secondary sites, notably the stratified epithelium of the mouth and feet, resulting in characteristic vesicular lesions. Host innate defences—principally type I interferons—are antagonised by viral proteinases, allowing rapid viral amplification. Clinical disease manifests as fever, salivation, lameness and weight loss. In ruminants a subclinical carrier state may ensue, with virus persisting in the nasopharynx for months, posing a threat to disease-free zones. Economic impact is vast, encompassing production losses, trade restrictions and the costs of stamping-out, vaccination and surveillance. Control relies on rapid detection, movement restrictions, biosecurity, ring vaccination with serotype-matched inactivated vaccines and, where feasible, emergence of marker (DIVA) vaccines. Advances in vaccine platforms, risk-based surveillance and molecular diagnostics underpin more precise epidemiological tracing and tailored immunisation strategies. A One Health perspective is essential, recognising socio-economic and ecological drivers of FMD spread and the public-good nature of veterinary services.

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Foot-and-Mouth Disease Pathogenesis and Control publication trend

The graph below shows the total number of articles in foot-and-mouth disease pathogenesis and control across all publications each year (not limited to Nature Index journals).

Technical terms

Autophagy: A cellular degradation pathway in which cytoplasmic material is sequestered in double-membrane vesicles and delivered to lysosomes, often subverted by viruses to modulate host immunity.

Carrier state: A subclinical phase in ruminants during which FMDV persists in the nasopharyngeal mucosa without overt disease, posing a risk for virus transmission.

Leader proteinase (Lpro): A viral protease that cleaves host translation factors and interferon pathway components, essential for FMDV virulence and immune evasion.

Interferon regulatory factor 3 (IRF3): A transcription factor activated in response to viral infection that drives the expression of type I interferon genes.

Vesicular lesions: Fluid-filled blisters on the tongue, lips, feet and teats of infected animals, characteristic of acute FMD.

References

1. Foot-and-mouth disease virus VP1 degrades YTHDF2 through autophagy to regulate IRF3 activity for viral replication. Autophagy (2024).
2. Leaderless foot-and-mouth disease virus serotype O did not cause clinical disease and failed to establish a persistent infection in cattle. Emerging Microbes & Infections (2024).
3. The Foot-and-Mouth Disease Carrier State Divergence in Cattle. Journal of Virology (2016).
4. The economic impacts of foot and mouth disease – What are they, how big are they and where do they occur?. Preventive Veterinary Medicine (2013).
5. Foot-and-mouth disease: past, present and future. Veterinary Research (2013).