Over a hundred thousand people have now died of Covid-19 in the UK alone; people around the world have been separated from their family and friends, and entire economies have come to a standstill. All of which raises an important question: how can the world prevent another pandemic?
The obvious place to start is at the beginning – before a pathogen has been seeded around the world and serious damage has been caused. If we can predict where the next pandemic will come from, perhaps we can stop it at its source.
It’s a simple idea, but is remarkably difficult to put into practice: infectious diseases can emerge from an enormous number of sources. Some are new strains of old pathogens – such as tuberculosis that has developed resistance to drugs, or malaria that is resistant to chloroquine. Others come out of laboratory accidents. More still stem from pathogens that are found in one region and then migrate into new places. The West Nile virus, for example, was first identified in Northern Uganda in 1937, before outbreaks occurred in Egypt and Israel, and eventually it flared up in Europe and North America over 60 years later. Since this virus is mainly transmitted by mosquitoes, which are vectors for the disease, it can spread around the world when the habitat of infected mosquitoes changes.
Above and beyond these possibilities, the most common source of a new infectious disease is “zoonosis”, when pathogens jump from animals to humans. Take the HIV/Aids pandemic: HIV originated from a virus called SIV, which infects primates. This primate virus is believed to have jumped from chimpanzees to humans many times during the hunting and trading of bushmeat, before it sparked an epidemic in West Africa and ultimately turned into a global pandemic.
In fact, many recent epidemics have been zoonotic, including Sars (which came from bats and palm civets), Mers (from camels), Zika fever (from monkeys), Ebola (from bats) and swine flu (from pigs). Zoonoses have been observed all around the world, but they are especially common in climates with tropical forests, in places that are home to a diverse range of mammals, and in land areas that have been recently converted for agricultural use.
The ways that we encounter animals have become riskier, with the rise of deforestation, agriculture, factory farming, bushmeat trade, urbanisation and climate change all making such contact more likely. These sorts of changes can fragment or transform the habitats of host species, pushing them into urban areas where they encounter humans.
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The construction of the large Argyle Dam in Western Australia in the 1970s, for example, set up a new habitat for various species of waterbirds (such as herons and egrets) and mosquitoes, which set in motion the life cycle of a virus called the Murray Valley encephalitis virus. As people moved into the region and farmed land around the dam, infected birds began to migrate outwards and new cases of a brain disease began to appear in urban areas. In 1974, this finally led to a large outbreak in south-eastern Australia, which for some patients resulted in permanent neurological disease and death.
Which of these risks should we be most concerned about? I spoke to Charles Kenny, an economist and the author of The Plague Cycle: The Unending War Between Humanity and Infectious Disease (2021), to understand what history tells us about infectious disease in the past and present.
If Kenny had to predict where the next pandemic would come from, factory farms would be near the top of his list. “Factory farms pack a lot of animals that carry infections shared with humans in a really small space,” he explained. “And then we feed those animals antibiotics, often in low doses. Most of the antibiotics produced each year worldwide are fed to animals. That’s just the perfect conditions to evolve and incubate mutated bacteria that are antibiotic-resistant.”
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In total, a diverse range of micro-organisms – such as viruses, bacteria, fungi, protozoa and helminths – can cause zoonotic diseases that are able to jump between humans and animals. Tens of thousands of virus species alone are potential sources of such disease, even though most have not yet been identified. Hot spots of zoonotic disease are found across vast areas of the world, in North and South America, Europe, Central Africa and most of Asia. The US National Institute of Allergy and Infectious Diseases (NIAID) maintains a list of now over a hundred pathogens that pose a major epidemic risk to humans, including ebolavirus, hantavirus, rickettsia, West Nile virus, Nipah virus, coronaviruses, and more.
In which case, why don’t new epidemics happen all the time?
Put simply, it takes more than a single human infection to cause an epidemic. New pathogens not only have to infect someone, they also have to be passed on to others – and most that can jump from animals to humans are rarely able to do so. Rabies, for example, has frequently passed from animals to humans (usually by dog bites), but has only spread between people in exceptional circumstances, such as during organ transplantation. Why?
The main reason is that even if viruses can jump between many species, they are usually only well-adapted to infecting a few of them. Sometimes, they can only attach to receptors found on the cells of certain species, but not others. Pathogens like these must jump between species many, many times before they stumble upon mutations that allow them to spread any further.
This means that when epidemics do arise, it is because pathogens have taken advantage of weaknesses in how we live. Zoonotic diseases tend to come from species that have a similar biological make-up to humans, with similar receptors on their cells. Or they come from species that we are in frequent contact with in risky settings, like the chimpanzees hunted for bushmeat that were the source of the HIV/Aids pandemic: circumstances such as these give pathogens more opportunities to jump between us and to get lucky with new mutations. As a consequence, the species that are most likely to carry zoonotic diseases are rodents, bats, shrews, primates and other mammals. Some pathogens also have their own tricks to bypass the constraints of species barriers – they might mutate rapidly, or have flexible features that enable them to infect a wide range of animals.
Using all of this knowledge, scientists have been screening animals and micro-organisms to predict the next pandemic in countless ways, including genetic sequencing, cell culture experiments, animal models and historical real-life case studies. This work is incredibly useful for narrowing down the search, and incidentally it helps scientists design new drugs and vaccines. But the possibilities that remain are still overwhelming.
Fortunately, there are other steps humans can take to intervene. It isn’t simply enough that a pathogen is able to transmit between people, it needs to be able to do so sufficiently that it doesn’t die out. This capacity can be measured and is described as the R0 (“R Nought”). This is the number of people who are expected to be infected by a single person carrying the disease, in a population that is susceptible to being infected. Pathogens with an R0 below 1 are expected to die out, while those with an R0 above 1 are expected to expand; a pathogen with a larger R0 spreads more rapidly in a population.
It’s crucial to understand that this value is not fixed. The number of people who would be infected by someone carrying a pathogen depends on the behaviour of those people, their environment, the length of time that they are infectious for, as well as the properties of the pathogen itself. And when the R wavers around 1, small changes in our behaviour can make a big difference.
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The way that pathogens are transmitted matters a great deal, whether it’s through direct contact with body fluids, breathing in droplets or particles, contaminated food or water, or vectors such as mosquitoes. Together, they reveal the possibility of approaching the problem in another way: by understanding how diseases are transmitted, we can prevent how far they spread.
We have been building the tools to do so for centuries, as Charles Kenny explained to me. “Some of the earliest cities were already, at least partially, using one of the best means we have to reduce infectious risk: keeping clean. Think of Rome’s aqueducts, baths and the Cloaca Maxima – the giant sewer that carried waste to the Tiber river. Over the centuries we added effective responses from quarantines and soap.”
Nowadays, few zoonotic diseases are caused by contaminated surfaces or environments, while transmission by vectors and airborne and oral routes are common. But even with airborne diseases we have progressed far beyond the 1918 Spanish flu pandemic, only a century ago, when doctors were unable to diagnose the disease correctly because it shared symptoms with so many other diseases, such as typhus. They weren’t even able to identify the pathogen that was responsible, as only optical microscopes were available at the time. The mysterious cause, a new strain of influenza A, was isolated for the first time in the 1930s.
Some diseases are now close to global eradication despite there being no vaccine or therapy available for them. Guinea worm disease, for example, which caused 3.5 million cases in 1986, has recorded less than a hundred cases per year since 2015, as the result of an aggressive campaign by the World Health Organisation and politicians such as former US president Jimmy Carter, who in 1995 negotiated the ceasefire of a civil war in South Sudan in order to get an elimination programme under way. The disabling disease, which is spread by parasitic worms carried by fleas in contaminated water, has now been almost wiped out by the simple act of filtering and treating water – a success that will also reduce the spread of other water-borne diseases.
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Modernity is full of examples of defences against infectious disease – from better sanitation and sewage, to pasteurisation, insecticides and physical barriers against infections, such as masks, mosquito nets and contraceptives. And now we have the benefit of new technology to detect pathogens, as well as new vaccines to inoculate ourselves against them.
In ways such as these, we can both prepare for specific pathogens that could put us at risk, while implementing broad defences against catalysts of transmission such as climate change and factory farming. We can implement measures that reduce the chances that entire classes of pathogens will lead to a pandemic. Perhaps we won’t be able to prevent pandemics from ever happening again, but we certainly can make them less frequent and devastating.
Saloni Dattani is a PhD candidate at King’s College London and the University of Hong Kong. She is also an editor of the magazine “Works in Progress” and a researcher on health at Our World in Data.
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