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