to have peaked in 1991, when 21.1 per cent of women attending antenatal clinics tested positive and some 1,200,000 people were thought to be infected.36 By then the virus had reached almost all parts of East Africa. In Tanzania, the area first affected after Kagera was probably Dar es Salaam. An expatriate may have contracted the disease there as early as 1980, but the first firm evidence was a prevalence of nearly 2 per cent in stored blood collected from pregnant women and blood donors in 1984–5. Thereafter antenatal prevalence in the city rose to 8.9 per cent in 1989 and 14.8 per cent in 1997.37 The disease was probably introduced from Kagera, perhaps by returning soldiers but more probably by Haya sex workers and bar girls from the region, who had been prominent throughout East Africa since the interwar period, driven perhaps by male control of land and income in a highly commercialised region. By 1986, 29 per cent of Dar es Salaam’s bar girls had HIV, with a prevalence of 35 per cent among the 33 per cent of them who came from Kagera. Two years later, 60 per cent of notified Aids patients in Dar es Salaam originated from Kagera, many of them no doubt people seeking treatment. Of Tanzania’s first 212 notified Aids cases, 60 per cent of males and 46 per cent of females said that they were heterosexually promiscuous.38 Yet this initial social profile was soon obliterated by the epidemic’s expansion. When women at family planning clinics in Dar es Salaam were surveyed in 1991–2, there was still a positive association between HIV infection and number of sexual partners, but even infected women had a median of only two partners within the previous five years, while married women claiming fidelity to husbands had a significantly greater risk of infection if the husband had not been faithful, a risk that increased with the woman’s own education and her partner’s.39
Dar es Salaam was a thousand kilometres from Kagera and almost as remote from Tanzania’s other borders, yet by August 1986, less than two years after HIV was recognised in the capital, its main hospital had admitted cases from each of mainland Tanzania’s twenty regions. Some were probably infected from Dar es Salaam. In 1988 the highest prevalence, after Kagera, was in Iringa region on the Tanzam road linking the capital to Zambia.40 Other areas, by contrast, acquired HIV by cross-border contact. In the south-western Mbeya region, for example, an explosive HIV and tuberculosis epidemic between 1986 and 1994 was caused by the C subtype of HIV-1, probably introduced from Zambia to the south and most prevalent at the border and in urban and roadside locations.41 Mwanza region, south of Lake Victoria, was probably infected from Kagera, but Mara region, on the eastern shore of the lake, appears to have shared the severe epidemic in the neighbouring Nyanza province of Kenya. In the Kilimanjaro and Arusha regions of northern Tanzania the disease was blamed on young, mobile traders returning from Kagera, Dar es Salaam, and Kenya. As everywhere in the continent, the epidemic there took its shape from the structure of the commercial economy, with a focus among urban bar girls and sex workers, high infection among young adults driven from fertile mountainsides by land scarcity, and prevalence declining as the disease radiated out into the countryside. In Arusha region in 1992, for example, adult infection was 10.7 per cent in the poorer parts of the regional capital, 5.2 per cent in the wealthier parts, 2.2 per cent in semi-urban areas, and 1.6 per cent in the countryside, where at this time the disease was still seen as a complaint of despised urban aliens.42 Because HIV entered Tanzania from all directions, the country had an unusual diversity of subtypes and unique recombinant forms.43 Twenty-five years after its first appearance in Kagera the disease was still spreading into remote parts of the country.
While the link from the west lake epidemic to Dar es Salaam was strong, that to Nairobi and the Kenyan epidemic is no more than probable. Kenya’s first Aids cases were concentrated in three locations: Mombasa on the coast, Nairobi in the centre, and the Nyanza province on the eastern shore of Lake Victoria. Any of these may have infected the others, or each may have been infected separately. If HIV reached the two cities directly from west of the lake, the main link, as in Dar es Salaam, was probably women from Kagera prominent in low-status sex work in Kenya since the interwar period. Of 418 women of this kind studied in Nairobi in 1985, 358 were Tanzanians and 37 Ugandans.44 Blood specimens tested retrospectively showed that even in 1981 some 4 per cent of the city’s sex workers were infected, a proportion that grew exponentially to more than 85 per cent in 1986. Of men with genital ulcer disease attending a Nairobi clinic, 3 per cent had HIV in 1981 and 15 per cent in 1985, leaving doubt whether women or men were first infected. In 1985, 2 per cent of women at antenatal clinics also tested positive, showing that infection was spreading to the general population.45 That was the year when the Kenyan authorities belatedly admitted that the disease was present.
For epidemiologists, HIV in Nairobi was a classic example of an epidemic rapidly transmitted within a core group and then passed on by a bridging group – the sex workers’ clients – to the general population. This happened in Nairobi, as not in Kampala, partly because the Ugandan epidemic began in the countryside and partly because of differences between the cities. In 1979 Nairobi’s 827,775 people included 138 males for every 100 females, with an even larger imbalance among adults. At least half its employed men had no wife in the city.46 Wealth and poverty were sharply juxtaposed and women with little education seldom found formal jobs. The result was an exceptionally overt, mercenary style of commercial sex, especially in the Pumwani red-light district, where a community of over a thousand sex workers, many from Kagera, sat outside their rooms waiting for brief encounters with working men at a price of 30–50 US cents. Each averaged nearly a thousand partners a year, working only by day because the night was too dangerous. Some 42 per cent had genital ulcer disease.47 Study of their clients in 1986–7, when the epidemic peaked, found that 8 per cent contracted HIV from them and that 96 per cent of infected clients were either uncircumcised or had genital ulcer disease or both. Five years later, 76 per cent of women in Nairobi seeking treatment for a sexually transmitted disease reported only one partner during the previous three months and had presumably been infected by him, indicating the potential for transmission to the general population. HIV prevalence at Nairobi’s antenatal clinics may have peaked in 1994 at about 17 per cent. Four years later over 40 per cent of Kenya’s new HIV infections were thought to come through commercial sex.48
The sex workers themselves suffered terribly. Nearly half of those hitherto uninfected contracted HIV each year. They then generally developed Aids within about half the normal time, perhaps owing to multiple infection or other sexually transmitted diseases.49 Their danger was discovered almost accidentally in 1985 during a preliminary survey of sexually transmitted diseases. When astonished researchers told sex workers that two-thirds of the 60 tested had HIV, they met ‘stunned silence’. Only five wanted to know their personal status, although most quickly adopted the free condoms pressed upon them. ‘When one gets beyond the initial prejudices and stereotypes,’ the organisers wrote, ‘one finds the prostitute knowingly risking AIDS, sacrificing her own hopes for the sake of her children or brothers and sisters.’50
The explosive epidemic in Nairobi almost monopolised attention in Kenya, so that little is known of HIV elsewhere during its first decade. Perhaps misleadingly, the coast region reported three times as many Aids cases as Nairobi in 1991, the great majority no doubt in Mombasa, where 54 per cent of 3,628 sex workers tested positive between 1993 and 1997 and adult prevalence in 2000 was 10.8 per cent.51 Elsewhere prevalence during the early 1990s was relatively low, except in towns along the trans-African highway between Nairobi and the Ugandan border. In 1993 both Nakuru and Busia reported higher antenatal prevalence than either Nairobi or Mombasa. From the mid 1990s there was also rapid growth in the Central and Eastern provinces around Nairobi. Kenya’s adult infection rate probably peaked around 1998, officially at 13.9 per cent although the true mark may have been substantially lower.52
Kenya’s anomaly was the Nyanza province bordering Lake Victoria, which experienced an explosive epidemic that is perhaps the least understood in Africa. The earliest infections may have come across the lake soon after the epidemic began on its western shore, for between 1986 and 1993 Nyanza reported 15,605 Aids cases – 31 per cent of all Kenya’s cases – implying widespread HIV prevalence in the early 1980s at least. By 1993, prevalence at antenatal clinics in Kisumu, the regional capital, was 20 per cent and rising quickly.53 In the absence
