A deadly parasite is on the loose. Like the predator in Alien, it has developed a taste for human flesh and has the ability to lurk undetected in its host for several weeks before emerging in a spectacular show of blood and gore. We try to contain it with the weapons at our disposal but there is little we can do to contain the fear and ignorance that accompanies the lurid reports of the outbreak and the spreading mortality.
Worse, when, as in the case of Ebola, the virus emerges in Africa and the majority of its victims are black, the outbreak is able to draw on primordial fears of the ‘jungle’ and European anxieties about racial contamination. Hitching a ride on planes, trains and automobiles, we worry that the parasite will succeed in evading our sophisticated Western detection systems, setting the stage for a Darwinian showdown between it and us in the heart of the modern metropolis. Sometimes, as in films like Contagion, disaster is averted at the last moment by the discovery of an antidote. But more often the result is Armageddon followed by an uneasy truce between the human survivors and some new mutant species, whether zombies or apes (I am thinking of films like I am Legend and Dawn of Planet of the Apes).
Whatever the ending, however, the moral is usually the same: the emergence of the predatory virus or parasite is our fault, the price we pay for blundering into alien ecosystems and disturbing the balance of nature. In the case of Alien, the crew of the Nostromo is ordered to investigate the predator by a shadowy corporation which hopes to harness it as a bioweapon. In the case of Ebola, the emergence of the virus is thought to be the result of our encroachment on the habitats where fruit bats breed. Indeed, with our insatiable demand for natural resources (meat, timber, oil, land), it is said, we are putting intolerable pressure on wild animal habitats across the globe, resulting not only in the emergence of Ebola but other zoonotic diseases, such as bird flu, SARS, and HIV/AIDs.
This ecological viewpoint is so prevalent today that few of us to think to question it, much less to ask where it came from. But infectious diseases were not always thought of as ‘emergent’ or having lives independent of our own. During the acme of bacteriology, from around 1880 to 1920, bacteria, viruses and parasites were ‘germs’ pure and simple. The task of medicine was to clean up the environments and bodies in which these microbes bred, or obliterate them with vaccines and chemical therapies. Consideration was rarely given to the microbe’s perspective or whether the biological relationship between these microbial invaders and their animal and human hosts served a wider ecological function.
Then, in 1940, the Australian immunologist Frank MacFarlane Burnet published Biological Aspects of Infectious Disease. Appearing at exactly the moment when infectious diseases were declining in social significance and chronic conditions were becoming the main focus of medical concern, Burnet’s book was the first to see disease in explicitly ecological and biological terms. In ‘constant environments’ Burnet argued that competition between parasites and hosts tended to favour low-level, immunising infections in which parasites enjoyed wide dispersal without causing overt disease (examples cited by Burnet were the common diseases of childhood such as measles, chickenpox and diphtheria). But should these relationships be disrupted by environmental challenges then the balance between parasite and host could shift, resulting in the re-emergence of old diseases or the emergence of deadly new pathogens. In particular, Burnet worried that overpopulation coupled with jet travel and international trade was disrupting these natural ecologies in unpredictable ways, leading to virulent new outbreaks of vector-borne diseases such as yellow fever. While a world in which everyone and everything was more closely linked in a biological sense should favour a ‘virtual equilibrium’ between humans and parasitical viruses, Burnet warned that ‘man… lives in an environment constantly being changed by his own activities, and few of his diseases have attained such equilibrium.’
Burnet was not the only medical thinker to warn about over-complacency in the battle against infectious disease. In the same period, Karl Meyer, a Swiss-born medical researcher based in California, was also drawing attention to the risks posed by what he called ‘latent’ infections. These infections included plague and psittacosis and existed in equilibrium in their principal animal host – squirrels and rats in the case of plague; parrots and parakeets in the case of psittacosis. But when humans tampered with the natural ecology by over-hunting squirrels or packing parakeets into crowded aviaries, then these infections could become virulent and jump species. Indeed, Meyer believed the worldwide pandemic of psittacosis in 1929-30 had started in just this way as breeders in California and other states had inadvertently mixed wild birds, who were latently infected with the ‘virus’, with domestic birds bred in captivity. The result was the emergence of a new strain of psittacosis that was lethal to humans, killing up to 40 percent of those infected.
Are we seeing something similar today with Ebola? Certainly, the virus has many of the hallmarks of a classic ‘spillover’ infection, including extremely high virulence (the case fatality rate in humans ranges from 60 to 90 percent). Though the ultimate reservoir of the virus has yet to be identified, fruit bats are the leading contender. The assumption is that in bats Ebola causes a low-level immunizing infection that allows it to be transmitted from one generation to the next. But when bats are dislodged from their roosting grounds by the destruction of orchards then this ecology is disturbed and the virus spills over into other animals, including humans. The hospitalization of patients and health care workers in Sierra Leone, and now the Royal Free Hospital in London, then can be seen as a form of ecological payback.
For all the media alarm about Ebola, however, most scientists and health professionals are relaxed about the threat. The usual explanation is that Ebola, unlike aerosol infections such as influenza, is transmitted through direct contact with bodily fluids, meaning the principle risk is to family members cast in the role of care-givers or doctors and nurses who treat patients in hospital settings. Moreover, because Ebola rapidly immobilizes its victims the chances are that the parasite will kill its host before it has an opportunity to spread to someone else. In this way, runs the theory, virulence is a dead-end for the parasite. The successful parasites are the ones that find a way to keep their hosts alive by trading virulence for transmissibility.
However, as the evolutionary biologist Paul Ewald argues, this is not always the case. For some vector-born diseases, such as malaria, high virulence may be a successful evolutionary strategy as immobilization of the host makes little difference to the parasite’s survival chances. Indeed, one reason falciparum malaria may have evolved to be so deadly is that its vector, the mosquito, is unaffected by the ingestion of the plasmodium, meaning that the parasite incurs no costs from increased virulence. On the contrary the more malaria parasites in a person’s blood and the more severe the infection the more likely it is to be passed on when the mosquito takes a blood meal.
Whether one subscribes to the view that long-term biological associations between hosts and parasites favour avirulent subclinical infections or one takes a dimmer view that parasites can mutate in either direction, the solution is clear: block transmission and you solve the problem. Unfortunately, in the case of Ebola, this is easier said than done. Whereas William Pooley, the British nurse transferred to the Royal Free Hospital from Sierra Leone this weekend, is now being treated in a negative pressure tent that ensures no virus can escape from his weakened body, no such facilities exist on the Ebola frontline where he contracted the virus. In Sierra Leone, Liberia and other countries in west Africa at the forefront of the epidemic clinics are chronically short-staffed and doctors do not have the benefit of state-of-the art containment facilities. Instead, they improvise with rubber gloves and plastic sheeting, doing their best to contain the virus with the rudimentary tools available. The risks to those individuals are considerable. For the rest of us, however, Ebola is likely to remain as remote a threat as the predator in Alien.
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