Although the data from Karonga are uniquely detailed, it was clearly not the first part of Malawi to experience HIV infection. Study of stored blood taken in southern Africa before 1974 has revealed no evidence of HIV, but the first 17 Aids cases were reported from Malawi’s health facilities in 1985, some with aggressive Kaposi’s sarcoma, and a year later nearly 4 per cent of Malawian mineworkers in South Africa were HIV-positive, the only national group from Central Africa significantly infected. Given the long incubation period before the appearance of symptomatic Aids, and given the wide extent of HIV infection evident by the mid 1980s, Malawi’s silent epidemic probably began before 1980, or only slightly after HIV can be discerned around Lake Victoria. Census data show that mortality in Malawi increased significantly between 1977 and 1987, but chiefly among children, who commonly died of Aids more quickly than adults.5
The virus may have reached Zambia slightly earlier than Malawi, although the evidence is indirect. In 1983 Anne Bayley, a surgeon in Lusaka, found herself treating unprecedented numbers of young adults afflicted with aggressive Kaposi’s sarcoma. When tested in 1984, 91 per cent of these were found HIV-positive. Bayley later thought that the first case might date back to 1980 and that HIV had probably reached Zambia in the mid 1970s, initially spreading slowly. She added – a conclusion presumably reached by retrospective testing – that in 1981 fewer than 1 per cent of women at Lusaka’s antenatal clinics were HIV-infected.6 Many early patients in Lusaka with Kaposi’s sarcoma had associations with the Copperbelt, where tuberculosis cases suddenly multiplied from 1984 and the first small HIV tests in the general population of mining communities in 1985 showed 13.5 per cent prevalence in males and 21 per cent in females. Of deaths from Aids reported from Zambia between March and July 1987, 46 per cent were from the Copperbelt and 18 per cent from Lusaka.7 Yet the situation in the capital was alarming enough, for tests there in 1985 showed that 8 per cent of pregnant women were infected. In February 1986 Aids patients were also dying in Livingstone on Zambia’s southern border with Zimbabwe.8
In reality, the silent epidemic had penetrated Zimbabwe some time before, although perhaps three or four years later than Zambia and Malawi as the virus was carried southwards. The first cases of Aids and aggressive Kaposi’s sarcoma were diagnosed in 1983. Alarm arose only when blood was first screened in 1985 and it was revealed that over 2 per cent of donors had HIV. Infection then concentrated in the northern city of Harare, with only 0.05 per cent of donors testing positive in Bulawayo, further south. Thereafter, however, expansion became general and rapid. At the district hospital at Hurungwe in Mashonaland West, the annual number of patients diagnosed with HIV rose between 1986 and 1988 from 16 to 292. In Manicaland province, on Zimbabwe’s eastern border, all districts recorded increased mortality from the late 1980s. By 1990 national antenatal prevalence was 12.9 per cent.9
Botswana was invaded next, slightly later than Zimbabwe and just as stealthily. Over 200 blood specimens collected in the north during 1984 showed no HIV. ‘It’s not a problem in Botswana,’ an official declared, ‘AIDS is primarily a disease of homosexuals and there is no homosexual in Botswana.’ The first case reported at that time was indeed a white homosexual.10 When the first Tswana tested positive a year later, the Minister of Health ‘allayed fears by mentioning that the modes of transmission of the disease means that it could not become a big epidemic’. Within another year, however, he was speaking of ‘a scourge that could decimate a large portion of the human race’ and recommending ‘a stable, faithful relationship with another uninfected person’. By then Botswana had 30 known HIV cases and feared that the real number might be more like 3,000. In 1990 tests showed that 5–7 per cent of blood donors in towns and 1–2 per cent in the countryside were infected.11
During the 1990s these four countries of Central Africa overtook East Africa as the chief focus of the global epidemic. Malawi experienced rapid growth of infection during the later 1980s in the major towns, led by Blantyre where infection rates at the hospital antenatal clinic rose from 2.0 per cent in 1985 to 25.9 per cent in 1991 and a peak of 32.8 per cent in 1996. A small study there in 1990–5 suggested an annual incidence of new infections among women of 4.21 per cent, or perhaps four times the rate during the Kinshasa epidemic. During that period, however, prevalence probably grew even faster in the countryside, narrowing the hitherto wide urban–rural differential. In 1996 adult prevalence was 23 per cent in urban, 18 per cent in semi-urban, and 12 per cent in rural areas. Given that only 12 per cent of Malawians lived in towns, most infections were rural.12
By the mid 1990s Zambia’s prevalence had overtaken Malawi’s. According to a later estimate, adult infection peaked in 1994–5 at about 17 per cent. As in Blantyre, the growth of the epidemic in the late 1980s was especially rapid in Lusaka, where antenatal prevalence rose to a roughly stable 22–27 per cent at different clinics in 1990–3. The difference was that 50 per cent of Zambians were urban and that overall prevalence in Copperbelt province almost equalled that in the capital.13
Yet Zambia, too, was soon overtaken. Zimbabwe’s prevalence figures are especially difficult to interpret, with wide variations between those quoted by national and international authorities and even wider fluctuations at individual sentinel sites. The most reliable data are probably for antenatal clinic attenders in Harare. Prevalence among them was 10 per cent in 1989 and 18 per cent in 1991, both figures substantially less than in the main cities of Malawi and Zambia, but it grew further to a peak of 32 per cent in 1995 and then fluctuated around that level. Yet only 28 per cent of Zimbabwe’s people were urban.14 The distinctive feature of its experience during the 1990s was the high level of prevalence outside the main cities, often so high that the statistics must be treated with caution. Three kinds of areas were worst affected. One contained towns on main roads close to borders, where truck drivers might socialise for several days while negotiating their way across the frontier. Beitbridge, on the South African border, recorded 59 per cent HIV prevalence in 1996, while the figure at Mutare, near the frontier with Mozambique, reached 37 per cent in 1997.15 Second, the trucking routes contributed to high prevalence in provinces and districts through which they passed. Masvingo province, which registered a barely credible provincial figure of 49.4 per cent among pregnant women in 2000, was bisected by the road from Harare to South Africa, while Midlands province, with a reported 45.1 per cent prevalence in 2000, straddled the route from Harare to Bulawayo.16 Yet this devastating provincial infection that distinguished Zimbabwe was not confined to transport routes but existed even in remote rural areas. In 1993–4 overall adult prevalence was already 24 per cent in the Honde valley, a fairly isolated part of Manicaland. Shortly thereafter, 22 per cent of pregnant women tested HIV-positive even at Tsholotsho in arid northern Matabeleland.17 As will be seen later, both its excellent transport system and its high levels of oscillating migration between country and town made rural Zimbabwe especially vulnerable to infection.
Those characteristics operated even more powerfully in Botswana. From only 2 or 3 per cent in 1990 its national adult prevalence soared to 23 per cent in 1995 and either 28 per cent (according to the government) or 36 per cent (according to UNAIDS) in 2000, the latter figure being the highest in the world.18 As the epidemic spread south, its momentum seemed to accelerate, suggesting the possibility that rapid passage of the virus from person to person might be increasing its virulence, although there was no hard evidence of this. The acceleration in Botswana was noticed first not at the capital, Gaborone, but at Francistown, where the main road crossed into Zimbabwe and antenatal prevalence reached 24 per cent in 1992 and 34 per cent in 1993. Gaborone soon followed, as did the mining town of Selebi Phikwe; in 2000 these three towns registered antenatal prevalences of 44, 36, and 50 per cent respectively.19 Yet this initial urban predominance was reversed as the epidemic grew. By 1999 prevalence among pregnant women was 22 per cent even in the Kgalagadi desert area, while the highest reported prevalence among them at that time was 51 per cent in the northern district of Chobe. Overall, according to the government, ‘the 2002 survey reveals slightly higher rates in rural than in urban areas’. The annual incidence of new infections for the whole country at that time was estimated to be 6 per cent, roughly three-quarters of the level reached among young people at Rakai
