Foot-and-Mouth Disease (FMD)

Occurrence: Africa, Asia, Eastern Europe; South America; notifiable in all countries.
Age affected: All ages.
Cause: FMD virus.
Effects: Lameness, blisters on tongue, snout and feet.


Foot-and-Mouth Disease is caused by the Foot-and-Mouth disease (FMD) virus, an aphthovirus. Seven distinct serotypes occur (A, O, C, S.A.T.1, S.A.T.2, S.A.T.3, Asia 1), each with several subtypes.

The virus may be cultivated in bovine or pig kidney cells, or bovine tongue epithelium. It is stable between pH 6 and pH 8, is rapidly destroyed by sunlight, remains for many months at 4-7°C, and for years when frozen. The virus can remain infective for 20 weeks on straw, is rapidly destroyed in meat, but may persist for up to 6 months in bone marrow and 4-5 months in lymph nodes.

Infection takes place by the respiratory and oral routes and through abrasions on the skin. Virus multiplies in the throat or at the point of entry and then in other parts of the body. Vesicles (blisters) develop, particularly on the coronary band and tongue. Virus is shed by aerosol within 24 hours of the first signs. Vesicles rupture and if uncontaminated, heal rapidly. Those on the feet may result in destruction of growing horn and loss of the hoof. Immunity develops within 3-7 days of the clinical signs, lasts only 6 months but only protects fully against the virus subtype involved.

Blisters at pig claw.
Photo credit: Central Veterinary Institute, the Netherlands.

Mode of transmission

Foot-and-Mouth Disease virus is shed by aerosol and from ruptured vesicles on tongue, snout and feet. It infects by direct contact with infected pigs, by inhalation and by the consumption of contaminated feed or water. The disease is extremely infectious for pigs and infection spreads rapidly within a farm, carried during pig movements, by aerosol within airspaces and by contaminated footwear, clothing, implements and even, passively, within the human respiratory passages.

As pigs are infectious before the clinical signs develop, spread may occur before the presence of the disease is recognised. Infection dies out in an individual pig within 30 days and no permanent carrier state is present. The virus survives outside the body for the times given above, and contaminated material is a major means by which the infection survives between hosts.

Spread between farms is by aerosol, and infected plumes carrying virus can travel for many km, especially across water. Spread occurs through pig movements from farm to farm, in transport especially through slaughterhouse traffic and through markets in the past. The virus disappears rapidly in muscle, but many outbreaks have resulted from the consumption of improperly cooked swill (garbage). The virus affects cattle and sheep which can infect pigs and may be carried passively from farm to farm by birds.

Clinical signs

The most obvious clinical sign is the sudden onset of severe lameness in a group of pigs which rapidly spreads to others in the same herd. The back may be arched, reluctance to move is common and movement may be accompanied by squealing. Affected pigs are often lying down, reluctant to rise, with feet which are obviously painful. Vesicles appear as raised, white areas 0.51 cm in diameter on the top of the tongue, on the snout and on the udder of the suckling sow and may rupture readily to leave small ulcers. Vesicles also develop on the coronet in the interdigital space, and on the supernumerary digits.

When they rupture, they cause shallow ulcers which heal as dark streak on the horn or even result in undermining of the horn. The damaged horn is shed to leave the sensitive claw uncovered. Fever (up to 41°C, 106°F) accompanies the earliest stages of the disease. Frothy saliva may be present. Affected animals are depressed, do not eat and lose condition. Mortality rarely exceeds 5%, but it may reach 50% in piglets when sudden death occurs before vesicles develop in either piglets or the sows.

Clinical signs of severe lameness spreading in a group or herd should lead to suspicion of FMD and inspection of the feet, snouts and tongues of lame pigs will confirm the presence of vesicles. This confirms the presence of a vesicular condition which could also be swine vesicular disease (or vesicular stomatitis or Seneca Valley Virus in America). Vesicles may be sufficient to confirm the diagnosis if the case is linked to a known outbreak of FMD. Chronic or recovering cases may be difficult to identify as marks in the hoof horn may be the only sign of disease. In most countries, suspect cases must be reported to the state veterinarian who will then supervise confirmation of diagnosis. Confirmation is by laboratory examination of fresh lesion material taken from suspected clinical cases. Virus may be detected and identified by: the complement fixation test using antibody to all 7 viral serotypes; a Polymerase Chain Reaction (RT-PCR) test for viral RNA; isolation in tissue culture; ELISA and radioimmunoassay. Serum from recovered cases and population may be tested for antibody.

Blister on the pig's nose. 
Photo credit: Central Veterinary Institute, the Netherlands.

Postmortem lesions

Post-mortem examination only confirms the presence of vesicles, a fevered carcase and patchy necrosis of the heart muscle in young pigs which have died. Marks in the hoof horn or loss of the horn from a digit may be the only sign of disease in recovered pigs. Vesicle fluid is taken for laboratory diagnosis if present.

Treatment and prevention

There is no treatment. Control in the European Union and many other countries is based on compulsory notification of suspected cases, followed by slaughter, disinfection of farm lorries and personnel using approved disinfectants, and strict control of movement of pigs. Occurrence must be reported immediately to OIE and agreed trade restrictions are promptly put in place.

As the virus can spread by wind for tens of kilometres over land, and up to 200 km over water and affect cattle and sheep, vaccination may be used strategically in areas surrounding an outbreak in combination with the existing slaughter policy. In countries where the disease is enzootic, annual vaccination is practised. Inactivated vaccines are used most frequently. Pigs are not readily immunised and require high concentrations of virus, although immunity has been demonstrated for up to 9 months using oil adjuvanted vaccines. These cause granulomatous reactions and should be given into the pinna of the ear or intraperitoneally.

More modern adjuvants such as montanide may also be used. One or more different serotypes may be included. Protection may take 7-20 days to develop and re-vaccination is required every 6-8 months. Piglets are difficult to protect. The disease is kept out of the European Union, North America and Australasia by control over the import of animals and animal products, quarantine, and by a ban on the use of waste foods containing animal products for feeding pigs. Where this is still allowed, waste food should be properly cooked and waste fed pigs go only to slaughter.

Claw horns letting loose is a result of secondary infections that occur in an FMD infection. Photo credit: RBI Beeldbank - Central Veterinary Institute, the Netherlands.

Special note

This is one of the most important diseases of pigs and suspicion of the disease MUST be reported immediately to the sate veterinary authorities who impose movement restrictions and confirm the diagnosis using an approved laboratory. If confirmed, OIE is informed immediately and trade in live pigs and pig products from the affected country/region is suspended. Government officials then impose a slaughter policy together with disinfection until the outbreak is deemed to be over. Any vaccination programme can only take place with government approval.