In South Africa, as in Europe, the information available regarding the prevalence of foot-and-mouth disease is not very conclusive.  In the past several references to the occurrence of a disease that can be interpreted as foot-and-mouth disease, have been made from time to time by different observers; but the descriptions given are not sufficiently detailed to allow of a definite decision.  In 1780 le Vailant (1795) described a disorder in cattle, “klowsiekte” which “attacked the feet of oxen causing them to swell prodigiously, and often producing suppuration, sometimes the hoofs dropped off.  It was not attended with any danger and generally terminated in a fortnight”.  Gordon Cumming (1850) also reported serious losses among his oxen from Mahura and his tribe.  From enquiries made by him it appeared that the disease was well known to his Hottentot servants.  In 1858 General S.J.P. Kruger reported on the campaign against Mahura along the Harts River, stating, “By this time our bullocks suffered much from the tongue and claw sickness.”  According to information obtained from some of the oldest inhabitants of the Transvaal and Free State, a disease resembling foot-and-mouth disease had been prevalent for a considerable time before it was recognized officially.  On the other hand, there seems to be very little doubt that some forms of blue-tongue have been mistaken for foot-and-mouth disease in the past (Bekker, de Kock, and Quinlan, 1934).


The first official record of foot-and-mouth disease in South Africa was made by Hutcheon in 1892 when an outbreak occurred in Griqualand West.  Although the source of the infection could not be traced, Hutcheon (1892) stated that the disease was first reported in parts of Mashonaland (Southern Rhodesia), from where it was considered to have spread along the traffic routes through Bechuanaland into Griqualand West, the Transvaal, the Orange Free State, and Natal.  Otto Henning (1892), who investigated the outbreak found the disease to be identical with the European disorder.  The scourge was well known to several farmers and, according to information obtained from some of the older inhabitants, it had been prevalent in South Africa for many years before this outbreak was reported.  Although over 75 per cent of the in-contact cattle contracted the disease, the mortality in adult animals did not exceed 3 per cent; but the losses in calves were reported to be considerably greater.  At first attempts were made to confine the disease to the North of the Orange River by preventing all movements of cattle from the north to the south of the river; but this was not possible, and as soon as Hutcheon (1893) realized that outbreaks were occurring in several districts south of the river, he withdrew the restrictions.  During the two following years mild epizootics occurred in different parts of the country (Hutcheon, 1894); but the disease never assumed serious proportions, and no further outbreaks were reported after 1895.  The advent of rinderpest in 1896 completely eclipsed foot-and-mouth disease in importance, and it may be that the devastation of the cattle population by that plague was responsible for its disappearance.


In April 1903 (Robertson, 1903) foot-and-mouth disease reappeared in South Africa.  The infection was introduced into the Cape Peninsula by means of shipments of cattle from the Argentine.  Fortunately the disease was confined to two places only, a farm where the imported cattle were kept and a local dairy that harboured a runaway heifer from the Argentine shipment.  Both areas were immediately placed under strict quarantine; the affected animals were dressed with antiseptic lotions and kept under as hygienic conditions as circumstances permitted; and the premises were thoroughly disinfected.  Although several of the Argentine animals succumbed to the secondary infection that resulted from their exposure to dirty, muddy surroundings, no deaths occurred in the local dairy herd.  At about the end of July of the same year there was no further evidence of the disease, and the quarantine restrictions were raised.


In April 1931, foot-and-mouth disease again made its appearance in southern Rhodesia when an outbreak occurred at the Nuanetsi Ranch, Chibi.  This was followed by more epizootics in Southern Rhodesia as well as in other parts of Southern Africa, including the Bechuanaland Protectorate, the Union of South Africa, Northern Rhodesia, and Portuguese East Africa.  The presence of the disease in southern Africa was established by means of guinea-pig inoculations by Bevan (1932), Robinson (1933) Lawrence (1935, 1937), Rossiter and Albertyn (1947), and by the Foot-and-Mouth Disease Research Committee (1937).  De Kock (1946) and Rossiter and Albertyn (1947) believe that the disease has become enzootic among some species of game, and that these animals are responsible for maintaining the infection in certain areas.  Through contact with infected game susceptible cattle pick up the infection and so start fresh outbreaks from time to time.


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Ruptured vesicles with raw surfaces, from a case produced experimentally by Dr. E.M. Robinson







Persons coming into intimate contact with diseased animals, e.g., milers, and those that handle infected discharges, are most commonly affected.  The infection may enter the body either through a coetaneous wound or abrasion, or through the mouth by means of infected milk.  Nuzzi (1948) reported five cases, three in children, who had partaken of milk from a cow during the incubation period.  The other two were adults who had handled the cow.


From the onset the patient is quite ill, often showing symptoms of headache, pyrexia, and hypersalivation, usually preceded by a dryness and warmth of the mouth.  After a day or two the characteristic vesicles appear, first on the buccal mucosa, and later elsewhere.  The lesions commence as small eruptions which later enlarge to form blisters of varying sizes containing a clear translucent fluid.  These are distributed on the mucous membrane of the tongue, the lips, the gums, and even in the pharynx, frequently causing considerable pain and swelling of the tongue and the pharynx.  The effect is to provoke salivation, which may be so intense as to cause serious discomfort to the patient.  In the course of two or three days the vesicles rupture to form ulcers with irregular borders, and these are surrounded by a red area.  The pharynx is often acutely inflamed and ulcerated, rendering swallowing painful and difficult.


Vesicles also develop on the volar aspect of the tips of the fingers, at the base of the nails, and between the fingers and toes.  In very severe cases the forearms and the legs may be involved, and rarely the conjunctiva, causing watering of the eyes and gumming of the eyelids.  Exceptionally, even the genital mucosae may be involved (van Rooyen and Rhodes, 1940).


The presence of the disease in man can be established by the inoculation of guinea-pigs or by means of cross-immunity tests.