foot-and-mouth disease in pigs
Don't need the entire report?
Generate a print friendly version containing only the sections you need.Generate report
PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- foot-and-mouth disease in pigs
International Common Names
- English: foot and mouth; foot and mouth disease in ruminants and pigs - exotic
- Spanish: aftosa; fiebre aftosa
- French: fièvre aphteuse
Local Common Names
- Argentina: fiebre
- Spain: glosopeda
- USA: hoof and mouth disease
OverviewTop of page
Foot-and-mouth disease (FMD) is a highly contagious viral disease of cloven footed animals (artiodactyls), characterised by fever, vesicles on the buccal mucosa and feet and sudden death in the young of susceptible species. FMD is caused by an aphthovirus, an RNA virus with a positive-sense single-stranded genome, in the family Picornaviridae. There are seven serotypes of FMD virus, namely O, A, C, ASIA 1, SAT (South African Territories) 1, SAT 2, and SAT 3. Domestic cattle, pigs, sheep, goats, buffalo and all species of wild ruminant and pig are susceptible. FMD is an OIE (Office International des Epizooties) List disease, and is probably the most important constraint to trade in live animals and their products (Kitching, 1998).
The distribution section contains data from OIE's World Animal Health Information Database (WAHID) on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Bos grunniens (yaks)||Domesticated host; Wild host|
|Bos indicus (zebu)||Domesticated host; Wild host||Cattle & Buffaloes: All Stages|
|Bos mutus (yaks, wild)||Domesticated host; Wild host|
|Bos taurus (cattle)||Domesticated host; Wild host||Cattle & Buffaloes: All Stages|
|Bubalus bubalis (Asian water buffalo)||Domesticated host; Wild host||Cattle & Buffaloes: All Stages|
|Camelus bactrianus (Bactrian camel)||Domesticated host; Wild host|
|Capra hircus (goats)||Domesticated host; Wild host||Sheep & Goats: All Stages|
|Lama glama (llamas)||Domesticated host; Wild host|
|Lama pacos (alpacas)||Domesticated host; Wild host|
|Ovis aries (sheep)||Domesticated host; Wild host||Sheep & Goats: All Stages|
|Ruminantia||Domesticated host; Wild host|
|Sus scrofa (pigs)||Domesticated host; Wild host||Pigs: All Stages|
Systems AffectedTop of page
digestive diseases of pigs
skin and ocular diseases of pigs
DistributionTop of page
FMD is endemic in Africa, most of Asia, the Middle East and parts of South America. Analysis of outbreak data over a number of years has demonstrated the global clustering of FMD viruses and identified 7 virus pools, where multiple serotypes occur but within which are topotypes that remain mostly confined to that pool (Hammond et al., 2011). The World Reference Laboratory for FMD (WRLFMD®) have defined 3 pools covering Europe, the Middle-East and Asia containing serotypes O, A and Asia 1, 3 pools covering Africa containing serotypes O, A, and SATs 1, 2 & 3 and 1 pool covering the Americas containing serotypes O and A. This distribution enables a regional approach to be taken to assist global control of FMD. An increased regional knowledge of FMD outbreaks and identification of these within particular reservoirs or pools of FMD activity can greatly assist globally informed regional FMD control programmes. It also follows that if vaccination is to be a major tool for control, each pool could benefit from investigation into the use of tailored or more specific vaccines relevant to the topotypes present in that pool, rather than a continued reliance on the currently more widely available vaccines.
Over recent years there has been a notable increase in the incidence of FMD outbreaks reported in Asia and the Middle East and a concurrent spread of the serotypes O (Pan-Asia 2 strain) and A (Iran 05 strain). In 2010-2011 Japan, Republic of Korea and Bulgaria all suffered type O FMD outbreaks, losing their status as countries listed by OIE as FMD-free without vaccination. In 2012 Japan and Bulgaria regained their status as free without vaccination but the Republic of Korea has embarked on a prolonged programme of vaccination.
Current trends show that globally the serotype most commonly identified is type O, with more than 80% of isolates characterized by the OIE/FAO FMD reference laboratory network in 2010-2011 being of this serotype (Hammond, 2012). However, in 2011-2012 there has been a marked increase in the number of reports of serotypes Asia 1 in pool 3 and in early 2012 a rapid spread of SAT 2 through North Africa into Libya and Egypt and on into the Middle East to the Palestine Autonomous Territories. In 2012 so far WRLFMD® have observed that more than 25% of samples tested were found to be type Asia 1 and 14% to be SAT 2 (Hammond et al., 2012).
Serotype C has not been reported since 2004 where it was detected in Brazil and Kenya. However, it may still be present in regions where surveillance is minimal or not possible due to difficult or restricted access. The SAT serotypes have never established outside of Africa, although in 2000, SAT 2 was found in Saudi Arabia and in 2012 spread from Egypt to Palestine Autonomous Territories.
The World Reference Laboratory for foot and mouth disease (WRLFMD®) located at the renamed Pirbright Institute, UK (formerly The Institute for Animal Health) is responsible for maintaining global surveillance and coordinating the OIE/FAO FMD reference laboratory network. Much of the information generated by WRLFMD® is available on their website located at http://www.pirbright.ac.uk/.
OIE publishes a report each year in which it lists FMD-free countries (see: www.oie.int/en/animal-health-in-the-world/official-disease-status/fmd/list-of-fmd-free-members/).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Cabo Verde||Absent, No presence record(s)|
|Central African Republic||Present|
|Côte d'Ivoire||Present||CAB Abstracts Data Mining|
|Djibouti||Absent, No presence record(s)|
|Guinea-Bissau||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Réunion||Absent, No presence record(s)|
|São Tomé and Príncipe||Absent, No presence record(s)|
|Seychelles||Absent, No presence record(s)|
|Brunei||Absent, No presence record(s)|
|China||Present||Present based on regional distribution.|
|Malaysia||Present||Present based on regional distribution.|
|-Sabah||Absent, No presence record(s)|
|-Sarawak||Absent, No presence record(s)|
|United Arab Emirates||Present||2003|
|Iceland||Absent, No presence record(s)|
|Isle of Man||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Barbados||Absent, No presence record(s)|
|Belize||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Costa Rica||Absent, No presence record(s)|
|Cuba||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|Dominican Republic||Absent, No presence record(s)|
|El Salvador||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Jamaica||Absent, No presence record(s)|
|Martinique||Absent, No presence record(s)|
|Nicaragua||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)|
|Trinidad and Tobago||Absent, No presence record(s)|
|French Polynesia||Absent, No presence record(s)|
|New Caledonia||Absent, No presence record(s)|
|New Zealand||Absent, No presence record(s)|
|Samoa||Absent, No presence record(s)|
|Vanuatu||Absent, No presence record(s)|
|Falkland Islands||Absent, No presence record(s)|
DiagnosisTop of page
Clinical signs and lesions
In pigs, clinical signs include fever, inappetance and reluctance to move. Vesicles may occur, particularly on the feet (coronets, interdigital skin) and may cause lameness. They may lead to separation of the keratinized layers of the hoof from the corium. Also, vesicles can develop on the snout and, in a lower frequency, on the tongue. Sows often develop vesicles on their teats. Pregnant sows may abort. The mortality may be high in sucking piglets.
FMD is indistinguishable from other vesicular viral diseases (vesicular stomatitis, swine vesicular disease, vesicular exanthema) and should be confirmed or excluded using suitable tests. Also, differential diagnoses should include rinderpest, mucosal disease, bovine viral diarrhoea, infectious bovine rhinotracheitis, bluetongue, bovine mamillitis and bovine papular stomatitis.
The best samples are epithelium of the vesicles from the mouth or foot, and vesicular fluid from the unruptured vesicles. Epithelium samples of between 1 and 2 cm² are satisfactory. Epithelial samples should be placed in a transport medium that maintains a pH 7.2-7.4 and is kept cool.
From ruminants, oesophageal-pharyngeal fluid (OPF) should be collected using a probang cup. The OPF should be diluted with buffer phosphate.
FMD virus causes an acute disease in over 70 species of cloven-hoofed animals but primarily it is the disease in farmed livestock such as cattle, sheep, goats, pigs and buffalo that requires laboratory diagnosis and confirmation. The disease is associated with the development of vesicles on epithelial surfaces of the mouth and feet and infection also generates a transient viraemia in infected animals that typically lasts for approximately five days (Alexandersen et al., 2003).
Tests that exploit these clinical windows in an infected animal form the basis of laboratory approaches currently used to diagnose FMD. These assays aim to detect FMDV in epithelium and fluid from vesicles, as well as in blood and swabs from mucosal surfaces (oral and nasal swabs). In addition, FMDV-specific antibody responses in exposed animals can be detected using serological assays.
Most commonly diagnosis is by observation of clinical signs (see Disease Course) and the subsequent isolation of live virus on tissue culture coupled with the identification of viral antigen by ELISA or viral nucleic acid by reverse transcription polymerase chain reaction (RT-PCR). Increase of specific antibody may also be used to indicate recovery from infection. Amplification of specific nucleic acid sequences using RT-PCR is now widely used for the laboratory detection of FMDV. These molecular assays are suitable for the diverse range of different samples that might be submitted for laboratory investigation (tissues, blood, swabs, oesophageal or pharyngeal (OP) scrapings, faecal samples and milk). Over the past 15 years, improvements have been made to RT-PCR protocols used for the detection of FMDV and real-time RT-PCR (rRT-PCR) assays have now largely replaced agarose gel based assay formats. These more rapid fluorescence-based approaches are highly sensitive enabling simultaneous amplification and quantification of FMDV specific nucleic acid sequences. In addition to enhanced sensitivity, the benefits of these closed-tube rRT-PCR assays over conventional endpoint detection methods include a reduced risk of cross-contamination, their large dynamic range, an ability to be scaled up for high-throughput applications and the potential for accurate target quantification. Several assays have been developed to detect FMDV that use 5’-nuclease assay (TaqMan®) system to detect PCR amplicons (Callahan et al., 2002; Oem et al., 2005; Reid et al., 2002). Other formats exploited for FMDV-specific rRT-PCR assays include the use of modified minor groove binder (MGB) probes (McKillen et al., 2011; Moniwa et al., 2007), hybridisation probes (Moonen et al., 2003), Primer-probe energy transfer (PriProET: Rasmussen et al., 2003) and RT-linear-after-the-exponential PCR (LATE PCR: Reid et al., 2010). In order to minimise human operator errors and increase assay throughput, these assays can be automated using robots for nucleic acid extraction (Moonen et al., 2003). Together with the implementation of quality control systems, these improvements have increased the acceptance of the rRT-PCR assays for routine diagnostic purposes.
More recently, lateral-flow devices (LFDs, also referred to as immuno-chromatographic strip tests or point of care tests) have been developed for the detection of FMD viral antigen. These simple-to-use and rapid tests utilise FMDV specific antibody reagents (normally monoclonal antibodies) in a format similar to the sandwich capture ELISA used for laboratory diagnosis. Positive test signal is generated by the diffusion of coloured, antibody-coated latex beads or colloidal gold particles through a membrane towards an immobilising band of trapping antibody. An LFD has been developed for the detection of all seven FMDV serotypes which uses a pan-serotypic monoclonal antibody (Ferris et al., 2009). In addition, sample preparation in field conditions can be achieved using simple disposable tissue homogenizers for preparing epithelial suspensions. In terms of diagnostic sensitivity and specificity, the overall performance of this LFD is similar to laboratory-based antigen ELISA, although the diagnostic sensitivity of the current test is lower for SAT 2 field strains (Ferris et al., 2009) and a separate Sat 2 LFD has been developed for this reason.
Epithelium from ruptured lesions is the most suitable sample to collect for diagnosis. This should be placed in 50% PBS-Glycerol plus antibiotics at neutral pH, and kept at 4°C or -20°C until submission to a laboratory capable of carrying out FMD diagnosis. This is usually the national laboratory, but samples may also be sent to the World Reference Laboratory for FMD at the Pirbright Institute (formerly The Institute for Animal health) Pirbright, UK. If submitting to the World Reference Laboratory, it is necessary to first contact for submission requirements (www.pirbright.ac.uk, Fax 00441483232621). The sample is prepared at the laboratory as a 10% suspension and inoculated onto a susceptible cell culture.
Primary bovine thyroid cells are the most sensitive indicator of virus presence, but lamb kidney may also be used. If the sample is fresh, and there are likely to be high levels of viral antigen present, the suspension may be used directly in an ELISA, which will also indicate the serotype. Virus recovered from tissue culture should also be typed by ELISA. Once isolated, the virus can be sequenced, if not locally, then at the World Reference Laboratory, to provide epidemiological data as to its likely origin, by comparison with other sequences in the Reference Laboratory database. It can also be used to help identify the most relevant vaccine strain to help control the outbreak by antigenic comparisons with existing vaccine strains (Kitching et al., 1989).
Serology for FMD virus antibodies is by ELISA (liquid phase blocking) (Hamblin et al., 1987), solid phase competition ELISA (Paiba et al., 2004) and non structural protein (NSP) antibody ELISA. The ‘gold standard’ test is still considered to be the virus neutralisation test (VNT), however, this test requires the use of tissue culture facilities and the handling of live FMD virus which may not be possible in some laboratories. The ELISA’s can give false positives which should be confirmed by VNT. The LPB and SPC ELISA’s and VNT are serotype specific, but several ELISAs for detecting antibodies to the NSP’s such as 3ABC have been developed which are non-serotype specific and some are now commercially available The NSP antibody tests do have the advantage of allowing the distinction of antibodies produced following infection and those induced by vaccination (Clavijo et al., 2004) and can be used for surveillance and demonstration of disease freedom. FMD vaccines are inactivated and, although they may contain some non-structural protein (particularly 3D), the antibody response to these proteins is much lower than following an infection.
The NSP tests are recommended by the OIE to support declaration of freedom from infection after emergency vaccination. Extensive validation of NSP tests has been carried out and demonstrates acceptable accuracy (for example Nanni et al., 2005; Sørensen et al., 2005; Brocchi et al., 2006); but the existing tests are still considered insufficiently sensitive and specific under field conditions to be used on an individual animal basis, and should be applied at herd level only (Bronsvoort et al., 2004; Brocchi et al., 2006).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Difficulty in prehending or chewing food||Pigs:All Stages||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Pigs:All Stages||Diagnosis|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Pigs:All Stages||Diagnosis|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:All Stages||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Sign|
|General Signs / Reluctant to move, refusal to move||Pigs:All Stages||Sign|
|General Signs / Sudden death, found dead||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Pain / Discomfort Signs / Forefoot pain, front foot||Pigs:All Stages||Diagnosis|
|Pain / Discomfort Signs / Hindfoot pain, rear foot||Pigs:All Stages||Diagnosis|
|Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain||Pigs:All Stages||Diagnosis|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Reproductive Signs / Mastitis, abnormal milk||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Pigs:All Stages||Diagnosis|
|Skin / Integumentary Signs / Nail, claw, hoof sloughing, separation||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Sign|
Disease CourseTop of page
The course of foot-and-mouth disease (FMD) is acute. The incubation period is variable and depends mainly on the strain and doses of virus, route of entry, and level of immunity. It may oscillate between 2-3 days and 10-14 days (Salt 1993; Sellers 1969).
The respiratory system is the usual primary site of FMDV infection (Burrows 1981). Early sites of FMDV replication are in the glandular cells of the mucous membrane and associated lymphoid tissues. Within 2-4 h, replicating virus can be detected in the upper respiratory tract secretions.
Following the primary virus replication, FMDV is disseminated to secondary sites that include the epithelial tissues in and around the mouth and feet, mammary glands, glandular organs and other lymphoid nodes, and cardiac muscle. This first stage of the infection is subclinical and large amounts of FMDV are shed in secretions and other body fluids.
After between 72 and 96 h the fever begins. As a result of the infection, the cells of the stratum spinosum of the epithelium vacuolate, swell and burst (Bekkum, 1959; Yilma, 1980). The intercellular fluid coalesces into vesicles. Affected animals show inappetance, lameness and reluctance to move, sudden death due to cardiac failure is common in piglets.
At 5 days post-infection (dpi), the vesicles in the coronets may extend round the top of the hoof so that the horn becomes separate. Vesicles can also appear in lips, tongue and teats. Pregnant sows may abort. Rising serum antibody titre coincides with a precipitous reduction in the titre of virus shed in external body fluids. Resolution is usually complete by 14 dpi. The lesions heal, although secondary bacterial infection can complicate these lesions.
Most excretion of the virus ceases about 4-6 days after the appearance of vesicles. The virus has been detected in the milk and semen of experimentally infected cattle for 23 and 56 days, respectively.
After clinical recovery, up to 60% of ruminant animals may become persistently infected. This persistent infection is established in the pharyngeal and cranial oesophageal tissues. The duration of the carrier state varies with, among other factors, species of animal affected, and strain of virus. The maximum reported carrier periods for different species are in cattle 2.5 years, sheep and goats for up to 9 months, African buffaloes, 5 years or more (Prato Murphy et al., 1994; Salt, 1993). Pigs do not become carriers.
The virus can be recovered intermittently from such animals by oesophageal-pharyngeal (OP) probang collections. The quantity and frequency of virus that can be collected decreases progressively with time.
Vaccinated animals may become infected. Although they are fully protected against clinical disease, they may develop carrier state (Prato Murphy et al., 1994; Salt, 1993).
EpidemiologyTop of page
Foot-and-mouth disease (FMD) is one of the most contagious of animal diseases. Cattle are the most susceptible of the domesticated species to FMDV, as little as 10 tissue culture infectious doses are required to establish infection by inhalation. Cattle are therefore the principal indicators of the disease. Pigs are important amplifiers because their capacity to excrete large quantities of virus (Sellers et al., 1971). Sheep are maintenance hosts since they can display very slight symptoms (Sellers et al., 1971).
The most common method of spread is by the movement of infected animals; however, FMD may also spread in products from infected animals (such as milk, semen and meat), by movement of people, vehicles or articles contaminated with virus from infected animals; or as an aerosol. The FMD virus is very susceptible to acid (pH 9) conditions, and the lactic acid in the meat of slaughtered animals that has been kept for 24 h at 4ºC to 'set' will kill the virus; but the virus will survive in the bone marrow and glands in which the pH remains close to neutral. With some strains the main means of transmission is as an aerosol, and infected animals, particularly pigs, can produce large amounts of virus in their breath, depending on the strain of virus - pigs may produce up to log10 8.6 TCID50 (tissue culture infectious doses) per day, and cattle and sheep, up to log10 5.2 TCID50 per day. Under the right weather conditions, an aerosol of infectious virus can spread as a discrete plume over considerable distances, having been recorded to have spread 250 km from France to southern England in 1981 (these outbreaks were quickly eliminated); over land, the plume is more likely to be disrupted, and spread in excess of 16 km is unlikely. The distance over which the virus can travel by the airborne route varies with virus strain and host species (Alexandersen and Donaldson, 2002). Cattle and sheep may be infected with as little as 20 TCID50 of virus by the respiratory route, while pigs require greater amounts (800 TCID50, but depends on strain of virus). All species are considerably less susceptible to infection by the oral route. FMD virus will quickly die at relative humidity below 60% RH, and is very susceptible to drying in the environment. At neutral pH and moist conditions, the virus can persist for a few weeks in contaminated premises or pasture (Donaldson, 1979; Donaldson, 1987).
FMDV infection of susceptible animals in the field occurs primarily through the upper respiratory tract by inhalation of airborne virus from an infected animal (Burrows et al., 1981; Donaldson et al., 1989; Eskildsen, 1969). Aerosol transmission usually occurs with animals in close proximity. However, there is circumstantial evidence that animals may be infected from several yards to many miles downwind from a source of infection (Hyslop, 1965; Sangar, 1979). The oesophageal-pharyngeal (OP) fluid, respiratory aerosols, saliva, vaginal and tracheal mucus, faeces, milk, and semen of infected animals may contain virus before appearance of clinical signs and lesions of the disease. Whilst lesions are present, FMDV is also present in the epithelium and vesicular fluids. Therefore, the disease may spread rapidly by movement of infected animals. Pigs do not become carriers. Other species after clinical signs may become persistently infected for variable periods (between 6 and 36 months in cattle, 4-9 months in sheep and goats and in the African Buffalo for at least 5 years) (Burrows et al., 1981, 1966; Prato-Murphy, 1994; Straver et al., 1970; Terpstra et al., 1990; Bekkum et al., 1960). Reports of field outbreaks indicate that convalescent cattle may transmit the disease when introduced into a FMD-free herd (Sangar, 1979). The role of carrier animals in the transmission has never been demonstrated experimentally in cattle and sheep. There is only one study that shows transmission of virus from carrier buffaloes to cattle under field conditions (Dawe et al., 1994; Hedger et al., 1985).
In many areas reservoir hosts are important factors in the epidemiology of foot-and-mouth disease. The African buffalo maintains the SAT serotype (in particular SAT1 and 3) in those countries which have a wild buffalo population, and there are many examples of transmission direct to cattle (Bastos et al., 1999) or transmission to impala, which then infect cattle (Bastos et al., 2000). Very little is known about the involvement of Indian buffalo in the epidemiology of FMD, although they will develop clinical disease and transmit infection to cattle. Other wild ruminants, such as deer, are susceptible to FMD, but usually as the recipient of FMD virus from cattle; there are no examples of FMD being maintained in a wild ruminant population other than in African buffalo.
Indirect transmission of infection is important because the virus can retain infectivity for a considerable time in the environment (Cottral 1969). The virus is inactivated in the meat of carcasses that undergo the normal post-slaughter acidification processes, but it persists for a very long time in frozen or chilled lymph nodes, bone marrow and residual blood clots. It also retains infectivity in uncooked, salted and cured meats, and unpasteurized milks (Cottral, 1969).
Higher titres of virus are required in all species to cause disease by ingestion. The virus may also gain entrance and establish the initial infection through abrasions in the mucous membranes or skin (Sellers, 1971; Sutmoller, 1976). Infection is also possible through the skin from a local trauma or abrasions.
Transmission is possible through artificial insemination, and contaminated embryos. However, embryo transplantation using properly collected and washed embryos does not constitute a risk (Sutmoller, 1976).
Transmission via arthropod or parasite vectors is possible, but is not considered important.
Generally, all susceptible animals in an exposed herd develop infection but under some circumstances, the incidence of disease is considerably less than 100%. Young animals are usually more susceptible than adults, unless protected by maternal antibodies arising from previous infection or vaccination. The climate may affect the spread of the virus. Hot, dry weather may slow the spread of epidemics.
Disease TreatmentTop of page
In recent years there has been a resurgence of interest in treatment as the huge cost of stamping out the disease has become much more expensive where the disease is out of control.
T-705 (favipiravir) is an experimental anti-FMDV drug that has been tested in pigs in Japan with activity and side-effects not fully understood at present (Furuta et al., 2009).
Prevention and ControlTop of page
Animals in endemic areas may be given some protection with prophylactic vaccination. The seven serotypes of FMD virus are immunologically distinct, and recovery from infection or vaccination with one serotype does not provide protection against the other six. In addition, within each serotype there are a large number of strains representing a spectrum of antigenic characteristics. It is therefore necessary to antigenically match the outbreak strain with a suitable vaccine strain, or even produce a new vaccine strain. Protection with even a closely matched vaccine will only last for approximately 6 months, and in endemic situations it is usually necessary to vaccinate cattle three times yearly, and sheep twice-yearly. Calves from vaccinated cows are protected for up to 4 months by colostral antibody, although this may be for a shorter time depending on the frequency of vaccination. The dose of vaccine varies according to the manufacturer and whether they are able to concentrate the antigen. There are no live vaccines officially in use worldwide. Adjuvant for ruminant FMD vaccines can be either aluminium hydroxide plus saponin or oil; for pigs it must be oil, either as a single or double emulsion. Other control measures should also be used to control outbreaks such as quarantine, disinfection and movement restrictions.
Countries usually free of FMD generally control outbreaks by slaughtering all infected and in-contact animals, and implementing strict movement controls and other zoosanitary measures (‘stamping out’). More extensive slaughter policies, including culling of animals on adjacent premises and small ruminants and pigs within 3 km of infected premises, were used during the UK epidemic in 2001. The effectiveness of such pre-emptive slaughter in controlling the spread of infection is controversial. It is important to note that vaccination is now expected to be considered as part of any response to an FMD outbreak in a free country and that those countries which hold FMD antigen banks should be prepared with practical contingency plans for deployment of vaccination should the situation arise.
Most FMD-free countries maintain the option to vaccinate by participating in FMD antigen banks, which they would take advantage of should the slaughter policy prove ineffective. There is still some reluctance to use vaccine because of the possibility that some of the vaccinated cattle that contacted live field virus would become carriers. However, recent scientific advances should allow a more rapid return to FMD-free status. This could be achieved through a combined approach involving improved vaccines and better use of rapid diagnostic tests to detect early infection and persistent infection accurately and competent data management. This is reflected by the increased priority given to vaccination in current FMD contingency plans, such as those of the European Union countries (Laddomada, 2003).
The use of vaccine delays the re-establishment of freedom from FMD status, as it affects international trade (Kitching et al., 1998; Barteling and Vreeswijk, 1991; Kitching, 1992; Kitching and Salt, 1995; Woolhouse et al. 1996; OIE, 1998). This restriction, however, is now less onerous: the OIE reduced the time period for regaining FMD-free status following emergency vaccination from the original 12 to 6 months, provided that non-structural proteins (NSP) tests are used to document that the remaining vaccinated population is free of infection.
ReferencesTop of page
African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp. http://www.au-ibar.org/index.php?option=com_flexicontent&view=items&cid=71&id=109&Itemid=56&lang=en
Alexandersen S, Quan M, Murphy C, Knight J, Zhang Z, 2003. Studies of quantitative parameters of virus excretion and transmission in pigs and cattle experimentally infected with foot-and-mouth disease virus. Journal of Comparative Pathology, 129(4):268-282.
Bachrach HL, 1968. Foot-and-mouth disease virus. Ann. Rev. Microbiology, 22:201-244.
Bastos ADS, Bertschinger HJ, Cordel C, Vuuren Cde WJvan, Keet D, Bengis RG, Grobler DG, Thomson GR, 1999. Possibility of sexual transmission of foot-and-mouth disease from African buffalo to cattle. Veterinary Record, 145(3):77-79; 16 ref.
Bastos ADS, Boshoff CI, Keet DF, Bengis RG, Thomson GR, 2000. Natural transmission of foot-and-mouth disease virus between African buffalo (Syncerus caffer) and impala (Aepyceros melampus) in the Kruger National Park, South Africa. Epidemiology and Infection, 124 (3):591-598.
Bekkum JG van, Straver PJ, Bool P, Frenkel S, 1959. Further information on the persistence of infective FMDV. Tijdschrift voor Diergeneekunde, 84:1159-1164.
Bekkum JG van, Straver PJ, Bool P, Frenkel S, 1960. Further information on the persistence of infective FMDV in cattle exposed to virulent virus strain. Bull. Off. Int. Epiz., 65:1949-1965.
Brocchi E, Bergmann IE, Dekker A, Paton DJ, Sammin DJ, Greiner M, Grazioli S, Simone Fde, Yadin H, Haas B, Bulut N, Malirat V, Neitzert E, Goris N, Parida S, Sørensen K, Clercq Kde, 2006. Comparative evaluation of six ELISAs for the detection of antibodies to the non-structural proteins of foot-and-mouth disease virus. Vaccine, 24(47/48):6966-6979. http://www.sciencedirect.com/science/journal/0264410X
Bronsvoort BM de C, Sørensen KJ, Anderson J, Corteyn A, Tanya VN, Kitching RP, Morgan KL, 2004. Comparison of two 3ABC enzyme-linked immunosorbent assays for diagnosis of multiple-serotype foot-and-mouth disease in a cattle population in an area of endemicity. Journal of Clinical Microbiology, 42:2108-2114.
Brown F, Cartwright B, 1960. Purification of the virus of foot and mouth disease by fluorocarbon treatment and its dissociation from neutralizing antibody. J. Immunol., 85:309-313.
Burrows R et al., 1981. The pathogenesis of natural and simulated natural FMD infection in cattle. J. Comp. Path., 91:599-609.
Callahan JD, Brown F, Osorio FA, Sur JH, Kramer E, Long GW, Lubroth J, Ellis SJ, Shoulars KS, Gaffney KL, Rock DL, Nelson WM, 2002. Use of a portable real-time reverse transcriptase-polymerase chain reaction assay for rapid detection of foot-and-mouth disease virus. Journal of the American Veterinary Medical Association, 220(11):1636-1642; 16 ref.
Clavijo A, Wright P, Kitching P, 2004. Developments in diagnostic techniques for differentiating infection from vaccination in foot-and-mouth disease. The Veterinary Journal, 167:9-22.
Cottral GE, 1969. Persistence of FMDV in animals, their products and the environment. Bull. Off. Int. Epiz., 71(3-4):549-568.
Dawe PS, Sorensen K, Ferris NP, Barnett ITR, Armstrong RM, Knowles NJ, 1994. Experimental transmission of foot-and mouth disease virus from carrier African buffalo (Syncerus caffer) to cattle in Zimbabwe. Veterinary Record, 134(9):211-215; 14 ref.
DEFRA, 2002. Department for Environment, Food and Rural Affairs, UK. http://www.defra.gov.uk/animalh/diseases/fmd/.
Donaldson AI, 1979. Airborne foot-and-mouth disease. The Veterinary Bulletin, 49:653-659.
Donaldson AI, 1987. Foot-and-mouth disease: The principal features. Irish Veterinary Journal, 41:325-327.
Eskildsen MK, 1969. Experimental pulmonary infection of cattle with FMDV. Nordisk Veterinaer Medicin, 21:86- 91.
Ferris NP, Nordengrahn A, Hutchings GH, Reid SM, King DP, Ebert K, Paton DJ, Kristersson T, Brocchi E, Grazioli S, Merza M, 2009. Development and laboratory validation of a lateral flow device for the detection of foot-and-mouth disease virus in clinical samples. Journal of Virological Methods, 155(1):10-17. http://www.sciencedirect.com/science/journal/01660934
Furuta Y, Takahashi K, Shiraki K, Sakamoto K, Smee DF, Barnard DL, Gowen BB, Julander JG, Morrey JD, 2009. T-705 (favipiravir) and related compounds: novel broad-spectrum inhibitors of RNA viral infections. Antiviral Research, 82(3):95-102. http://www.sciencedirect.com/science/journal/01663542
Hamblin C, Kitching RP, Donaldson AI, Crowther JR, Barnett ITR, 1987. Enzyme-linked immunosorbent assay (ELISA) for the detection of antibodies against foot-and-mouth disease virus. III. Evaluation of antibodies after infection and vaccinations. Epidemiology and Infection, 99(3):733-744; 14 ref.
Hammond JM, 2012. OIE/FAO FMD Reference Laboratory Network Annual Report 2011. http://www.wrlfmd.org/ref_labs/fmd_ref_lab_reports.htm
Hammond JM, Ferris NP, Li YanMin, Knowles NJ, King DP, Paton DJ, 2011. The global situation of foot and mouth disease occurrence - an overview. In: First OIE/FAO global conference on foot and mouth disease: the way towards global control, Asunción, Paraguay, 24-26 June, 2009. Paris, France: OIE (World Organisation for Animal Health), 11-20.
Hammond JM, King D, Knowles N, Mioulet V, Li Y, 2012. Analysis of the worldwide FMD situation, trends and regional differences. In: Second OIE/FAO Global Conference on foot and mouth disease, Bangkok, Thailand, 27-29 June 2012.
Hedger RS, Condy JB, 1985. Transmission of foot and mouth disease from African buffalo virus carriers to bovines. Vet. Rec., 117, 205.
House C, House JA, 1989. Evaluation of techniques to demonstrate foot-and-mouth disease virus in bovine tongue epithelium: comparison of the sensitivity of cattle, mice, primary cell cultures, cryopreserved cell cultures and established cell lines. Veterinary Microbiology, 20(2):99-109; 26 ref.
Hyslop NSTG, 1965. Ariborne infection with with the virus of FMD. J. Comp. Path., 75:119-126.
Kitching RP, 1992. The application of biotechnology to the control of foot-and-mouth disease virus. British Veterinary Journal, 148: 375-388.
Kitching RP, 1992. Viral diseases. Foot-and-mouth disease. Bovine medicine: diseases and husbandry., 537-543; 4 ref.
Kitching RP, 1998. A recent history of foot-and-mouth disease. Journal of Comparative Pathology, 118:89-108.
Kitching RP, Knowles NJ, Samuel AR, Donaldson AI, 1989. Development of foot-and-mouth disease virus strain characterisation - A review. Tropical Animal Health and Production, 21:153-166.
Kitching RP, Salt JS, 1995. The interference of maternally derived antibody with active immunization of farm animals against foot-and-mouth disease. British Veterinary Journal, 151:379-389.
Laddomada A, 2003. Control and eradication of OIE List A diseases: The approach of the European Union to the use of vaccines. In: Brown F, Roth J, eds. Vaccines for OIE List A and Emerging Animal Disease. Developmental Biology. Basel, Switzerland: Karger, 114:269-280.
Loeffler F, Rrosch P, 1898. Berichte deer Kammission zur Erforschung der maul-und Klauenseuche bei dem institut fur Infektions krankheiten in Berlin. Zentralbatt fur Bacteriologie, Parasitenkunde und Infektionskrankheithen, 1(23):371-391.
Mackay DKJ, 1988. Differentiating infection from vaccination in FMD. The Vet. Quarterly, 20(Supplement 2, May).
McCauley EH et al., 1977. A study of the potential economic impact of foot and mouth disease in US Proceedings of United States Animal Health Association, 81st Annual Meeting, 284-305.
McKillen J, McMenamy M, Reid SM, Duffy C, Hjertner B, King DP, Bélak S, Welsh M, Allan G, 2011. Pan-serotypic detection of foot-and-mouth disease virus using a minor groove binder probe reverse transcription polymerase chain reaction assay. Journal of Virological Methods, 174(1/2):117-119. http://www.sciencedirect.com/science/journal/01660934
Meyer RF, Brown CC, House C, House JA, Molitor TW, 1991. Rapid and sensitive detection of foot-and-mouth disease virus in tissues by enzymatic RNA amplification of the polymerase gene. Journal of Virological Methods, 34(2):161-172; 14 ref.
Moniwa M, Clavijo A, Li MingYi, Collignon B, Kitching PR, 2007. Performance of a foot-and-mouth disease virus reverse transcription-polymerase chain reaction with amplification controls between three real-time instruments. Journal of Veterinary Diagnostic Investigation, 19(1):9-20.
Moonen P, Boonstra J, Hakze-van der Honing R, Boonstra-Leendertse C, Jacobs L, Dekker A, 2003. Validation of a LightCycler-based reverse transcription polymerase chain reaction for the detection of foot-and-mouth disease virus. Journal of Virological Methods, 113(1):35-41.
Nanni M, Alegre M, Compaired D, Taboga O, Fondevila N, 2005. Novel purification method for recombinant 3AB1 nonstructural protein of foot-and-mouth disease virus for use in differentiation between infected and vaccinated animals. Journal of Veterinary Diagnostic Investigation, 17:248-251.
Oem JaeKu, Kye SooJeong, Lee KwangNyeong, Kim YongJoo, Park JeeYong, Park JongHyeon, Joo YiSeok, Song HeeJong, 2005. Development of a Lightcycler-based reverse transcription polymerase chain reaction for the detection of foot-and-mouth disease virus. Journal of Veterinary Science, 6(3):207-212.
Office International Des Epizooties, 1998. International Animal Health Code.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
OIE, 1999. Resolution XI and XII 64th General Session. International Committee.
OIE, 2001. Handistatus II. Office International des Epizooties. World Wide Web page at http://www.oie.int/eng/info/en_bdd.htm.
OIE, 2003. Foot and mouth disease in Bolivia: follow-up report No. 4 (final report). Disease Information. 16(41).
OIE, 2003. Foot and mouth disease in the United Arab Emirates. Disease Information, 16(19):111.
OIE, 2004. Foot and mouth disease in Brazil. Disease Information. 17(25).
OIE, 2004. Foot and mouth disease in Israel. Follow-up report No. 2 (final report). Disease Information. 17(19).
OIE, 2004. Foot and mouth disease in Libya. Follow-up report No. 6 (final report). 17(3).
OIE, 2004. Foot and mouth disease in Mongolia. Follow-up report No. 2 (final report). 17(43).
OIE, 2004. Foot and mouth disease in Peru. Follow-up report No. 2 (final report). 17(38).
OIE, 2004. Foot and mouth disease in Russia. Follow-up report No. 1. Disease Information, 17(18).
OIE, 2004. Foot and mouth disease in Zambia. Follow-up report No. 5. 17(25).
OIE, 2004. Foot and mouth diseases in Tajikistan. Disease Information, 17, No. 7.
OIE, 2005. Foot and mouth disease in Hong Kong, special administrative region of the People’s Republic of China. Virus type Asia 1. Disease Information. 18(12).
OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int/wahis_2/public/wahid.php/Wahidhome/Home
Paiba GA, Anderson J, Paton DJ, Soldan AW, Alexandersen S, Corteyn M, Wilsden G, Hamblin P, MacKay DKJ, Donaldson AI, 2004. Validation of a foot-and-mouth disease antibody screening solid-phase competition ELISA (SPCE). Journal of Virological Methods, 115:145-158.
Pereira HG, 1981. Foot and mouth disease. In: Gibbs EPJ, ed., Virus disease of foot animals. London, UK: Academic Press Inc, 333-363.
Prato-Murphy ML et al. , 1994. Analysis of sites of foot-and-mouth disease virus persistence in carrier cattle via the polymerase chain reaction. Arch. Virol., 136:299-307.
Rasmussen TB, Uttenthal A, Stricker Kde, Belák S, Storgaard T, 2003. Development of a novel quantitative real-time RT-PCR assay for the simultaneous detection of all serotypes of Foot-and-mouth disease virus. Archives of Virology, 148(10):2005-2021.
Reid SM, Ferris NP, Hutchings GH, Zhang ZhiDong, Belsham GJ, Alexandersen S, 2002. Detection of all seven serotypes of foot-and-mouth disease virus by real-time, fluorogenic reverse transcription polymerase chain reaction assay. Journal of Virological Methods, 105(1):67-80.
Reid SM, Pierce KE, Mistry R, Bharya S, Dukes JP, Volpe C, Wangh LJ, King DP, 2010. Pan-serotypic detection of foot-and-mouth disease virus by RT linear-after-the exponential PCR. Molecular and Cellular Probes, 24:250-255.
Rodriguez LL, Gay CG, 2011. Development of vaccines toward the global control and eradication of foot-and-mouth disease. Expert Review of Vaccines, 10(3):377-387.
Rueckert RR, 1985. Picornaviruses and their replication. In: Fields BN, ed. Virology. New York, USA: Raven Press.
Ryan MD, Belsham GJ, King AMQ, 1989. Specificity of enzyme-substrate interactions in foot-and-mouth disease virus polyprotein processing. Virology, 173:33-45.
Salt JS, 1993. The carrier state in foot-and-mouth disease - an immunological review. British Veterinary Journal, 149:207-223.
Sangar D, 1979. The replication of Picornaviridae. Journal of General Virology, 45:1-13.
Sellers RF et al., 1969. Exposure of vaccinated bulls and steers to airborne infection with FMD. Vet. Rec., 85(7):198-199.
Sellers RF, 1971. Quantitative aspects of the spread of foot-and-mouth disease. Vet. Bull., 41(6):431-439.
Sellers RF, Herrniman KAJ, Mann JA, 1971. Transfer of foot-and-mouth disease virus in the nose of man from infected to non-infected animals. Vet. Rec., 89(16):447-449.
Straver PJ, Bool PH, Claessens AM, van Bekkum JG, 1970. Some properties of carrier strains of FMDV. Arch. Ges. Virusforsch, 29:113-126.
Sutmoller P, Gaggero CA, 1965. Foot and Mouth Disease carriers. The Veterinary Record, 77:968-969.
Sutmoller P, McVicar, 1976. Pathogenesis of FMD: the lung as an additional portal of entry of the virus. Journal of Hygiene, Cambridge, 77:235-243.
Sørensen KJ, Stricker K de, Dyrting KC, Grazioli S, Haas B, 2005. Differentiation of foot-and-mouth disease virus infected animals from vaccinated animals using a blocking ELISA based on baculovirus expressed FMDV 3ABC antigen and a 3ABC monoclonal antibody. Archives of Virology, 150:805-814.
Terpstra C, Maanen Cvan, Bekkum JGvan, 1990. Endurance of immunity against foot-and-mouth disease in cattle after three consecutive annual vaccinations. Research in Veterinary Science, 49(2):236-242; 24 ref.
Yilma T, 1980. Morphogenesis of vesiculation in FMD. Am. J. Vet. Res., 41:1537-1542.
CABI, Undated. Compendium record. Wallingford, UK: CABI
CABI, Undated a. CABI Compendium: Status inferred from regional distribution. Wallingford, UK: CABI
CABI, Undated b. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
OIE, 2004. Foot and mouth disease in Brazil. In: Disease Information, 17 (25) Paris, France: World Organisation for Animal Health.
OIE, 2004a. Foot and mouth disease in Libya. Follow-up report No. 6 (final report). In: Disease Information, 17 (3) Paris, France: World Organisation for Animal Health.
OIE, 2004b. Foot and mouth disease in Peru. Follow-up report No. 2 (final report). In: Disease Information, 17 (38) Paris, France: World Organisation for Animal Health.
OIE, 2004c. Foot and mouth disease in Russia. Follow-up report No. 1. In: Disease Information, 17 (18) Paris, France: World Organisation for Animal Health.
OIE, 2005. Foot and mouth disease in Hong Kong, special administrative region of the People's Republic of China. Virus type Asia 1. In: Disease Information, 18 (12) Paris, France: World Organisation for Animal Health.
Distribution MapsTop of page
Select a dataset
CABI Summary Records
Unsupported Web Browser:
One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/