The Origins of AIDS

by Pepin

  Adapted from Pepin.46

  Map 5 Map of Cameroun Français and the four colonies that comprised the Afrique Équatoriale Française federation.

  It seems plausible that not all medical injections carried the same risk of HCV transmission. Again, data gathered during studies of healthcare workers occupationally exposed to their patients’ blood can be informative. Healthcare workers exposed to HCV experience a higher risk of infection when a hollow-bore needle had been placed in the index patient’s vein and when they sustain a deeper injury; these risk factors presumably reflect the higher number of viral particles accidentally inoculated. Extrapolating to the potential iatrogenic transmission between patients, the risk must have been higher with IV, intermediate with IM, and lower with SC or ID injections. And obviously the risk must have been proportional to the total number of injections received. The same conclusions can be extended to the transmission of HIV. In Cameroon, researchers looked for HIV-1 nucleic acids in discarded needles and syringes that had been used on HIV-infected patients less than six hours earlier. One third of the syringes used for IV injections contained detectable virus, versus only 2% of those used for IM injections.47–49

  Inoculation hepatitis

  Now we will go back in time to try to assess what medical doctors and nurses working in central Africa in the first half of the twentieth century could have known concerning the potential transmission of viruses during medical care. Presumably, understanding these risks might have made them more careful. We can assume that the level of understanding among these pioneers of tropical medicine was no higher than among their counterparts working in Europe. Most of the knowledge about blood-borne viruses that eventually trickled down to medical practitioners in Africa originated from Europe.

  During this period of interest, little was known about viruses in general and even less about putative viruses potentially causing hepatitis. Unlike bacteria and parasites, viruses were too small to be seen during direct or stained microscopic examinations of specimens. Their culture required the support of cells, while for bacteria an agar plate with the right nutrients would suffice. Nor were clinicians at the time able to measure liver enzymes in the blood, which is essential to the diagnosis of hepatitis, whatever its aetiology. These enzymes are released when there is inflammation in the liver.

  In practice, ‘hepatitis’ was diagnosed when a patient developed jaundice for which there was no other apparent explanation (in the tropics, this investigation would include negative smears for malaria). Cases of hepatitis not severe enough to cause jaundice would be missed, while some patients with other conditions associated with jaundice were misdiagnosed as having hepatitis. The diagnoses were pretty reliable, however, when outbreaks occurred: if dozens or hundreds of somehow-related patients developed jaundice within a limited time frame, there was no doubt that this corresponded to hepatitis caused by an infectious agent.

  ‘Inoculation hepatitis’ or ‘serum hepatitis’ began to be described in textbooks from the 1940s as appearing after various medical interventions including, in Europe, the treatment of syphilis with arsenic-based drugs, usually administered as a series of weekly IV injections. Clinicians distinguished between early arsenical hepatitis, occurring around day 9 and presumed to be drug-related, and late hepatitis, occurring after about 100 days, which was thought to be infectious.50–55

  Before WWII, only 1% of syphilitics treated with IV arsenical drugs developed jaundice, but wartime conditions and shortages led to a quicker turnaround of syringes and needles. In several military clinics in Britain, between 50% and 75% of men treated for syphilis developed jaundice! Similar epidemics occurred in civilian hospitals after the virus had been introduced by returning soldiers who had received initial doses of some IV drug in a military clinic. This was attributed to the re-use of glass syringes, which were in short supply, so they could not be boiled between patients (it would have taken too long for the syringes to cool down before they could be handled again); they were put into a disinfectant briefly or they were merely rinsed with water. Before a drug was injected IV, the nurse had to aspirate a small quantity of blood to make sure that the needle was properly located within a vein. When the drug was pushed into the vein, a minute quantity of blood remained in the syringe and the needle, some of which ended up being injected into the vein of the next patient(s).54–57

  When outbreaks of jaundice were described after the treatment of syphilis and other infections with penicillin, then a revolutionary drug, it became more and more difficult to attribute these cases to anything other than a transmissible agent. Furthermore, a viral cause was suspected when it became apparent that the nurses who administered the IV injections, as well as the laboratory technicians who handled the blood samples sent for testing, were themselves at risk of developing jaundice. These outbreaks certainly corresponded to infection with HBV, since most cases of acute infection with HCV do not develop overt jaundice. Obviously, to reach a risk of hepatitis of 50–75%, a vicious circle with exponential amplification of HBV was created. A first HBV-infected patient transmitted the virus to a few more; each of these second-generation cases infected a few additional patients, and so on.58

  Around 1942, batches of a yellow fever vaccine which had been suspended in human serum (obtained from medical students) during its production caused 50,000 cases of jaundice among American civilians and soldiers. With this massive epidemic, the second major form of viral hepatitis was given its current name. Strongly associated with injections and not displaying any seasonality, it became known as hepatitis B, to distinguish it from the other form of infectious hepatitis, hepatitis A, which was not associated with injections but displayed marked seasonal variations in incidence. When US army veterans who had developed hepatitis in 1942 after receiving the yellow fever vaccine were tested in 1985, four decades later, 97% of them had antibodies against HBV, as did 73% of those who had been vaccinated without developing overt hepatitis, compared to only 13% of those not vaccinated. If those who were infected but did not develop jaundice are added to the symptomatic cases, it can be estimated that 330,000 vaccine recipients were iatrogenically infected with HBV. Other vaccines, blood sampling through a common syringe (in clinics for diabetics or in a sanatorium), transfusions and administration of convalescent sera, plasma or injectable drugs were in turn all recognised as causing hepatitis B.59–60

  There is no evidence that medical officers working in central Africa in colonial times became aware of these risks. The risk of inoculation hepatitis was not mentioned in any of the reports of the health systems of AEF and Cameroun that will be reviewed in the next chapter, while in the Belgian Congo its first description was published in 1953. Acute HCV infection is often asymptomatic or causes non-specific symptoms, without overt jaundice, and could not possibly have been recognised by the colonial clinicians. Infection with HBV is nearly universal in central Africa and generally acquired during childhood (when it rarely causes jaundice), which leaves little potential for its iatrogenic transmission to adults, in contrast to Britain, where most adults treated for syphilis had hitherto not been infected with HBV and were susceptible to an iatrogenic infection. Furthermore, when iatrogenic HBV infection did occur in sub-Saharan Africa, symptoms would have developed after a one- to four-month incubation period, making it difficult for doctors to recognise that this was related to a previous episode of medical care.

  Reports of health services in Cameroun and AEF give no indication regarding how re-usable syringes and needles were sterilised between patients or how many times a syringe/needle might be used on any given day. A textbook for nurses, written by the chief medical officer of Gabon in 1931, gave instructions regarding how syringes and needles were to be sterilised, but these required an autoclave or a dry heat incubator, available only in hospitals and large health centres. What mobile teams and nurses working in small facilities without electricity were expected to do was unclear. Most injections were given by practical nurses with limited scientific trainin
g. Given the huge caseloads, the sterilisation process may have been shortcut or bypassed, as in Egypt. We will see later that, at least in the Belgian Congo, syringes and needles were not even boiled between patients. It seems likely that this was the rule rather than the exception.61

  With this in mind, to estimate their potential role in the transmission of blood-borne viruses and particularly SIVcpz/HIV-1 and HCV, we will review the major disease control programmes implemented in central Africa from 1921 to 1959, the topic of the next two chapters.

  8 The legacies of colonial medicine I: French Equatorial Africa and Cameroun

  We have just seen how HIV and other blood-borne viruses can be transmitted through injections. Here we will examine the history of colonial medicine in the French territories of central Africa, where remarkable public health interventions ultimately proved successful in reducing the burden of tropical diseases, but at the same time caused the parenteral transmission of HCV, the HTLV-1 retrovirus and presumably SIVcpz/HIV-1 as well. The core of the problem was that since the early drugs against infectious diseases were not very effective, they all had to be administered by injections, often IV, so as to maximise the drug concentration in the blood and in other tissues. As we will see now, tens of millions of IV injections were administered within the crucible of HIV-1, at exactly the right time.

  The system

  A remarkable peculiarity of French colonial history is the way medicine was organised: as part of the military. Young Frenchmen interested in a medical career in the colonies would usually get their degree at a medical school run by the armed forces in Bordeaux, before moving on to the tropical medicine institute in Marseilles, known as Le Pharo, after the name of the park where it is located near the old port. Overseas, they would start as a médecin-lieutenant and progressively, for the more talented, patient or motivated, move up the ladder to become perhaps a médecin-colonel or médecin-général at the end of their careers. Very few of them would be posted to the barracks to provide care for the colonial armed forces. Instead, they were posted to the hospitals and disease control units, working among civilians but remaining military doctors so that a strict hierarchy was maintained. Disease control interventions and modes of healthcare delivery would be decided at the top of the pyramid, by the médecin-général, and implemented in a similar fashion throughout the colony following detailed protocols. There were precise definitions of what had to be reported and in what form, and the reports from each hospital or district would be merged into an annual report for the colony, containing an extraordinary number of tables, maps and graphs about the diseases of interest, their distribution, the treatments administered, the exact number of injections for each drug, and so on. Some of these annual reports contained 800 pages. Their format was the same for all colonies, so that they could be consolidated into an annual summary of the health status of overseas France.1

  The other important feature of French colonial medicine was its population-based approach. While elsewhere in Africa colonial doctors were satisfied with providing care to whoever managed to show up at the local hospital or dispensary, the French wanted to provide basic health care to everybody, through the treatment of common and chronic tropical diseases. They kept reliable medical censuses of the population (their target), and their intent was to detect and treat all cases of a few selected diseases among this entire population. To do so, they funded and staffed mobile disease control teams who would roam through the bush, day after day, village after village, to examine everyone, find the cases and treat them in order to reduce the human reservoir of these infections and decrease transmission to the point where the disease would eventually disappear. Attending case-finding sessions was compulsory, and a medical certificate was issued for each person. This public health approach, with massive numbers of individuals treated in their own villages with injectable drugs against a few diseases, offered a unique opportunity for the transmission of blood-borne viruses, whose existence was unknown at the time, to a degree much higher than could have occurred in British and Portuguese colonies.

  Fixed health care in hospitals and health centres was fairly limited initially, and it was just too bad for patients who developed an acute illness between the biannual visits of the mobile teams. Eventually, tensions arose between the champions of the ‘vertical’ approach (disease-specific mobile teams) and those who wanted to develop multipurpose fixed centres providing basic care available year round (the ‘horizontal’ approach, later renamed primary health care). The latter, of course, was necessary to provide care for acute and treatable conditions such as malaria, pneumonia, gastroenteritis, women with obstructed labour, and so on.

  The mother of all tropical diseases

  Eugène Jamot became the most famous French colonial doctor in Africa, and his biography illustrates the colonial medicine system as well as the development of the disease control interventions. Born in 1879, the first in his family to go to college, he studied natural sciences, taught for a few years in high schools in Algeria and Montpellier to accumulate some savings and then obtained his medical degree from Montpellier in 1908. After practising in France for two years, he decided he had other ambitions, partially prompted by an unhappy marriage, a difficult relationship with his mother and some problems with the justice system following a violent argument with his stepfather.2–5

  After the tropical medicine course in Marseilles, his first posting was to Tchad, following which he received further training in Paris, and became deputy director of the nascent Institut Pasteur in Brazzaville. Two weeks after his arrival, WWI broke out and he was designated to serve as the medical officer of a column that invaded Kamerun from the AEF. After the successful conclusion of this campaign, he returned to Brazzaville from 1917 to 1921. By then a médecin-capitaine, he developed the overriding interest of his professional life: the control of sleeping sickness, which he conceived around specialised mobile teams. He led the first one which operated in Oubangui-Chari.6

  Sleeping sickness (African trypanosomiasis), caused by a parasite called Trypanosoma brucei gambiense, was the first communicable disease for which large-scale control interventions were implemented in central Africa. The disease was first described in a European text in 1803 by Thomas Winterbottom, a British physician in Sierra Leone. One of its clinical signs, the presence of enlarged lymph nodes in the neck, was known to slave traders as an adverse prognostic sign, and the price of such slaves was reduced accordingly. After weeks or months of intermittent fever, patients develop chronic meningo-encephalitis characterised by profound daytime somnolence, hence its name, which would last for several months until the fatal outcome, which was universal if untreated.

  Sleeping sickness did not spread to the Americas with the slaves due to the absence of its tsetse fly vector in the New World. It is thought that the massive displacements of populations that accompanied the European colonisation of central Africa in the late nineteenth century facilitated the dissemination of the parasite. Trypanosomes were imported into regions where the disease had hitherto been absent or uncommon, and spread rapidly in such immunologically naive populations. The high incidence of sleeping sickness preoccupied French and Belgian colonial authorities who, in some regions because of the morbidity and mortality caused by this disease, were running out of their labour force. Furthermore, a high incidence among Africans implied a high risk of transmission to Europeans, who often developed this lethal disease.

  Indeed, the aim of many of the disease control initiatives implemented during the early colonial era was to protect the Europeans by decreasing the reservoir of the pathogen in the African population around them. Institutes of tropical medicine were established in Marseilles, London, Liverpool and Brussels to find technological solutions that would lower the mortality of Europeans in Africa, which was even higher in the centre of the continent than on the coast. A British government publication stated that ‘in the days when the west coast was the white man’s grave, the Congo forest would have been his pu
rgatory’. The annual medical reports of each French colony started with a detailed section on health problems of the Europeans, with a list of all those who had died during the previous year, along with the cause of death: it was just too bad for your reputation if you had died from alcoholic cirrhosis or complications of syphilis.7

  Substantial resources were allocated to the control of sleeping sickness, organised around what became known as the Jamot doctrine. The idea was simple: mobile teams would visit each village, examine everyone, detect as many cases as possible using simple methods (microscopic examination of blood or lymph node aspirate) and treat them on the spot with whatever drugs were available. Initially, drugs were not very effective for the patients themselves, who often died despite treatments which could not get rid of the parasites in the brain. However, the drugs reduced the patients’ infectiousness by suppressing the presence of trypanosomes in the blood. For a long time trypanosomiasis treatment was geared more towards a collective benefit than improving the individual fate of the patient receiving these toxic arsenical drugs.

  In these early days, members of the case-finding mobile teams did heroic work under harsh conditions. For instance, in the space of eighteen months in 1917–19, Jamot examined 89,743 individuals in Oubangui-Chari, diagnosing and treating (mostly with SC drugs) 5,347 trypanosomiasis cases, and did all this with only three microscopes and six syringes. They would spend twenty days per month in villages, sleeping in huts provided by the local population, with no facilities whatsoever. Much of the travelling between villages, many of which were inaccessible by road, was done by foot. They were taking a substantial risk themselves as they spent two-thirds of their lives in locations harbouring a lot of tsetse flies infected with trypanosomes. Several healthcare workers developed trypanosomiasis and died from the disease or its treatment. As a contribution to medical knowledge, some published their own cases, describing the progression of their symptoms in a type of scientific paper which has fortunately disappeared: the auto-observation. By shortening the period during which a patient was infectious, their interventions quickly proved effective, reducing the incidence of and mortality from trypanosomiasis by more than 65%. In 1922, Jamot was transferred to Cameroun Français, recently acquired by the French during WWI, where the authorities were discovering the extent of the trypanosomiasis problem inherited from the Germans.6,8–9