In this Insight, Yingying Wang, a Postdoctoral researcher at the University of Jyväskylä, discusses her  paper Phylogenetic structure of wildlife assemblages shapes patterns of infectious livestock diseases in Africa – recently shortlisted for the Haldane Prize for Early Career Researchers.

Yingying Wang
Yingying Wang

About the paper

More than half of infectious diseases originate in animals, mostly wildlife, and many of these diseases have multiple host species. So, biodiversity (e.g., species richness, the number of different species) plays a very important role in disease risk (e.g., the probability that a specific disease can occur). I am very interested in the relationship between disease risk and wildlife biodiversity, especially in the current scenario of biodiversity loss. There is one famous hypothesis about this relationship called the dilution effect (Ostfeld & Keesing, 2000). This hypothesis suggests that more species leads to less disease. In other words, higher number of different species protect people from being exposed to zoonotic diseases. How interesting! However, not everyone is convinced. Sometimes more species brings more disease. This debate made me wonder: is species richness a good indicator for disease risk? If not, which index or indices are more informative given that biodiversity can be measured in different ways? For example, phylogenetic diversity, which conserves information about host-pathogen interactions, might relate more directly to disease transmission in animal assemblages. Moreover, disease risk can also be measured in different ways, and different measurement of disease risk may respond differently to species richness (Huang, van Langevelde, Prins, & de Boer, 2015). In our study in Functional Ecology (Wang et al., 2019), we used a dataset of African livestock diseases from the world organisation for animal health (OIE) to explore the relationship between different indices of biodiversity (i.e., host richness and the phylogenetic relationships among wildlife species) and disease risk. We considered two ways to measure disease risk: the occurrence of individual diseases and the total disease burden (i.e., accumulated number of different diseases).

Photos of some animals in Africa (photo by Jasper Eikelboom; the zebra, buffalo and tsessebe were all photographed in Kruger National Park, South Africa and the sabels in Welgevonden Game Reserve, South Africa)
Photos of some animals in Africa (photo by Jasper Eikelboom; the zebra, buffalo and tsessebe were all photographed in Kruger National Park, South Africa and the sabels in Welgevonden Game Reserve, South Africa)

There are two main results in our study. First, species richness alone was inadequate when analysing disease–diversity relationships, as we found that species richness responds differently to the different measures of disease risk. There was a significant positive relationship between species richness and total disease burden but no relationship between species richness and occurrence of individual diseases. The positive relationship between species richness and total disease burden supports ideas about “diversity begets diversity” (Hechinger & Lafferty, 2005): high species richness supports more niches for pathogens and leads to more different diseases. The second main result in our study was that phylogenetic relatedness consistently affected both occurrence of individual diseases and the total disease burden. Phylogenetically closely related assemblage showed more diseases and a higher probability to have a disease. One reason might be that closely related species share similar immunological defences, so pathogens can spill over very easily from one species to another. On the other hand, those closely related species might also have similar habitat requirements. A higher encounter rate of those species could also lead to a higher disease risk.

About the research

Understanding the mechanisms behind disease-diversity relationships is critical for disease prevention and management. My study suggests that phylogenetic relationships among host species play an important role, one that is even more important than host species taxonomic diversity, in shaping the risk patterns of infectious diseases. Studying this phylogenetic relatedness may help to explain why the relationship between species richness and disease risk is sometimes negative (i.e., dilution effect) and sometimes positive (i.e., diversity begets diversity). For example, if increasing species richness makes an assemblage more phylogenetically narrow (by adding more relatives of the original species), then pathogens can spread more easily, and disease risk can increase. However, if increasing species richness makes an assemblage more phylogenetically diverse, disease risk may decline. Therefore, in addition to the simple number of species in an assemblage, phylogenetic information of assemblages should also be considered when studying disease-diversity relationships.

I am now studying other systems to better understand the generality of the effect of phylogenetic relatedness on disease risk. For example, Lyme disease is a model system for many studies on the dilution effect. Does phylogenetic relatedness have a larger effect than species richness in this system, too? I think so. Also, some studies suggest that the relationship between species richness and disease risk is scale-dependent. I think it is very interesting to test whether the effect of phylogeny is consistent over different spatial scales.

About The Author

Yingying Wang
Yingying Wang

I have always been interested in wildlife and wildlife health. I got involved in animal ecology as a bachelor’s student. My BSc thesis project was about the spatial occurrence of Ixodes persulcatus along the China-Russia border in Inner Mongolia, China. I like the process of asking a scientific question and answering it. I started my PhD at Wageningen University (the Netherlands) in 2015. I was thrilled to have the chance to continue my interest in animals and animal health in the Resource Ecology Group (now called Wildlife and Conservation Ecology) primarily under the supervision of Dr Willem Fred de Boer and Dr Kevin D. Matson. My research focused on disease patterns in wildlife. Unlike previous studies that have emphasized specific host-parasite interactions, my work considered the full suite of mammal species that influence infection dynamics. More specifically, I studied the main factors that shape patterns of infectious diseases and how disease risk change under changes in biodiversity. A key part of my PhD work was this study, which shows that phylogenetic relatedness of assemblages is more important than the number of hosts species present in an area.

Currently, I am working as a postdoctoral researcher together with Dr Eva R. Kallio at the Department of Biological and Environmental Science, University of Jyväskylä (Finland). My project focuses on the drivers of zoonotic tick-borne pathogens in natural populations. We aim to predict and mitigate future risks of tick-borne pathogens. We ask questions such as what are the roles of large mammals (e.g., deer) and small mammals (e.g., bank vole) in population dynamics or infection rates of ticks under different scenarios of species richness and phylogenetic relatedness among those species.

What project are you most proud of?

I am really proud of the projects during my PhD where I studied the relationships between disease risk and biodiversity and identified the importance of phylogenetic relatedness. This paper in Functional Ecology plays a fundamental role in my PhD work. To our knowledge, this paper is the first one studying phylogenetic structure of wildlife assemblages and disease patterns at a regional spatial level. I am happy to see that my work offers fresh insights into disease-diversity relationships.

What is the best thing about being an ecologist?

When it comes to “the best thing about being an ecologist,” the first word that comes to my mind is “surprise.” It is exciting and always surprising to explore the mysteries of nature, although I must admit it is not easy. The process of research is, simply speaking, asking questions and answering them. But asking a question is not as easy as it sounds: one needs to ask appropriate but innovative questions based on the existing ecological knowledge. Then, when trying to answer your newly formulated question, in my experience, some surprise often is revealed. For example, in the analyses related to our Functional Ecology paper, we expected that species richness would be positively related to total disease burden and negatively related to occurrences of single diseases. As it turned out, this is not what we found.

Moreover, ecosystems are very complex. Hosts and non-hosts and pathogens all interact with each other and with environmental conditions. This complexity means that ecosystems and ecological interactions are full of surprises! I love those surprises because they can give you a new way to understand nature. And these surprises also remind us about the limits of our current understanding.

You can find Yingying’s paper here, along with our other shortlisted papers.

Hechinger, R. F., & Lafferty, K. D. (2005). Host diversity begets parasite diversity: bird final hosts and trematodes in snail intermediate hosts. Proceedings of the Royal Society B: Biological Sciences, 272(1567), 1059–1066. doi: 10.1098/rspb.2005.3070

Huang, Z. Y. X., van Langevelde, F., Prins, H. H. T., & de Boer, W. F. (2015). Dilution versus facilitation: Impact of connectivity on disease risk in metapopulations. Journal of Theoretical Biology, 376, 66–73. doi: 10.1016/j.jtbi.2015.04.005

Ostfeld, R. S., & Keesing, F. (2000). Biodiversity series: The function of biodiversity in the ecology of vector-borne zoonotic diseases. Canadian Journal of Zoology, 78(12), 2061–2078. doi: 10.1139/z00-172

Wang, Y. X. G., Matson, K. D., Prins, H. H. T., Gort, G., Awada, L., Huang, Z. Y. X., & de Boer, W. F. (2019). Phylogenetic structure of wildlife assemblages shapes patterns of infectious livestock diseases in Africa. Functional Ecology, 33(7), 1332-1341. doi: 10.1111/1365-2435.13311