The African AIDS Epidemic. John Iliffe

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The African AIDS Epidemic - John Iliffe

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Sudan in 1976, 0.9 per cent subsequently revealed HIV.1 Such low levels of infection may well have existed in other rural areas of the equatorial region during the 1970s. They apparently existed also in Kinshasa. One of those testing positive at Yambuku had probably contracted the disease in the capital during the early 1970s. Of 805 blood specimens taken from pregnant women in Kinshasa in 1970, two later revealed HIV infection. So did blood taken there in 1972 from two of four patients with Kaposi’s sarcoma.2

      The conversion of this low-level infection into an expansive epidemic probably took place in the urban environment of Kinshasa during the 1970s. The key may well have been the exceptional infectivity of the newly infected, which meant that if the virus entered a network of sexual relationships in which partners were exchanged rapidly and extensively, it could build up a momentum of infection sufficient to reach epidemic levels. That is probably what happened in the United States, where HIV prevalence among homosexual men attending a sexually transmitted disease clinic in San Francisco rose between 1978 and 1984 from 1 per cent to 65 per cent.3 It happened at much the same period, although less explosively, among heterosexuals in the East African cities of Bujumbura, Kigali, and Nairobi, as also in rural south-western Uganda and in Abidjan in West Africa. The first occasion, however, was in Kinshasa, where HIV first encountered rapid partner exchange in urban sexual networks wider, although not necessarily much more promiscuous, than those of the countryside.

      Map 1 Western Equatorial Africa

      The first person to notice the change may well have been Dr Kapita Bila, the Congolese physician heading the internal medicine department at Kinshasa’s huge, 2,000-bed Mama Yemo Hospital. ‘Something dramatic happened in 1975,’ he recalled a decade later, referring especially to a doubling of cases of Kaposi’s sarcoma, a tumour that could take aggressive forms when the immune system was damaged and hence often became a conspicuous symptom of Aids. Other hospitals in the region observed this increase only in the later 1970s and early 1980s, but Kapita Bila dated it at Mama Yemo from 1975 and claimed that hospital records revealed cases at that time. The records also confirmed Congolese doctors’ recollections that in the mid 1970s they had first noticed numerous cases of the severe wasting and diarrhoea that became the most common symptoms of Aids in African patients.4 In the late 1970s doctors across the river in Brazzaville observed similar cases. Physicians in Kinshasa initially attributed these symptoms to tuberculosis, which spread epidemically in the region during the 1970s and 1980s, perhaps in synergy with HIV. By 1985, one-third of tuberculosis patients in Kinshasa’s hospitals also had HIV.5 A more distinctive indicator of Kinshasa’s emerging HIV epidemic was cryptococcal meningitis, an agonising and commonly fatal infection of the brain. Hitherto generally confined to children, it spread in a distinctively urban form to adults with damaged immune systems and became increasingly common at Mama Yemo from the late 1970s.6

      When blood taken in 1980–1 from antenatal clinic attenders in Kinshasa was later tested, it showed that HIV prevalence among them had grown during the 1970s from 0.2 per cent to 3 per cent.7 The world’s first HIV epidemic among a heterosexual population had begun before the existence of the virus was even suspected. That, more than anything else, was why Africa was to suffer so terribly during the following decades. Yet enlightenment now came quickly. In June 1981 American doctors published the first account of an epidemic of pneumocystis carinii pneumonia among American homosexuals. On reading it, physicians in Brussels and Paris realised that they had treated similar conditions since the mid 1970s, chiefly in Africans from the equatorial region or Europeans who had visited it. Of the first 96 recorded Aids patients seen in Europe, 54 were Africans, 40 of them from the DR Congo.8 In contrast to infected Americans, however, they were heterosexuals in roughly equal numbers of men and women, they did not take drugs, and they had no obvious risk factor in common except their geographical origin. In October 1983 joint American and Belgian teams left for Kinshasa and Kigali.

      At Mama Yemo, Kapita Bila showed the visitors the patients he suspected to be suffering from Aids. ‘The moment I walked into the hospital in Kinshasa I realised something terrible was happening,’ recalled Peter Piot, later the first head of UNAIDS.9 ‘Meningitis was only one manifestation of the disease,’ wrote his colleague Joseph McCormick:

      Some developed such exquisitely sore mouths and tongues that they were unable to eat. Those who could manage a few bites of food were suddenly stricken by cramps and disgorged a copious amount of diarrhea. Their skin would break out in massive, generalised eruptions. Infected fungating masses would appear inside and outside their bodies. When the infection didn’t consist of voracious yeast cells [as in cryptococcal meningitis], there were many other parasites ready to eat the brain alive. None of the victims could comprehend in any way what was happening to them or why. And we? All we could do was watch in horror, our roles as physicians reduced to scrupulous observers and accurate recorders of documentation. Our one hope was that if we could understand the processes we were observing, someone, somewhere, might find some solution.10

      Diagnosing by symptoms, the team identified 38 Aids cases in Kinshasa’s hospitals, 20 men and 18 women. Of these, 29 were from Kinshasa itself, but others came from all parts of the country, indicating how far the virus had spread. On 3 November the team presented its findings at a medical meeting at Mama Yemo, warning that the disease appeared to be sexually transmitted, incurable, and fatal. ‘If there is a misfortune spreading terror in Kinshasa in the last few days, it is assuredly AIDS,’ a local editor wrote five days later. ‘It is spoken of in the most varied ways . . . at the office, at the market, in bars, in families . . . Never in my memory as a journalist have I seen such concentration on a subject as disagreeable as strongly feared.’11 It was his last such comment, for President Mobutu’s increasingly unpopular and insecure government banned the subject for the next four years. ‘For the four million Kinois,’ a foreign journalist wrote in 1986, ‘the disease, for lack of any official information, still has no name. Signs, therefore, suspicions, often infantile beliefs. Aids all the same.’12

      Reactions abroad to evidence that the disease was widespread in a heterosexual population were equally hostile. American medical journals rejected Piot’s report and it took over a year to convince the American government. In the meantime the World Health Organisation cautiously endorsed the discovery by French scientists that Aids was caused by a retrovirus. McCormick persuaded the Centers for Disease Control in Atlanta to fund a research project in Kinshasa.13

      Projet Sida, as it became known, began work in June 1984 and defined the epidemiology of the urban disease in a form that still dominated medical thought two decades later. A collaboration between American, Congolese, and Belgian specialists, initially led by an idealistic public health expert named Jonathan Mann, the Project had nearly 300 staff at its peak and the advantage of newly devised equipment to test blood for HIV. Its most important finding was that between 6 and 7 per cent of pregnant women at Kinshasa’s antenatal clinics were already infected with HIV, whereas earlier estimates of the epidemic had observed only the much smaller numbers with advanced Aids. Mann warned in 1986 that ‘one to several million Africans may already be infected’. He reckoned the annual incidence of new infections at between 0.5 and 1.5 per cent of hitherto uninfected people.14 The Project also identified the means of transmission as sexual intercourse, exchange of blood by injection or transfusion, and infection from mother to child, excluding aerial transmission, insect vectors, and casual contact.15 Sexual transmission was bidirectional, whereas the possibility of women infecting men had hitherto been uncertain. Among new infections, eleven were women to every ten men, although women in their twenties outnumbered men by three to one.16 In other respects those infected did not have a strong social profile. The earliest observed cases had often been prosperous people who could afford multiple partners and medical treatment, but antenatal prevalence at Mama Yemo was somewhat higher than at a fee-paying hospital. The age profile, however, was distinctively bimodal, peaking in infants and young adults.17

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