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Foot-and-Mouth Disease VirusOn this page: Description & Distribution Clinical signs Diagnosis Transmission Treatment & Control
Description and Distribution
The foot-and-mouth disease virus (FMDv) is in the family Picornaviridae. Foot-and-mouth disease is caused by a small RNA virus which is very infectious and can spread very quickly if not controlled.
The natural hosts of FMD virus are cloven-hoofed animals: specifically cattle, antelope, sheep, goats, deer, pigs and camels. Foot-and-mouth disease causes fever and damage to the epithelial cells around the mouth and feet, and the mucous membrane lining the mouth and gut system. FMD morbidity is high, but mortality is usually low in adult animals. In young animals mortality can be high because the disease damages heart muscle cells.
Electron micrograph of the foot-and-mouth disease virus
There are seven different serotypes of foot-and-mouth disease virus (A, O, C, Asia 1, and South African Territories [=SAT] 1, 2, and 3). Multiple subtypes occur within each serotype. The different serotypes all produce symptoms of foot-and-mouth disease and are distinguishable only in the laboratory. Once an animal has had FMD caused by one serotype, it is still susceptible to attacks by the other serotypes and major different strains within the same serotype. Likewise, each FMD serotype or major strain must be vaccinated against separately. When animals recover from infection by one type of virus they have little or no protection against attacks by any one of the others.
Countries in which foot-and-mouth disease virus serotype O was reported to the World Organization for Animal Health (OIE) between 1990 and 2002
Foot-and-mouth disease has historically occurred across most of the world, but has never been reported from a few isolated countries such as New Zealand and Iceland. FMDv types O, A and C have occurred in Europe, South America, Central America, Asia, Africa. Types SAT1, SAT2, SAT3 mainly occur in Africa although SAT1 caused an extensive epizootic in the Middle East. Type Asia 1 has occurred in Asia. Within a virus type, antigenic drift occurs and demarcations between foot-and-mouth disease virus subtypes are not clear-cut. The map shows the geographical distribution of just the serotype O foot-and-mouth outbreaks up to 2005 - note, grey areas do NOT indicate the absence of FMD virus, but absence of reported outbreaks.
Clinical signs in cattle
Fever is one of the first signs of foot-and-mouth disease, with raised temperature and shivering. If at pasture, the animal will be away from the rest of the herd. A cow in milk will show a sudden drop in yield.
Blisters begin to develop, usually within a few hours, most frequently on the upper surface of the tongue and the bulbs of the heels. Feeding and cuddling may cease and the animal is 'tucked up' with 'staring' (rough-textured) coat.
There is quivering of the lips and uneasy movement of the lower jaw, with copious, frothy saliva around the lips that drips to the ground. A characteristic smacking sound is produced by partial opening of the mouth. Loss of condition is marked, partly on account of the fever and partly because the mouth is so painful that the animal is afraid to eat.
Infra-red detection of raised temperatures around mouth and feet can be used to screen animals for early stages of foot-and-mouth disease. (Agricultural Research Service, 2009)
Infrared image of a cow with foot-and-mouth disease;
If the mouth is examined, blisters will be found on the upper surface of the tongue on the dental pad, inside the lips, and sometimes on the muzzle. At first the blisters are seen as small raised areas, whitish in colour and containing fluid: they quickly increase in size until they eventually burst and collapse, leaving the 'skin' loose and wrinkled, with a dead appearance. On handling, the 'skin' is easily removed, leaving a raw surface underneath. When the blisters have burst the temperature falls, pain decreases and the animal may start to eat again.
The age of FMD lesions on the tongue can be assessed from their appearance. Recently formed vesicles will be intact, but tend to rupture when the tongue is drawn from the mouth. 2-day-old lesions have sharp margins and the exposed dermis has a red raw appearance. 3-4 day old lesions show sero-fibrinous exudation into the lesion with progressive loss of lesion margination as can be seen in the picture below.
Lesions on gum of cow with foot-and-mouth disease in Kenya 1996
Lesion on tongue of cow with foot-and-mouth disease in Kenya 1996.
About the same time there is evidence of pain in the feet. The animal lies down constantly and, when forced to move, walks very tenderly. Lameness usually gets worse, until the animal can only hobble when moving on hard or uneven surfaces. The blisters develop on the feet about the same time as in the mouth. Most commonly they occur at the bulbs of the heels, at the front of the cleft of the hoof, and in the cleft itself. They usually burst fairly quickly through movement of the feet, and then appear as a ragged tear exposing a raw surface as shown in the picture below.
Lesion in cleft of hoof of cow with foot-and-mouth disease in Kenya 1996
Cows and heifers may develop blisters on the teats (as seen on the picture below) and resent any attempt at milking. Because of this, and damage to the milk-secreting cells of the udder, there is a very marked drop in milk yield.
Lesions on teats of cow with foot-and-mouth disease
Clinical signs in animals other than cattle
In sheep the main symptom is a sudden, severe lameness. The animal looks sick, lies down frequently and is very unwilling to rise. When the animal is made to rise, it stands in a half-crouching position, with the hind legs brought well forward. Mouth symptoms are not often noticeable, but may form on the dental pad and the tongue. There are usually blisters on the feet at the top of the hoof, where the horn joins the skin in the cleft of the foot. Unless complicated by foot rot, the foot is clean and there is no offensive smell.
In pigs the main symptom in pigs is sudden lameness. The animal prefers to lie down and when made to move hobbles painfully. Blisters form on the upper edge of the hoof where the skin and horn meet (see picture right), and on the heels and in the cleft. Mouth symptoms are not usually visible, but blisters may develop on the snout or on the tongue. Swine Vesicular Disease has identical symptoms to FMD and hence must be treated as suspected foot-and-mouth disease until laboratory tests prove otherwise.
More details on clinical signs of foot-and-mouth disease are given in DEFRA (2007).
Coronary band vesicles on the feet of a pig with foot-and-mouth disease.
Usually a definitive diagnosis of FMD is based on the presence of FMD virus or antigen (immuno-reactive substances produced by the virus). Tests identify whether or not virus is present, and the specific serotype. In the absence of tissue samples, diagnosis can be made based on the demonstration of specific antibodies in serum (antibodies are proteins produced by the animal to combat the virus).
Detection of virus (virus isolation or detection of virus antigen) is generally carried out on epithelium from intact vesicles (blisters), fluid from vesicles, or the tags of epithelium from the edges of ruptured vesicles (erosions). Blood may also be tested for the presence of virus (viraemia); sometimes other tissues/secretions are used. Cells and mucus from the pharynx may be used for the detection of virus in subclinically infected animals and carriers.
For material expected to contain large amounts of FMD virus, virus typing is carried out by the complement fixation test, enzyme-linked immunosorbent assay (ELISA) or polymerase chain reaction (PCR). FMDv negative samples must then be tested by growth in cell culture followed by virus typing of the cell culture supernatant. Samples which are less likely to contain large amounts of FMD virus are tested by growing the virus from the sample in cell culture, followed by virus typing. Tests such as the complement fixation test or ELISA, performed on fresh material from vesicles (blisters) or vesicular fluids, allow a definitive diagnosis on virus-positive samples within a few hours. Direct serotyping using ELISA is able to produce a positive result within three hours from the time the test is set up, dependent on the presence of sufficient FMDv antigen in the sample. If a test result is negative at this stage, a cell culture is required which will either amplify antigen to a level where it can be detected or confirm the negative result.
Detection of antibodies raised against foot-and-mouth disease virus is carried out on serum samples. Traditional tests detect antibody to structural proteins of the FMD virus, and the serum must be tested for each of the seven different types of virus. These tests can be used to determine which types of FMD virus are/have been present in an area. More recently, tests have been developed which detect non-structural proteins. These tests detect infection with any type of FMD virus and do not distinguish between virus types. The oldest of the tests for non-structural antibodies detect antibodies to "virus infection associated antigen" (D3). However, animals which have been vaccinated repeatedly with inactivated vaccines may be positive with this test (for example due to contamination of some impure vaccines with this non-structural protein and because FMD virus particle contains some of this protein in its capsid (V.w23)). In the last several years, tests (mainly ELISAs) have been developed to detect various non-structural FMDv protein antigens. These tests are sensitive, specific and suitable for screening large numbers of serum samples. They are able to distinguish between animals which have been infected with foot-and-mouth disease (had virus replicating in them) and those which have not, whether or not the animals have been vaccinated against FMD.
A detailed account of available diagnostic tests is given in OIE (2009).
Foot-and-mouth disease virus is shed from an infected live animal in many different ways - in air-borne droplets from the lungs and the fluid-filled vesicles, in the saliva, urine, faeces, semen and milk, in secretions from the eyes, nose, prepuce and vagina, and through direct contact with skin or pieces of infected skin that may drop off the animal. FMD virus may also be transmitted in milk and infected carcasses on meat, hides, and bones which are frequently transported locally, regionally and between continents. Virus may be produced by an infected animal before the damage to the skin and mucous membranes is evident. Occasionally, outbreaks are associated with escapes of foot-and-mouth virus from a laboratory.
FMD virus can be spread by moving infected animals, or by any other animals, or man, that have contacted the above body substances, or breathed in the infected airborne droplets. The wind may move the air-borne droplets containing the virus up to 250 km over water and shorter distances over land. FMD virus may also multiply in, and thereby be spread by, some animals which do not have clinical signs (subclinically affected animals) and may multiply in and possibly be spread from carrier animals.
The virus then enters a susceptible animal through inhalation (the lungs), ingestion (the gut system), sexual transmission, conjunctival membranes (eye), inoculation (injection) or damaged skin. The interval between exposure to infection and the appearance of symptoms varies between twenty-four hours and ten days, or even longer. The average time, under natural conditions, is three to six days.
Notice requesting walkers to disinfect their boots
Animals have been recorded to "carry" the FMD virus without appearing clinically ill. This may occur after recovery from clinical disease, after undetected subclinical disease, and on exposure of vaccinated animals to virus. The duration of the carrier-state varies with species and has been recorded in African buffalo for at least five years, cattle for up to 3 years, sheep and goats for up to 9 months. Pigs have never been reported to become foot-and-mouth carriers. In Africa there is good evidence that carrier buffalo can transmit the SAT FMD viruses to cattle, but there is as yet no evidence for transmission of FMD virus from carrier cattle, sheep or goats to susceptible animals.
Treatment and Control
The earliest method of foot-and-mouth disease control consisted of slaughter (culling) of infected and susceptible in-contact animals, restricting animal movement, and disinfection. This is sometimes termed the 'stamping out' method of FMD control. Using this method the disease was eliminated from North America by 1929. However, stamping out was much less successful in Europe and outbreaks occurred repeatedly until the 1960s. Development of an inactivated whole-virus preparation then led to a successful FMD vaccination program in Western Europe, and by 1989 disease outbreaks had virtually ceased.
In 1992 the European Union adopted a no-vaccination policy, with most of Europe recognised as 'free of FMD without vaccination'. Any incursions of the disease were rapidly terminated by slaughter of infected and susceptible in-contact animals. Similar strides in disease control were also made in South America, utilizing annual vaccination campaigns and animal culling. By the end of the 1990s, Argentina, Chile, Uruguay, the southern part of Brazil, and Guyana were recognized by the international community as being 'free of FMD without vaccination'.
Near the end of the 20th century it appeared that, at least in countries that engaged in international trade of animals and animal products, FMD was under control. As a result, many of these countries discontinued foot-and-mouth vaccination entirely, and research efforts in many European and South American countries were significantly reduced. However, FMD still occurred in the Middle East and many countries in Africa and Asia.
Then FMD re-emerged in developed countries. In 1997 an FMD outbreak caused by a type O virus was reported in Taiwan, a country that had been free of the disease for 68 years. This outbreak resulted in the slaughter of more than 4 million pigs, almost 38% of the entire pig population, at a cost of approximately U.S. $6 billion. Starting in late 1999 and 2000, a series of FMD outbreaks occurred in a number of countries in East Asia. This was followed by an outbreak in South Africa and the devastating outbreak in the United Kingdom which then spread to the European continent.
In the UK 2001 epizootic over 10 million sheep and cattle were killed in an attempt to halt the disease. With the intention of controlling the spread of foot-and-mouth disease, public footpaths over wide tracts of the British countryside were closed. This had a disastrous effect on the rural economy, and tourism in general. By the end of that outbreak the crisis was estimated to have cost the UK $16 billion.
The U.K. did not vaccinate to control the 2001 outbreak, on the grounds that it would not be possible to distinguish vaccinated from infected animals and that some may become carrier animals - and thus risk the UK's no-vaccination disease-free status. However, the large-scale slaughter of animals, many of which were probably not infected, raised considerable public concern.
Burning of cattle carcasses slaughtered during foot-and-mouth disease outbreak in UK.
The UK 2001 outbreak was one of the first times that extensive use was made of modelling both to predict the disease dynamics and inform control measures. This approach was not popular amongst much of the veterinary establishment, and was blamed for the excessive slaughter of animals. In particular this modelling justified pre-emptive culling of all susceptible animals on farms adjacent to infected premises. Keeling (2005) provides a useful review of the three models used, and assesses the advances needed if models are to be successfully applied during any subsequent epidemic. A much more critical approach is taken by Kitching (2006) who believed the culling policy was driven by unvalidated predictive models, and provides a salutary warning of how models can be abused in the interests of scientific opportunism.
The UK outbreak supposedly resulted in a change in policies to a more prominent role for vaccination, with emergency vaccination, vaccination-to-live policies, and antiviral approaches now actively encouraged by measures recently approved by the OIE (Grubman & Baxt, 2004). Some of the novel strategies available to tackle FMD are described by Grubman (2005). Despite this some countries are still using mass slaughter as their only response to disease outbreaks (the UK's policy remains to be tested).
In the last several years, type O virus has caused foot-and-mouth disease epidemics in a number of countries throughout the world which have previously been designated FMD Free (with or without vaccination), including Japan, Korea, Taiwan, Uruguay, Argentina and southern Brazil. Turkey reported the most outbreaks(261 total)in 2010, but the most disastrous outbreak was in South Korea with an estimated 3.5 million livestock culled. Vaccines were prohibited at the time of the outbreak, but South Korea has since initiated a vaccination campaign targeting nine million pigs and three million cattle. In the United States concern has been expressed (Whitcomb, 2011) that large-scale farming operations, unrestricted animal movement and a shortage of public health and large-animal veterinarians make re-emergence of the disease in America inevitable.
In other words, pursuing a no-vaccination disease-free status, instead of reducing the risk of a serious FMD outbreak, is achieving exactly the opposite - and vastly increasing the cost when it happens.
Meanwhile over much of Asia and Africa things continue essentially as before. FMD is considered an serious - but not particularly disastrous - disease, from which animals usually recover with few after-effects. We end with a picture of Maasai children butchering a calf that died of foot-and-mouth disease - the meat will be roasted and eaten.
Maasai children butchering a calf that died of foot-and-mouth disease in Kenya