Instead of writing my own post this week, I’m going to link you to a post about one of the coolest things I’ve learned about in months: microhylid frogs and tarantulas may have a defense mutualism! Frogs living and breeding in the same holes with tarantulas may be protected from predators, and tarantula eggs may be protected by frogs from ant predation or parasitism. HOW DID I NOT KNOW ABOUT THIS UNTIL NOW? Please read every amazing detail here. You can also see some cool photos of spiders and frogs hanging out together here. Also, someone already posted a relevant cartoon to Imgur: enjoy!
Do you study parasites or other symbionts? Would you like some exposure for a cool paper that you published? Do you want practice communicating your work to other disease ecologists, students, and the general public? Then I have a deal for you!
In my about page, I encourage people to send me cool parasite ecology papers that I should blog about. I’m still happy to receive those suggestions, but I’m starting to get such a high volume of suggestions that I can’t keep up with them all. That’s sad, because you are all doing awesome work, and I would love to feature that work on this blog. So, I’m inviting you – ALL OF YOU! – to write a post about a recent paper (or a suite of related papers) that you have published, which I then will gladly post on Parasite Ecology!
If you’re interested, there are a few posting guidelines that I’d like you to follow:
- The paper you cover must involve symbiont ecology in some way.
- The paper you cover must be published (at least in press).
- The post must be original – no copyright violations! – meaning that you can’t copypaste an abstract that you have used for a conference or the paper.
- The post must be written in such a way that someone outside the field of disease ecology (e.g., a freshmen undergrad) could understand it. This can be tricky, but it can often be achieved by reducing jargon and by linking your post to previous posts explaining background concepts.
- The post must contain a cartoon! Now, before you let that deter you, let me say that if you really, really, really don’t want to make a cartoon for your post, I’ll make one for you. But making the cartoons is fun, so I encourage you to do it! Don’t worry about your art skills. I trace. A lot. And you can, too.
Please be aware that (1) I can’t pay you to write a post, and (2) I reserve the right to turn down potential posts that don’t follow the above guidelines. Other than that, anything goes – haikus, you name it! – and I’m looking forward to featuring your awesome science!
You can email your posts to me at firstname.lastname@example.org or ask me questions in the comments or via email. Happy writing!
Admit it, the title of this post made you cringe! Or it set off a little fuse in your brain and you’re just seconds away from your head exploding. Take a zen moment, and then continue reading for some interesting science.
If you don’t know what the dilution effect hypothesis is or why disease ecologists are debating the hypothesis, you might want to check out some of my previous posts before reading this one. But briefly: scientists have found a negative relationship between host biodiversity and the risk of infection to particular host species in some disease systems in some areas. That negative relationship is called the “dilution effect,” because host biodiversity is “diluting” parasite transmission. The debates have arisen because disease ecologists can’t agree on is how often the dilution effect occurs in natural systems: always, sometimes, or never? I’ve described the core arguments on both sides of the debate in this post.
Meta-analyses are one way to figure out how commonly the dilution effect occurs in natural systems. By collecting all of the available empirical and/or observation studies that consider biodiversity-disease relationships and lumping them together into one analysis, we can figure out whether the dilution effect always, sometimes, or never occurs in natural systems. Before my last post on the dilution effect debates was published, two such meta-analyses argued that the dilution effect only sometimes occurs (it’s “idiosyncratic”) in systems where the focal hosts are humans and non-human primates. Additionally, in the meta-analysis regarding how biodiversity influences human risk of infection with zoonotic pathogens, Salkeld et al. (2013) found evidence of a publication bias for studies that find a dilution effect, suggesting that studies finding neutral or amplification effects are less likely to be published.
Fast forward to Civetello et al. (2015), who did a larger meta-analysis that included more studies in more host-parasite systems. As I posted about a few weeks ago, Civetello et al. (2015) found broad support for the dilution effect, which I suppose we can say means that the dilution effect “often” or “usually” occurs, which puts us somewhere between “always” and “sometimes.”
Now back to the “debate” part of this post: Salkeld et al. (in press) responded to the Civetello et al. (2015) paper with some concerns regarding the larger meta-analysis. In particular, they worried that including laboratory studies might muddle the analysis, because the way that we manipulate systems in the lab doesn’t necessarily correspond to what really happens in nature. Also, they pointed out that if there is a publication bias – as they previously found – then it might not be particularly meaningful that the dilution effect is commonly reported in the ecological literature. However, Civetello et al. (2015) didn’t evaluate whether there was a publication bias in their analysis. (Note that McCallum et al. 2015 also pointed out some of these possible concerns.)
Civetello et al. (in press) responded to these worries by doing another meta-analysis. They used only a subset of the studies from their previous paper, so that they were including only field studies of human pathogens, like in Salkeld et al. (2013). Civetello et al. (in press) still found an overall dilution effect, and they suggested that adding in the studies published since Salkeld et al. (2013) provided more statistical power to see the dilution effect than Salkeld et al. (2013) had. Civetello et al. (in press) also looked for publication bias in their subsetted dataset and didn’t find any evidence for bias, but they point out that the analysis to look for a publication bias had to violate some assumptions of independence, so it might not be particularly meaningful.
It’s unlikely that things are totally resolved here, but I think everyone is on the same page regarding the future directions for diversity-disease relationships: we’ve spent time looking for general trends and determining how common the dilution effect is in natural systems, and now it’s time to switch our focus to the mechanisms underlying the dilution effect.
Civitello DJ, et al. (2015) Biodiversity inhibits parasites: Broad evidence for the dilution effect. Proc Natl Acad Sci USA 112:8667–8671.
McCallum H. (2015) Lose biodiversity, gain disease. Proc Natl Acad Sci USA 112: 8523–8524.
Salkeld DJ, Padgett KA, Jones JH (2013) A meta-analysis suggesting that the relationship between biodiversity and risk of zoonotic pathogen transmission is idiosyncratic. Ecol Lett 16(5):679–686.
Salkeld DJ, Padgett KA, Jones JH, Antolin MF (2015) Public health perspective on patterns of biodiversity and zoonotic disease. Proc Natl Acad Sci USA, 10.1073/pnas.1517640112.
Thought experiment time! Let’s say you could somehow (1) find/identify/locate and (2) eliminate every parasite on the planet. In this case we’ll lump pathogens and viruses and parasitoids and maybe even micropredators/vectors into the category of “parasites.” If you waved your magic wand and eliminated parasites from the planet, what effects would that elimination have on individuals, populations, communities, and ecosystems? I think that’s a great disease ecology prelim question, and you should all start using it immediately.
If you’re interested in the answers that other people have proposed to answer that question, I have some links for you! You can check out Wood and Johnson’s recent Frontiers in Ecology and Evolution paper (“A world without parasites: exploring the hidden ecology of infection“), and the similar and wonderful “soapbox” paper written by Bob Holt (“A World free of parasites and vectors: Would it be heaven, or would it be hell?“). Then there are these thought-provoking papers parasite conservation by Gomez et al. (“Parasite conservation, conservation medicine, and ecosystem health” and “Neglected wild life: Parasitic biodiversity as a conservation target“). Doughtery and colleagues also have a parasite conservation paper out in press that you might be interested in (“Paradigms for parasite conservation”).
If you haven’t seen it yet, there’s a recent Science paper by Johnson et al. (2015) entitled, “Why infectious disease research needs community ecology.” If you’re a disease ecologist, it probably won’t come as a surprise to you that infectious disease research needs community ecology. If you’re not a disease ecologist, check out this paper for a quick, informative read!
I was happy to see that Johnson et al. (2015) emphasized the importance of looking at symbiont communities as well as host communities when considering the spread of parasites and pathogens. The importance of symbiont communities is still not as widely recognized as I think it should be, and this paper does a great job of giving concrete examples of systems where coinfection by parasites/pathogens or the presence of non-pathogenic symbionts influence the spread of a single parasite within a host population or community.
If you’re looking for more examples where understanding the spread of parasites and pathogens required a detailed understanding of community ecology, check out some of these previous blog posts:
Considering symbiont communities is important:
Considering host communities is important:
Considering heterogeneity among individuals and species is important:
Johnson, P.T.J., J.C. de Roode, and A. Fenton. 2015. Why infectious disease research needs community ecology. Science 349(6252): 1259504.
Observing transmission events – and knowing that you just observed a transmission event – can be really tricky, but it’s a really important step in understanding parasite ecology in any given system. For instance, last week I talked about the Mg pathogen that causes conjunctivitis in house finches, and I told you that the pathogen might be transmitted among birds via bird feeders (=fomites). This possibility is corroborated by evidence that the number of direct contacts made by individual birds didn’t influence the probability of infection; that is, bird feeders seem more plausible than bird-bird contacts. But it’s still hard to say that Mg is never transmitted by direct contacts between birds, or how often that kind of transmission might occur. And that’s in a system where they’ve really spent a lot of time figuring out how the pathogen is transmitted!
Another good example is of this uncertainty in transmission routes comes from gastrointestinal pathogens. Pathogens that cause all kinds of diarrhea seem to be utilizing a strategy where they get out there and contaminate the environment and thereby make contact with other potential hosts. Based on that idea, we usually assume that fecal-oral transmission is really important to gastrointenstinal pathogens, whereas direct contacts among hosts are less important. Is that really true?
In a recent study, Blyton et al. (2014) quantified how long pairs of possums hung out at night, whether they were pair-bonded (=sex presumably happened), whether they shared dens during the day, and how much spatial overlap they had in their ranges. They related those potential drivers of transmission to the probability that the possums shared strains of non-pathogenic E. coli. Surprisingly, spatial proximity wasn’t important to strain-sharing, but the total time that pairs spent interacting was important, which is counter intuitive for transmission based on environmental contamination. But Blyton et al. (2014) posit that the most important kinds of contacts were brief nocturnal associations, rather than all-day den sharing or long-term pair-bonding. That’s seems really crazy, until you remember that possums probably aren’t defecating in their dens. It might be that the brief nocturnal associations are likely to result in contact with fresh, contaminated poo and E. coli transmission than den-sharing or simply living near an “infected” possum. Neat! But notably, we still don’t know exactly how E. coli is being transmitted in that system!
Anyone have any other notable examples of pathogens whose transmission routes we haven’t totally figured out yet? Here are two examples from systems with vector-based transmission:
Blyton, M.D.J., S.C. Banks, R. Peakall, D.B. Lindenmayer, and D.M. Gordon. 2014. Not all types of host contacts are equal when it comes to E. coli transmission. Ecology Letters 17: 970–978
For simplicity, we often assume that all hosts have an equal probability of becoming infected by and transmitting parasites and pathogens. But of course, we know that it isn’t how real systems work. For instance, in real systems, hosts vary in their propensity to become infected by pathogens, and that variation is one probable cause of the parasite ecology “law” that macroparasites are aggregately distributed among hosts. We call hosts that are highly susceptible to a given pathogen “superreceivers,” and hosts that are highly likely to transmit a pathogen are “superspreaders.”
Here’s a question for you to ponder: are superspreaders usually superreceivers and/or are superreceivers usually superspreaders? For instance, sex workers are at high risk for contracting HIV (=superreceivers) because they frequently change sex partners, and they’re also highly likely to spread HIV (=superspreader), if they have it, in comparison to the average person. In that case, the superreceivers are also superspreaders. When that happens, we might predict really explosive epidemics whenever “patient zero” is a superreceiver+superspreader, because R0 will be very, very high.
But consider the Tasmanian devil example that I posted about recently. Tasmanian devils that bite lots of individuals are highly likely to contract Tasmanian devil facial tumor disease; they’re superreceivers. But being bitten by an infected individual doesn’t seem to transmit the infectious cancer to the receiving host, so devils that bite frequently don’t transmit any more frequently than devils that don’t bite frequently. Therefore, the superreceivers in that system aren’t superspreaders.
Now let’s talk about a really cool system that I somehow haven’t blogged about yet. House finches are hosts for an emerging bacterial pathogen (Mycoplasma gallisepticum – Mg) that jumped from poultry into house finches in the 1990s. This pathogen causes conjunctivitis in the house finches – a symptom you don’t often think about in wildlife! In a really neat recent paper, Adelman et al. (2015) showed that birds that spent more time on bird feeders were more likely to become infected by (superreceivers) and transmit (superspreaders) Mg. This is a really cool example of a pathogen that appears to be transmitted by “fomites”: inanimate objects that the pathogen can survive on when off the host.
We probably don’t have enough examples in the literature to determine whether superspreaders are usually superreceivers or to look for generalities in systems where this occurs. But we’re accumulating more examples all the time! Stay tuned.
…if academics were at higher risk of developing conjunctivitis when they sought out free food, I’d have some very squinty-eyed colleagues.
Adelman, J.S., S.C. Moyers, D.R. Farine, and D.M. Hawley. 2015. Feeder use predicts both acquisition and transmission of a contagious pathogen in a North American songbird. Proc Biol Sci. 282(1815): 20151429.