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Preferred Scientific Name
foot-and-mouth disease in ruminants
International Common Names
bovine foot-and-mouth disease, FMDV infection, foot-and-mouth disease, ovine foot-and-mouth disease, foot and mouth disease in ruminants and pigs - exotic
foot-and-mouth disease virus
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 probably the most important constraint to trade in live animals and their products (Kitching, 1998; Mann and Sellers, 1990).
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). 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: http://www.oie.int/.
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 in Palestine Autonomous Territories.
Foot-and-mouth disease is one of the most widespread TAD on the African continent where serotypes A, O, SAT 1 and SAT 2 were reported in 2011 (AU-IBAR, 2011). Some exceptional epidemiological events relating to FMD were notified from the southern part of the continent (South Africa, Botswana, Namibia) due to serotypes O, SAT 1 and SAT 2.
A total of 902 outbreaks of FMD were reported to the African Union Interafrican Bureau for Animal Resources (AU-IBAR) from 28 countries in 2011 compared to 454 outbreaks from 24 countries in 2010 and 378 outbreaks from 26 countries in 2009 (see table below). In 2011, a total of 86,185 cases leading to 2804 deaths, with an estimated case fatality rate of 3.25% were reported from the infected countries. Ethiopia (721), followed by Eritrea (404), Benin (355), Burkina Faso (305) and Uganda (137) reported the highest number of fatalities within the year.
All the countries listed, except Cote d'Ivoire, Eritrea and Uganda, have been reporting FMD outbreaks over the past several years.
Countries reporting FMD to the AU-IBAR
|Central African Republic||12||1330||115||0||0|
With regards to the monthly distribution in Africa, FMD appears to occur throughout the year. However, the level of FMD occurrence showed a sharp increase between April and September, and a decreasing trend between October and April. It is difficult to explain this trend without undertaking a comprehensive study to understand the temporal distribution of the main risk factors underpinning FMD occurrence on the continent.
The table below shows the confirmed serotypes that were involved in some of the outbreaks that occurred between 2006 and 2011 (AU-IBAR, 2011). In 2011, only 6 out of 28 (6/28) countries that reported FMD outbreaks provided information about the serotypes, compared to 4/23, 2/20 and 7/24 in 2008, 2009 and 2010, respectively. It is evident that the serotypes of the majority of outbreaks are not known, an indication of either the weakness of the laboratory capacity or lack of laboratory support to FMD outbreak investigations in the continent. It is also apparent that the majority of the reported cases were diagnosed based on clinical signs, further demonstrating the weak link between field epidemiological investigation and laboratory diagnosis. For countries that use vaccination as a control measure, effectiveness of the vaccination campaign largely depends on knowing the serotype involved as there is no cross protection between different serotypes. Other control measures reportedly used include movement control, slaughter and quarantine.
Countries that confirmed to AU-IBAR FMD serotypes in Africa from 2006 to 2011
|Country||2006 & 2007||2008||2009||2010||2011|
|Benin||NS||O, SAT 1 & 2||O, SAT 1 & 2||A, O, SAT 1, SAT 2||A, O, SAT 1, SAT 2|
|Botswana||SAT 1 & 2||SAT 2||NS||NS||NS|
|Egypt||A, O||NS||A, O||NS||NS|
|Mozambique||NS||NS||NS||SAT 2||SAT 2|
|Rwanda||NS||A, O, SAT 2||A, O, SAT 2||A, O, SAT2||NS|
|South Africa||SAT 1 & 3||NS||NS||SAT 2||A, O|
|Togo||NS||O, SAT 1||O, SAT 1||O, SAT 1||NS|
|Zimbabwe||NS||NS||NS||SAT 1,SAT 2||NS|
NS: Not specified
During 2011, Mauritius and Madagascar maintained their "FMD freedom without vaccination" status as per the OIE code, whereas Botswana and Namibia maintained "FMD free zones where vaccination is practiced". However, the FMD free zone status of South Africa without vaccination is no longer recognized by the OIE as it was suspended on the 25th February 2011 following outbreaks of FMD in the districts of Jozini and Umhlabuyalingana in KwaZulu-Natal province.
It is probably the geographical location of Madagascar and Mauritius as islands that enabled them to establish and maintain their FMD country freedom status. Cattle production systems across Africa largely fall either in the pastoral or sedentary categories. The predominantly sedentary system in Southern Africa has enabled Botswana, Namibia and South Africa to establish OIE recognized free zones. Furthermore, these zones have largely been supported by the erection of fences which are not practical in the predominantly pastoral systems of production practised elsewhere in Africa.
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/. The OIE publish a report each year in which it lists FMD-infected countries (see: OIE Official disease status, FMD).
= Present, no further details = Widespread = Localised
= Confined and subject to quarantine = Occasional or few reports
= Evidence of pathogen = Last reported... = Presence unconfirmed
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 information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.
|Country||Distribution||Last Reported||Origin||First Reported||Invasive||References||Notes|
|Algeria||Last reported||1999||OIE, 2012|
|Angola||OIE, 2012; Kitching, 1998|
|Benin||Present||NULL||OIE, 2012; Kitching, 1998|
|Botswana||Restricted distribution||OIE, 2012; Kitching, 1998|
|Burkina Faso||Present||OIE, 2012; Kitching, 1998|
|Burundi||Reported present or known to be present||Kitching, 1998; OIE Handistatus, 2005|
|Cameroon||Present||OIE, 2012; Kitching, 1998|
|Cape Verde||Absent, never occurred||OIE, 2012|
|Central African Republic||Present||OIE, 2012; Kitching, 1998|
|Chad||Present||OIE, 2012; Kitching, 1998|
|Congo||No information available||NULL||OIE, 2009; Kitching, 1998|
|Congo Democratic Republic||No information available||Kitching, 1998; OIE Handistatus, 2005|
|Côte d'Ivoire||Restricted distribution||OIE, 2012; Kitching, 1998|
|Djibouti||Disease not reported||NULL||OIE, 2009; Kitching, 1998|
|Egypt||Present||OIE, 2012; Kitching, 1998|
|Equatorial Guinea||OIE, 2012; Kitching, 1998|
|Eritrea||Present||NULL||OIE, 2009; Kitching, 1998|
|Ethiopia||Present||OIE, 2012; Kitching, 1998|
|Gabon||Disease never reported||NULL||OIE, 2009; Kitching, 1998|
|Gambia||No information available||NULL||OIE, 2009; Kitching, 1998|
|Ghana||Present||OIE, 2012; Kitching, 1998|
|Guinea||Disease not reported||200612||OIE, 2009; Kitching, 1998|
|Guinea-Bissau||No information available||NULL||OIE, 2009; Kitching, 1998|
|Kenya||Present||OIE, 2012; Kitching, 1998|
|Lesotho||Absent, never occurred||OIE, 2012|
|Libya||Present||Native||OIE, 2012; Kitching, 1998; OIE, 2004c; OIE Handistatus, 2005|
|Madagascar||Absent, never occurred||OIE, 2012|
|Malawi||Last reported||2011||OIE, 2012; Kitching, 1998|
|Mali||Restricted distribution||NULL||OIE, 2009; Kitching, 1998|
|Mauritania||Reported present or known to be present||Kitching, 1998|
|Mauritius||Absent, never occurred||OIE, 2012|
|Morocco||Last reported||1999||OIE, 2012|
|Mozambique||Present||OIE, 2012; Kitching, 1998|
|Namibia||Restricted distribution||OIE, 2012; Kitching, 1998|
|Niger||Restricted distribution||OIE, 2012; Kitching, 1998; OIE Handistatus, 2005|
|Nigeria||Present||OIE, 2012; Kitching, 1998|
|Réunion||Disease never reported||OIE Handistatus, 2005|
|Rwanda||OIE, 2012; Kitching, 1998|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Senegal||Present||OIE, 2012; Kitching, 1998|
|Seychelles||Absent, never occurred||OIE, 2012|
|Sierra Leone||Last reported||1958||OIE, 2012; Kitching, 1998|
|Somalia||Present||OIE, 2012; Kitching, 1998|
|South Africa||Restricted distribution||OIE, 2012; Kitching, 1998|
|Sudan||Restricted distribution||OIE, 2012; Kitching, 1998|
|Swaziland||Last reported||2001||OIE, 2012|
|Tanzania||Present||OIE, 2012; Kitching, 1998|
|Togo||Present||OIE, 2012; Kitching, 1998|
|Tunisia||Last reported||1999||OIE, 2012|
|Uganda||Present||OIE, 2012; Kitching, 1998|
|Western Sahara||Present||Kitching, 1998|
|Zambia||Present||NULL||OIE, 2009; Kitching, 1998; OIE, 2004g|
|Zimbabwe||Present||OIE, 2012; Kitching, 1998|
In endemic situations, local breeds frequently show a degree of resistance to clinical disease, although there is no evidence that they have increased resistance to infection. Infected zebu cattle in Africa rarely show many disease signs. High-yielding dairy cattle appear very susceptible to severe clinical FMD, frequently leading to secondary complications such as mastitis and chronic lameness. Sheep and goats may not show obvious clinical signs of FMD and have been responsible for taking disease across international borders and disseminating infection within countries because they have not been recognized as infected (Hedger, 1981; Kitching, 1998; Mansley et al., 2003). Some strains of FMD virus have shown host specificity, such as the isolate found in South-East Asia affecting pigs (Dunn and Donaldson, 1997). The Arabian camel is probably resistant to all strains of FMD virus, while the Central Asian camel is susceptible. Other camelid species can be infected under experimental conditions, but usually resist infection in the field (Wernery and Kaaden, 2004).
|Bos grunniens (yaks)||Domesticated host, Wild host|
|Bos indicus (zebu)||Domesticated host|
|Bos mutus (yaks, wild)||Domesticated host, Wild host|
|Bos taurus (cattle)||Domesticated host|
|Bubalus bubalis (buffalo)||Domesticated host, Wild host|
|Camelus bactrianus (Bactrian camel)||Domesticated host, Wild host|
|Capra hircus (goats)||Domesticated host, Wild host|
|Lama glama (llamas)||Domesticated host|
|Lama pacos (alpacas)||Domesticated host|
|Ovis aries (sheep)||Domesticated host, Wild host|
|Sus scrofa (pigs)||Domesticated host, Wild host|
Bones (& Feet) - Large Ruminants
Bones (& Feet) - Pigs
Bones (& Feet) - Small Ruminants
Digestive - Large Ruminants
Digestive - Pigs
Digestive - Small Ruminants
Mammary Glands - Large Ruminants
Mammary Glands - Pigs
Mammary Glands - Small Ruminants
Respiratory - Large Ruminants
Respiratory - Pigs
Respiratory - Small Ruminants
Skin - Large Ruminants
Skin - Pigs
Skin - Small Ruminants
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).
In some endemic 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 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 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.
Ruminants which have recovered from infection, or vaccinated animals which have contact with live virus without developing disease, can become persistently infected, goats for up to 3 months, sheep up to 9 months, cattle sometimes over 3 years, and African buffalo over 5 years. The virus can be recovered from the pharynx using a metal sampling cup (probang). Although under experimental conditions it has not been possible to demonstrate transmission from these carrier animals to susceptible in-contact animals, there is considerable field evidence that they can initiate fresh outbreaks of disease. Pigs do not become carriers (Salt, 1993 - review).
Virus excretion in semen and milk may occur up to 4 days before the appearance of clinical signs, although it is maximum when signs are first seen.
Countries infected with FMD are constrained from trade in live animals and animal products with FMD-free countries. As it is predominantly the developing world in which FMD is present, the disease has prevented many of the poorer countries from exploiting the rich markets of Europe, North America and Japan. In 1997 FMD entered Taiwan; the consequent control programme involved widespread vaccination and slaughter of over 4 million pigs. The loss of the export trade to Japan and Korea cost the country over US $2 billion (US $2 x 109) in the first year. It is possible they may never recover their export market as other countries have taken this over. The 2001 epidemic in the UK cost over US $20 billion in lost trade, cost of animal slaughter, disposal and disinfection, and due to the effect in the tourist industry. A large epidemic in the USA could cost over US $100 billion.
Although the cost of the disease in poorer countries does not justify the cost of a control and eradication programme in terms of increased production, the cost/benefit becomes positive when access to lucrative export markets is included (James and Ellis, 1978). In countries such as Zimbabwe, Botswana and South Africa, which export meat to Europe and in which FMD is present in wildlife, fences and vaccinated buffer zones have been established to separate domestic buffalo and the cattle from wild ungulates. FMD had been eradicated from many South American countries in order to take advantage of new export markets, but there has been a recent re-introduction of FMD into Argentina, Uruguay and Southern Brazil. Control programmes have been started in India and South-East Asia.
FMD can severely disrupt dairy production by reducing milk yield and causing secondary complications. In intensive sheep flocks, it can cause up to 90% mortality in lambs.
Although there are reports in the literature of human infection with FMD virus, this is extremely rare, and the clinical signs very mild. More commonly humans develop a hand and foot disease due to coxsackie B virus infection. There is no danger to humans from eating FMD virus-infected or vaccinated meat, other than the poor condition of the carcass due to the disease process (Donaldson, 1979; Donaldson, 1987; Salt, 1993).
The FMD virus has a predilection for epithelial cells, causing ballooning degeneration and vesicle formation. In young animals it invades the myocardial cells of the developing heart, causing necrosis and death of the affected cells and consequent heart failure, which can be seen as white scars post mortem (tiger heart). In the carrier animal, the virus can be found in the basal layer of the stratified squamous epithelium of the dorsal soft palate. It is not clear why it is non-lytic in these animals. Viraemia lasts 3 to 4 days, detectable 48 h before the onset of clinical signs. Recovery follows the development of specific antibodies in the blood (IgM and IgG) and secretions (IgA), detectable from 10 days after infection (Kitching, 1992a).
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 (http://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, (OIE, 2005c). 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).
There is no totally reliable method for detecting carrier animals; single probang samples probably detect only 50% of carriers, and sampling should be repeated after a 2-week interval.
Differential diagnosis for FMD in cattle includes: bovine virus diarrhoea, vesicular stomatitis, rinderpest, malignant catarrhal fever, papular stomatitis, cowpox and pseudocowpox, and any traumatic or corrosive injury to the mouth. In sheep, bluetongue, pest of small ruminants, orf, interdigital dermatitis, capripox and non-specific mouth lesions, often due to trauma. FMD is often difficult to diagnose clinically in sheep because the disease is generally mild (Watson, 2004). Sudden death in young animals can be due to a variety of viral, bacterial or deficiency diseases.
The incubation period for FMD can be between 2 and 11 days, depending on the infecting dose, the strain of virus and the host susceptibility. Initially, a fever develops and vesicles appear on the tongue and buccal mucosa, the coronary band and heels of the feet, and on the udder. On the tongue, these quickly rupture, leaving a raw, exposed submucosa, and causing the animal to salivate and avoid feeding. The vesicles on the feet take longer to rupture, and are prone to secondary infection; those on the udder interfere with milking and predispose to mastitis. The extent of clinical signs is very variable, and with low infecting doses the infection may be subclinical. Once disease is established on a farm, the virus challenge increases (the within-farm epidemic), the incubation period is shortened and clinical signs become more severe. Dairy cattle may lose 50% of the epithelium from their tongues. In uncomplicated cases, healing is usually rapid, and adult cattle return to normal usually within 10 days of onset of disease, although they will suffer a 20% or greater loss of their total lactation. Young ruminants may die without any clinical signs, and yearling cattle may fail to mature properly because of damage to glandular organs such as thymus and thyroid. Abortion is not usually seen (see Donaldson, 1987). The course of the clinical disease in sheep rarely exceeds three days in uncomplicated cases, and the infection is frequently subclinical.
|Drug||Dosage, administration and withdrawal times||Life stages||Adverse affects||Drug resistance||Type|
|foot-and-mouth disease vaccine||Variable. Usually subcutaneous administration of aqueous vaccines for ruminants; intramuscular route for oil-adjuvanted products. Use of vaccine may result in international trade restrictions. Generally, primary course of two vaccinations 4-5 weeks apart. Booster after 6 months in low-risk areas; 4 months in high-risk. Seek veterinary advice and information from vaccine manufacturer.||All Stages/All Stages||Anaphylaxis (in cattle)||No||Vaccine|
There is no specific treatment once disease has become established, other than supportive therapy, and antibiotics to prevent secondary infections.
Various novel approaches for treatment and prevention of FMD and other viral infections have been proposed. Inhibition of FMD virus replication and reduced production of escape mutants can be demonstrated in vivo using, for example, small interfering RNA targeting the conserved regions of viral genome (Liu et al., 2005) or lethal mutagenesis using pre-extinction viral RNA (Gonzalez-Lopez et al., 2004). Other experimental options include mutagenic antiviral drugs such as ribavirin, or targeting drugs at viral components such as the highly conserved 3C protease of FMDV, which is required to cleave the precursor virus into functional proteins (Birtley et al., 2005).
|Vaccine||Dosage, Administration and Withdrawal Times||Life Stages||Adverse Affects|
|foot-and-mouth disease vaccine||Variable. Usually subcutaneous administration of aqueous vaccines for ruminants; intramuscular route for oil-adjuvanted products. Use of vaccine may result in international trade restrictions. Generally, primary course of two vaccinations 4-5 weeks apart. Booster after 6 months in low-risk areas; 4 months in high-risk. Seek veterinary advice and information from vaccine manufacturer.||Anaphylaxis (in cattle)|
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 (OIE, 2006).
Modern FMD vaccines perform very well both for regular prophylactic vaccination programmes and for the control of outbreaks. Modern inactivated vaccines require adjuvants, usually aqueous aluminium hydroxide/saponin for ruminants or mineral oil-based for pigs or ruminants. Emergency use 'high potency' vaccines are always expected to be formulated with oil regardless of species to be vaccinated. Vaccination inhibits local virus replication and excretion in the oropharynx and thus reduces or prevents virus transmission. It may also inhibit the development of the carrier state (Barnett et al., 2004). Emergency vaccines contain higher antigen payloads than conventional vaccines; they induce rapid immunity (often within 4 days) and offer wider antigenic coverage. It is important to identify the optimum cross-protective vaccine strain for use in an outbreak (Barnett and Carabin, 2002).
Many FMD-free countries now have strategic reserves of concentrated, purified vaccine antigen at ultra-low temperatures for use in an emergency situation (Barnett and Carabin, 2002). The purification of FMD viral antigens to remove non-structural proteins (NSP) allows differentiation between vaccinated and infected animals. Consequently, the combined use of purified vaccine and anti-NSP tests essentially provides a 'marker' system (Barteling, 2004).
Other approaches, such as synthetic peptide and DNA vaccines, are under investigation, (see for example Guo-HuiChen et al., 2005).
Acharya R, Fry E, Stuart D, Fox G, Rowlands DJ, Brown F, 1989. The three-dimensional structure of foot-and-mouth disease virus at 2.9 Å resolution. Nature, 337:709-716.
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/pan-african-animal-health-yearbook
Alexandersen S, Donaldson AI, 2002. Further studies to quantify the dose of natural aerosols of foot-and-mouth disease virus for pigs. Epidemiology and Infection, 128(2):313-323; 43 ref.
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.
Alexandersen S, Zhang ZhiDong, Donaldson AI, 2002. Aspects of the persistence of foot-and-mouth disease virus in animals - the carrier problem. Microbes and Infection, 4(10):1099-1110.
Barnett PV, Carabin H, 2002. A review of emergency foot-and-mouth disease (FMD) vaccines. Vaccine, 20(11/12):1505-1514; 28 ref.
Barnett PV, Keel P, Reid S, Armstrong RM, Statham RJ, Voyce C, Aggarwal N, Cox SJ, 2004. Evidence that high potency foot-and-mouth disease vaccine inhibits local virus replication and prevents the 'carrier' state in sheep. Vaccine, 22:1221-1232.
Barteling SJ, 2004. Modern inactivated foot-and-mouth disease (FMD) vaccines: historical background and key elements in production and use. In: Foot-and-mouth Disease: Current Perspectives. Wymondham, UK: Horizon Bioscience, 305-333.
Barteling SJ, Vreeswijk J, 1991. Developments in foot-and-mouth disease vaccines. Vaccine, 9(2):75-88; 191 ref.
Bartley LM, Donnelly CA, Anderson RM, 2002. Review of foot-and-mouth disease virus survival in animal excretions and on fomites. Veterinary Record, 151(22):667-669.
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.
Birtley JR, Knox SR, Jaulent AM, Brick P, Leatherbarrow RJ, Curry S, 2005. Crystal structure of foot-and-mouth disease virus 3C protease: new insights into catalytic mechanism and cleavage specificity. Journal of Biological Chemistry, 280:11520-11527.
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, 1984. Chemical basis of antigenic variation in foot-and-mouth disease virus. Biochemical Society Transaction, 12:705-708.
Brown F, 1985. Antigenic structure of foot-and-mouth disease virus. In: Regenmortel MHVV, Neurath AR, eds. Immunochemistry of viruses. The basis for serodiagnosis and vaccines. Elsevenier Science Publishers, BV, 265-279.
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.
Dawe PS, Flanagan FO, Madekurozwa RL, Sorensen KJ, Anderson EC, Foggin CM, Ferris NP, Knowles NJ, 1994. Natural transmission of foot-and-mouth disease virus from African buffalo (Syncerus caffer) to cattle in a wildlife area of Zimbabwe. Veterinary Record, 134(10):230-232; 11 ref.
DEFRA, 2002. Department for Environment, Food and Rural Affairs, UK. http://www.defra.gov.uk/animalh/diseases/fmd/.
Doel TR, 2003. FMD vaccines. Virus Research, 91(1):81-99.
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.
Dunn CS, Donaldson AI, 1997. Natural adaption to pigs of a Taiwanese isolate of foot-and-mouth disease virus. Veterinary Record, 141(7):174-175; 12 ref.
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
Gonzalez-Lopez C, Arias A, Pariente N, Gomez-Mariano G, Domingo E, 2004. Preextinction viral RNA can interfere with infectivity. Journal of Virology, 78:3319-3324.
Grubman MJ, Baxt B, 2004. Foot-and-mouth disease. Clinical Microbiology Reviews, 17(2):465-493.
Guo-HuiChen, Liu-ZaiXin, Sun-ShiQi, Bao-HuiFang, Chen-YingLi, Liu-XiangTao, Xie-QingGe, 2005. Immune response in guinea pigs vaccinated with DNA vaccine of foot-and-mouth disease virus O/China99. Vaccine, 23:3236-3242.
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, 1981. Foot-and-mouth disease. In: Davis JW, Karstad LH, Trainer DO, eds. Infectious Diseases of Wild Mammals. Ames, IA: USA, Iowa State University Press, 87-96.
James AD, Ellis PR, 1978. Benefit-cost analysis in foot-and-mouth disease control programmes. British Veterinary Journal, 134:47-52.
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.
Letshwenyo M, Mapitse N, Hyera JMK, 2006. Foot-and-mouth disease in a kudu (Tragelaphus strepsiceros) in Botswana. Veterinary Record, 159(8):252-253. http://www.bvapublications.com
Liu MingQiu, Chen WeiZao, Ni Zheng, Yan WeiYao, Fei LiAng, Jiao Ye, Zhang Jun, Du QingYun, Wei XueFeng, Chen JiuLian, Liuc YuMei, Zheng ZhaoXin, 2005. Cross-inhibition to heterologous foot-and-mouth disease virus infection induced by RNA interference targeting the conserved regions of viral genome. Virology, 336(1):51-59.
Mann JA, Sellers RF, 1990. Foot-and-mouth disease virus. Virus infections of ruminants., 503-512; 26 ref.
Mansley LM, Dunlop PJ, Whiteside SM, Smith RGH, 2003. Early dissemination of foot-and-mouth disease virus through sheep marketing in February 2001. Veterinary Record, 153:43-50.
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
Minor PD, Brown F, Domingo E, Hoey E, King A, Knowles N, Lemon S, Palmenberg A, Rueckert RR, Stanway G, Wimmeri E, Yin-Murphy M, 1995. Virus Taxonomy. In: Murphy et al. eds. Picornaviridae. Wien, New York, Springer-Verlag, 329-336.
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.
Moraes MP, Chinsangaram J, Brum MCS, Grubman M, 2003. Immediate protection of swine from foot-and-mouth disease: a combination of adenoviruses expressing interferon alpha and a foot-and-mouth disease virus subunit vaccine. Vaccine, 22:268-279.
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.
Office International Des Epizooties, 2000. Manual of Diagnostic Techniques.
Office International des Epizooties, 2001. Disease outbreaks reported to the OIE. Bulletin. Office International des Epizooties. 2001, 113.
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, 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 Nigeria. Paris, France: Office International Des Epizooties, Disease Information, 17(49).
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 South Africa. Virus type SAT2 in the FMD controlled area. Follow-up report No. 4. Paris, France: Office International Des Epizooties, Disease Information, 17(44).
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, 2004. Manual of Diagnostic Techniques. Paris, France: Office International Des Epizooties.
OIE, 2005. Foot and mouth disease in Botswana. Follow-up report No. 2 (final report). Paris, France: Office International Des Epizooties, Disease Information, 18(44).
OIE, 2005. Foot and mouth disease in Congo (Dem. Rep. of the...). Paris, France: Office International Des Epizooties, Disease Information, 18(37).
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, 2005. Foot and mouth disease in Israel. Follow-up report No. 1. Paris, France: Office International Des Epizooties, Disease Information, 18(52).
OIE, 2005. Foot and mouth disease in Mongolia. Follow-up report No. 2. Paris, France: Office International Des Epizooties, Disease Information, 18(42).
OIE, 2005. Foot and mouth disease in Myanmar. Virus type Asia 1. Paris, France: Office International Des Epizooties, Disease Information, 18(34).
OIE, 2005. Foot and mouth disease in Russia. Paris, France: Office International Des Epizooties, Disease Information, 18(51).
OIE, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
OIE, 2006. Foot and mouth disease in Brazil. Follow-up report No. 15. Paris, France: Office International Des Epizooties, Disease Information, 19(3).
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
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.
Pay TWF, 1984. Factors influencing the performance of foot-and-mouth disease vaccines under field conditions. In: Applied Virology [ed. by Kurstak, E. \Al-Nakib, W. \Kurstak, C. ..]. New York, USA: Academic Press, 73-86.
Porta C, Kotecha A, Burman A, Jackson T, Ren J, Loureiro S, Jones IM, Fry EE, Stuart DI, Charleston B, 2013. Rational engineering of recombinant Picornavirus capsids to produce safe, protective vaccine antigen. PLoS Pathogens, 9(3):e1003255.
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, Brüning A, Hutchings GH, Kowalska Z, Åkerblom L, 2001. Development of a rapid chromatographic strip test for the pen-side detection of foot-and-mouth disease virus antigen. Journal of Virological Methods, 96:189-202.
Reid SM, Ferris NP, Hutchings GH, Samuel AR, Knowles NJ, 2000. Primary diagnosis of foot-and-mouth disease by reverse transcription polymerase chain reaction. Journal of Virological Methods, 89(1/2):167-176.
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.
Roeder PL, Le Blanc Smith PM, 1987. Detection and typing of foot-and-mouth disease virus by enzyme-linked immunosorbent assay: a sensitive, rapid and reliable technique for primary diagnosis. Research in Veterinary Science, 43(2):225-232.
Salt JS, 1993. The carrier state in foot-and-mouth disease - an immunological review. British Veterinary Journal, 149:207-223.
Shaw AE, Reid SM, King DP, Hutchings GH, Ferris NP, 2004. Enhanced laboratory diagnosis of foot and mouth disease by real-time polymerase chain reaction. Revue Scientifique et Technique Office International des Epizooties, 23:1003-1009.
Sørensen KJ, Madsen KG, Madsen ES, Salt JS, Nqindi J, Mackay DKJ, 1998. Differentiation of infection from vaccination in foot-and-mouth disease by the detection of antibodies to the non-structural proteins 3D, 3AB and 3ABC in ELISA using antigens expressed in baculovirus. Archives of Virology, 143(8):1461-1476; 23 ref.
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.
Thomson GR, Vosloo W, Bastos ADS, 2003. Foot and mouth disease in wildlife. Virus Research, 91(1):145-161.
Watson P, 2004. Differential diagnosis of oral lesions and FMD in sheep. In Practice, 26:182-191.
Wernery U, Kaaden OR, 2004. Foot-and-mouth disease in camelids: a review. Veterinary Journal, 168(2):134-142.
Woolhouse MEJ, Haydon DT, Pearson A, Kitching RP, 1996. Failure of vaccination to prevent outbreaks of foot-and-mouth disease. Epidemiology and Infection, 116(3):363-371; 17 ref.
Yadav S, Sharma R, Chhabra R, 2005. Interleukin-2 potentiates foot-and-mouth disease vaccinal immune responses in mice. Vaccine, 23(23):3005-3009.
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