Although rinderpest has periodically invaded Egypt in the past, the disease was not known in southern Africa before 1896.  According to Lugard (1893) the plague was introduced along the East Coast of Africa, opposite Aden, in 1889.  The infection was probably introduced from Arabia or India.  It was believed that the disease was carried southward along the Nile in 1890 by the Italian armies.  It reached Masailand and Uganda during the same year and the north of Lake Nyasa about July, 1892.  It destroyed not only domestic bovines, but also many of the indigenous antelopes along its southward course.  Early in February, 1896, large numbers of cattle and game were reported to be dying from an obscure disease on both sides of the Zambesi River.


On March 3rd it reached Bulawayo, where Gray made a diagnosis of rinderpest.  From there the plague was rapidly conveyed southwards by means of transport oxen.


Referring to the mortalities in Masailand, Lugard (1893) states that “never before in the memory of man, or by the voice of tradition, have the cattle died in such numbers; never before has the wild game suffered”.


The scourge reached Mafeking, some 500 miles south of Bulawayo, early in April, and about the same time it crossed the Limpopo into the Transvaal where the cattle population was rapidly decimated.  As soon as rinderpest made its appearance at Mafeking every effort was made by the Government of the Cape of Good Hope to confine the infection locally and to prevent its extension further southward.  Several herds of cattle were shot; two lines of fences were erected beyond (i.e., south of) the seat of infection; and cordons of mounted police were stationed at various points to prevent movements of cattle from infected areas to parts south of the line.  But, in spite of the most strenuous precautions, the disease penetrated the barriers, and reached Vryburg in May; Herbert, Hay and Barkly West in September; and Kimberley in October of the same year.


A final determined attempt to check the extension of the scourge further southward was then made at the Orange River.  A barbed-wire fence, about a thousand miles long, was erected along the northern boundaries of the Cape Colony, about 1,000 yards south of the Orange River.  The fence started near the south-western extremity of Bechuanaland and extended eastwards as far as Basutoland; then along the Cape-Basutoland and Cape-Natal boundaries as far as the coast.  Police patrols were stationed all along the line, and any communication between the infected country on the north of the line and the Cape Colony was most carefully supervised.  European travelers from the Colony was most carefully supervised.  European travelers from the north were admitted only after disinfection of their clothes, and the entrance of natives was practically prohibited.  As a result of these precautions the invasion of the Cape was delayed, but on March 24th, 1897, an outbreak occurred unexpectedly in the Herschel district, south of the line.  After an investigation into the possible source of the infection the following information was obtained:  The leader of a span of oxen, travelling on a main road near Aliwal North, south of the line, picked up a sack containing, amongst other things, dried meat and a pair of blood-stained trousers.  He put on the trousers, and a few days afterwards the leading oxen showed symptoms of rinderpest.  But before a diagnosis was made the infection had already spread to other cattle that had been in contact with the infected span of oxen.


The authorities, realising the impossibility of preventing the spread of the disease by means of the measures so far adopted, resorted to other prophylactic methods.  Meanwhile Robert Koch (1897), who had been investigating rinderpest at Kimberley on the invitation of the Cape Government, had confirmed the immunizing properties claimed by cattle farmers for the bile of animals that had died of the disease.  In February, 1897, this method of immunization was adopted all over the country, and before the end of 1898 more than two million head of cattle had been successfully inoculated.  At the end of 1898 rinderpest was under control and temporarily disappeared from South Africa, the last reported outbreak occurring on the Transvaal-Bechuanaland border in August, 1899.  (Hutcheon, 1897, 1899, 1900).


During this virulent epizootic, rinderpest caused ruin and devastation over extensive stretches of country, destroying not only the majority of domestic bovines along its route, but also considerable numbers of indigenous antelopes.  It was estimated that more than two-and-a-half million head of cattle succumbed to it in South Africa alone.


In May, 1901, cattle plague reappeared in Basutoland (Maseru), and in parts of the Eastern Orange Free State.  It was believed that these fresh outbreaks were due to the introduction of infected cattle from German South-West Africa, where the infection had persisted after the original epizootic of 1896 (Hutcheon, 1902).  Although the scourge rapidly spread to other parts of the country it appeared in a less virulent form than in 1896, and it was more easily controlled by the more reliable prophylactic measures available.  By the end of 1903 cattle plague was completely eradicated from the Cape Province, but it still persisted for a while in South-West Africa and in parts of Natal and Zululand.  Soon afterwards, however, the disease entirely disappeared from South Africa and has never made its appearance again.  But rinderpest has remained enzootic in several parts of Africa.


During the military operations in East Africa during the First World War, rinderpest was carried southwards by the movements of infected cattle.  In 1917 the Union Government justifiably became alarmed and dispatched a veterinary commission, under the leadership of Principal Veterinary Officer Gray, to combat the disease in the danger zone.  The operations were carried on over a belt of country about 200 miles long between the infected and the clean territory.  This belt extended right across the gap between the northern extremity of Lake Nyasa and the southern end of Lake Tanganyika.  All the cattle were removed from a strip of country in this belt, about 10 to 20 miles wide.  North of this strip all the bovines over an area of about 30 to 40 miles wide were inoculated with the serum-simultaneous method.  In this way an attempt was made to establish an immune zone between the infected country to the north of this belt and the clean area to the south.  During the course of a year more than 100,000 head of cattle were immunized.  At one time the disease was carried through the immune belt, but no serious outbreak of rinderpest occurred, and the disease soon disappeared.  Unfortunately a heavy mortality of native cattle followed the operations of the commission.


After this extension of rinderpest into the south the authorities in Tanganyika, by immunizing all the cattle south of the railway line from Dar-es-Salaam to Lake Tanganyika, attempted to create an immune zone between the enzootic areas in the north and the southern boundaries of the Colony.  But, as Lowe (1942) states, it is futile to maintain a rinderpest-free area in the East African Territories as long as it is contiguous to regions where the disease is allowed to remain uncontrolled.  Because the dissemination of the infection is effected by indigenous game as well as bovines, the problem of the eradication of rinderpest in East Africa is a more formidable undertaking than in other parts of the world.  Lowe points out that many of the extensions of rinderpest into the south must be attributed to game.  According to Mitchell and Le Roux (1946), the southern Highlands of Tanganyika are thickly populated by game.  There are no cattle and game along the eastern and western boundaries of the cattle zone.  Mitchell and Peevie (1945) believe that this contact between game and cattle was responsible for the southward spread of rinderpest during 1939.  As this extension was regarded as a menace to Nyasaland, to the Rhodesias, and to the Union of South Africa, prompt co-operative action was taken by these countries, and in collaboration with Tanganyika a campaign of mass immunization was organized under the leadership of D.T. Mitchell.  This led to the vaccination of approximately one million head of cattle, and a solid block of immune animals was thus created south of the railway line.  When a fresh outbreak occurred in the south during 1941 it was decided, in addition, to erect a 10-foot high game-proof fence between the southern end of Lake Tanganyika and the north of Lake Nyasa – but only 100 miles of this fence was completed (Lowe, 1942), as the menace of rinderpest’s extending further southward had meanwhile disappeared.

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The ravages of rinderpest in South Africa in 1897.  (Onderstepoort collection).







In South Africa a number of outbreaks of swine fever was recorded during the period 1903-1935.  Robertson (1905) thought that outbreaks had actually occurred before 1900, but the nature of the disease apparently was not recognized until Hutcheon (1903) reported a virulent epizootic at Groot Constantia, Cape.  Soon afterwards several outbreaks of swine fever which were probably connected with those at the Cape were described in the Transvaal by Stockman (1904), Gray (1905, 1906), and Theiler (1907).  Theiler produced evidence to show that the disease resembled the hog cholera of America and the swine fever of Europe.  He, however, could not find Salmonella cholerae suis in any of the animals examined, and concluded that this organism was not necessary for the development of the disease.  By means of blood inoculations he was able to produce typical swine fever in pigs with pathological changes characterized by hemorrhage in the lymphatic glands and the internal organs, necrotic diphtheritic deposits and button-like ulcers on the mucosa of the gastro-intestinal tract.  Further outbreaks that were diagnosed solely on clinical grounds were reported by Gray up to 1919.


Meanwhile Montgomery (1921) was studying an extremely virulent disease in East Africa occurring in localities where contact with other domestic pigs could be definitely excluded.  The disease was first noticed in 1910 and was characterized by haemorrhages in the internal organs and a mortality rate of close on 100 per cent.  Wild pigs notably warthogs (Phacochoerus sp.) and bush pigs (Potamochoerus sp.), were incriminated as inapparent carriers, from which domestic pigs obtained the infection.  Steyn (1928, 1932) reported a similar disease in South Africa and showed that it was prevalent in certain bushveld areas where opportunities existed for cohabitation between wild pigs and domestic hogs.  He was able to transmit this disease to swine by means of blood obtained from a warthog shot in the Koedoesrand area, where sporadic outbreaks had been occurring.


During 1934-1935 de Kock, Robinson, and Keppel (1940) investigated extensive epizootics of swine fever in the Western Province and lesser ones on the Witwatersrand.  They found that the pathological changes presented by this disease resembled those of the acute form of European swine fever and of those described by Montgomery (1921) in East Africa.  Evidence was obtained which suggested that the infection responsible for these outbreaks had been carried to the Rand from endemic areas in the Northern Transvaal, where contact with wild pigs sometimes occurred.  From the Rand the disease was conveyed by means of infected pigs to the Western Province.  By inoculating susceptible pigs with blood collected from a number of apparently healthy warthogs, shot in the Potgietersrus area, de Kock and his co-workers produced fatal swine fever.  But blood obtained from warthogs in some other areas, e.g. Zululand, proved to be non-infective.


De Kock, Robinson, and Keppel (1940) thought that the disease reported by Hutcheon (1903), Robertson (1905) and Theiler (1907) was reported by Hutcheon (1903), Robertson (1905) and Theiler (1907) was the same as that investigated by Steyn (1928, 1932) and by themselves in 1934-1935; and that it resembled the acute form of European swine fever.  It should, however, be pointed out that the necrotic diphtheritic deposits and button-like ulcers described by Theiler (1907) were entirely absent in the disease studied by Montgomery (1921), Steyn (1928, 1932), Walker (1933), and by de Kock and his co-workers.


Montgomery (1921) found that pigs immunized or even hyperimmunized with the European form of swine fever could not withstand an injection of the African virus, nor could pigs injected with antisera prepared from the English, Hungarian, or American strains of swine fever virus be protected against exposure to infection with the African virus.  Montgomery, therefore, labeled the African disease as a hyperacute form of swine fever.  Neither could Geiger (1937) protect susceptible pigs against the African virus by means of European swine fever antisera, and he experienced very severe losses amongst his hyperimmune pigs when the African disease spread accidentally among his experimental pigs.


De Kock, Robinson, and Keppel (1940) also reported negative results with cross-immunity tests performed with the African and European viruses, but they obtained evidence to show that, as a result of a common antigenic factor, some antigenic relationship existed between the causal agents of the two diseases.  Moreover, de Kock and his associates showed that the pathological changes presented by the South African disease resembled not only those of the East African disease but also those of the acute form of European swine fever.  They concluded, therefore, that more than one strain of virus might be found in swine fever and that the South African disease was caused by an extremely virulent strain.  Walker (1933) believed that there were probably several different strains of virus causing African swine fever.