This post was originally published on BioDiverse Perspectives – a research blog aimed at fostering communication about biodiversity.
Few studies have had as large of an impact on me as Charles Mitchell’s study of the impacts of plant species diversity on fungal diseases at the Cedar Creek grassland in Minnesota, USA.
Ok; quick caveat, Charles Mitchell is my advisor. But I’m not saying this to put my advisor on a pedestal. This study is in large part the reason that I study what I do, and that I am a graduate student where I am. By evaluating disease impact in an experiment that directly manipulated host species diversity, Mitchell was able to provide empirical evidence that decreased host diversity should increase the abundance of many diseases. Not only did it key in on the link between biodiversity loss and health risk, but the study showed me that such a complicated question could be approached in a way that was experimentally tractable.
But I don’t want to focus on Mitchell’s research here. See, although his study provided evidence to support the diversity-disease hypothesis, I am highlighting it here because it led to the search for general mechanisms behind that phenomenon. Instead I want to focus on a paper that I consider a true frontier in biodiversity science. This is a paper that took an often disjointed and complicated field, grounded it in a very simple theoretical model, and then generated some clear, testable hypotheses to move the field forward.
In their 2006 paper, Effects of species diversity on disease risk, Keesing, Holt, and Ostfeld provided a synthesis that would address the key question that underlies the diversity-disease hypothesis: What is the mechanism by which biodiversity influences disease risk? By generating 5 discrete mechanisms from a litany of previous research, they provided what would hopefully become a roadmap for future research aiming to understand and possibly mitigate for the relationship between biodiversity loss and increased disease risk.
I’m not going to get into the nitty-gritty details of this paper. Rather, I want to highlight one really cool aspect of it that I think was truly innovative and inspirational: that they take something almost immeasurably complicated (the ecology of plant and animal hosts, and the epidemiology of specialist, generalist, and vector born pathogens) and reduce it to the simplest system possible (a simple epidemiological susceptible-infected model) to identify the specific mechanisms by which diversity can influence disease risk. From this simplified model, they are then able to scale up in complexity to explain patterns observed in far more complicated systems.
So obviously, this paper is important to disease ecologists and conservationists aiming to prevent the spread and emergence of infectious diseases (not a trivial thing in and of itself). But I think this paper has value to all biodiversity researchers. It’s so easy to get bogged down in our own subfields and forget that we can often look to other disciplines or simple theory to synthesize our own research. Keesing, Holt, and Ostfeld used a simple epidemiological model to decompose nearly 100 years of research into 5 testable hypotheses. Biodiversity, with it’s multiple dimensions, drivers, results, and feedbacks, can often seem immeasurably complicated. Is there a simple, ecological theory that can unify this field as well?
Update: The PEGE Journal Club just posted a review of a recent empirical study of biodiversity and disease risk in a trematode parasite of amphibians that was published in Nature. Pieter Johnson’s lab at CU Boulder is doing a lot of really cool research in disease ecology, and this recent paper is a great example! Here, they argue that there’s an emergent property of host diversity that can decrease disease risk that acts independent of host density.