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.
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.