A way forward: an ecological hypothesis to understand and predict disease spillover events

Zohdy, S., T. S. Schwartz, and J. R. Oaks. 2019. The Coevolution Effect as a Driver of Spillover. Trends Parasitol. 35.https://doi.org/10.1016/J.PT.2019.03.010

As the COVID-19 pandemic worsens throughout many parts of the country, there’s no doubt that you’ve encountered discussion of just where the virus (SARS-COV-2) originated. While there are a handful of hypotheses circulating (as well as conspiracy theories, unfortunately), the explanation supported by molecular evidence and that scientists currently accept is this: the novel coronavirus originated in wildlife (likely a bat, pangolin, or other wild species) in the area of Wuhan (Hubei Province), China, and then spilled over – either directly to or by means of a bridge species – into humans, where it underwent further genetic change before becoming the virus that is causing the COVID-19 pandemic (Andersen et al. 2020). An earlier envirobites post by Dr. Andrew Barton discusses in detail that the problem in infectious disease outbreaks lies squarely in the human interaction. Either human encroachment into the habitat or harvesting species for the wildlife trade or markets is what creates potentially lethal disease outbreaks.

What is spillover?

The term spillover describes when a virus, bacteria, or some other potential disease-causing agent (we’ll call it a pathogen) that is harbored by one species “jumps,” or is transmitted to, another species. The pathogen doesn’t always make the new species sick; sometimes they can coexist. But if you haven’t heard the term spillover before, you’re likely familiar with examples that occurred between wildlife and humans – think swine flu, Ebola, or toxoplasmosis – and know that these diseases can be very serious, even deadly.

What causes these spillover events to happen?

As with most things, it’s complicated. One major factor involved in the emergence of infectious diseases that originate from wildlife and jump to humans is habitat fragmentation. This occurs as humans alter the landscape for development, or natural disasters damage habitats. What used to be large sections of uninterrupted forest or other natural space becomes broken up into smaller and smaller “islands” of the original habitat type. Wildlife and other organism communities are altered, and animals that may have never come into contact with humans are suddenly more exposed to human habitat. Pathogens maintained within these fragments are then more easily transmitted to humans either directly, or sometimes by means of an intermediate organism, called a vector. Ticks and mosquitoes are prime examples of these disease-transmitting organisms, and are responsible for numerous human illnesses like Lyme disease, Rocky Mountain spotted fever, yellow fever, Zika virus, et cetera, et cetera, et cetera. Diseases that can be transmitted from wildlife to humans are called zoonoses.

Deforestation and habitat fragmentation are large drivers of spillover events.
Photo by roya ann miller on Unsplash

It is critical that we understand all of the pieces of spillover events so that they can be predicted and ideally prevented. Scientists at Auburn University recently considered the two main hypotheses for spillover, and asked how do pathogens with the potential to spillover from wildlife to humans arise in damaged or altered landscapes? 

Current spillover hypotheses

The two main ideas behind how these outbreaks currently occur based on landscape health and species diversity are the dilution effect and amplification effect. Do these sound opposing? Well, they are.

Dilution effect: this hypothesis says that when there is more diversity of species, there is a greater chance that a disease will be spread out among all of the different species, or only infect some. There is less chance for transmission. This is well-supported on a small scale, and is a major way the bacteria that cause Lyme disease is understood to transmit in a forest ecosystem.

Under the dilution effect, when there are more species of animals present in a habitat it means that there is less disease, because it gets spread out among animals that may not be able to transmit it.

In this image, different colors represent different animal species. The silver, spiky shapes represent infection.

Amplification effect: this idea says that when you have more species, there are more opportunities for a disease to spread out and infect more animals.

Amplification effect is the opposite of dilution effect, and predicts that more species present mean that there are more animals capable of becoming infected and transmitting the pathogen.

In this image, different colors represent different animal species. The silver spiky shapes represent infection.

These explanations work for some disease systems and not for others. And in some cases, both dilution and amplification can be happening at the same time depending on different ways the disease transmits among mice at different times (Luis et al. 2018).

New spillover hypothesis: the coevolution effect

Zohdy and colleagues describe both of these hypotheses as ends of a spectrum that fail to take important factors into consideration, such as how ecosystem interactions and habitat fragment size contribute to spillover. Most notably, how do the host, vectors, and pathogens evolve together? The rate of genetic change in the disease and likelihood of spillover into human populations increases when vectors — which act as a bridge from the  are inserted into the equation. Therefore, the authors proposed a hypothesis called the coevolution effect. This hypothesis states that disease spillover is a product of coevolution of hosts and vectors, and the fragmented habitats they live in – a more complex combination of the factors involved that were unaddressed in the previous hypotheses.

In particular, each habitat fragment acts as an island where separate coevolution cycles among pathogens and vectors occur. With increasingly more “islands,” there exists a greater chance that a pathogen with the ability to jump to humans evolves.

Figure and caption adapted from Zohdy et al. 2019

The authors also suggest several animal disease systems that are ripe for the testing of this new, detailed hypothesis. In particular (and perhaps most relevant right now), bats are widely known to host a multitude of zoonotic viruses due to their high metabolic rates and protection against fevers, migratory behavior, and tendency to cluster in large groups. Bats also are hosts to numerous parasites like ticks and sucking flies that can easily transmit disease from a bat to another animal or human. Disease systems that do not involve vectors can also test this hypothesis as numerous fecal-oral route parasites (like giardia for example) may also be impacted by habitat fragmentation. 

A new hypothesis is exciting and provides many, many questions for researchers to answer. In this case, is habitat fragmentation associated with increased genetic diversity amongst hosts and pathogens, and does this lead to spillover events? Perhaps more importantly, then, the question is what do we do to fix it? If the COVID pandemic has taught us anything, it’s that there’s a lot of work to do all around.

References

Andersen, K. G., A. Rambaut, W. I. Lipkin, E. C. Holmes, and R. F. Garry. 2020. The proximal origin of SARS-CoV-2. Nat. Med. 26: 450–452. https://doi.org/10.1038/s41591-020-0820-9

Luis, A. D., A. J. Kuenzi, and J. N. Mills. 2018. Species diversity concurrently dilutes and amplifies transmission in a zoonotic host-pathogen system through competing mechanisms. Proc. Natl. Acad. Sci. U. S. A. 115: 7979–7984. https://doi.org/10.1073/pnas.1807106115

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Heather Kopsco

Heather Kopsco

I'm a disease ecologist interested in infectious disease emergence and spillover from wildlife to humans (and vice versa) as a result of human-induced climate and landscape alterations. I completed my PhD in May 2020 at the University of Rhode Island where I researched tick-borne disease socioecology. Currently, I am a postdoctoral research associate in the Smith lab at the University of Illinois Urbana-Champaign College of Veterinary Medicine where I am working on species distribution models of ticks and tickborne disease in Central Illinois.

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