A Short History of Disease

by Sean Martin

  By the time an international team, comprised of people from the CDC, the WHO and a team of Belgians, including Piot, arrived in October, they found that the Yambuku Mission Hospital had closed, as most of the staff had either died from the disease, or were sick. The case fatality rate was 88 per cent, making it one of the most lethal diseases ever known. One of the team admitted that he was ‘no Marlboro Man’ and was ‘scared shitless… I’m really frightened. As, I think, we all should be.’481 They would not only have to make a thorough inspection of the mission hospital, but also visit every village that had been infected, all of which were now under quarantine. They put on their protective suits and began work.

  Blood and tissue samples were sent to Europe and the US for analysis, where the new disease was found to be a virus, somewhat similar to Marburg. In the quest to find the virus’s reservoir, hundreds of animals were tested to see if they were the reservoir: 818 types of bug went under the microscope, as did mosquitoes, ten pigs, one cow, six monkeys, two duikers, seven bats, 123 rodents, including 69 mice, 30 rats, and eight squirrels. None of them carried any signs of the disease.482 The lab work was also not without its risks: just as Jordi Casals had fallen victim to Lassa while studying it at Yale, so one scientist at Porton Down in the UK became ill while examining samples from Zaire. The team of experts warned ‘No more dramatic or potentially explosive epidemic of a new acute viral disease has occurred in the world in the past 30 years.’483

  Peter Piot decided the new disease should not be named Yambuku, to spare the village the stigma of being associated with the horrific outbreak, and so it was named Ebola, after the river some sixty miles from the Yambuku Mission Hospital where Mabalo Lokela had been immediately prior to becoming ill, and possibly where he had also contracted the disease.

  After further outbreaks in Zaire and Sudan, Ebola had effectively disappeared by 1979. Its next reported case occurred in very different circumstances. In 1989, in echoes of the 1967 Marburg outbreak in Belgrade, a shipment of lab monkeys from Luzon in the Philippines died of Ebola in a quarantine facility in Reston, Virginia, in the Washington DC metro area. The animals appeared to have died of an airborne variant of the disease, and panic ensued. The building was locked down and sterilised by the US Army Medical Research Institute of Infectious Diseases (USAMRIID). Luckily, none of the staff in Reston developed Ebola. Further research into the virus determined it was a different strain to the one that had proved so fatal in Yambuku, and was christened Reston virus. Despite fieldwork in the Philippines and Indonesia, the source of the outbreak was never found, and no one knows how the virus got to the Philippines in the first place. Alternatively, the virus could have been endemic, but only broken cover when the monkeys were caught and sent to the labs for research. Reston remains one of Ebola’s puzzles. As David Quammen noted, ‘the good news about Reston virus, derived both from the 1989 US scare and from retrospective research on Luzon, is that it doesn’t seem to cause illness in humans, only in monkeys. The bad news is that no one understands why.’484

  Scientists have, however, been able to piece together how Ebola gets transmitted to humans. As with the animal to human jump that HIV made, Ebola is passed to humans by close contact with infected animals. This usually means animal blood or other secretions entering the human body, or the eating of meat from an infected animal. Chimpanzees, gorillas, fruit bats, monkeys, forest antelope and porcupines are all susceptible to Ebola. (Some scientific studies have focussed on die-offs in these animal populations, in an attempt to predict Ebola’s movements and incidence.485) The disease is spread between people through direct contact with bodily fluids, or clothes or bedding contaminated with them. Anyone coming into contact with an infected person, such as a nurse or person preparing a body for burial, is at extreme risk. But even shaking someone’s hand might pass on the disease. People remain infectious for as long as the virus remains in their blood and bodily fluids, although men who have recovered can still transmit Ebola in their semen for up to seven weeks after recovery.

  Further strains of Ebola have been found. In 1994, Taï Forest ebolavirus affected a Swiss scientist in Côte d’Ivoire (she survived); and in 2007 the Bundibugyo ebolavirus emerged in Uganda. The two original strains of the disease have remained active, the Yambuku strain (also known as Zaire ebolavirus), which has remained the most widespread and lethal, and the Sudan strain (Sudan ebolavirus). The Sudan variant is actually the ‘original’ form of Ebola, breaking out in a cotton factory in Nzara, in what is now South Sudan, and then affecting neighbouring areas between June and November 1976. This outbreak wasn’t quite as bad as Yambuku, with a mortality rate of ‘only’ 53 per cent.486

  One of the major problems scientists have had in finding Ebola’s reservoir is that outbreaks were sporadic until the mid-1990s, when they began to increase in frequency. Indeed, apart from the 1989 outbreak of Reston virus, there was a 15-year silence (1979–1994) from the Zaire strain. A major outbreak in Kikwit in the Democratic Republic of Congo in 1995 became an immediate emergency: Kikwit is a city with a population of over 300,000, the first time Ebola had struck an African city. It was the worst since Yambuku, with 254 deaths – a case fatality rate of 81 per cent. There was a massive trapping operation to find the reservoir: thousands of small mammals, birds, reptiles and amphibians were caught, killed and sampled. Blood was also taken from dogs, cows and pet monkeys. In total, 3,066 samples were sent to the CDC for analysis.487 The Ebola virus wasn’t found in any of them.

  Despite this result, the team at CDC were able to make some assumptions: that the reservoir is a mammal, possibly one with a forest habitat – all Ebola outbreaks in Africa had been in or near forests – and that, due to the sporadic nature of the outbreaks, either the reservoir is a rare animal, or it’s one that only rarely makes contact with humans. The importance of reservoirs is that if you know where the reservoir lives, you know where the outbreak is likely to occur. But the more scientists studied Ebola, the more blanks they drew.

  Studies of Ebola have not focused exclusively on the science. The American medical anthropologist Barry Hewlett visited areas affected by the 1994 outbreak in Gabon, and also the 2000 outbreak in Gulu, Uganda. Hewlett learned from the local people in Gabon that they believed Ebola to be ezanga, meaning a vampire-like evil spirit. One villager told Hewlett that ezanga are ‘“bad human-like spirits that cause illness in people” as retribution for accumulating material goods and not sharing.’488 (A possible reference to the fact that one of the epicentres of the 1994 outbreak in Gabon was a gold mine.) For those sufficiently versed in magic, ezanga could be summoned and directed at an enemy. The effect of ezanga was to eat away a person’s insides until they died. In Uganda, the Acholi people told Hewlett they thought Ebola was caused by supernatural agency. They called the spirit gemo, and it arrived periodically to cause sickness and death. The gemo did not cause just Ebola, but also measles and smallpox, which the Acholi had also suffered. Hewlett learned that the disrespect of nature spirits could awaken the gemo and make it decide to pay a visit.

  Hewlett discovered that once a gemo was known to be present in a community, the sick were quarantined, and could only be nursed by a survivor of the same illness (if there were any); people were not allowed to travel to other villages; had to abstain from sex; could not eat rotten or smoked meat; and ordinary burial practices – which included not only washing the body but voiding the stomach and bowels of the deceased – were proscribed. Dancing was also forbidden. Given that most of these activities can put a person in danger of contracting Ebola – even dancing, given that the disease can be spread by sweat, spittle, and expectoration – David Quammen speculates that these cultural practices may have helped contain the 2000 outbreak in Gulu.489

  The 2014 outbreak of Ebola was the worst yet recorded, and marked the first time the disease has reached epidemic proportions. It also marked the first time Ebola cases had been reported in West Africa. The epidemic began in the Guéckédou prefecture of southern G
uinea in December 2013, with the death of a two-year-old child and his mother. The virus spread throughout the family, and seems to have been disseminated further at the various funerals, and also by doctors treating the sick, who then themselves died of Ebola. On 10 March 2014, the local health authorities reported the crisis to the Guinean Ministry of Health, at which time the epidemic came to the notice of international health bodies. On 8 August, the World Health Organization declared the epidemic to be a Public Health Emergency of International Concern (PHEIC), the WHO’s equivalent of a red alert.

  Despite heroic efforts to contain the epidemic, there were serious problems in getting aid to the sick. Much of this had to do with the poor infrastructure in the affected countries. Liberia, Guinea, and Sierra Leone were all countries recovering from decades of civil wars, unrest and instability. As might be expected, levels of public health care were very low, and none had much in the way of immediate resources to throw at the crisis. Unlike the Acholi in Uganda during the 2000 outbreak, people were reluctant to abandon traditional burial practices and stay put. The relative closeness of affected areas to big cities, and their transport networks, meant that the epidemic spread easily. And international aid, when it came, was too late to stop the situation getting out of control.490 By the start of 2015, the World Health Organization had recorded over 24,000 cases and around 10,000 deaths. The case fatality overall was in the region of 70 per cent.491

  Studies published during the epidemic noted some important features. A paper published in The New England Journal of Medicine found that the virus was not Taï Forest virus, which was the ‘local’ form of Ebola (Côte d’Ivoire, where Taï Forest virus had broken out in 1994, shares a border with Guinea), but was a variant of the Zaire strain. A second study, published in Science Express (a satellite publication of the journal Science), noted that the Ebola virus is mutating, and that the 2014 epidemic was probably the result of a single spillover from the animal reservoir to humans. Five of the co-authors of the Science Express paper had died of Ebola before publication, giving it, as David Quammen notes, ‘a certain extra gravitas.’492

  Both papers agreed that Ebola’s reservoir could be bats. A large number of diseases are known to come from bats, including Marburg, rabies, SARS (see below), Nipah (see below) and a group of relatively little-known viruses such as Kyasanur Forest virus, Menangle virus, Hendra virus, Tioman virus and Australian bat lyssavirus. Bats make good reservoirs because they have existed in their present form for around fifty million years, meaning that their association with disease is of extremely long standing, more than enough time to develop possible immunity to just about everything, or at least a higher level of resistance. Bats are also very social, and live in close proximity to each other, meaning that any disease one picks up is very easily spread within the community. Bat communities are also sufficiently large for a disease to remain within them, rather than die out. (Known as Critical Community Size: see Chapter 1.) There are also many bats in many species: one in four mammals is a bat. Bats can also cover surprisingly large distances each night on their forages for food.

  It seems possible that Ebola has been spreading through the bat colonies of central and west Africa for decades, mutating as it goes. How many bats are infected, no one knows. As to where it will strike next, that too is unknown. And, perhaps most remarkably of all, scientists still don’t know exactly how Ebola kills people. The most likely route is by causing immune system collapse, and then flooding the body with replicating viruses. As David Quammen notes, ‘The current scientific understanding of ebolaviruses constitutes pinpricks of light against a dark background.’493

  Other New Diseases: The Coming Plagues

  Ebola, Lassa and Marburg are – along with HIV/AIDS – perhaps the most well-known of the new diseases that have appeared since the 1960s. But there are many more. Arno Karlen lists another twenty-four that have appeared since 1951, among them: Korean, Dengue, Bolivian, Argentine and Venezuelan haemorrhagic fevers, Kyasanur Forest disease, Chikungunya, Human babesiosis, O’nyong-nyong fever, Oropouche, LaCrosse Encephalitis, intestinal capillariasis, Pontiac fever, human toxoplasmosis, Lyme disease, Rift Valley fever, toxic shock syndrome, Brazilian purpuric fever and human ehrlichiosis. Karlen notes that this list is only a fraction of the new diseases that have appeared.494

  Not all new diseases have come out of the forests of Africa. Legionnaires’ disease first appeared in 1976, striking a convention of the American Legion at a hotel in Philadelphia. Caused by the bacteria of the Legionella genus, unknown prior to 1976, the disease can cause fatal pneumonia. Initially thought to be caused by toxic chemicals or even sabotage – American authorities were on high alert at the time due to fears of a possible swine flu epidemic – it transpired that the bacteria had been spread by the hotel’s air conditioning.

  Intensive factory farming methods are also implicated. Bovine spongiform encephalopathy (BSE, otherwise known as mad cow disease) first appeared in the UK in 1984. BSE is a neurodegenerative condition that is thought to have been caused by feeding cows – normally herbivorous beasts – all manner of refuse from slaughtered animals. Some of this fodder – brains and spinal cords in particular – are thought to have been infected with the sheep disease scrapie, which then made the species jump into cattle. Because of the forced feeding of other animals to cows, BSE has been dubbed ‘high-tech cannibalism’.495 BSE can cause new variant CJD in humans, sometimes called the ‘human mad cow disease’, through eating the meat of infected animals. It causes the rapid onset of dementia and death, and is incurable.

  The study of CJD led to the discovery of a new form of infection – the prion – in 1982, by the American neurologist Stanley Prusiner. An aberrant form of protein, the prion is able to self-replicate and causes a number of diseases in animals aside from BSE. In humans, prions cause the various forms of CJD (including new variant CJD), Kuru, fatal familial insomnia and the extremely rare Gerstmann–Sträussler–Scheinker syndrome. The discovery of prions won Prusiner a Nobel Prize in 1997.

  Factory farming also spread Nipah virus, which first appeared in Indonesia in 1999. As noted above, this disease originally came from bats. Initially causing fever, vomiting and flu-like symptoms, Nipah then attacks the nervous system, and can cause brain damage and hallucinations before death occurs. One pig farmer who survived the 1999 outbreak reported seeing pigs running around his hospital bed.496 The outbreak caused 257 cases in humans, 100 of them fatal. Over a million pigs were culled to stop Nipah spreading.

  Intensive farming is also linked to the first pandemic of the twenty-first century, SARS (Severe Acute Respiratory Syndrome). It began simply enough, with a man visiting the hospital in the Chinese town of Foshan, in Guangdong province, with flu-like symptoms on 16 November 2002. The doctors were puzzled by his condition, but as he didn’t die, no one was worried. The man was discharged after treatment, and was never heard from again. But he seems to have inadvertently set up a chain of infection that started working immediately. Then, in January 2003, a seafood merchant in the province’s capital, Guangzhou, was taken ill. Retrospectively, the World Health Organization realised he was what’s known as a ‘super-spreader’ – a modern-day equivalent of Typhoid Mary, capable of infecting many more people than would normally be the case. The seafood merchant infected staff in three hospitals, and also infected a professor who was travelling to Hong Kong. The professor then turned the ninth floor of the Hotel Metropole in Hong Kong into a locus of disease, before dying in early March. Other people staying at the Metropole spread the infection across Hong Kong, while others flew abroad, to Vietnam, Canada and Singapore, carrying SARS with them.

  The World Health Organization had first been alerted to the new disease in late February by their man in Hanoi, an Italian doctor by the name of Carlo Urbani. He had been rushed off his feet by the new disease, reporting to Geneva that it produces initial flu-like symptoms before developing into pneumonia. Urbani reported that the disease was also affecting hospital
staff at an alarming rate. One of his patients had been staying at the Metropole hotel in Hong Kong. By the end of March, both the man from the Metropole and Dr Urbani himself had died from the new disease.

  Alarmed at how fast ‘atypical pneumonia’ was spreading around the world, the WHO issued an emergency travel alert on 15 March 2003. Cases had been reported in Canada, Spain, Germany and the UK, and there were fears it could spread further. Screenings at airports were introduced, some people were placed in quarantine, and the white cotton face mask – so much a feature of the Spanish Flu of 1918 – became a common sight in China.

  The WHO believed ‘atypical pneumonia’ might be an influenza-type disease, as it was marked by similar symptoms – a high temperature, aching muscles, chills and a sore throat. Some even thought it might be pneumonic plague. Tests soon showed that the new, as yet unnamed disease caused severe damage to the lungs, and didn’t respond to antibiotics. The WHO coordinated an international team of experts to study the new disease, which was christened SARS. It was found to be a coronavirus, of the same family as the common cold. No one was able to explain why SARS should be so much deadlier, or why it appeared. In June 2003 an international conference on SARS was held in Kuala Lumpur, Malaysia, with 900 participants from 44 countries. By the end of the month, the pandemic was declared officially over.

  As with its origins, SARS had an equally sudden and mysterious end. 32 countries had been affected, with 8000 cases and more than 900 deaths.497 The speed of SARS shows how modern travel has sped up the development of pandemics to ‘fast forward’. It took the Black Death over ten years to travel along the Silk Road to the West; now it would arrive in ten hours (or less) on a plane. The pandemic also demonstrates how seriously the WHO and international health authorities took the outbreak, with work starting on analysing the virus immediately. The first paper on SARS – identifying it as a new, deadly coronavirus – was published on 8 April 2003, less than six weeks after Carlo Urbani had first reported the Hanoi outbreak.