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Except from: Knowles, N.J. (1990). Molecular and antigenic variation of foot-and-mouth disease virus. M.Phil Thesis, March, 1990, Council for National Academic Awards.

Foot-and-mouth disease (FMD) is a highly contagious, economically devastating disease of cloven-hoofed animals. Its host range is extremely wide being capable of infecting nearly 70 species within 20 families of mammals (Hedger, 1981). Although rarely fatal FMD can be an economically devastating disease due to serious loss of condition.

In cattle the disease is characterized by fever and vesicular lesions on the mouth, tongue, muzzle, hooves and udder. These lesions lead to salivation and lameness. Secondary bacterial infections frequently occur, especially on the feet. Myocarditis may occur in young animals sometimes resulting in death. The clinical picture in pigs is similar, however, sheep and goats are usually less severely affected.

The earliest description of what was probably FMD was that by Hieronymi Fracastorii (1546). He described the disease, which occurred in Northern Italy in 1514, as being unusual and affecting only cattle. In 1780 in Southern Africa, Le Vaillant (1795) described a disease in cattle which "attacked the feet of oxen causing them to swell prodigiously and after producing suppuration, sometimes the hooves dropped off". Gordon Cumming (1850) and General S.J.P. Kruger (1858) also described a disease in Southern Africa which was probably FMD. Foot-and-mouth disease was present in Rhodesia (Sinclair, 1922) and Swaziland (Edmonds, 1922) in 1892 and in Rhodesia in 1894-5 (Edmonds, 1922). Hutcheon (1894) records an outbreak in South Africa, originating in Mashonaland and the Northern part of the Transvaal in 1893.

In 1896 a panzootic of rinderpest swept through Southern Africa and only isolated pockets of wildlife and cattle survived, the total ruminant population was probably reduced by 95%. There are no reports of FMD in Southern Africa from this time until 1931 when the disease was observed in Rhodesia, except for outbreaks of disease in Cape Town in 1903 which originated from the importation of live, diseased animals from the Argentine and were successfully controlled (Robertson, 1904).

In Germany the existence of FMD was first reported by Adami in 1754 (see Henning, 1956), while in Great Britain it was first recorded in August 1839. By the end of that 1839 the disease had spread to most districts of England and some parts of Scotland (M.A.F.F., 1965). The disease continued during 1840 and 1841 but during 1842-44 there was a marked reduction in the incidence of the disease. During the latter part of 1845 and in 1846 the incidence again increased followed by a gradual fall in incidence until 1851. A very severe epidemic occurred in 1852, but during the remainder of the decade the disease incidence was low. In 1869 there was an increase in incidence which built up to 27,254 cases in 1870 and 52,164 cases in 1871. Foot-and-mouth disease was endemic in Continental Europe during this period and outbreaks were recorded for the first time in Canada and the United States. This was also the period when FMD was first introduced into South America (Argentina) in the late 1860's and early 1870's along with the cattle taken by European immigrants (Machado, 1969). The disease spread to Brazil in 1895 and to Uruguay and probably Peru and Chile in 1910. The disease may not have spread to Ecuador until 1943 while Venezuela and Colombia remained free until type O was introduced into the former country in 1950 via imported cattle from Argentina. Type A was introduced soon after in 1951, possibly from Europe.

In Ceylon (now Sri Lanka) FMD appears to have been present before 1842 (Cattle Disease Commission Report of 1869-70, quoted by Fernando, 1969).

In 1898 Loeffler and Frosch discovered that the agent of FMD was filterable and in 1922, Vallée and Carré first showed the existence of two immunological types of FMDV by cross-immunity tests in cattle. They were designated by their areas of origin, O (Oise, a department in northern France) and A (Allemagne - Germany). Soon after Waldmann and Trautwein (1926) reported the existence of three immunologically distinct types, A, B and C. Comparison of these virus types revealed that Waldmann and Trautwein's types A and B were the same as Vallée and Carré's types O and A, respectively; type C was distinct. Thus the three types became known, by international agreement, as Vallée O, Vallée A and Waldmann C and later simply as O, A and C. Many atypical virus strains were later described, mainly from Africa, until in 1948 a sample submitted to the WRL from Bechuanaland yielded a virus (BEC/1/48) which in cross-protection tests in cattle and guinea pigs was found to be distinct from O, A and C. Subsequently a virus isolate from Northern Rhodesia (RHO/1/48) was identified as yet another distinct type. Retrospective testing of viruses isolated between 1931 and 1937 revealed isolates from Southern Rhodesia in 1937 (RV/11/37) and 1931 (RV/1/31) which were similar to the 1948 isolates from Bechuanaland and Northern Rhodesia, respectively (Brooksby, 1958). A further virus isolate from Southern Rhodesia in 1934 (RV/7/34) was found to be a third new type. These new types were designated SAT (Southern African Territories) types 1, 2 and 3. The seventh serotype, designated Asia 1, was first recognised in the early 1950's as viruses isolated from India in 1951 and 1952 (Dhanda et al., 1957) and Pakistan in 1954 (Brooksby and Rogers, 1957).