Foot and Mouth disease



Highly contagious disease affecting cloven-hoofed animals, responsible for the outbreak of vesicles and erosion on the buccal mucosa, between the claws and on udders.



Direct loss:

- High morbidity but low mortality

- Significant loss in milk and meat production

- High cost of disease control measures

Indirect loss:

- Prohibition of animal movement and sale of products

- Obstruction to international commerce (embargo of infected countries)

- Drop in prices

Susceptible species: 

Cloven-hoofed animals:

Domestic: bovines, ovines, caprines, porcines.

Wild: ruminants (cervidae, buffalos) and wild boars.


Highly resistant. Rare infection occurring through massive exposure.

Asymptomatic affection the most often. Rarely, fever, headache, sore throat and ulcers.

Etiological agent: 

Naked RNA virus from the family Picornaviridae Aphtovirus genus.

7 immunologically distinct serotypes offering no cross-protection: A, O, C, SAT1, SAT2, SAT3, Asia1.


Survives in the outside environment and resists cold but is sensitive to heat and to acid and basic pH. It is destroyed in meat through the maturation process but persists in the spinal cord and lymph nodes.

Methods of transmission

Early viral excretion occurs after the appearance of symptoms.

Infected, pre-symptomatic infected, asymptomatic infected and chronic or recovered carriers are all sources of the virus. As are animal products: unpasteurised milk, cured meat, unsterilized swill.

Virulent matter:

Breath, all secretions and excretions: ulcers, saliva, expectoration, blood, milk, semen, embryos and runts.


Direct: through contact. Rapid dissemination of the virus in susceptible populations, accentuated where animal population is dense (intensive farming, fairs and animal markets)

Indirect: animate vectors (people, other animals), inanimate vectors (vehicles, airborne). Diffusion of the virus between farms over long distances.

NB: In tropical regions it seems that transmission occurs more through direct contact than through airborne vectors. Weather conditions are less favourable to virus survival than in temperate countries.

Method of contamination: 

Contamination mainly through oropharyngeal mucosa. Bovines become contaminated mainly by respiratory route and suidae by oral route.

Receptivity and sensitivity factors

• Pigs: amplifying hosts. Massive viral excretion in breath. Play an important role in airborne/windborne dissemination of the virus.

• Bovines: Reveal virus circulation. Extreme susceptibility and high capacity for infection through respiratory route.

• Small ruminants: disease reservoir. Low susceptibility, asymptomatic infection, favourable to silent viral propagation.


Incubation period: 2 to 14 days.


Viremia stage: hyperthermia, exhaustion, inappetence, drop in milk production.

Stable phase: painful ulcers (vesicles then ulcers)

- in the mouth (tongue, gums, cheeks, palate) leading to dysphagia, chewing and abundant saliva.

- between the claws, responsible for stamping and lameness.

- on the udders (teats)

Final stage: recovery in 8-15 days, prolonged convalescence and persistence of sequelae (hoof deformation, udder lesions, decreased production). Even recovered animals lose their economic value.

Complications: weight-loss, secondary bacterial infections, mastitis, claw loss, myocarditis, calf death

Ovines and caprines:

Less severe clinical progression which may go unnoticed except where ovine virus strain tropism induces marked symptoms.

Less marked lesions in the mouth, primarily foot lesions, agalactia, casting, death of young stock.


Fever, loss of appetite, refusal to move.

Sometimes exclusive serious foot lesions, visible easy limping on hard ground.

Groin and teats affected, casting, high mortality among piglets.

Macroscopic lesions: 


Ulcers: superficial vesicles that burst within 24 hours leaving ulcers that heal (mouth) or become infected (feet).


Myocarditis: heart muscle necrosis in young animals, "tiger heart" appearance

Rumen pillar vesicular lesions.

Clinical diagnosis: 

Ulcers, salivation, stamping, lameness, mammilitis and death of young animals are all signs of foot and mouth disease which should be confirmed by a laboratory rapidly given the degree of contagiousness.

Differential diagnosis: 

Foot and mouth disease should not be confused (depending on the species) with:


mucosal disease

gangrenous coryza

papular stomatitis

vesicular stomatitis

infectious rhinotracheitis

mouth traumatism



blue tongue

contagious ecthyma

sheep pox

foot rot




vesicular disease

vesicular stomatitis

vesicular exanthema

foot rot

biotin deficiency

Virological diagnosis: 

- Samples:

Carried out on ulcer, foot or other lesions on several animals. Possibility of brush sampling of oesopharyngeal fluid.

Ideally: ulcers before they burst (liquid + epithelium > 2 cm2) or the most recent ulcers.

Refrigerated transfer at a pH of 7.2 – 7.4.

! Make sure regulations are respected with regards to ulcer sample transport.

- Techniques:


• Complement fixation

• Virus isolation on cell culture


Serological diagnosis: 

- Samples: blood sample in a dry tube.

- Techniques:

• ELISA: The latest ELISA tests developed distinguish between vaccine antibodies (ELISA 3D, 3C, 3ABC).

• Virus neutralisation test

• VIAA (virus infection-associated antigen) tests are being progressively replaced by the more sensitive ELISA tests.


No specific treatment is available.


Refer to the legislation and strategy in force in the country concerned.

Sanitary prophylaxis

This is difficult as the virus is highly contagious and resistant and affects numerous susceptible species through various methods of dissemination.

Defensive measures:

Protection of disease-free areas:

- Monitoring and control of animal movements on area borders.

- Prohibition of live animals and animal products from affected countries.

- Quarantine on importation of live animals.

- Prohibition of the use of unsterilized swill.

Offensive measures :

- Isolation and culling of infected animals and susceptible animals having entered into contact with infected animals.

- Destruction of carcasses, litter and products from susceptible animals

- Cleaning and disinfection of premises and equipment + depopulation.

- Controlled human and animal movement.

- Increased monitoring of herds.

- Sterilization of swill.

Medical prophylaxis

Routine vaccination

This strategy is based on the efficacy and harmlessness of the vaccine and requires high vaccinal coverage of the susceptible population.

Combined with a culling and restriction of animal movement policy in the case of an outbreak this strategy limits virus propagation and greatly reduces the number of outbreaks

Strategic vaccination

Strategy employed in countries where prevalence is too high for culling and/or wide scale vaccination to be implemented.

The aim is to limit the impact of the disease by combing strategic vaccination with other measures (monitoring, quarantine, zoning, etc.).

Emergency vaccination

• Covering vaccination for the infected area:

The aim is to reduce the quantity of virus produced by infected animals at the source of the disease (e.g.: pigs) and to limit disease dissemination while waiting for the infected herd to be slaughtered.

• Covering vaccination around the infected area:

The aim is to create a "belt" of vaccinated animals around a source and to limit dissemination of the infection outside this area.


Two types of monovalent or multivalent inactivated virus vaccines exist:

• Vaccine with an aluminium hydroxide - saponin emulsion (ruminants)

• Oil emulsion vaccine (pigs and ruminants)

The vaccine strain is to be chosen according to the strain present in the affected area.


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