Zoonotic diseases
When Karl Johnson boarded a plane in La Paz, Bolivia, he could barely contain his excitement. This was the moment the US virologist had been waiting for. Having qualified as a doctor, he had spent six years at the US National Institutes of Health in Maryland, where his brief was to study the viruses that cause the common cold, bronchitis and pneumonia. During those tedious days cooped up in the lab, he had longed for some adventure. So when he was accepted for a position at the Middle America Research Institute (MARI), Panama, he hoped
his luck would change.
Above the roar of the engines, Johnson pondered what lay ahead. He was travelling to the remote hilltop town of San Joaquín to investigate a mysterious disease known as el typho negro that had emerged in the Machupo River region. There was little to go on. He knew that its victims were dying in horrific circumstances – delerious, convulsing, bleeding from the eyes and vomiting blood – and that these symptoms were similar to those of a virus that had attacked farmers in Argentina ten years earlier. But that was it. Even Hercule Poirot would have been stumped.
Having set up makeshift laboratories among San Joaquín’s white-washed houses, Johnson and his two MARI colleagues set to work. The key to unravelling the mystery and stopping the epidemic was identifying the pathogen, where it had come from and how it was infecting people.
Despite the lack of evidence, their initial progress was good. An autopsy on the body of a two-year-old boy revealed the disease was caused by a member of the Arenavirus family. The next step was to identify its origins. The assumption was that, like malaria, it was transmitted by biting insects. But an exhaustive biodiversity survey in the town and the surrounding area unmasked a different culprit: the vesper mouse.
All that was left was to determine how the disease was transmitted to humans. However, this final piece of the puzzle proved more elusive. None of the victims had had direct contact with the animals. The insect route appeared most likely – the obvious parallel was with bubonic plague, which is transmitted from rats to humans by fleas. But over a year, the team collected 10,000 fleas, mites, ticks and mosquitoes; none were carrying the Machupo virus, as it became known.
For months, the scientists pored over their notes, hoping to find the missing clue. Johnson’s colleague, ecologist and veterinarian Merl Kuns, insisted that they should redouble their survey efforts, and continue to scour the foothills around San Joaquín to apprehend the offending insect. But Johnson wasn’t so sure. Convinced that the answer lay in experimentation, he returned to
his lab in Panama.
Johnson’s suspicions were eventually confirmed when he found that caged hamsters were infecting one another by excreting the virus in their urine. A cull of mice in San Joaquín subsequently confirmed this hypothesis, and two weeks later the epidemic was ended for good.
At the time, the medical world saw the emergence of such zoonotic diseases as anomalies, freakish events confined to exotic parts of the world that were of considerable scientific interest but of little real concern. But there is now growing evidence to suggest otherwise.
New research shows there was a steady increase in the number of new emerging infectious diseases at the end of the last century. And that almost three quarters have come from animals. Indeed, scientists believe that with the emerging threats of Ebola, HIV, SARS and now avian influenza, combined with the resurgence of established diseases such as malaria and dengue fever, we are now entering a new age of zoonotic pestilence last seen in Biblical times.
A long-running narrative
The microbes that cause infectious disease were among the first forms of life on Earth. They have been around for more than a billion years, far longer than humans, or indeed any animal. Since then, they have ensured their survival in much the same way as any other organism, adapting to new environments by mutating and jumping from one host to another and surviving therein.
Tony McMichael, director of the Australian National Centre for Epidemiology and Population Health, explains that the emergence and re-emergence of infectious diseases is part of a long-running narrative. “Microbes are always jumping across species barriers, usually unsuccessfully,” he says. “The more often they get the chance, the greater the probability that one – perhaps with a fortuitous mutation that suits it better to the new host – will establish a foothold, manage to achieve onwards-transmission, and become a circulating ‘human’ infection.”
In such cases, it’s the unfamiliarity of the relationship that causes the pathogen to kill its host. Indeed, it isn’t in the interest of a microbe to be so virulent that it causes death: the idea of the malevolent virus has been largely dreamed up by the media. A successful pathogen, instead, develops a more ‘healthy’ relationship by adapting to become less deadly. At the same time, the host evolves to develop its own resistance.
Historically, new diseases emerged among our ancestors when changing patterns of human activity disturbed the biological equilibrium. Early humans exposed themselves to unfamiliar pathogens when they began eating meat regularly and, later, when they spread from Africa into new environments and climates.
During the past 10,000 years, the rate of zoonotic disease emergence has accelerated since humans took up agriculture and animal husbandry, living in increasingly close contact with domesticated animals and pests. In his book Human Frontiers, Environments and Diseases, McMichael describes three “great transitions” in the relationship between humans and microbes.
The first occurred among the early civilisations of the Middle East, Egypt, East Asia and Central and South America. During this time, humans would have acquired many of today’s familiar ‘crowd’ diseases – measles, mumps, chickenpox, influenza, smallpox, tuberculosis, leprosy and the common cold. After a period of adjustment, during which epidemics usually killed off large numbers of naïve populations, evolution would create a new balance, as humans gained resistance and the pathogens became less deadly. In this way, city states would have eventually acquired immunity against localised infections. But as contact increased through commerce and conflict, pathogens would have been exchanged, with devastating consequences.
The second period saw the great civilisations of Eurasia swapping diseases over longer distances, “when branches of the human family came into contact again after tens of thousands of years of separation following the ancient hunter–gatherer dispersals”, says McMichael.
Finally, the conquest by European explorers of the New World from the late 15th century saw the indigenous populations of Latin America and, later, Australia and the Pacific devastated by diseases such as smallpox, measles and influenza. These peoples had no herds of wild animals, so had remained relatively free of ‘crowd’ diseases. At the same time, the trans-Atlantic slave trade introduced African, mosquito-borne infections (malaria and yellow fever) to the Americas.
During the 20th century, the world returned to a state of relative equilibrium. By the 1960s, the medical establishment felt that it had outwitted infectious disease for good. We had learned to avoid disease by treating water, improving hygiene standards and controlling vector organisms, to prevent it through vaccinations and to fight it with antibiotics and antiviral treatments. Sensing the battle was over, scientists turned their attention elsewhere. Today, however, that decision appears somewhat naïve.
The microbe returns
When Peter Daszak boarded the plane from New York’s JFK airport to Washington DC on 14 January 2004, he had a lot on his mind. As director of the Consortium for Conservation Medicine (CCM), he had been invited to speak at a meeting of the National Centre for Ecological Analysis and Synthesis. But, at that moment, it was the last thing he needed. He was in the middle of coordinating an investigation into the SARS outbreak in China: his inbox was bulging and his phone wouldn’t stop ringing.
His workload wasn’t the only thing on his mind. Ever since his days as a postgraduate student in the early 1990s, Daszak had been interested in patterns of disease emergence, particularly relating to wildlife. He would escape the boredom of the lab by visiting London Zoo, where he helped the head pathologist identify unusual parasites found among the animals.
Daszak had never bought into the idea that infectious disease was on the decline. In fact, he believed the opposite was true. The World Health Organization was reporting that infectious disease was claiming more lives than ever. Malaria and tuberculosis, diarrhoeal and respiratory diseases were resurgent, and HIV was about to become the worst of all. But that wasn’t all. His experience told him something else was happening.
Daszak had emigrated from the UK to the USA in 1997, when his wife got a job with a biotech company in Atlanta. At the time, epidemiologists were pointing out that not only were the old pathogens resurgent, but the number of newly emerging diseases seemed to be rising. Since joining the CCM in 2000, Daszak had seen the evidence for himself: Hendra virus in Australia, Nipah virus in Malaysia, new strains of influenza, West Nile virus in the USA and now SARS.
What concerned him was that no-one appeared to know what to do about it. Epidemics were addressed – very efficiently – in terms of disaster management. But if infectious disease was as big a threat as it appeared to be, he thought, surely we should be doing something about preventing such diseases emerging in the first place.
Daszak had been so busy recently that he hadn’t had time to plan his talk that day. It was only now, as the plane levelled off in the bright winter sun, that he began to think about what he might say. He opened his diary and looked down at the address he had written down: Conservation International, 1919 M Street, Washington DC.
And that’s when it hit him. Conservation International had developed the concept of hotspots to identify areas where biodiversity is most at risk. If we knew where and why diseases were emerging, he thought, perhaps we could develop a way to predict where and how new diseases were likely to emerge.
As soon as he got back to the CCM office in New York, Daszak sat down with his colleagues to see if his idea was workable. He knew that Mark Woolhouse at Edinburgh University had recently published a database of emerging diseases, and that Kate Jones at the Institute of Zoology in London had been analysing large databases on diversity and extinction. So he hatched a plan to collect data on all recent emergence events, and analyse them to identify patterns that would enable him to make predictions for the future.
Fast forward two years, and Daszak’s team has collected information about the origin and cause of every disease emergence event since 1940 – a total of 409. Among these are new strains of ‘old diseases’ such as influenza, some of which, such as bubonic plague and streptococcus, have emerged as a result of the widespread use of antimicrobial treatments. However, a significant number are genuinely new to science.
What is perhaps most surprising is that at least 62 per cent were contracted from animals. In fact, some analyses reveal that this is as high as 73 per cent. These include exotic pathogens such as Ebola, Marburg, Nipah and West Nile virus, as well as those that we might consider more mundane – salmonella, E. coli and variant CJD. Indeed, it’s safe to say that those emerging diseases that have caused the most alarm in recent years have all originated from animals: SARS from bats, avian influenza from waterfowl and HIV-1 from chimpanzees.
Although developments in medical science have created more opportunities to discover new diseases, Daszak says his research proves that something unusual is happening. “These aren’t random events,” he says. “There’s a clear pattern that shows that the rate of emergence events has increased gradually over the past 50 years or so. What we’re seeing now is a return to the kind of patterns humans experienced in Biblical times. If we don’t do anything about it, it won’t be long before we have another disaster on our hands.”
Changes in human ecology
According to the Book of Revelations, the Four Horsemen of the Apocalypse will bring pestilence, as well as war, famine and death, at the end of the world. But these new pathogens haven’t been conjured up by an act of God, nor have they sprung from thin air. Instead, they’ve emerged as they always do, because changes in human ecology have presented microbes with new opportunities.
In many cases the disruptions in human ecology take the form of changes in the interface between humans and domestic animals on the one hand and wildlife on the other.
Jonathan Epstein, an epidemiologist with the CCM, explains that increasing urbanisation and agricultural expansion have both played a part. “As cities and towns grow,” he says, “they expand into previously wild habitats, so you get increased interaction between people and urbanised wildlife, such as robins, which carry West Nile virus, and raccoons, which carry rabies.”
Nipah virus emerged in 1998, when the intensification and expansion of livestock management allowed more contact between domestic animals and wildlife. “Nipah has probably been present in flying foxes for a very long time, but it has never had the opportunity to spread to humans,” says Epstein. “Like many pathogens, it depends on a certain density of susceptible individuals before a sustained outbreak is possible.” The growth of pig farming in Malaysia in the 1980s and ’90s provided those very conditions. “The farm where the virus first emerged was one of the country’s largest, with around 30,000 animals, so the virus was able to spread quickly and maintain itself among the pigs for long enough that humans could be infected.”
The SARS virus was transmitted to humans in a similar way at livestock markets in China. Epstein was involved in the investigation that last year identified Chinese horseshoe bats as its reservoir. “These bats were being brought into the markets, where there was a high density of live wild animals and humans, with lots of contact between them all through the butchering and unhygenic handling by the vendors,” he says. In this case, it’s likely that the virus jumped from the bats into civets and then to humans.
One of the principal factors to have influenced the rise in emerging zoonotic diseases is environmental disturbance. Deforestation has been shown to increase incidences of malaria,
by providing ideal conditions for mosquitoes to breed. There is also a theory that the loss of Malaysian rainforest forced fruit bats carrying Nipah virus to feed in orchards next to pig pens.
The transmissions of such high-profile diseases as Ebola, HIV, Lassa, Marburg and monkeypox, and others, have been facilitated by the bushmeat trade in Africa. This in itself is nothing new,
says Wolfe. “Humans have been hunting for thousands of years, and our ancestors for millions of years before that,” he says. “And long as people have exposed themselves to the bodily fluids of wild animals by hunting and butchering, there has been cross-species transmission of diseases.”
Today, however, consumers in Central Africa alone eat an estimated 579 million animals a year. This has increased the odds of a pathogen making the jump, says William Karesh, director
of the Wildlife Conservation Society’s Field Veterinary Program. “The rise in human population, and contact with and consumption of wildlife increases the chance that pathogens can achieve species-to-species transmissions.”
The likelihood of successful transmission is increased further in Africa because of the animals involved. “Chimpanzees and gorillas,” says Wolfe, “have a similar physiology to humans, so we’re all susceptible to the same kinds of diseases.”
Wolfe has recently discovered a series of new retroviruses among hunting communities in Cameroon. This suggests that these events may be occurring regularly. “This is only the tip of the iceberg,” he says. “Africa’s rainforests are home to extraordinary levels of biodiversity, and that means viruses and bacteria as well as plants and animals. We’ve only identified a small percentage of the viruses being transmitted from animals to humans.” The same is true in the live animal markets of China, says Daszak, as well as locations where humans are disturbing the established ecology and biodiversity is high. “The more opportunities we present to these pathogens, the more likely it is that they will make the leap.”
Transmission, prediction and prevention
Last year, Uige province in northeastern Angola suffered the worst outbreak of Marburg fever
on record. Of 374 cases, 329 died. In that case, virologists found that miners had probably contracted the disease from bat droppings while working in caves. Once infected, they transmitted the virus to members of their family.
The outbreak in Angola was more widespread because of one crucial factor: the victims in Uige reached a health facility. Once there, unsafe medical practices spread the virus – rapidly.
This form of nosocomial spread has been the principal reason behind the larger outbreaks of zoonotic diseases, says Laurie Garrett, author of The Coming Plague: Newly Emerging Diseases in a World Out of Balance. “In Africa, people stagger into these terrible hospitals and clinics that are desperately out-of-date, run-down, under-staffed and under-supplied, where there’s almost no infection control. So these ghastly places become the amplification system.”
Transmissions of Ebola, Marburg and Lassa may have been going on for thousands of years, she says. But because these cases would have been relatively isolated, the pathogen never had a chance to spread. “In ancient times, a hunter would just stagger off and die,” says Garrett. “In the worst case, his village would have been wiped out.” Today, however, changes in human migration have given diseases the chance to spread.
The same is happening on a global scale. Nowadays, we’re not only moving ourselves around the world faster than ever, but we’re moving animals, plants, soil, bacteria and viruses as well. The rapid spread of SARS and the more insidious creep of HIV/AIDS offer no better examples. SARS also reveals that it isn’t just the run-down health facilities in the developing world that amplify infectious disease, but also the state-of-the-art hospitals in wealthy countries. “Once these microbes get entrenched in a hospital they have mutated to the point where they can live on a bar of soap or even in antibacterial formulations. This issue isn’t about exotic and terrifying zoonotic events outside the First World. It’s about how we are changing our ecology and creating bridges for the microbes,” says Garrett.
Daszak says that if current practices continue, it will be only a matter of time before a new zoonotic disease has the same impact as HIV/AIDS. Certainly, the H5N1 strain of avian flu has the potential. And sooner or later the health services won’t be able to cope, says Garrett.
“The use of increasingly powerful antimicrobials is only going to create more problems,” she says. “We now have broad-spectrum, nuclear-bomb-level antibiotics available in black markets in the Third World. And we’re routinely treating minor infections in pre-schoolers with formulations of antibiotics that 15 years ago would have been reserved for intensive care. We’re digging our own graves.” The result is a race to reinvent the weapons we need to fight the microbes. “We’re working on scales of years and decades, while the microbes are working in hours and days. We’re never going to win.”
There is now a growing belief that the public health and global scientific communities need
to look beyond disaster management and move towards the prediction and prevention of disease emergence. “We’ve embraced it when it comes to medicine on an individual level,” says Wolfe. “We know that it’s a lot easier to encourage people to change their diet than it is to deal with heart disease. But we haven’t got that far with disease emergence. If we’d had five years notice on HIV, we wouldn’t be in the position we’re in today.”
Daszak’s database is the first step in the attempt to predict and prevent the emergence of new zoonotic diseases. “We have to bring together ecologists and virologists to talk about prediction,” he says. “Ecologists understand how changes to the environment affect wildlife populations and disease dynamics. And virologists have the capacity to test for new viruses and identify those that are most likely to achieve species-to-species transmission. By combining their skills, we can develop models that will enable us to predict where diseases are most likely to emerge in the future.”
Wolfe’s study of hunting communities in Cameroon is the first application of this kind of work. His success, says Daszak, is proof that it should be replicated around the world in the hotspots for zoonotic disease emergence. “I’d like to get to a stage where we could identify the diversity of viruses within a certain region and assess the risk of their emergence. That way we could advise governments planning to expand their livestock or timber industries, for example, to avoid those areas where these pathogens exist. That’s the vision. It’s early days, and our first attempts will be very basic and very rough. But it’s the first step in what I think will become a fantastic and very valuable new science.”
his luck would change.
Above the roar of the engines, Johnson pondered what lay ahead. He was travelling to the remote hilltop town of San Joaquín to investigate a mysterious disease known as el typho negro that had emerged in the Machupo River region. There was little to go on. He knew that its victims were dying in horrific circumstances – delerious, convulsing, bleeding from the eyes and vomiting blood – and that these symptoms were similar to those of a virus that had attacked farmers in Argentina ten years earlier. But that was it. Even Hercule Poirot would have been stumped.
Having set up makeshift laboratories among San Joaquín’s white-washed houses, Johnson and his two MARI colleagues set to work. The key to unravelling the mystery and stopping the epidemic was identifying the pathogen, where it had come from and how it was infecting people.
Despite the lack of evidence, their initial progress was good. An autopsy on the body of a two-year-old boy revealed the disease was caused by a member of the Arenavirus family. The next step was to identify its origins. The assumption was that, like malaria, it was transmitted by biting insects. But an exhaustive biodiversity survey in the town and the surrounding area unmasked a different culprit: the vesper mouse.
All that was left was to determine how the disease was transmitted to humans. However, this final piece of the puzzle proved more elusive. None of the victims had had direct contact with the animals. The insect route appeared most likely – the obvious parallel was with bubonic plague, which is transmitted from rats to humans by fleas. But over a year, the team collected 10,000 fleas, mites, ticks and mosquitoes; none were carrying the Machupo virus, as it became known.
For months, the scientists pored over their notes, hoping to find the missing clue. Johnson’s colleague, ecologist and veterinarian Merl Kuns, insisted that they should redouble their survey efforts, and continue to scour the foothills around San Joaquín to apprehend the offending insect. But Johnson wasn’t so sure. Convinced that the answer lay in experimentation, he returned to
his lab in Panama.
Johnson’s suspicions were eventually confirmed when he found that caged hamsters were infecting one another by excreting the virus in their urine. A cull of mice in San Joaquín subsequently confirmed this hypothesis, and two weeks later the epidemic was ended for good.
At the time, the medical world saw the emergence of such zoonotic diseases as anomalies, freakish events confined to exotic parts of the world that were of considerable scientific interest but of little real concern. But there is now growing evidence to suggest otherwise.
New research shows there was a steady increase in the number of new emerging infectious diseases at the end of the last century. And that almost three quarters have come from animals. Indeed, scientists believe that with the emerging threats of Ebola, HIV, SARS and now avian influenza, combined with the resurgence of established diseases such as malaria and dengue fever, we are now entering a new age of zoonotic pestilence last seen in Biblical times.
A long-running narrative
The microbes that cause infectious disease were among the first forms of life on Earth. They have been around for more than a billion years, far longer than humans, or indeed any animal. Since then, they have ensured their survival in much the same way as any other organism, adapting to new environments by mutating and jumping from one host to another and surviving therein.
Tony McMichael, director of the Australian National Centre for Epidemiology and Population Health, explains that the emergence and re-emergence of infectious diseases is part of a long-running narrative. “Microbes are always jumping across species barriers, usually unsuccessfully,” he says. “The more often they get the chance, the greater the probability that one – perhaps with a fortuitous mutation that suits it better to the new host – will establish a foothold, manage to achieve onwards-transmission, and become a circulating ‘human’ infection.”
In such cases, it’s the unfamiliarity of the relationship that causes the pathogen to kill its host. Indeed, it isn’t in the interest of a microbe to be so virulent that it causes death: the idea of the malevolent virus has been largely dreamed up by the media. A successful pathogen, instead, develops a more ‘healthy’ relationship by adapting to become less deadly. At the same time, the host evolves to develop its own resistance.
Historically, new diseases emerged among our ancestors when changing patterns of human activity disturbed the biological equilibrium. Early humans exposed themselves to unfamiliar pathogens when they began eating meat regularly and, later, when they spread from Africa into new environments and climates.
During the past 10,000 years, the rate of zoonotic disease emergence has accelerated since humans took up agriculture and animal husbandry, living in increasingly close contact with domesticated animals and pests. In his book Human Frontiers, Environments and Diseases, McMichael describes three “great transitions” in the relationship between humans and microbes.
The first occurred among the early civilisations of the Middle East, Egypt, East Asia and Central and South America. During this time, humans would have acquired many of today’s familiar ‘crowd’ diseases – measles, mumps, chickenpox, influenza, smallpox, tuberculosis, leprosy and the common cold. After a period of adjustment, during which epidemics usually killed off large numbers of naïve populations, evolution would create a new balance, as humans gained resistance and the pathogens became less deadly. In this way, city states would have eventually acquired immunity against localised infections. But as contact increased through commerce and conflict, pathogens would have been exchanged, with devastating consequences.
The second period saw the great civilisations of Eurasia swapping diseases over longer distances, “when branches of the human family came into contact again after tens of thousands of years of separation following the ancient hunter–gatherer dispersals”, says McMichael.
Finally, the conquest by European explorers of the New World from the late 15th century saw the indigenous populations of Latin America and, later, Australia and the Pacific devastated by diseases such as smallpox, measles and influenza. These peoples had no herds of wild animals, so had remained relatively free of ‘crowd’ diseases. At the same time, the trans-Atlantic slave trade introduced African, mosquito-borne infections (malaria and yellow fever) to the Americas.
During the 20th century, the world returned to a state of relative equilibrium. By the 1960s, the medical establishment felt that it had outwitted infectious disease for good. We had learned to avoid disease by treating water, improving hygiene standards and controlling vector organisms, to prevent it through vaccinations and to fight it with antibiotics and antiviral treatments. Sensing the battle was over, scientists turned their attention elsewhere. Today, however, that decision appears somewhat naïve.
The microbe returns
When Peter Daszak boarded the plane from New York’s JFK airport to Washington DC on 14 January 2004, he had a lot on his mind. As director of the Consortium for Conservation Medicine (CCM), he had been invited to speak at a meeting of the National Centre for Ecological Analysis and Synthesis. But, at that moment, it was the last thing he needed. He was in the middle of coordinating an investigation into the SARS outbreak in China: his inbox was bulging and his phone wouldn’t stop ringing.
His workload wasn’t the only thing on his mind. Ever since his days as a postgraduate student in the early 1990s, Daszak had been interested in patterns of disease emergence, particularly relating to wildlife. He would escape the boredom of the lab by visiting London Zoo, where he helped the head pathologist identify unusual parasites found among the animals.
Daszak had never bought into the idea that infectious disease was on the decline. In fact, he believed the opposite was true. The World Health Organization was reporting that infectious disease was claiming more lives than ever. Malaria and tuberculosis, diarrhoeal and respiratory diseases were resurgent, and HIV was about to become the worst of all. But that wasn’t all. His experience told him something else was happening.
Daszak had emigrated from the UK to the USA in 1997, when his wife got a job with a biotech company in Atlanta. At the time, epidemiologists were pointing out that not only were the old pathogens resurgent, but the number of newly emerging diseases seemed to be rising. Since joining the CCM in 2000, Daszak had seen the evidence for himself: Hendra virus in Australia, Nipah virus in Malaysia, new strains of influenza, West Nile virus in the USA and now SARS.
What concerned him was that no-one appeared to know what to do about it. Epidemics were addressed – very efficiently – in terms of disaster management. But if infectious disease was as big a threat as it appeared to be, he thought, surely we should be doing something about preventing such diseases emerging in the first place.
Daszak had been so busy recently that he hadn’t had time to plan his talk that day. It was only now, as the plane levelled off in the bright winter sun, that he began to think about what he might say. He opened his diary and looked down at the address he had written down: Conservation International, 1919 M Street, Washington DC.
And that’s when it hit him. Conservation International had developed the concept of hotspots to identify areas where biodiversity is most at risk. If we knew where and why diseases were emerging, he thought, perhaps we could develop a way to predict where and how new diseases were likely to emerge.
As soon as he got back to the CCM office in New York, Daszak sat down with his colleagues to see if his idea was workable. He knew that Mark Woolhouse at Edinburgh University had recently published a database of emerging diseases, and that Kate Jones at the Institute of Zoology in London had been analysing large databases on diversity and extinction. So he hatched a plan to collect data on all recent emergence events, and analyse them to identify patterns that would enable him to make predictions for the future.
Fast forward two years, and Daszak’s team has collected information about the origin and cause of every disease emergence event since 1940 – a total of 409. Among these are new strains of ‘old diseases’ such as influenza, some of which, such as bubonic plague and streptococcus, have emerged as a result of the widespread use of antimicrobial treatments. However, a significant number are genuinely new to science.
What is perhaps most surprising is that at least 62 per cent were contracted from animals. In fact, some analyses reveal that this is as high as 73 per cent. These include exotic pathogens such as Ebola, Marburg, Nipah and West Nile virus, as well as those that we might consider more mundane – salmonella, E. coli and variant CJD. Indeed, it’s safe to say that those emerging diseases that have caused the most alarm in recent years have all originated from animals: SARS from bats, avian influenza from waterfowl and HIV-1 from chimpanzees.
Although developments in medical science have created more opportunities to discover new diseases, Daszak says his research proves that something unusual is happening. “These aren’t random events,” he says. “There’s a clear pattern that shows that the rate of emergence events has increased gradually over the past 50 years or so. What we’re seeing now is a return to the kind of patterns humans experienced in Biblical times. If we don’t do anything about it, it won’t be long before we have another disaster on our hands.”
Changes in human ecology
According to the Book of Revelations, the Four Horsemen of the Apocalypse will bring pestilence, as well as war, famine and death, at the end of the world. But these new pathogens haven’t been conjured up by an act of God, nor have they sprung from thin air. Instead, they’ve emerged as they always do, because changes in human ecology have presented microbes with new opportunities.
In many cases the disruptions in human ecology take the form of changes in the interface between humans and domestic animals on the one hand and wildlife on the other.
Jonathan Epstein, an epidemiologist with the CCM, explains that increasing urbanisation and agricultural expansion have both played a part. “As cities and towns grow,” he says, “they expand into previously wild habitats, so you get increased interaction between people and urbanised wildlife, such as robins, which carry West Nile virus, and raccoons, which carry rabies.”
Nipah virus emerged in 1998, when the intensification and expansion of livestock management allowed more contact between domestic animals and wildlife. “Nipah has probably been present in flying foxes for a very long time, but it has never had the opportunity to spread to humans,” says Epstein. “Like many pathogens, it depends on a certain density of susceptible individuals before a sustained outbreak is possible.” The growth of pig farming in Malaysia in the 1980s and ’90s provided those very conditions. “The farm where the virus first emerged was one of the country’s largest, with around 30,000 animals, so the virus was able to spread quickly and maintain itself among the pigs for long enough that humans could be infected.”
The SARS virus was transmitted to humans in a similar way at livestock markets in China. Epstein was involved in the investigation that last year identified Chinese horseshoe bats as its reservoir. “These bats were being brought into the markets, where there was a high density of live wild animals and humans, with lots of contact between them all through the butchering and unhygenic handling by the vendors,” he says. In this case, it’s likely that the virus jumped from the bats into civets and then to humans.
One of the principal factors to have influenced the rise in emerging zoonotic diseases is environmental disturbance. Deforestation has been shown to increase incidences of malaria,
by providing ideal conditions for mosquitoes to breed. There is also a theory that the loss of Malaysian rainforest forced fruit bats carrying Nipah virus to feed in orchards next to pig pens.
The transmissions of such high-profile diseases as Ebola, HIV, Lassa, Marburg and monkeypox, and others, have been facilitated by the bushmeat trade in Africa. This in itself is nothing new,
says Wolfe. “Humans have been hunting for thousands of years, and our ancestors for millions of years before that,” he says. “And long as people have exposed themselves to the bodily fluids of wild animals by hunting and butchering, there has been cross-species transmission of diseases.”
Today, however, consumers in Central Africa alone eat an estimated 579 million animals a year. This has increased the odds of a pathogen making the jump, says William Karesh, director
of the Wildlife Conservation Society’s Field Veterinary Program. “The rise in human population, and contact with and consumption of wildlife increases the chance that pathogens can achieve species-to-species transmissions.”
The likelihood of successful transmission is increased further in Africa because of the animals involved. “Chimpanzees and gorillas,” says Wolfe, “have a similar physiology to humans, so we’re all susceptible to the same kinds of diseases.”
Wolfe has recently discovered a series of new retroviruses among hunting communities in Cameroon. This suggests that these events may be occurring regularly. “This is only the tip of the iceberg,” he says. “Africa’s rainforests are home to extraordinary levels of biodiversity, and that means viruses and bacteria as well as plants and animals. We’ve only identified a small percentage of the viruses being transmitted from animals to humans.” The same is true in the live animal markets of China, says Daszak, as well as locations where humans are disturbing the established ecology and biodiversity is high. “The more opportunities we present to these pathogens, the more likely it is that they will make the leap.”
Transmission, prediction and prevention
Last year, Uige province in northeastern Angola suffered the worst outbreak of Marburg fever
on record. Of 374 cases, 329 died. In that case, virologists found that miners had probably contracted the disease from bat droppings while working in caves. Once infected, they transmitted the virus to members of their family.
The outbreak in Angola was more widespread because of one crucial factor: the victims in Uige reached a health facility. Once there, unsafe medical practices spread the virus – rapidly.
This form of nosocomial spread has been the principal reason behind the larger outbreaks of zoonotic diseases, says Laurie Garrett, author of The Coming Plague: Newly Emerging Diseases in a World Out of Balance. “In Africa, people stagger into these terrible hospitals and clinics that are desperately out-of-date, run-down, under-staffed and under-supplied, where there’s almost no infection control. So these ghastly places become the amplification system.”
Transmissions of Ebola, Marburg and Lassa may have been going on for thousands of years, she says. But because these cases would have been relatively isolated, the pathogen never had a chance to spread. “In ancient times, a hunter would just stagger off and die,” says Garrett. “In the worst case, his village would have been wiped out.” Today, however, changes in human migration have given diseases the chance to spread.
The same is happening on a global scale. Nowadays, we’re not only moving ourselves around the world faster than ever, but we’re moving animals, plants, soil, bacteria and viruses as well. The rapid spread of SARS and the more insidious creep of HIV/AIDS offer no better examples. SARS also reveals that it isn’t just the run-down health facilities in the developing world that amplify infectious disease, but also the state-of-the-art hospitals in wealthy countries. “Once these microbes get entrenched in a hospital they have mutated to the point where they can live on a bar of soap or even in antibacterial formulations. This issue isn’t about exotic and terrifying zoonotic events outside the First World. It’s about how we are changing our ecology and creating bridges for the microbes,” says Garrett.
Daszak says that if current practices continue, it will be only a matter of time before a new zoonotic disease has the same impact as HIV/AIDS. Certainly, the H5N1 strain of avian flu has the potential. And sooner or later the health services won’t be able to cope, says Garrett.
“The use of increasingly powerful antimicrobials is only going to create more problems,” she says. “We now have broad-spectrum, nuclear-bomb-level antibiotics available in black markets in the Third World. And we’re routinely treating minor infections in pre-schoolers with formulations of antibiotics that 15 years ago would have been reserved for intensive care. We’re digging our own graves.” The result is a race to reinvent the weapons we need to fight the microbes. “We’re working on scales of years and decades, while the microbes are working in hours and days. We’re never going to win.”
There is now a growing belief that the public health and global scientific communities need
to look beyond disaster management and move towards the prediction and prevention of disease emergence. “We’ve embraced it when it comes to medicine on an individual level,” says Wolfe. “We know that it’s a lot easier to encourage people to change their diet than it is to deal with heart disease. But we haven’t got that far with disease emergence. If we’d had five years notice on HIV, we wouldn’t be in the position we’re in today.”
Daszak’s database is the first step in the attempt to predict and prevent the emergence of new zoonotic diseases. “We have to bring together ecologists and virologists to talk about prediction,” he says. “Ecologists understand how changes to the environment affect wildlife populations and disease dynamics. And virologists have the capacity to test for new viruses and identify those that are most likely to achieve species-to-species transmission. By combining their skills, we can develop models that will enable us to predict where diseases are most likely to emerge in the future.”
Wolfe’s study of hunting communities in Cameroon is the first application of this kind of work. His success, says Daszak, is proof that it should be replicated around the world in the hotspots for zoonotic disease emergence. “I’d like to get to a stage where we could identify the diversity of viruses within a certain region and assess the risk of their emergence. That way we could advise governments planning to expand their livestock or timber industries, for example, to avoid those areas where these pathogens exist. That’s the vision. It’s early days, and our first attempts will be very basic and very rough. But it’s the first step in what I think will become a fantastic and very valuable new science.”
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