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FOOT-AND-MOUTH DISEASE

FOOT-AND-MOUTH DISEASE

Foot-and-mouth disease (FMD) is a highly contagious disease of domesticated and wild ungulates characterized by vesicles in the mouth and on the feet. Hedgehogs and very rarely man may also become infected.

Aetiology

Foot-and-mouth disease is caused by infection with a virus of the genus aphthovirus, in the family Picornaviridae. There are seven antigenically distinct types of FMD virus, identified as types A, O, C, SAT (South African Territories) 1, SAT 2, SAT 3 and Asia 1.Within each of these seven types there are a large number of strains which form an antigenic spectrum, from closely related strains to strains so antigenically different as to almost justify the establishment of additional types.

Distribution

Foot-and-mouth disease is endemic throughout sub- Saharan Africa as far south as Tanzania, and also Equador, Bolivia, Peru, part of Brazil, Columbia and Venezuela in South America and most of the Middle and Far East. Canada, Central and North America,Australia, New Zealand, Japan, Argentina, Chile and South Korea are free of FMD. Most of Europe is also free of FMD, but suffers occasional outbreaks of disease in spite of strict import regulations. In Southern Africa FMD virus is usually restricted to wildlife in the game parks, although it rarely escapes into cattle areas bordering the parks.

Types O and A of FMD virus are the most widespread, especially in S. America, the Middle East and Asia; types SAT 1, SAT 2 and SAT 3 are generally restricted to Africa, although they have periodically spread into the Middle East; Asia 1 occurs in the Far East and India, although it also has spread into the Middle East. Type C only rarely causes outbreaks in Asia and has all but disappeared.

Epidemiology

Foot-and-mouth disease is an extremely contagious disease, with as few as ten infectious units being able to initiate disease in a bovine by the respiratory route. The virus can survive in dry faecal material for 14 days in summer, in slurry up to six months in winter, in urine for 39 days and on the soil between three days in summer and 28 days in winter. FMD virus is, however, very susceptible to inactivation by extremes of pH, i.e. below pH 6.0 and above pH 10.0. It is most stable between pH 7.2 and 7.6. Within this range at 4°C the virus can survive in suitable media up to a year but, as the temperature is increased, its survival time is reduced to eight to ten weeks at 22°C, ten days at 37°C and to less than 30 minutes at 56°C. The survival of airborne virus is optimal when the relative humidity is above 60 per cent. Natural ultraviolet light in sunlight has little direct effect on the FMD virus.

Like many diseases, FMD is most commonly spread by the movement of infected animals; of particular significance are sheep, goats and wild ungulates, because disease in them can be mild, and pigs because of the amounts of virus they can excrete. An infected pig excretes up to 400 million infectious units per day, 3000 times more than an infected bovine, sheep or goat. In infected cattle, milk products and semen many contain FMD virus up to four days before the appearance of clinical signs and can also be responsible for the spread of disease. Pigs can carry virus for ten days before disease is manifested. Lorries, fomites and stockmen may also be contaminated with virus from infected carcases, although the reduced pH of the carcase following rigor mortis is sufficient to inactivate the virus in the meat.

The possibility of windborne spread of FMD virus has been given considerable significance, particularly in temperate countries where the climate is conducive to the survival of the virus. There is evidence to indicate that FMD virus has been carried up to 250km over the sea and up to 60km over land. The spread of disease by the wind is dependent on the amount of virus generated by infected animals, the weather conditions, the topography over which it is carried and the susceptibility of the animals contacting the airborne virus. A plume of virus will be subjected to vertical and horizontal dispersion, which is related to wind speed and turbulence, the vertical air temperature gradient and ground topography; the survival of the airborne virus will depend on relative humidity. Cattle have a large respiratory tidal volume compared with other FMD susceptible stock and can be infected following inhalation of relatively low quantities of virus and thus are most at danger to infection from the airborne virus.Windborne spread of FMD virus is believed to have occurred in 1981 when infected pigs in Brittany, France, spread disease to cattle in the Isle of Wight, England, over a distance of 250km, predominantly over sea.

Cattle recovered from FMD and vaccinated cattle in contact with FMD virus may retain virus in their pharyngeal region for many months. This is the carrier state. Vaccinated cattle which have had contact with disease may also develop a pharyngeal infection without showing any clinical signs. The significance of these carrier animals is not clear but, although it has proven difficult to show transmission from a carrier to a susceptible animal under experimental conditions, there is considerable circumstantial evidence supported by sequencing of carrier and outbreak strains suggesting that carriers may have initiated outbreaks.

Transmission and pathogenesis

Cattle are most susceptible to FMD by inoculation of the virus intradermally into the tongue. However, natural infection is most frequently by inhalation of droplets containing FMD virus or by ingestion of FMD virus contaminated material. One infectious unit of FMD virus is sufficient to infect a bovine by intradermolingual inoculation, while between 10 and 100 infectious units can initiate disease in a bovine following inhalation. Many thousand infectious units may be required to infect an adult bovine by ingestion, although less will be required by a calf following insufflation of infected milk.

The primary site of replication of inhaled virus is in the pharynx and lymphoid tissue of the upper respiratory tract. FMD virus then enters the blood stream, is distributed around the body and following secondary replication in other glandular tissues appears in the body fluids such as milk, urine, respiratory secretions and semen, before the appearance of frank clinical signs of FMD. However, it is during the early vesicular stage of the disease that the majority of virus is excreted into the environment. Milk may contain log106.7 infectious doses50/ml, semen log106.2 infectk6ious doses50/ml, urine log104.9 infectious doses50/ml and faeces log105.0 infectious doses50/g. An infected bovine can excrete up to log105.1 infectious doses50/day by the respiratory route and can provide a potent source of FMD virus to the remaining uninfected cattle in the herd. This may be sufficient to overcome a waning vaccinal immunity.

 

The incubation period for FMD can be up to 14 days with low infecting doses and with strains of virus of low virulence. However, as the quantity of virus in the environment of an FMD outbreak increases, the incubation period in cattle decreases. For susceptible cattle in contact with an infected animal it is frequently between two and four days.

Clinical signs

The incubation period is between two and 14 days, depending on the route of infection, the dose, the strain of virus and the susceptibility of the host. Following an initial pyrexia in the region of 40°C (104°F), lasting one or two days, a variable number of vesicles develop on the tongue, hard palate, dental pad, lips, muzzle, coronary band and interdigital space. Vesicles may also be seen on the teats, particularly of lactating cows. Young calves may die before the development of vesicles because of a predilection by the virus to invade and destroy the cells of the developing heart muscle. The vesicles in the mouth quickly rupture, usually within one to two days of their formation, leaving a shallow ulcer surrounded by shreds of epithelium. The vesicles on the tongue frequently coalesce and a large proportion of the dorsal epithelium of the tongue may be displaced. The vesicles on the feet may remain for two to three days before rupturing, depending on the terrain or floor surface of the cattle accommodation.

Healing of the mouth lesions is usually rapid; the ulcers fill with fibrin and by day 10 after vesicle formation they appear as areas of pink fibrous tissue, still, however, without normal tongue papillae. Healing of the lesions on the feet is more protracted and the ulcers are susceptible to secondary bacterial infection. The horn of the heels may become under-run, as a consequence of both the initial vesicle and secondary bacterial infection.

Acutely infected cattle salivate profusely and develop a nasal discharge, at first mucoid and then mucopurulent, which covers the muzzle. They stamp their feet as they try to relieve the pressure on first one foot and then another. They may prefer to lie down and resist attempts to raise them. Lactating cattle with teat lesions are difficult to milk and the lesions frequently become infected, predisposing to secondary mastitis.

Affected cattle quickly lose condition; the drop in milk yield can be dramatic and will not be recovered during the remaining lactation. Some animals fail ever to completely regain their previous condition, due to the development of lesions in the thyroid gland – ‘hairy panters’.

An outbreak of FMD can be economically devastating in an intensively farmed region. However, in the extensive husbandry systems of South America and Africa, where expectations of cattle productivity are low, FMD may seem insignificant compared with the prevalent clostridial, haemoparasitic and deficiency diseases. This attitude frustrates programmes to completely control FMD and attempts to introduce intensive farming or a dairy industry.

Pathology

The epithelial cells of the stratum spinosum of the skin undergo ballooning degeneration. As the cells disrupt and oedema fluid accumulates, vesicles develop which coalesce to form the aphthae and bullae that characterize FMD. The cells of the squamous epithelium of the rumen, reticulum and omasum may also become involved. In young animals the virus invades the cells of the myocardium and macroscopic grey lesions may be seen particularly in the wall of the left ventricle, giving it a striped appearance (tiger heart). Cells of the skeletal muscles may also undergo hyaline degeneration.

Diagnosis

Initial diagnosis is usually on the basis of clinical signs, with or without a history of contact between the herd and an infected animal or reports of FMD in the vicinity. In a fully susceptible herd the clinical signs are frequently severe and pathognomonic. However, in endemic regions in herds which have a partial natural or vaccinal immunity, clinical signs may be mild and may be missed. All vesicular lesions in cattle should be investigated as potential FMD.

The success of the laboratory confirmation of a presumptive diagnosis of vesicular virus infection depends on the submission of adequate material, sent under suitable conditions. A minimum of 2 square cm of epithelium from a ruptured vesicle in a 50/50 mixture of glycerine and 0.04 molar buffered phosphate (pH 7.4–7.6) should be sent to a laboratory designated for handling FMD virus and equipped with the reagents required to type a positive sample.

Diagnosis of FMD is usually controlled by a government department. Where laboratory diagnosis cannot be adequately carried out within a country, samples should be sent by the relevant government department to the regional FMD laboratory or to the World Reference Laboratory (WRL) for Foot-and-Mouth Disease, Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright,Woking, Surrey, GU24 ONF, UK. Even when diagnosis is performed within a country, it is recommended that duplicate samples also be sent to the WRL or regional laboratory for confirmation of diagnosis and strain identification. Details of the method of submission of samples are described by Kitching and Donaldson (1987), although new regulations now also apply to sending pathological specimens by air.

Foot-and-mouth disease virus is very sensitive to pH values away from neutrality and is, for example, quickly inactivated below pH 6. Virus can also be isolated with heparin from vesicular fluid or from whole blood collected from the viraemic animal (up to four days after the initial appearance of vesicles). Although high titres of virus can be recovered from milk and internal body organs such as lymph nodes and muscle, these specimens should only be sent in addition to, and not instead of, epithelium samples. Negative tests on these tissues could be misleading and cause a false sense of security.

On receipt at the WRL, epithelial samples are prepared as 10 per cent suspensions for the enzyme linked immuno-sorbent assay (ELISA). This test identifies virus antigen within the sample and can distinguish between the seven FMD virus types; it has now replaced the classical complement fixation test for FMD diagnosis. Results from this test are available within three hours of arrival. At the same time as the ELISA test is being prepared, samples of the epithelial suspension are inoculated onto primary bovine thyroid cells and pig kidney cells (IB-RS-2 cells). If a clear positive is not obtained from the ELISA test, virus growth on either or both of these two cell systems would provide sufficient antigen after 24 or 48 hours for a second ELISA test. In the absence of virus growth on thyroid or pig kidney cells after 48 hours (first passage) the cells are inoculated onto fresh thyroid and pig kidney cells (second passage). Samples are considered negative following negative ELISA and failure of virus growth after 48 hours on second tissue culture passage, i.e. after a minimum of 96 hours following arrival at the WRL. The polymerase chain reaction (PCR) is also available for detection of FMD virus genome in diagnostic samples.

In countries which use vaccination to control FMD, there is a requirement to relate the outbreak strain to existing vaccine strains. This can be shown using a two way microneutralization test. Mixtures of field virus and antisera to a vaccine virus, usually prepared in guinea pigs, are incubated at 37°C for one hour and then inoculated with BHK-21 cells into the wells of a microtitre plate. The plates are placed in a 37°C incubator and examined daily for evidence of a virusinduced cytopathic effect in the cells. The titre of serum which neutralizes 100 tissue culture infective dose (TCID)50 of virus is calculated and compared with the titre of the same serum which neutralizes 100 TCID50 of the vaccine virus. The ratio of titre of serum against field virus to titre of serum against vaccine virus is the r1 value, and gives an indication of the antigenic relationship between the field and vaccine strains and therefore the probable usefulness of that vaccine in controlling the outbreak of FMD.

A similar r1 value can be derived using the ELISA. The serum antibody titre against FMD virus of cattle vaccinated against FMD can also be measured using the virus neutralization (VN) or ELISA test. Immunity in cattle to FMD can be correlated with the level of serum antibody at 30 days after primary vaccination, although the relationship is not absolute, being dependent on the challenge dose of virus and the closeness of its antigenic relatedness to the vaccine strain. The VN and ELISA are FMD virus type-specific, so that when used to determine whether an animal has had contact with FMD the

tests must be performed separately against each of the FMD serotypes with which the animal may have had contact. In some parts of the world, e.g. Africa, this could be any one of up to six different FMD serotypes. Such testing can be time-consuming, expensive and present results difficult to interpret. A non-type-specific screening test has been developed which estimates the presence of antibody to the non-structural proteins of FMD virus; these are formed in an infected animal as the virus replicates and the non-structural proteins are expressed.

Control

The control of FMD depends on prevention of the introduction of virus, prevention of infection of stock and the prevention of spread of virus from infected animals. How this is achieved by individual countries depends on a variety of economic and practical considerations.

Economic importance

The economic importance of FMD is hard to quantify accurately. The direct costs of vaccination, slaughter of infected animals, movement restrictions and closure of markets can be measured. The indirect local and national costs, e.g. loss of potential export markets, may be the most significant and yet most uncertain cost.

Assuming that a country wishes to prevent FMD remaining or becoming endemic, two options are available. Either all cattle (and possibly sheep, goats and pigs) are routinely vaccinated or no vaccination is carried out and outbreaks are controlled by slaughter as they occur. Which policy is the most economic can be assessed by critical point analysis or by estimating the critical point at which the cost of one policy equals the cost of the other policy. Costs that must be considered are the cost of vaccine and its administration or its storage as a strategic reserve. If it is also assumed that neither policy will eliminate the possibility of FMD outbreaks, the cost of controlling an outbreak must be assessed and multiplied by the estimated total number of outbreaks.

The cost of an FMD outbreak must include the cost of controlling the outbreak, including ring vaccination, the cost of slaughtered animals, the loss of production and the interruption of domestic and international trade. The international trading status of a country that vaccinates already will be considerably less affected than that of a country that does not vaccinate. Similarly, the status of a country that does not use routine FMD vaccine but vaccinates in order to control an FMD outbreak may be affected by lengthy trade restrictions with other non-vaccinating countries following the cessation of vaccination. The difficulty in assessing these uncertain costs may be illustrated by an analysis of the cost of annual vaccination (policy A) and the cost of a stamping out with ring vaccination (policy B) carried out in the Federal Republic of Germany (Lorenz, 1987). The average annual cost of policy A was estimated to be between 52 and 286 million DM, while the average annual cost of policy B was between 2.5 and 321 or more million DM. The wide range reflected the number of assumed FMD outbreaks that could occur under each regime. The estimates considered most likely, however, were between 183 and 227 million DM for policy A and between 47 and 61 million DM for policy B.

Any scenario for assessing the cost of FMD control must ultimately assume the existence of an efficient veterinary service, capable of diagnosing the disease and with facilities available to control it. Without this infrastructure any, even approximate, estimate of the economic significance of FMD becomes academic.

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