Parasites and host body condition

Yesterday, as I was swabbing an eastern small-footed bat for the first time, I noticed something startling: it’s ears were orange! I was alarmed, because under UV light, orange spots show regions of the bat that are infected by the white-nose syndrome fungus. But when I looked at my nearby colleague, he was not holding the UV flashlight. Confused, but excited, I whispered to him (you always whisper when you’re around hibernating bats), “This bat has orange ears!”

He was totally unphased. Apparently Myotis leibii pretty much always have ectoparasitic mites, which are orange. I’m so intrigued by these mites, but my lit searching has yet to answer my many questions: why do so many M. leibii have them? Do other species not have mites because they rarely cuddle with M. leibii during hibernation? And, most importantly, are the mites parasites, commensals, or mutualists? It might seem safe to assume that the mites are parasites, but these two awesome stories have taught me to be cautious:

(1) Even groups with parasitic origins can contain species that aren’t parasites. The New Zealand bat fly (Mystacinobia zelandica) is a good example of this. You should read this whole fascinating story about the people who discovered that the New Zealand bat fly doesn’t suck bat blood, like related genera in other places, but rather lives in social groups that feed on bat guano (Holloway 1976). M. zelandica only hang out on bats when they’re catching rides to roosts.

(As a side note, one of the people quoted in that article is Ricardo Palma – a retired, Honorary Research Associate at the Museum of New Zealand Te Papa Tongarewa – who has the best automated email response I’ve ever seen:

“I will be happy to deal with your message, but only if it refers to parasitic lice (Phthiraptera) or to ornithological nomenclature.”

I cannot wait until I get to that part of my career.)

(2) Bird mites aren’t parasites. I’ll give you a minute…

Yeah, I was shocked, too! In what I imagine was incredibly painstaking work, Doña et al. (2018) found that the tiny guts of bird mites didn’t contain bird blood or feathers. Instead, they contained bird uropygial gland oil, fungi, and bacteria; mites are little cleaner symbionts! This probably explains why a large correlational study found that in most bird species, there were positive relationships between mite loads on birds and birds’ body condition. Unlike parasites, mites seem to have a net beneficial effect on their hosts (Galván et al. 2012).

This all reminds me of why I started writing this post in the first place: I wanted to ponder whether we look for relationships between symbionts and host body condition too often or not often enough. The examples that I’ve given so far suggest that we might not quantify how symbionts affect their hosts often enough, because we often assume that all symbionts are parasites until someone comes along and demonstrates otherwise. On the other hand, looking for correlations between symbiont loads and host body condition is probably not a great way to quantify how symbionts affect hosts, especially when the correlations are from a cross-sectional survey at just one time point. These correlational studies might be suboptimal and even misleading for many reasons:

  1. Symbiont loads today might not noticeably affect host condition until some point in the future, so time-lagged correlations might be more appropriate.
  2. Body condition metrics are alluring – wouldn’t it be great to measure one or two things and know how healthy or evolutionarily fit an animal is? – but studies often find that our favorite body condition metrics predict little to nothing about host fitness.
  3. As always, correlation doesn’t imply causation. Instead of symbionts decreasing host body condition, it might be that hosts with low body condition are more likely to acquire parasites or that a shared driver affects both body condition and parasite load.

I also worry that many correlational studies between symbiont loads and host body condition occur as afterthoughts. Now that I’ve switched to study vertebrates, I can relate to this. If you can only catch a few individuals (because they’re rare, or because IACUC said so, or because they’re hard to catch), you want to measure everything that you can about each individual, especially anything that might tell you about that animal’s future health and fitness (things you probably won’t get to measure later). Over the years, you accumulate tons of parasite data this way, even if you weren’t originally interested in parasites, so you decide to analyze it, and maybe publish it if you find that parasites decrease host body condition. Maybe this scenario isn’t as common as I think it is, but there is a publication bias in the literature: we’re less likely to publish positive relationships between symbiont loads and host body condition (Sánchez et al. 2018).

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In conclusion, I think that we don’t quantify the effects of symbionts on their hosts often enough, and that when we do, we often do it in a suboptimal way. If we really want to quantify these effects, we should (1) figure out what the symbionts eat (is it the host or something else?), and (2) experimentally manipulate symbiont loads and quantify host fitness (rather than body condition) – otherwise, we should put a lot more caveats in our discussion sections. If you’re interested in more details about parasite loads and host body condition that I didn’t cover here, check out this recent meta-analysis by Sánchez et al. (2018)!

References: 

Doña, J., H. Proctor, D. Serrano, K. P. Johnson, A. O. Oploo, J. C. Huguet‐Tapia, M. S. Ascunce, and R. Jovani. 2018. Feather mites play a role in cleaning host feathers: New insights from DNA metabarcoding and microscopy. Molecular Ecology.

Galván, I., E. Aguilera, F. Atiénzar, E. Barba, G. Blanco, J. L. Cantó, V. Cortés, Ó. Frías, I. Kovács, L. Meléndez, A. P. Møller, J. S. Monrós, P. L. Pap, R. Piculo, J. C. Senar, D. Serrano, J. L. Tella, C. I. Vágási, M. Vögeli, and R. Jovani. 2012. Feather mites (Acari: Astigmata) and body condition of their avian hosts: a large correlative study. Journal of Avian Biology 43:273–279.

Holloway, B. A. 1976. A new bat‐fly family from New Zealand (Diptera: Mystacinobiidae). New Zealand Journal of Zoology 3:279–301.

Sánchez, C. A., D. J. Becker, C. S. Teitelbaum, P. Barriga, L. M. Brown, A. A. Majewska, R. J. Hall, and S. Altizer. 2018. On the relationship between body condition and parasite infection in wildlife: a review and meta-analysis. Ecology Letters 21:1869–1884.

Cryptic connections and pathogen transmission

Happy Thanksgiving, Everyone! The origins of this holiday aside, I find it worthwhile to spend a day feasting and reflecting on all of the things that I’m thankful for. This year, one of those things is my new postdoc position studying white-nose syndrome (WNS). I’ve blogged about WNS before (e.g., here and here), but I’ve yet to blog about my favorite WNS paper, because it only just came out this week in Nature! I might be a bit biased in my evaluation, but it was certainly worth coming out of my blogging torpor to write about. Give it a read!

Let me tell you about a lovely dream that I share with many other disease ecologists: a new wildlife pathogen emerges; funding to study it becomes immediately available; we rush in and quickly figure out how the pathogen is transmitted by observing how hosts contact other hosts and/or pathogens in the environment; we thus quickly figure out how to interrupt pathogen transmission, our control efforts save an imperiled host species, and the crowd goes wild. Most of that scenario is still just wishful thinking, but today I’ll focus specifically on the difficulties associated with observing and quantifying the contacts that matter for pathogen transmission. There are two scenarios that can turn my lovely dream into a nightmare: the contacts I can observe are not important for transmission and/or the contacts that I cannot observe are important for transmission. Here are some examples: 

(1) The mycoplasma pathogen that causes house finch conjunctivitis seems like it should be transmitted from one bird eyeball to the next when birds physically contact each other. Direct contacts between birds aren’t necessarily easy to observe, but they can be quantified with proximity loggers and similar technology. But those obvious, quantifiable bird–bird contacts don’t really explain mycoplasma transmission dynamics. Instead, transmission seems to occur only when birds visit the same bird feeders subsequently – an infected bird visits, deposits some pathogen, and leaves, and then a susceptible bird visits later and gets exposed. These infected and susceptible birds are “connected” across time in a way that would be completely missed if we didn’t record videos of bird feeders or do feeder RFID experiments.

(2) Mountain brushtail possums spend their days in tree hollow dens and often share their dens with other individuals, especially their pair-bonded mates. Obvious contacts! But contact networks based on den-sharing contacts did a poor job of predicting E. coli strain sharing among possums. Spatial overlap in home ranges (and thus exposure to the same E. coli contaminated environments) wasn’t a great predictor of E. coli strain sharing either. Instead, brief (~4 min), nocturnal, cryptic contacts best explained E. coli transmission.

(3) And finally, we have the new white-nose syndrome example. It’s hard to imagine a more adorable and obvious contact than two bats snuggling for days at time while they hibernate. On average, each cave-hibernating bat in the Midwest is snuggled up with ~2% of the other bats in the cave during visual surveys. But if you cover individual bats in ultraviolet-fluorescent powder and leave them for a few months, you’ll come back to find that during their occasional bouts of arousal, they have actually contacted ~15% of the other bats and much of the cave environment, leaving little puffs of powder in their wakes. And it turns out that those cryptic contacts – the ones that were illuminated by powder trails but not by counting snuggling bats – do a much better job of predicting fungus transmission within and between bat species. For instance, northern long-eared bats were usually seen roosting alone, but the powder revealed a wealth of cryptic connections to individuals of the same and other species. Those cryptic connections likely explain why most northern long-eared bats are infected by the white-nose syndrome fungus by the end of the hibernation season. In contrast, tri-colored bats are rarely seen cuddling and were rarely contaminated by powder from other bats, confirming that they’re the loners of the cave world and explaining why so few tri-colored bats are infected by the end of the hibernation season. Really cool stuff!

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These examples illustrate an important point that is easy to forget: if you have gone into the field and quantified a contact network for a host species, you have not necessarily also quantified a transmission network for that host species. To construct transmission networks, you need to know all contact types, and you need to actually quantify transmission.

References:

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.

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

Hoyt, J. R., K. E. Langwig, J. P. White, H. M. Kaarakka, J. A. Redell, A. Kurta, J. E. DePue, et al. In press. Cryptic Connections Illuminate Pathogen Transmission within Community Networks. Nature.

Top 15 cited infectious disease ecology papers of the past decade

I’m a bit behind on blogging (and everything else), but I’d never forget your parasite ecology Halloween treat! Since nothing scares me quite as much as comparing my impact metrics to those of my colleagues, I thought it’d be horrifyingly fun to post a list of the 15 infectious disease ecology papers that were published and most cited in the past decade. I’m sure the suspense is already killing you, so here it is: 

  1. Gilman et al. 2010. A framework for community interactions under climate change. TREE. Cited 486 times.
  2. Lafferty 2009. The ecology of climate change and infectious diseases. Ecology. Cited 435 times.
  3. Lafferty et al. 2008. Parasites in food webs: the ultimate missing links. Ecology Letters. Cited 378 times.
  4. Alizon et al. 2009. Virulence evolution and the trade-off hypothesis: history, current state of affairs and the future.Journal of Evolutionary Biology. Cited 314 times.
  5. Fincher et al. 2008. Pathogen prevalence predicts human cross-cultural variability in individualism/collectivism. Proceedings of the Royal Society B – Biological Sciences. Cited 255 times.
  6. Kilpatrick et al. 2010. The ecology and impact of chytridiomycosis: an emerging disease of amphibians. TREE. Cited 229 times.
  7. Harris et al. 2009. Skin microbes on frogs prevent morbidity and mortality caused by a lethal skin fungus. ISME Journal. Cited 228 times.
  8. Smith et al. 2009. The role of infectious diseases in biological conservation. Animal Conservation. Cited 202 times.
  9. Crowl et al. 2008. The spread of invasive species and infectious disease as drivers of ecosystem change. Frontiers in Ecology and the Environment. Cited 200 times.
  10. Kelly et al. 2009. Parasite spillback: A neglected concept in invasion ecology? Ecology. Cited 196 times.
  11. Martinez 2009. The role of natural environments in the evolution of resistance traits in pathogenic bacteria. Proceedings of the Royal Society B – Biological Sciences. Cited 191 times.
  12. Angela et al. 2013. A comparison of bats and rodents as reservoirs of zoonotic viruses: are bats special? Proceedings of the Royal Society B – Biological Sciences. Cited 184 times.
  13. Tompkins et al. 2011. Wildlife diseases: from individuals to ecosystems. Journal of Animal Ecology. Cited 170 times.
  14. Plowright et al. 2008. Causal inference in disease ecology: investigating ecological drivers of disease emergence. Frontiers in Ecology and the Environment. Cited 168 times.
  15. Hoberg et al. 2008. A macroevolutionary mosaic: episodic host-switching, geographical colonization and diversification in complex host-parasite systems. Journal of Biogeography. Cited 166 times.

To generate this list, I searched Web of Science for papers with “infectious disease*” as a topic, and I filtered the results by ecology as a subject. A different search strategy would likely alter the results, but this list seems relevant to me. If you’re a grad student preparing for prelims, this would make a great reading list! Happy Halloween!

Parasites and host movement behaviour

A few weeks ago, we talked about the three parasite-themed organized oral sessions at ESA 2018. When I attended the “Uniting Predator-Prey and Parasite-Host Theory session, I saw Dr. Dave Daversa from the University of Liverpool give a talk for the first time. He was mostly talking about a neat meta-analysis regarding the effects of predators versus parasites on prey/hosts, but he mentioned some of his work about “behavioural fever” in amphibians infected by the chytrid fungus. I made a note to look up the paper he mentioned, but then I didn’t need to, because he made a trip to Virginia Tech a week later to give a talk focused on that work. So convenient! His dissertation work tells a great story about disease ecology and research conundrums and successes. I thought y’all might be as interested as I was, and Dave kindly agreed to write a guest post about that work for us. So, without further ado, here’s the story of Dave’s dissertation and more:

Many wildlife species can be observed moving across the landscape when spending time outdoors.  Observing the movements of their parasites is less straightforward. My head began to ache as I gazed at my field data.  I had been tracking the movements of alpine newts (Ichthyosaura alpestris) among a network of ponds in Central Spain in hopes of clarifying the spread of the pathogenic fungus parasite, Batrachochytrium dendrobatidis (Bd), known also as “chytrid” for the disease chytridiomycosis that it causes. Chytrid had reached global distributions and was decimating populations of its amphibian hosts.  How this microscopic fungus managed to spread across the landscape remained a mystery.

Alpine newts were ideal candidates for being chytrid vectors.  Newts were susceptible hosts of chytrid, but chytrid infections were not highly lethal to newts. Furthermore, newts routinely moved to different ponds during the breeding season, in contrast to most amphibians that tend to pick a pond and stay put.  Together, these traits screamed “superspreader”. By characterizing newt movements, I therefore expected to characterize the spread of chytrid as well. That is not what the data were indicating though.  Rather, the hundreds of newts that I followed exhibited only weak chytrid infections, if any, leaving no signature of infection spread among the ponds. What was going on?

For newts, even localized movements to neighbouring ponds mark a significant change in habitat from fully aquatic ponds to dryer, terrestrial habitat like the mossy grasslands that surrounded the montane ponds in Spain. Perhaps switching habitats affects chytrid in ways that inhibited its spread from pond to pond? Movement of hosts onto land reduces how frequently newts contact (i.e., are exposed to) infective chytrid spores because the spores rely on moist environments to survive. Given these moisture requirements, terrestrial activity may also compromise the ability of chytrid to grow on newts after infecting them.  Since seasonal terrestrial migrations of common toads (Bufo spinosus) at these same sites allowed them to recover from chytrid infections (read more here), these potential terrestrial effects did not seem so far-fetched.

My colleagues and I decided to bring newts into the lab to take a closer look at their movement and infections. Doing so uncovered convincing evidence that terrestrial activity was detrimental to chytrid. Firstly, frequent exposures that came with prolonged time in water were an important condition for infections to develop; infrequent exposures to even high concentrations of spores did not pose a high risk of infection.  Secondly, when we kept newts in terrariums, they contracted fewer infections than when we kept them in aquariums.  Any infections that did pop up in terrestrial newts were weak and didn’t last long, while those in aquatic newts were stronger and more robust.  Terrestrial activity therefore hindered chytrid in two ways: by reducing frequency of contact between newts and spores and by inhibiting survival and reproduction of chytrid on newts.

We then put newts in tanks with both land and water containing chytrid spores, allowing them to move freely between the two habitats, and we videotaped their activity for a week. Upon reviewing the videos we noticed an interesting pattern.  After about four days, just about the time it takes for chytrid to fully establish an infection, newts that contracted infections spent increasingly more time in the terrestrial habitats, particularly newts that developed severe infections.  Yet, newts that remained uninfected didn’t change their activity much. Chytrid infections appeared to cause newts to head for land, a behaviour that, as we showed previously, can kill off those infections.

The effects of terrestrial habitat, combined newt behavioural responses to infection, may be a reason why newts are not superspreaders of chytrid. To definitively determine that will, as always, require more research.  However, what is clear from this work is that behaviours exhibited during routine activities can play a big role in shaping parasitism risk, especially when those activities span multiple habitats.  Parasites in turn, may influence day-to-day behaviours more than one might expect.  So, the next time you are commuting to work, whether by car, bike or train, note the different environments you are traversing.  Consider how the commute might affect your encounters with parasites, and how those parasites could be actually influencing the route that you take.

Many thanks to Dave for sharing his work! He offered to give us a newt photo as a visual, but it’s been awhile since I tortured people with puns, so instead, ponder this:

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Parasite Ecology at ESA 2018

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ESA 2018 in New Orleans was filled with opportunities to learn about some great parasite ecology research, meet new people, and catch up with existing colleagues. (Speaking of colleagues, Chelsea Wood won the Unofficial Parasite Ecology Cartoon Contest with her animated Haeckel parasite drawings!) ESA 2018 was especially great because there was not one, not two, but THREE organized oral sessions about parasites! Julia Buck and Grace DiRenzo (both of UCSB) kindly agreed to help me write this post summarizing the three organized oral sessions for those who couldn’t be at ESA (and for those who had to choose between sessions, since two were unfortunately scheduled concurrently).

OOS 25: Uniting Predator-Prey and Parasite-Host Theory Under a General Consumer-Resource Framework

Organizer: Dr. Julia Buck (author of this summary)

Co-organizers: Tara Stewart Merrill, Dr. Armand Kuris

A year ago, I watched jealously on twitter as everyone attending ESA 2017 posted about the amazing science being presented there. One tweet in particular described an invited talk by Andy Dobson, and upon reading his abstract, I realized that I needed to organize a session for ESA 2018. I decided that applying predator-prey theory to parasite-host dynamics would be a broad enough topic to attract a large audience, while still being narrow enough to have meaningful boundaries. My session was motivated by the need for more cross-talk between predator-prey and parasite-host ecologists.

I invited Armand Kuris to parasitize the first couple of minutes of my talk so that he could introduce the consumer framework in Lafferty and Kuris 2002 (TREE). Once we had distinguished the different types of consumers from one another, I delved into their direct and indirect effects. Like predators, parasites can cause DMIEs through their consumptive effects and TMIEs through their nonconsumptive effects, but unlike predators, they can also cause TMIEs through their consumptive effects. Next up, Dave Daversa presented the results of a meta-analysis on the nonlethal effects of predators vs. parasites. In general, predators elicit stronger avoidance responses than parasites, but their net effects may be similar in magnitude than those of predators because the response to parasites is integrated through time. Next up, Janet Koprivnikar presented the results of several studies that Dave included in his meta-analysis. Specifically, she found that tadpoles avoid parasites and predators, but when forced to choose between them, they prefer to forage in the presence of parasites – the less lethal threat. Although avoidance of trematode cercariae by tadpoles might be motivated by fear, Caroline Amoroso showed that parasite avoidance by lemurs might be more strongly motivated by disgust, an emotion previously thought to be unique to humans.

Next up, Kevin Lafferty presented our theoretical work on the functional and numerical responses of predators vs. parasites, showing that whether we detect the functional or numerical response depends, in part, on study scale. Mike Cortez also presented theoretical work showing that differences between predators and parasites whose victims compete for resources are due, in part, to the fact that predators are immediately lethal to prey but parasites are not immediately lethal to hosts. Next Cherie Briggs shook things up by asking where all the parasitoid talks have gone. Parasitoids are similar to predators in that they are lethal to their victims, but they attack a single host during a life stage and establish a durable relationship with it, so they are a type of infectious agent. Apparently, ecologists used to study (and publish on) parasitoids in ecology journals, but most parasitoid work is now found in entomology journals. Tom Raffel presented a fascinating comparison of the thermal biology of parasitism vs. predation – a topic I never would have considered if not for this session. Finally, Andy Dobson and John McLaughlin presented their work on parasites in food webs. Andy applied the Lafferty et al. 2015 general consumer-resource model to the Yellowstone food web, while John compared predators vs. parasites in terms of their diversity, biomass, and impact on network structure.

Overall, the attendance at and reception to the talks in this session was excellent. Despite the fact that several speakers panicked when they realized what they had agreed to (sorry!), I found these talks inspiring. Thanks to all who presented, and to Tara Stewart Merrill for moderating.

OOS 32: Novel Modeling Approaches in Disease Ecology

Organizer: Dr. Graziella DiRenzo (author of this summary)

Co-organizer: Dr. Cherie Briggs

In disease ecology, there are so many statistical and mathematical models that can be used to answer a number of ecological/evolutionary questions that it can be difficult to pick “the right one”. There likely isn’t a right model – because as George Box said, “all models are wrong, but some are useful”. When I started my post-doc with Dr. Cherie Briggs at UCSB, I started thinking about compiling an organized oral session at ESA where we could learn about a bunch of cool and emerging models in disease ecology.  

We kicked off the session with Monique Ambrose, a graduate student, talking to us about spillover events and R0 in monkeypox from Dr. Jamie Lloyd-Smith’s Lab at UCLA. She had very interesting methods on how to account for a number of parameters in her likelihood model – and this was one of the only wildlife applications we saw in the session along with Dr. Kim Pepin. Dr. Kim Pepin spoke to us about methods the USDA-APHIS is trying to treat the leading edge of rabies in the eastern United States with vaccines. When is the best time to vaccinate raccoons? Questions like this and others were answered during her talk.

The remainder of the talks fell into the category of vector-borne diseases. Dr. Miguel Acevedo began with a great anecdote from a class he taught, telling us that a set of students from a class did not like a host-predator model because it was too simple BUT they liked the simple output,  reminding us about the tradeoffs in complexity, realism, and interpretation. Dr. Michaela Martinez followed-up with the awesome data collection methods they are employing in their lab to understand polio outbreaks and other human diseases from medical records. And along those same lines, Dr. Felicia Magpantay explained the differences that vaccination methods can have on the number of infected hosts using simulated data.

Dr. Mercedes Pascual, Dr. Victoria Romeo, Dr. Nicole Mideo, and Dr. Leah Johnson discussed malaria and other vector-borne diseases. Who knew the interactions between mosquitoes and temperature could make models so complicated?

We ended the session with an amazing presentation on integral projection models by Dr. Jessica Metcalf followed by a discussion/Q&A with Dr. Hal Caswell. This name may sound familiar because of his work on population matrix models.  

In the end – it was a successful session with between 80 and 150 people in the room at any particular talk. The presenters were engaging, animated, and made the material they were discussing easily accessible to everyone in the audience, regardless of career stage. Thank you to everyone who came, participated, and tweeted!!!

OOS 33: Parasite Conservation in the Face of Global Change: Opportunities, Challenges, and Next Steps

Organizer: Dr. Skylar Hopkins (author of this summary)

Co-organizer: Dr. Colin Carlson

When I told people about our parasite conservation session, most had the same questions: “Conserving parasites? Aren’t they bad? Why would you want to do that?” I’m happy to admit that some parasites are “bad” for people, our domesticated species, and wildlife. For instance, I don’t want to be infected by Guinea worm and I don’t want my dog to be infected by heartworm. But I also don’t want to get eaten by a lion, and I still think that large carnivore conservation is important. Therefore, I think that the question that we need to answer is not, “Should we conserve parasites?”, but rather, “Which parasite species should we conserve, and how will we accomplish those conservation goals?” Though parasites have historically been neglected and even persecuted by conservation research and practice, scattered groups of people have begun to tackle the pressing parasite conservation questions in the past decade or so, and my co-organizer (Colin) and I thought it was finally time to get a bunch of us in one place to try to coalesce as a subfield. Thus, roughly one year ago, the plan for the Parasite Conservation OOS was hatched! On extremely short notice, we cobbled together an international group of people from diverse institutions and career stages, and we were so pleased with the outcome at ESA! Here’s a synopsis of the session:

Giovanni Strona opened our session with a rousing discussion of community structure, community disassembly, and (co)extinction rates: he previously found that the order in which host species become extinct determines parasite co-extinction rates, and more recently, he found that removing parasites from systems accelerates biodiversity loss via a positive feedback loop, whereas reintroducing parasite species slows total biodiversity loss. But we might lose fewer parasite species than we expect if parasites can switch host species instead of going down with the ship. For instance, Jorge Doña told us that even in groups that are thought to be highly specific, like the bird feather mites that he studies, ~5% of symbionts are found on unexpected host species, suggesting that (1) the bipartite networks that we base our co-extinction simulations on might contain many stragglers; and (2) host switching deserves further study, because even though major switches are rare, they are a means by which symbionts might escape co-extinction. Speaking of specificity and host range, Tad Dallas followed with a discussion of how well we can estimate host range from host–parasite co-occurrence data, concluding that 20-40% of parasite ranges are currently unknown. Despite these big gaps in our knowledge of parasite ecology (e.g., host specificity), we might be able to use general parasite biodiversity patterns to make parasite conservation decisions. For instance, Chelsea Wood reminded us that a general law in parasite ecology is that parasite biodiversity increases with host biodiversity, suggesting that parasite and host biodiversity hotspots will coincide. However, Chelsea also showed us how fishing can decouple this classic relationship; when complex life cycle parasites are lost with their fished hosts, parasite and fish diversity are no longer correlated! And Mark Torchin showed us that unlike the classic latitudinal gradients that we see in free-living species, parasite biodiversity and interaction intensity can be higher in temperate regions.

If we already know a lot about host and parasite distributions, we can specifically model how global change will affect primary and secondary parasite extinctions, which Colin Carlson told us would be better than just relying on predictions from simulations with bipartite networks. And then I argued that no matter which kinds of models we’re using, we’re going to want to test their predictions regarding parasite extinction patterns on long-term, high-resolution host–parasite datasets; I used Chesapeake Bay fish parasites to illustrate how museum specimens might let us build those long-term datasets retrospectively. Kayce Bell followed my talk with a much broader discussion of all of the parasite museum collections available for parasite ecology and conservation research. And then Roger Jovani reminded us that not all symbionts are parasites, like feather mites that clean bird feathers (!!), and we should really embrace all symbionts for conservation purposes. And finally, Kelly Speer reminded us that symbionts even have their own hyper-symbionts, like microbes living in bat flies, and environmental changes that alter symbiont microbiomes might be important conservation considerations.

Overall, it was a very fun session, and I’m so excited for the new collaborative plans that we all put in motion.

Again, thanks to everyone who participated in and/or came to our parasite-themed organized oral sessions at ESA 2018! And if you want to schedule a parasite-themed OOS for next year, you’ll need to submit your proposal by September 13th, 2018. If you have questions about the process, we’d be happy to try to answer them!

Unofficial ESA 2018 Parasite Ecology Cartoon Contest

ESA 2018 is right around the corner, so it’s time to start polishing up your best cartoons for the Unofficial ESA 2018 Parasite Ecology Cartoon Contest. My favorite cartoonist will be awarded an almost entirely worthless prize (i.e., some publicity for their cool science and bragging rights for a year). I might also pick a real prize to send you in the mail, if I get some good recommendations.

To participate, all you need to do is put a cartoon in your talk. The cartoons don’t need to be funny! They also don’t need to be your personal artwork; borrowing with permission and attribution is fine. I’m just looking for cartoons that help communicate your work to the audience. That being said, anything punny is worth mega bonus points.

I believe that I’m going to be at ESA Monday-Thursday. If you have an amazing cartoon that you want me to see, you can tell me in advance in the comments, via email, or on Twitter, and I’ll try my best to be there!

To anticipate some questions:

Can you use cartoons from this site, if you use proper attribution? Yes! You don’t need to ask me in advance.

Can the judge be swayed by offers of free lattes or future academic positions? No! (Except yes. So much yes.)

Good luck!!