by Pepin
Bonobos are less aggressive and more mutually tolerant than P.t. troglodytes, and males and females have similar social ranks (some primatologists even describe an unusual situation of female dominance). Bonobos are not territorial so that males do not stalk or attack males from other troops and interactions with other communities are generally peaceful. They have a particularly intense, peculiar – and dare I say – quasi-human sexual activity: they do it for fun rather than just for reproductive purposes, and they have sex mostly in what biologists call a ‘ventral–ventral mount’ (the ‘missionary position’). Among other practices that have been described by highly dedicated primatologists, they practise mutual genital–genital rubbing, genital massages, mouth kisses and even oral sex. Another unique feature of bonobos is their bisexuality, seen in both males and females.34–36
About half of intercourses are preceded by some form of courtship, but once they copulate fifteen seconds suffice. Intercourse is used to solve conflicts and maintain social interactions, and female bonobos are known to accept sex in exchange for food, a process quite similar to some human behaviour that we shall describe later. The period of sexual receptivity of female bonobos is twice as long as for Pan troglodytes and bonobos are more likely to have promiscuous matings outside their own group. In principle, these factors could facilitate the sexual transmission of viruses.
Until recently only thirty-two bonobos, all but four living in zoos or primate centres in Europe and the US, had been tested for SIVcpz infection and none was infected. The main problem in studying bonobos in the wild is that they are close to extinction, with between 10,000 and 20,000 individuals scattered around a large area of the DRC. Their distribution is discontinuous and bonobos are well aware that their main predator is humans. Just last year, samples from around sixty wild-living bonobos, obtained from two sites in the DRC, have finally been tested and were all negative for SIV. Given the heterogeneity in the distribution of SIV among Pan troglodytes, one would like a larger number of Pan paniscus troops to be tested, but in the meantime it is fair to say that there is no evidence that this primate played a role in the emergence of HIV-1.28,37–38
Origins of SIV in chimpanzees
What was the source of SIVcpz infection in chimpanzees lies outside the scope of this book, which is to understand the early twentieth-century events that led to the current HIV-1 pandemic. To finish the story quickly, I will just add that, as reviewed elsewhere, SIVcpz probably originated from the recombination of distinct SIVs infecting smaller monkeys, principally the SIVrcm of red-capped mangabeys and a SIV which seems to infect greater spot-nosed monkeys, moustached guenons and mona monkeys. The most likely opportunity for such a recombination occurred when chimpanzees hunted and ate smaller monkeys. Perhaps the two SIVs that gave rise to SIVcpz were transmitted independently to different chimpanzees and spread for some time before an ape became infected with both, allowing recombination to occur. Alternatively, one of the SIVs could have established itself within the chimpanzee population, the recombination occurring when one of the chimps infected with the original SIV acquired a second SIV from a small monkey, again via predation.25–27,39
3 The timing
Having identified the source of HIV-1, the next question is: when did the virus manage to cross species from chimps to humans? It has often been said that AIDS was a new disease on the African continent. Apart from the published cases mentioned in Chapter 1, clinicians working in central Africa, for instance Dr Bila Kapita, chief of internal medicine at Hôpital Mama Yemo in Kinshasa, reported that, at least since the mid-1970s, they started seeing cases that in retrospect were very likely to have been AIDS. This would be consistent with some degree of dissemination of the virus during the mid-1960s, given the average ten-year interval between infection and symptomatic disease. But could the disease have been present even earlier?1,2
Bush medicine
In most district or regional hospitals of countries inhabited by P.t. troglodytes, the diagnostic facilities during the colonial era (and even now) were so minimal that it would have been difficult, even for astute and experienced clinicians, to recognise the emergence of a new disease characterised by intermittent fevers and profound wasting. Most such institutions did not have any kind of half-decent microbiology laboratory. No cultures were done, either for common bacterial pathogens or the agent of tuberculosis, and diagnoses were based on stains made directly on the specimens, or solely on the combination of symptoms and signs found during the clinical examination. Fifty years later, I found the same situation at the Nioki hospital in Zaire: nothing had changed. This approach was relatively effective for diagnosing parasitic diseases (malaria, sleeping sickness, filariasis, intestinal parasites) but very insensitive for most bacterial diseases. Little radiological investigation was available either; only in the best hospitals was it possible to get something as elementary as a chest x-ray. The first x-ray machine in Brazzaville was installed in 1931, two years before one became available in Léopoldville.
Thus a patient with fever, chronic diarrhoea and wasting might initially have been administered an antibiotic active against, say, typhoid fever. An old antibiotic, chloramphenicol, used to be popular for this indication. If this did not work, then extra-pulmonary tuberculosis would be suspected and the patient started on antituberculosis drugs (only after 1950 because, prior to that, there was no drug treatment for tuberculosis). Several weeks would be required to determine whether the patient improved on this second empirical medication. Some responded, and probably indeed suffered from occult tuberculosis. Others did not and would slowly die, often at home after it had become clear that the hospital could not provide a solution, and the families did not want to waste all their meagre resources on unsuccessful therapeutic trials. The doctors would presume that these patients died from some form of cancer, the diagnosis of which was well beyond the scope of bush hospitals. A final diagnosis would never be made, as doctors had too many other things to worry about to try to determine the actual cause of a particular death by performing an autopsy. The capacity to recognise an emerging disease was minimal, for the simple reason that there was a long list of serious diseases, already recognised in every medical textbook of the time, that these hospitals could not diagnose.
In the capitals, diagnostic facilities were better but still far from the European standards of the time, even in the clinics whose main (or only) role was to provide care for Europeans. These hospitals had a few specialists, mostly surgeons who could carry out biopsies if some form of cancer was suspected. The histopathological slides would be sent to a collaborating hospital in Europe, and the results would come back months later. One such surgeon who worked in Brazzaville thought he had perhaps recognised a new disease, as we will see now.
A colonial tragedy
Léon Pales was not an ordinary colonial doctor. He graduated from Bordeaux in 1929, aged twenty-four. During his medical studies, to earn some money Pales worked as an anatomical assistant at the medical school, helping with autopsies and the dissection of cadavers for medical students learning anatomy, an experience that would later prove very useful. While the usual MD thesis at the time consisted of a 60–80 pages literature review of some narrow medical topic, his was 429 pages long and addressed a very unusual field, palaeopathology: the study of diseases of prehistoric humans through examination of their bones. It would remain the standard French-language textbook for three decades. One of its main themes was that the study of ancient diseases could provide knowledge useful in understanding modern health problems. After the tropical medicine course in Marseilles, Pales was posted to Moyen-Congo (1931–3) and Tchad (1934–7). Back in France, he worked in Marseilles, taught anatomy and ethno-anthropology at the École du Pharo, and directed a field surgical unit during the invasion of France in 1940. Made a prisoner, he was repatriated to France the following year. He became assistant director of the Musée de l’Homme in Paris but does not seem to have been involved in the resistance movement organised ar
ound this institution. After WWII, the rest of his career (in France, and a few years in West Africa) would be devoted to palaeopathology, his first love, to anthropology and nutrition.3,4
During his two-year term in Brazzaville, Pales’ career intersected with a colonial tragedy for the sake of ‘economic development’: the building of a railway between Brazzaville and Pointe-Noire, the Chemin de Fer Congo–Océan (CFCO), whose main purpose was to avoid depending on the Belgian railway. In a region with little infrastructure, a second railway was built only 100 kilometres from the Matadi–Léopoldville line, at the same time as the latter was expanded (Map 4). Started in 1921, the 511-kilometre railway would not be completed until 1934. Ninety-two bridges or viaducts had to be erected, as well as twelve tunnels, with the longest stretching over 1.5 km. During construction, the regions immediately west of Brazzaville and east of Pointe-Noire presented no major logistical problem; food could easily be delivered and the sick evacuated. In the middle, however, the 100-kilometre stretch in the Mayombe, a dense and hilly equatorial rain forest, became a nightmare. The Mayombe was thinly populated and the workforce had to be imported, creating a huge melting pot of all AEF ethnic groups, forced to live in squalid conditions highly propitious for the spread of microbial agents, perhaps including HIV-1.5
Map 4 Itinerary of the Brazzaville–Pointe-Noire and Léopoldville–Matadi railways.
Initially in Moyen-Congo, and later in Oubangui-Chari and Tchad, 127,250 adult men were conscripted to work on the CFCO. Paid 1.5 francs per day, less than 1% of what their French foreman received, they worked ten hours a day, six days a week. Daily rations of food were inadequate, and the workers often received less than they were supposed to. They were housed in mud-brick buildings, where 50–60 men slept in the same room. As rumours spread concerning the fate of CFCO workers, it became increasingly difficult for the local chiefs to recruit their target numbers, for many fled to safer areas. The colonial authorities lowered the age limit, increased the duration of forced labour and coerced some unfortunate men in returning up to five times. Some workers absconded, usually in groups, but escape was harder to envision for men from Oubangui-Chari and Tchad. How could they possibly get back to their villages, a thousand kilometres away, without a penny in their pockets or any understanding of the local languages?6,7
Slave owners had an obvious interest in keeping their slaves alive: it was expensive to replace those who died. The situation was different with the CFCO. By contract, the AEF government had to supply the Société de Construction des Batignolles with 8,000 workers year round. Their recruitment, transportation, lodging and feeding was the responsibility of the state. As soon as a worker died, the state had to provide another and pay a penalty to the company if the minimum number of workers was not available. This was an early example of a public–private partnership in which the private company got excellent terms.
Grossly underpaid, underfed, overworked and housed in appalling conditions, between 15,000 and 23,000 workers died in the process, ten times the death toll of the Léopoldville–Matadi railway thirty years earlier. The most murderous section, and the most difficult from the engineers’ point of view, was the Mayombe. On top of the work accidents, epidemics broke out in the workers’ camps. Mortality among the Mayombe workers was a staggering 496 per 1,000 men-years in 1926 (in other words, half would be dead within a year), 454 in 1927 and 384 in 1928. It declined to 173 per 1,000 men-years in 1929, when sanitary conditions improved after this scandal was revealed in France by writer André Gide and journalist Albert Londres. In absolute terms, the peak mortality occurred in 1927, when 2,892 workers died: eight per day. Mortality was highest among those recruited in Tchad.6–9
Inspection missions were sent by the French government to investigate whether the newspaper reports were true, and to come up with solutions. Two military doctors, General Lasnet and Lieutenant-Colonel Ferris, led these inspections. Ferris described the pathetic conditions of the primitive hospitals set up near the building sites, where huts erected for twelve patients could house thirty, causing transmission of pathogens between patients. Someone admitted for pneumonia ended up with dysentery a few days later, or vice versa. The main causes of mortality were: dysentery (bloody diarrhoea), caused by Shigella dysenteriae, endemic in the Mayombe; pneumonia, caused by a bacterium known as the pneumococcus; beriberi, a vitamin B1 deficiency which causes heart failure; other ill-defined febrile illnesses; and what the doctors called ‘physiological misery’, with some features (apathy, nostalgia) suggestive of major depression.6,10
The scandal in France and the inspection visits forced the AEF government to improve the workers’ sanitary conditions. Governor Raphael Antonetti knew that he was in trouble and spent months writing detailed replies to the inspectors’ reports. Instructions about how to take proper care of the workers were issued. Wages were increased, and some women were allowed into the workers’ camps. Naturally, prostitution quickly developed, and STDs, hitherto inexistent, appeared among the workers. Prostitutes were noted to collect ‘their fees on paydays amidst long palavers’.9
Instructive autopsies
When Léon Pales arrived in Brazzaville in 1931 as the colony’s surgeon and obstetrician, the CFCO workers’ health situation had already improved. Surgical facilities in Brazzaville were limited, so Pales had a lot of free time to do what he had learned in Bordeaux and which nobody in AEF had done before: autopsies. He had access to the Institut Pasteur laboratory, where bacteriological cultures were available (for instance, to look for pathogens causing diarrhoea, such as Shigella and Salmonella) and where guinea pigs could be inoculated to look for the aetiological agent of tuberculosis. The Pasteur laboratory was even able to characterise pneumococci (the main agent of pneumonia) into serotypes.
Pales eventually published a few scientific papers on this necropsic work. First, he reported the findings from eighty-five patients who had died from pneumococcal infections, sixty-four of whom were CFCO workers. The pneumococcus was grown from the blood cultures, the cerebrospinal fluid, pleural fluid, pericardial fluid or other specimens obtained either pre-mortem or during autopsy. Pales described the autopsy findings, from the adrenals to the brain, which often revealed disseminated pneumococcal infections. This did not imply that the patients were immunologically impaired, but reflected the absence of an effective treatment which allowed this virulent pathogen to spread throughout the body. It certainly demonstrated Pales’ unique competence and motivation in performing detailed autopsies and his access to the only laboratory in AEF where bacteriological cultures could be performed.11–12
He subsequently published a paper on tuberculosis in AEF, and more detailed information is available from a thesis written by medical student Jean Auclert in Marseilles using material provided by Pales. Pales described a new condition that he called Cachexie du Mayombe. Cachexia means profound weight loss. Adult male patients with Cachexie du Mayombe weighed as little as 30–5 kg, and were described as ‘an assembly of bones held together by skin . . . whose only sign of life lay in their gaze’. They had a normal appetite and experienced no vomiting but suffered from chronic non-bloody diarrhoea. However, repeated examination of their stools failed to reveal a parasitic agent, and stool cultures performed at the Institut Pasteur were negative for the enteric pathogens known at the time, especially the Shigella dysenteriae which had killed many of the CFCO workers.13–14
Pales autopsied fifty such patients who, by his definition of the syndrome, had worked on the Mayombe part of the railway and sought care in Brazzaville after being declared unfit for service due to poor health. In thirteen autopsies, he found confirmation of a tuberculosis that had been diagnosed pre-mortem, in seven others he found occult tuberculosis undiagnosed pre-mortem (tuberculosis of the intestine or the intra-abdominal lymph nodes), in four he found other diseases which killed the patient, but in twenty-six autopsies he did not find any macroscopically obvious medical condition explaining the profound wasting. He did note, however, tha
t many of these patients had cerebral atrophy, very unusual for young adults, and that they also had generalised lymphadenopathy, including large mesenteric (around the small bowel) lymph nodes, which failed to reveal the tuberculosis bacillus via staining and/or guinea pig inoculation. We do not know the actual incidence of the Cachexie du Mayombe, but Pales presumably autopsied only a small fraction of cases, as many must have died elsewhere than at the Brazzaville hospital.
This new syndrome was certainly suggestive of AIDS. We can be pretty sure that these twenty-six patients did not have disseminated tuberculosis or cancer, which should have been easy to recognise during the autopsy. Severe malnutrition was also unlikely, because the patients’ condition should have improved when properly fed in Brazzaville. The concentration of cases among patients who had worked in a well-defined area suggests a transmissible agent. Brain atrophy is common in patients with AIDS, and leads to a complication called AIDS dementia. Generalised lymphadenopathy is a hallmark of HIV infection, caused either by the virus itself or a variety of opportunistic infections which supervene. Such findings, as well as their chronic diarrhoea, would not have been noted had the patients died of major depression or some other severe psychological disturbance related to the hardship they had to endure.
