The African AIDS Epidemic. John Iliffe

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The African AIDS Epidemic - John Iliffe

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1983 cryptococcal meningitis, Kaposi’s sarcoma, tuberculosis, and other opportunistic infections became increasingly common in Bujumbura and doctors suspected Aids, which was confirmed serologically in 1984.4

      Map 2 Eastern Africa

      Bujumbura’s epidemic grew remarkably fast during the early 1980s. By 1986 some 16.3 per cent of women tested at antenatal clinics were infected. Thereafter growth slowed temporarily, rising only to an urban prevalence of 18.3 per cent in 1992, which nevertheless implied a high incidence of new cases.5 One reason for the epidemic’s virulence may have been its close association with tuberculosis, long prevalent in Burundi. In 1986, 55 per cent of tuberculosis cases treated in Bujumbura were HIV-positive, while tuberculosis cases in Burundi as a whole increased between 1985 and 1991 by 140 per cent. The epidemic’s most striking feature, however, was its urban concentration. While urban antenatal prevalence in 1992 was 18.3 per cent, it was only 5.2 per cent in semi-urban and 1.9 per cent in rural areas.6 Rwanda’s first rough sample survey of people of all ages in 1986 showed a similar contrast between 17.8 per cent prevalence in towns and only 1.3 per cent in the countryside. The highest rates among pregnant women were in Kigali, where they rose even more quickly than in Bujumbura, reaching 33 per cent in 1993.7

      The rapid infection of Kigali and Bujumbura took place in countries where sexual behaviour among the overwhelmingly Christian general population was remarkably strict. In a survey conducted during the late 1980s, only 10 per cent of men and 3 per cent of women aged 15–19 in Burundi reported sexual intercourse during the last twelve months, compared with 51 per cent and 30 per cent respectively in the Central African Republic.8 The result was a different epidemic pattern, dominated not by widespread partner exchange but by commercial sex. Sex workers had long been Africa’s urban witches, blamed for all manner of social ills, so that there is a danger of stereotyping their role in the epidemic. Yet everywhere in eastern Africa, except Uganda, they were the first focus of infection. In 1984 a study of 33 sex workers in Butare, Rwanda’s second town and home to a military base and university, found 29 infected with HIV, along with 28 per cent of their clients, who frequented a median number of 31 sex workers a year. Of 300 Aids patients in Bujumbura in 1987–9, 106 of the 184 men had frequented sex workers and 21 of the 116 women had themselves been sex workers.9 Both countries were overwhelmingly monogamous, with exceptional numbers of unmarried women. In the early 1990s Kigali had 50 per cent more men than women aged 20–39. Fifteen years earlier the city also had an estimated minimum of 2,000 femmes libres, many of them uprooted by the destruction of Tutsi power since the revolution of 1961.10 On average, men in Kigali made their sexual debut at 18 but married at 24–28; in the meantime, since other young women in this ‘austere Catholic town’ were carefully protected, they frequented sex workers and often continued to do so after marriage. Circumcision was rare, condoms despised, sexually transmitted diseases widespread, sexual coercion common, and women depended overwhelmingly on a male partner for income.11 Although epidemics in both countries initially focused around sex workers, therefore, their clients quickly spread the disease to their regular partners. In the late 1980s, 80 per cent of infected women and 76 per cent of infected men in Kigali had an infected partner.12

      On the eve of the genocide of 1994, antenatal prevalence in the Rwandan countryside – ‘in the hills’, as they said in Kigali – remained less than 5 per cent. In rural Burundi it was even lower.13 The contrast with the relatively equal urban–rural prevalence that will be seen in Central Africa is difficult to explain in small countries with excellent transport systems, dense rural populations, and large income differentials between town and country. The towns did spread infection to their rural environs. A study in the Butare region in 1989–91 showed no association between HIV prevalence among rural women and the frequency with which they visited the town, but a significant association if their regular partner visited it daily.14 Yet these were small towns. The largest, Kigali, had only 220,000 inhabitants in 1986, only some 3 per cent of Rwanda’s population. They had no industry to attract the long-staying migrant workers who were probably most responsible for spreading infection to Central African villages. Whatever the reason, Aids in Rwanda and Burundi began and remained until the mid 1990s essentially an urban disease.

      The contrast elsewhere in the Lake Victoria region was remarkable. In the lakeshore districts of Masaka and Rakai in south-western Uganda and the Kagera region of north-western Tanzania, Africa experienced its first rural-based Aids epidemic, a product of a prosperous peasant society at a moment of profound crisis. In East Africa during the 1970s the post-independence order was beginning to unravel. General Amin seized power in Uganda in 1971, precipitating eight years of violence and a magendo economy of illegality and self-help until the Tanzanian invasion overthrew him in 1979. Tanzania, although politically more stable, suffered severe economic decline as a result of the socialist strategy adopted in 1967, a decline accentuating Kagera’s long-standing problems of isolation, land scarcity, and agricultural decay. In Kenya, too, the prosperous era of Jomo Kenyatta gave way from 1978 to growing stringency and corruption under Daniel arap Moi.

      HIV penetrated first into the borderland between Uganda and Tanzania west of Lake Victoria. Some have believed that the virus had been present in Uganda since the late 1950s or 1960s, pointing especially to occasional cases of the aggressive form of Kaposi’s sarcoma later found in some Aids patients. This is possible, but aggressive Kaposi’s sarcoma was a consequence of immune suppression rather than necessarily of HIV; nobody at the time noticed any change in the epidemiology of the disease, as they did in the early 1980s, and no stored blood from the region prior to the late 1970s has shown HIV antibodies.15 Without stronger evidence it seems more in accord with the continental pattern of the epidemic to think that Aids first appeared on the Uganda–Tanzania border in the late 1970s and HIV a few years earlier.

      Its arrival cannot now be identified exactly. According to Uganda’s chief epidemiologist, symptoms later characteristic of Aids were first reported late in 1982,

      when several businessmen died at Kasensero, an isolated small fishing village on Lake Victoria. This small town was also known for smuggling and illicit trade, and when these deaths occurred fellow traders shrugged it off as witchcraft. Others thought it was natural justice against those who had cheated. The only common characteristic the victims had was that they were all young and sexually active and stayed away from home for several days chasing wealth and presumably using it generously for their recreation and merriment.16

      Across the border in Tanzania the first three Aids cases in Kagera region entered hospital in 1983. Retrospectively, however, medical workers believed that they had seen earlier cases. Kitovu Mission Hospital in Masaka district of Uganda was later said to have recorded 84 during 1982 alone. An African doctor in Rakai district believed that his uncle had died of the disease in 1980. The leading expatriate specialist later thought he had seen the corpses of Aids victims in Kampala in 1979 or 1980. Taken as a whole, the evidence suggests that HIV entered the region during the 1970s and became epidemic in the early 1980s.17

      Local people called the new disease ‘Slim’ because wasting was commonly its most visible symptom. ‘In the first six months,’ Dr Anthony Lwegaba reported from Rakai in 1984,

      the patient experiences general malaise, and on-and-off ‘fevers’. For which he may be treated ‘self’ or otherwise with Aspirin, chloroquine and chloramphenicol etc. In due course, the patient develops gradual loss of appetite.

      II. In the next six months, diarrhoea appears on-and-off. There is gradual weight loss and the patient is pale. Most patients at this point in time will rely on traditional healers, as the disease to many is attributed to witchcraft.

      III. After one year, the patient develops a skin disease . . . which is very itchy. Apparently it is all over the body. The skin

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