Parasite ecology cartoon feedback

The main goal of this blog is to communicate recent symbiont ecology science to people in the field and to students and non-scientists outside of the field. Judging by the feedback that I’ve received already, the cartoons that accompany (most of) my posts are one of the main draws for scientists visiting the blog. They’re also the most important selling point for educators using my posts in their classes and other educational material. I have a few years of cartoon experimenting under my belt, but it is still difficult to guess which cartoons will be crowd pleasers. So, if you’re a regular visitor and/or you’re an educator using my cartoons for educational purposes, I’d greatly appreciate it if you could take a moment to give me some cartoon feedback. Thank you in advance!

First, you can visit last week’s post and vote on the best parasite ecology cartoon from 2015. I really use that feedback to think about what kinds of cartoons to make in the future.

Second, you can post in the comments of shoot me an email to tell me what you like and/or what could be improved to make my cartoons more accessible to students.

One recent experiment has been embedding movie/TV references in my cartoons. The downside of this is that not everyone will get all of the references. (I fear I’m getting old….) Stay tuned next week for my best and most timely movie reference yet!

Forrest Gump

House, MD

Home Improvement

Terminator

Monty Python and the Holy Grail

Fringe

300

Best parasite ecology cartoon of 2015?

Happy New Year!

It’s the first day of the new year, which means that you get to vote on the best parasite ecology cartoon from last year! In 2013, the winner was “Social Networking in Lemurs,” a cartoon about this study that painted lice on lemurs to infer lemur contacts. In 2014, the winner was “Oldest Trick in the Book,” a romantic cartoon about a snail who was castrated by trematodes. Which 2015 cartoon was best?! I’m opening up the voting for these candidates:

Dispersal is like a box of chocolates

Tethered love

Tastes like chicken

Crappy relationships:

House (finch), M.D.:

When snails feel sluggish:

The host plant is always greener on the other side:

Hasta la vista, Biomphalaria:

You don’t guano know:

Bring out yer dead (prairie dogs)!:

Do you REALLY know how parasites are transmitted in your system?

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:

What is the predominant transmission route by which prairie dogs contract the plague?

What was the predominant transmission route by which humans contracted the Bubonic plague?

Reference:

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

The coextinction of parasites, commensals, and mutualists – a call for more natural history studies!

By definition, mutualists, commensals, and parasites (hereafter “affiliates” in this post) depend on their hosts for resources or services. Therefore, if a host species goes extinct, the affiliates associated with that host may go extinct, too. And in fact, coextinction events like this should be as common as – or even more common than – extinctions of hosts, because we know that every host species has many mutualists, commensals, and parasites. Just think about the mites living in your eyebrows, the bacteria living in your intestines, and that one time that you had lice in third grade. If humans disappeared, all of those affiliate species might also go extinct!

Of course, you might not believe in the intrinsic value of all species; you might be wondering why you should care if some tiny species that you’ve never heard of goes extinct. Extinctions of mutualistic species – such as the gut microbes that help you digest food and the pollinators that keep our agricultural systems running – have obvious implications for our economy and health. But parasites, too, play important roles in our lives. For instance, they regulate populations of wildlife host species, and they may prevent you from having allergic reactions to things that you shouldn’t be allergic to. And of course, species exist in intricate webs of interactions, and by accidentally (or purposely!) adding or removing species from ecosystems, we have often learned that one species can have huge impacts on ecological communities.

So, coextinctions of affiliates are important, and these coextinctions should be common. That means that we have documented tons of these coextinction events, right? Actually, we haven’t! There are very few examples of documented coextinctions (Dunn 2009, Colwell et al. 2012), and some of those are not entirely open and shut cases. But why?

Say that you document the extinction of a particular host species: Host A. Should every affiliate associated with Host A also go extinct? Because some affiliates likely use multiple host species, some of the affiliates of Host A probably survived on other host species. Also, even an affiliate that historically only used Host A might be able to continue existing if it can switch to a new host species. For instance, maybe Host B, a close relative of Host A, is a suitable alternative host.

Now imagine that you’re trying to document affiliate coextinctions as Host A disappears. What evidence might you use to figure out which affiliates have also disappeared? There might be published accounts of some of the affiliates of Host A, but there are very few host species (if any) for which every affiliate species has been documented. Therefore, the loss of one host species means that several unnamed and undescribed invertebrate species will be lost before ever being documented by humans. Even if you had a perfect list of every affiliate species, it might be really difficult to confirm whether each affiliate was now extinct. That’s because we rarely (if ever) have perfect lists of every host species used by a given affiliate species. So, if one affiliate species frequently uses three host species, but you think it is a specialist on Host A, you might think the affiliate has gone extinct, only to find it happily hanging out on Hosts B and C when you survey those species three decades later.

To summarize, we predict many coextinctions of affiliates to occur as hosts go extinct, but we have hardly documented any such coextinctions. It may be that that affiliate species are much less vulnerable than we expect due to the use of multiple host species or host species switching as a primary host goes extinct, and/or it may be that we are just very poorly equipped to observe and document these coexinctions. Clearly, if we’re going to get better estimates of affiliate coextinction rates, we need more data! Specifically, we need:

• Better understanding of the natural histories of these systems. We need complete lists of affiliates for each host species, complete lists of host species for each affiliate species, preserved specimens of affiliates for genetic identification, and information on the strengths of the interactions between each affiliate and host species.
• Better estimates of how frequently affiliates shift host species, and whether jumps to new host species are associated with declines in the availability of the current species. In other words, how often do we expect affiliates to sink with the ship versus swimming to safety? (For further reading about this, see Kiers et al. 2010.)

(It’s been too long since my last pirate worm cartoon….)

Some related reading:

Conservation – save the parasites along with the hosts?

Are pubic lice going extinct?

References:

Colwell, R.K., R.R. Dunn, N.C. Harris, and D.J. Futuyme. 2012. Coextinction and Persistence of Dependent Species in a Changing World. Annual Review of Ecology Evolution and Systematics 43: 183-203.

Dunn, R.R., N.C. Harris, R.K. Colwell, L.P. Koh, and N.S. Sodhi. 2009. The sixth mass coextinction: are most endangered species parasites and mutualists? Proc. R. Soc. B 276: 3037–3045.

Kiers, E.T., T.M. Palmer, A.R. Ives, J.F. Bruno, and J.L. Bronstein. 2010. Mutualisms in a changing world: an evolutionary perspective. Ecology Letters 13(12): 1459-1474.

Parasites and Snail Personality

When individual animals show consistent behavioral responses in different scenarios or in similar scenarios across time, and individuals vary in their responses, we can say that there are behavioral ‘types’ or personalities in that animal population. For instance, some animals might have aggressive personalities, where those individuals are consistently more aggressive than other individuals in the population. Personality is getting a lot of attention in disease ecology right now because particular animal behavioral traits (or suites of personality traits = behavioral syndromes) might increase an individual’s risk of becoming infected by a pathogen or the probability that an infected individual transmits a pathogen. For instance, I recently blogged about how Tasmanian devils that receive many head wounds in aggressive encounters (=lower social rank individuals) are less likely to become infected by Tasmanian devil facial tumor disease than individuals with fewer head wounds (=more aggressive/higher social rank individuals).

In a recent study, Seaman and Briffa (2015) set out to determine (1) whether snails have personalities and (2) whether snail personality traits are related to trematode infection status. The personality trait that they considered was “re-opening” time, which was a measure of how reluctant the snail was to re-open it’s operculum after being poked by the investigator. I’m not ashamed to say that this reads like an excerpt from the description of my dream job: “All observations were carried out by a single observer who had practised touching snail’s feet with a consistent level of pressure.”

Seaman and Briffa (2015) found that snails did have consistent responses to the mock predation encounters, where individual snails took consistently more or less time than average to re-open their operculum. Additionally, snails that were first intermediate hosts for trematodes (i.e., castrated snails) had longer re-open times, on average.

Because Seaman and Briffa (2015) used uninfected and infected field snails – as opposed to experimentally infecting their snails – it is unclear whether the differences in snail opening times is driven by infection, or whether the differences in opening times somehow affects the probability of becoming infected. Even if infection is driving the different mean response times, it doesn’t mean that the parasites are manipulating the snails. For instance, it might just be that infected snails are showing a sickness response, which makes them act sluggish. (Heh, get it?) Or it could be that the trematodes are manipulating the snails to make them behave more cautiously, thereby decreasing the probability that the host (and parasites!) gets eaten by a predator.

Because there are multiple potential mechanisms at work, I couldn’t decide on the dialogue of this cartoon. So, pick your favorite!

 

Reference:

Seaman, B., and M. Briffa. 2015. Parasites and personality in periwinkles (Littorina littorea): Infection status is associated with mean-level boldness but not repeatability. Behavioural Processes.

Inferring intra and interspecific parasite transmission from parasite population genetic structure

It’s often important to know how frequently parasites are transmitted among hosts of the same species (intraspecific transmission) or among hosts of different species (interspecific transmission). But observing parasite transmission events can be very difficult in wildlife populations, so we often have to use proxies instead of measuring transmission rates directly. For instance, we might use the frequency with which two bird species share a nesting site as a proxy for how frequently we think that transmission should happen between the two species.

But of course, transmission doesn’t necessarily happen when two species contact each other. So how can we determine whether interspecific transmission is really happening? There’s more than one method, but today, I just want to talk about a cool method that I’ve seen in a bunch of recent papers: comparisons of parasite population genetic structure within and among host species. If parasite populations are highly genetically differentiated among host populations or among host species (or even among individual hosts!), then there is evidence for low parasite transmission and thus genetic mixing among host populations or among host species (or individual hosts). Conversely, if there is no genetic differentiation in parasite populations among host populations or host species, then there may be high parasite transmission among host populations or host species. Here are a whole bunch of examples of how this idea has been explored in the literature recently:

Ectoparasitic flies on bats (Olival et al. 2013):

Olival et al. (2013) sampled bat flies on three species of bats in the Pteropus genus at eight sites in Malaysia, Cambodia, and Vietnam. Almost all of the bat flies were from a single species: Cyclopodia horsfieldi. An analysis of the molecular variance in the sampled bat flies showed that very little of the variation was explained by geographic region or host species. This suggests high rates of interspecific transmission of this bat fly species among the three Pteropus bat species. Previously, interactions between the three bat species, including roost sharing, were thought to be uncommon. But because the bat flies pupate off the host in the roosts, Olival et al. (2013) suggest that perhaps interspecific transmission can happen when the different bat species share the same roost locations sequentially, rather than at the same time.

Even though there was low genetic structuring in the sampled Cyclopodia horsfieldi bat flies, for one bat host species (Pteropus hypomelanus), there was relatively low gene flow in the parasite population at some isolated island sites. It turns out that bat gene flow is also low at those smaller, more isolated island sites. But if that’s the case, then why don’t those parasites have distinctly different genetic lineages from other sites and host species?  Olival et al. (2013) suggest that one of the bat species, Pteropus vampyrus, visits those more isolated island populations of Pteropus hypomelanus during long-distance dispersal, and that those visits provide enough population mixing to prevent divergence in the parasite lineages among sites and host species.

Ectoparasitic mites on bats (van Schaik et al. 2014):

Let’s stick with bats, but shift our geographic focus to central Europe and our parasite focus to mites in the genus Spinturnix. S. myoti mites live on Myotis myotis bats and S. bechsteini mites live on Myotis bechsteinii bats. Both mites have similar life histories, and they are only transmitted during direct contact; they can only survive for a few hours off a host bat, unlike the bat flies discussed above. S. myoti mites had high genetic diversity and panmictic genetic structure, with no differentiation among bat populations. S. bechsteini mites had low genetic diversity and high differentiation among bat populations. van Schaik et al. (2014) suggest that the differences in the genetic structure of the two mite species can be explained by the differences in the social systems of the two bat species. Myotis myotis bats have larger colony sizes, more inter-colony visits during the maternal season, and closer intraspecific associations during the mating season, and all of these factors could lead to more intraspecific transmission of S. myoti mites, both within and among colonies. That is so cool! (By the way, check out this post for more information about the relationship between host contacts and parasite transmission.)

Ectoparasitic flies on birds (Levin and Parker 2013):

In the Galapagos, great frigatebirds (Fregata minor) are parasitized by Olfersia spinifera hippoboscid flies, and Nazca boobies (Sula granti) are parasitized by Olfersia aenescens hippoboscid flies. The great frigatebirds have distinct genetic population structure among islands, but their hippoboscid flies and a pathogen transmitted by the flies (Haemoproteus iwa) have no genetic differentiation among islands (Levin and Parker 2013). Also, of the few Olfersia spinifera hippoboscid flies sampled on a second frigate species (F. magnificens), all flies had the most common fly haplotype on great frigatebirds. Similarly, the Nazca boobies had distinct genetic lineages among sites, whereas the hippoboscid flies on boobies showed no genetic differentiation among sites or among multiple booby host species.

So, what’s going on? How could the parasites be so well-mixed among sites, while their bird hosts are not? Levin and Parker (2013) suggest two hypotheses: 1) maybe alternative host species that weren’t considered in this study are doing lots of island hoping and carrying flies around with them. Remember that Pteropus vampyrus bats may play that kind of role in the bat fly example above. 2) Host genetic structure is distinct among islands because the birds are philopatric; they like to mate at their natal breeding site. But juvenile birds may still visit other sites without mating, and thus without influencing bird population genetic structures, and those visits could spread the parasites among the islands, thus mixing the parasite lineages.

Feather lice on birds (Koop et al. 2014):

Let’s stick with birds in the Galapagos, but let’s change our focal host to hawks (Buteo galapagoensis) and our focal parasites to feather lice (Degeeriella regalis). Hawks are thought to cross open water far less often than the frigatebirds and boobies in the previous example. Unsurprisingly, Galapagos hawk populations have high genetic differentiation among islands, where the genetic differences among populations increase with the distance among islands (Koop et al. 2014). Hawk feather lice also show high genetic differentiation among islands, unlike in our previous parasite examples. This suggests that there is very little interpopulation dispersal of lice, and there isn’t an alternative host carrying lice to different islands, either. Furthermore, lice are mostly vertically transmitted from parent to offspring, rather than the host-roost-host or horizontal host-host transmission routes in the previous systems. As a result, there is also genetic differentiation of lice among individual hosts, so that each host acts like a parasite island! Neat!

Feather mites on birds (Dabert et al. 2015):

Birds again, but now let’s talk about feather mites on two species of skuas (arctic and long-tailed skuas) in Svalbard. The mites are thought to be transmitted only during direct host contact, either vertically from mother to offspring or horizontally among hosts. Even though the two skua species nest at the same sites during the breeding season, nests tend to be spaced far apart, so Dabert et al. (2015) predicted that the two skua species would have distinct mite species. Both skua species had mites in the Alloptes genus, which were morphologically very similar, but which were genetically distinct enough between the two host species to be classified as two different species. However, both skua species also had Zachvatkinia isolata mites, and those mites had a well-mixed population with no evidence for genetic differentiation among host species. How could that be? Well, the two skua species do contact each other, during very brief but common aerial fights. And it may be that Zachvatkinia isolata mites, which are more abundant on the host and specialize on a relatively external region of the feathers, are more likely to be transmitted during those brief aggressive encounters than the Alloptes mites that hang out in more protected parts of the plumage. UHM, AWESOME.

You might be wondering if similar studies have been done with host species that don’t fly, or with endoparasites instead of ectoparasites. There is some endoparasite work, like with schistosomes and whipworms, but I’m not going to cover it here. As for non-flying host species, check back next week for an example of how the insight gained from studies like this can be used in an applied way to manage parasite transmission.

(I was watching a lot of Fringe when I made this cartoon.)

References:

Dabert, M, SJ Coulson, DJ Gwaizdowicz, B Moe, SA Hanssen, EM Biersma, HE Pilskog, and J Dabert. 2015. Differences in speciation progress in feather mites (Analgoidea) inhabiting the same host: the case of Zachvatkinia and Alloptes living on arctic and longtailed skuas. Exp Appl Acarol 65:163–179.

Olival, KJ, CW Dick, NB Simmons, JC Morales, DJ Melnick, and K. Dittmar. 2013. Lack of population genetic structure and host specificity in the bat fly, Cyclopodia horsfieldi, across species of Pteropus bats in Southeast Asia. Parasites & Vectors 6:231

Koop, JA, KE DeMatteo, PG Parker, and NK Whiteman. 2014. Birds are islands for parasites. Biology Letters 10: 20140255.

Levin, II, and PG Parker. 2013. Comparative host–parasite population genetic structures: obligate fly ectoparasites on Galapagos seabirds. Parasitology 140: 1061–1069.

van Schaik, J, G Kerth, N Bruyndonckx, and P Christe. 2014. The effect of host social system on parasite population genetic structure: comparative population genetics of two ectoparasitic mites and their bat hosts BMC Evolutionary Biology 14:18.

Migration and Parasites

Birds that migrate are infected by more nematode species than birds that do not migrate. Why is that? Well, it could be because migrating birds visit many more habits than non-migrating birds, and they therefore encounter many more nematode species. It might also be that migrating birds are more susceptible to nematodes due to the stress associated with migrating. Or, both explanations might be important!  Check out the recent paper that described this pattern, and/or check out the summary of the paper on the Oikos blog!

Reference:

Koprivnikar, J., and T. Leung. Flying with diverse passengers: greater richness of parasitic nematodes in migratory birds. Oikos.

Snail Fitness

Just something silly for April Fool’s Day. Have you seen my posts about snails and their parasitic castrators? Check them out here, here, and here!

Predator vs. Parasite vs. Parasitoid vs. Mutualist– A Simple Classification Scheme

One of the most frequently accessed posts on this blog defines the terms “predator,” “micropredator,” “parasite,” and “parasitoid” and then presents a classification scheme for differentiating among those natural enemies (Lafferty and Kuris 2002). If you haven’t read that post yet, I recommend taking a look before you read this one. I obviously fancy the dichotomous key presented in the previous post quite a bit. However, it is not be the best classification scheme for all situations. For example:

1. Check out Britt Koskella’s comments on the previous post – it is difficult to classify the bacteriophages that she studies using that classification scheme.
2. The previous key may be difficult to use for educational purposes. For instance, it requires explaining castration and trophic transmission, which are concepts that might be unnecessarily complicated for explaining the distinction between parasites and predators to non-specialists.
3. The previous key only deals with natural enemies, so we can’t use it to explain how mutualists and commensalists fit into this group of trophic relationships.
4. The previous key doesn’t show how relationships can vary with life stages, ecological conditions, and environmental conditions.
5. The previous key doesn’t have any pictures of snails on it. (Priorities.)

Therefore, having an additional classification scheme that specializes in some of the aforementioned areas would be useful. And – you guessed it – one was recently(ish) published (Parmentier and Michel 2013)! This classification scheme uses two continuous variables to designate relationships: the relative duration of the association (RDA) and the fitness effects on the ‘host.’

The relative duration of association ranges from 0 to 1, where 0 means that the ‘symbiont’ (including predators) spends none of its lifetime associated with the ‘host’ (or prey), and 1 means that the symbiont spends all of its lifetime associated with the host. For instance, predators and micropredators have RDA’s close to zero – a lion spends only a small portion of its life with a single zebra prey. Conversely, an adult trematode parasite (the worm in the orange section of the figure) will spend that entire life stage in association with a single host. The RDA is the Y axis on the figure below.

In recent months, we’ve talked a lot about the fitness effects that symbionts have on their hosts. Briefly, symbionts may have both negative and positive effects on hosts, and it is the net effect that determines how we classify the relationship. However, the net effect can vary with ecological and environmental conditions (see here, here, and here). Therefore, whenever we place a point on this graph, we need to remember that it might slide left or right as conditions vary.

Parasitoid wasps spend the entirety of their larval life stage in the host, and they ultimately kill the host. In this figure, parasitic castrators – like the trematodes that castrate snails – end up in the same region as the parasitoids. And this is where bacteriophages and Cordyceps fungi would fall out, too. However, like we discuss in the previous post, the term “parasitoid” is probably not a good one for this group, because that term is usually used to refer specifically to the unique life cycles of parasitoid wasps. In this figure, it means any parasite that reduces host fitness to zero.

Predators like lions, frogs, and crayfish also reduce prey fitness to zero. However, micropredators and herbivores (e.g., mosquitoes and cows) are special classes of predators that do not kill their prey. Then there is a group of animals that consume plants, but are probably more appropriately classified as parasites because they spend the majority of their life span (or a single life stage) on a single host plant. Therefore, things that eat plants will typically fall out somewhere between the aphids and the micropredators. (I should note that herbivores can have more than minimal impacts on host plant fitness, but many grazers have small impacts.) Similarly, Mark Siddall – the man who went on a quest for the hippo ass leech – doesn’t like classifying leeches as micropredators, because some spend most of their time on a single host. Therefore, most leeches would also fall out somewhere along that line between aphids and mosquitoes. Except, yaknow, the ones that are actually predators, and fall out near the lions.

On the mutualism side of things, we have symbionts like pollinators, which are only very briefly associated with each host; they’re like micropredators, but with positive fitness effects on their hosts. And then there are symbionts that are associated with single hosts for most of their lifespans, like ants on Acacia trees or guard crabs on corals. But again, remember that those relationships might shift left on the X axis as conditions vary.

Speaking of which, finding an example of a commensalist is hard. I used the example of epibionts on hermit crab shells, which help protect the hermit crabs from some predators but make the hermit crabs more susceptible to other predators. The net effect is unclear, but the positive and negative effects might balance out to a zero net effect.

So, there you have it. I think this figure should be really useful, especially as a general framework.

References:   

Lafferty, K.D., and A.M. Kuris. 2002. Trophic strategies, animal diversity and body size.  TREE 17(11): 507-513. (Direct link to PDF download)

Parmentier, E., and L. Michel. 2013. Boundary lines in symbiosis forms. Symbiosis 60: 1-5.

50 Shades of Symbionts

When we “sell” our science to journals and policy makers and even the general public, we often pitch our work in broad, abstract strokes (“trait-mediated indirect effects of…”) and/or in a highly applied context (“acid runoff tolerance of two functionally important species”).  I’m not saying that’s wrong.  But I think that most scientists – and most non-scientists – fall in love with ecology because the systems (the actual plants/animals/etc.) are cool, and then we have to gloss over the insanely awesome systems that we study in order to talk about the general applicability of our results.  Well, no more brushing cool systems under the rug!  Parasite Ecology is taking action by doing a few weeks of Odes to Awesome Systems.

The best way to prove that you have an awesome study system is to graphically illustrate the unquestionable adorableness of your study species.  EXHIBIT A – Hermit Crabs with Pink Afros:

Photo from here.

Did you know that hermit crabs have over 500 symbiont species?  More than 100 of those symbionts are obligate symbionts, meaning that they are only found on/in/with hermit crabs.  I learned that while perusing a heartwarming tale entitled, “”The Not So Lonely Lives of Hermit Crabs: Studies on Hermit Crab Symbionts.”

One of those obligate symbionts is the pink afro (also called “snail fur”) in the photos above.  Those colonial hydroids (genus Hydractinia) are found exclusively on gastropod shells, and especially shells that are occupied by hermit crabs.  Unsurprisingly, scientists who go out and find hermit crabs with pink afros just have to ask this question:  do the hydroids affect their hermit crab hosts?

As I’ve blogged about before (here and here), some symbionts protect their hosts from natural enemies.  Buckley and Ebersole (1994) wondered if the hydroids could protect hermit crabs from being eaten by blue crabs.  They found that blue crabs were just as likely to attack hermit crabs with or without hydroids, so the hydroids didn’t have any effect on predator preference.  However, blue crabs were much more successful when attacking hermit crabs with hydroids.  Having hydroids actually made hermit crabs more susceptible to predation!

BUT… gastropod shell strength wasn’t associated with the presence of hydroids.  So what was it about hydroids that made it easier for blue crabs to successfully attack hermit crabs?  Well, a second, parasitic symbiont – shell-boring Polydoran worms – decreased shell strength, and those worms were more likely to be present if the shells had hydroids.  So, one symbiont mediated the occurrence of a second symbiont, which in turn mediated blue crab predation success.  Nuts!

This could be the part of the story where we conclude that hydroids decrease hermit crab fitness.  But remember how most symbioses are context-dependent, where the strength and even the sign of the interaction depends on environmental and ecological conditions?  Well, it turns out that hydroids protect hermit crabs from a different enemy: ectoparasitic slipper limpets.  Therefore, Buckley and Ebersole (1994) suggest that the relationship between hydroids and hermit crabs changes throughout the year, depending on whether blue crabs and/or limpets are abundant.  That really emphasizes the importance of studying symbioses across broad time scales and under varying ecological and environmental conditions.

So, there you have it.  You can’t figure out hermit crab ecology without thinking about hermit crab symbionts.   Pink afros are more than just fashion statements.

Reference:

Buckley WJ, Ebersole JP (1994) Symbiotic organisms increase the vulnerability of a hermit crab to predation. J Exp Mar Bio Ecol 182:49–64.