Zoonoses happen when a disease-causing pathogen – bacteria, virus, fungus – leaps from non-human animals to humans. The novel coronavirus is the most recent in a list of high-profile zoonoses that includes the SARS, MERS, Ebola, Zika and Nipah viruses. Zoonoses make up over 60% of all emerging infectious diseases around the world, and nearly 72% originate in wildlife. This feature requires us to develop a deeper understanding of where, when and how zoonoses become a public health problem, and this is where disease ecology can help.
Take, for instance, growing concerns that biodiversity loss can increase zoonoses. This is true – but the links between biodiversity and disease are complicated. One key factor in disease spillover is pathogen load. How biodiversity regulates pathogen loads can be understood through ecological theory. Some animal species, called reservoirs, maintain high pathogen loads. However, the chance that a pathogen load soars or jumps from reservoirs to humans often involves species other than the reservoir.
Now, the disease risk reduces, or becomes ‘diluted’, when the animal species called the hosts become a dead-end for a pathogen. Lyme disease offers a well-studied example. The disease-causing bacterium Borrelia burgdorferi is transmitted by ticks that feed on reservoir animals – such as deer mice – and then bite humans. Ticks of the genus Ixodes are less likely to spread the pathogen when there are so many different animal hosts to feed from. When forest loss knocks out some host species, the population of deer mice increases (because they have more resources now), and with them so does the incidence of Lyme disease.
Disease dilution also happens for the West Nile virus in birds, the hantavirus in rodents, Bartonella bacteria in wood mice, and tick-borne encephalitis in rodents. Closer home, dilution may happen with tick-borne diseases like the Kyasanur forest disease (KFD). One study found higher KFD burden with more mammal species but the analysis was too coarse to assess mechanisms. We need field-level studies to see how mammal diversity is linked to ticks that spread KFD.
Adding to the complexity, zoonoses can be regulated by microbes other than the disease-causing pathogens as well, and animals carry lots of microbes. Some of these, like the good ones in our guts, may actually keep the bad ones in check. So there is the ironic possibility that more microbes may mean less disease. Studying entire communities of microbes on animal hosts may shed more light on how biodiversity links to disease.
The relationship of disease with larger scale factors like deforestation can also be equivocal. Forest loss can increase zoonotic outbreaks – but after a threshold of deforestation, some diseases like malaria actually decline as forest cover falls. We don’t know why, but humans’ access to healthcare, sanitation or other factors may be involved. Without clear knowledge, we must not think that turning natural ecosystems into cities will contain disease spillover – just as it may be foolish to react to zoonoses by culling a species that may have played host to the pathogen.
Consider the case of rabies in bats, already a much-maligned mammal. In Latin America, the vampire bat is the main reservoir of rabies. To control rabies, people destroyed bat roosts, but recently researchers found that viral loads were higher in roosts that had a history of culling. Similarly, culling bison didn’t have an effect on the spread of brucellosis nor (hypothetically) culling wild boars on the spread of swine fever.
Indeed, there is no evidence that eliminating reservoirs will eliminate disease. If one species, say the flying fox, harbours a potential pathogen, killing it doesn’t guarantee that the disease will be eliminated. Instead, we need to further study reservoir species in different habitats, and their interactions with other species to identify the mechanisms that regulate diseases and affect humans.
Ecology holds the promise of helping us understand spillovers and predict outbreaks, but this knowledge has gaps that need to be filled. It would be naïve to assume more biodiversity always means lower disease risk or that biodiversity loss invariably leads to disease spillover. Loss of some host species may well reduce disease transmission, and other hosts may serve as intermediaries. Pathogens evolve. There is much more to know.
It’s possible this uncertainty makes us uncomfortable, but zoonoses will not just disappear if we rush out and kill bats, rodents or other wildlife. In fact, such drastic disturbances could push pathogens to spillover to new hosts. Indiscriminately culling wildlife or destroying ecosystems could also bring about new diseases – what the science writer David Quammen called “shaking the viral tree”.
Destroying ecosystems and wildlife has other costs. Ecosystems clean the air, regulate climate, store carbon, cycle nutrients, recharge groundwater and maintain watersheds. Animals like bats and birds provide essential functions like pollination and pest control. When they are killed, we may beat back a local disease but what about their ecosystem functions? Will the trade-off be worth it? We don’t know.
We must desist from drastic reactions until we know enough – but we shouldn’t not act either. Until the time is right to act, we should endeavour to develop a clearer picture of emerging infections and potential zoonoses. We could investigate how animal hosts and microbial communities interact, how different host species shape different groups of potential pathogens, if particular host species have disproportionate effects, and the specific mechanisms by which land-use change and human behaviour mediate disease spillover.
Some of this science may seem obscure, without immediate use. We often respond to a pandemic in emergency mode, focusing on seemingly clear targets: sequence the genome, treat the symptoms, make a vaccine, etc. But tackling zoonoses has to begin much before they occur and requires research combining disease ecology, human behaviour, pathogen biology and public health.
According to EcoHealth alliance, a global consortium of researchers studying zoonoses, “We have to look at systems not from the standpoint of specific hazards but for the dynamics of the systems themselves, and a spectrum of possible outcomes.” Such layered knowledge can help us design plans to track host-pathogen dynamics and look for diseases. Research has to be coupled with targeted outreach to communicate the science, dispel myths and convey best practices.
India especially needs a multi-pronged approach to zoonoses. In 2002, India was the world’s top hotspot for zoonoses. In 2020, a higher burden of zoonoses and increased risk factors show that we urgently need research, monitoring, planning and shoring up our public health infrastructure to face future outbreaks.
Emerging and existing zoonoses should make us reconsider our current ways of life. Breaching forest frontiers, large-scale bushmeat hunting, animal markets, gargantuan livestock farms, climate change – all provide fertile grounds for pathogens to leap from animals and plants to humans. Zoonoses remind us that the human world and natural world don’t operate independently of each other.
Meghna Krishnadas is an ecologist at the Laboratory for Conservation of Endangered Species at the CSIR-Centre for Cellular and Molecular Biology.