Biological control of schistosomiasis: prawn terminators

Schistosomiasis is the second most common parasitic disease infecting humans. (The first is malaria.) According to The Global Network for Neglected Tropical Diseases, 240 million people in 78 countries are infected by schistosomes at this moment. This disease kills hundreds of thousands of people each year.

Of course, most of the people afflicted by schistosomiasis live in tropical and subtropical regions, especially in poor regions with limited water availability and inadequate water sanitation. Therefore, the average US citizen probably hasn’t even heard of schistosomiasis. So, briefly, schistosomiasis is a disease caused by a parasitic worm, called a trematode. Schistosome trematodes have complex life cycles, as depicted by the CDC diagram here. When infected humans urinate or defecate in bodies of water, the eggs of the parasite are released and hatch in the water. A free-living larval parasite, called a miracidium, swims around until it finds a snail to infect. Later, the infected snail releases more free-living larvae, called cercariae, and these swim through the environment until they find a human to infect. In water bodies with infected snails that are releasing cercariae, humans can get infected whenever they contact water for swimming, bathing, or water-collecting purposes.

The global burden of schistosomiasis is huge, so there is great imperative to figure out a way to control transmission of schistosomes to humans. The most common control strategy is an antihelmentic drug for humans (praziquantel). When entire communities of people are treated, the health of the treated individuals improves, and the chain of transmission from humans to snails is broken. Another control method involves using chemicals (molluscicides) to kill the snails in particular water bodies. However, those chemicals can have unintended adverse effects on non-snail organisms living the same water bodies. Additionally, both control methods tend to be temporary in nature – if the treatments aren’t kept up, snails can be reintroduced into the water bodies and/or humans can become infected with new adult parasites.

This brings me to the topic of this post: biological control of schistosomiasis as a supplement to existing control strategies. As far as I know, biological control of schistosomiasis isn’t being used in a major way in any control programs. But there is a lot of interest in this type of control, and I’ve seen several recent papers on this topic that I wanted to share:

  • Introduce snail parasites: Duval et al. (2015) recently discovered a bacterial pathogen of snails (Paenibacillus glabratella) that causes high snail mortality. The pathogen is also transmitted from adult snails to eggs, and infected eggs are less likely to hatch successfully. So, this bacterium might be a promising biocontrol option! However, it’s unclear at this point whether the bacteria are specific to the snails that are intermediate hosts for schistosomes, or if the bacteria would infect many invertebrate species.
  • Introduce snail competitors or predators: There has been interest in using competing snail species and predators of snails to control snail populations for a long time. Of course, these biocontrol agents need to have a strong enough effect on the target snail species that they greatly reduce or eliminate populations of the target species. And ideally, the biocontrol agents won’t wreak havoc on any other species, even after the target species has been eliminated. Sokolow et al. (2014) recently showed that river prawns are voracious predators of snails when the two are maintained together in the laboratory. Furthermore, Sokolow et al. (2014) point out that prawns are nutritious, delicious, and sell for high prices, and local people could harvest the larger prawns for food while leaving the small and medium prawns to do their snail terminating. WIN-WIN.
  • Introduce parasite predators: The free-living larvae that trematodes use for transmission between hosts are susceptible to predation by all kinds of animals: fish, dragonfly and damselfly larvae, filter-feeding invertebrates, etc. My personal favorite is an oligochaete worm (Chaetogaster limnaei) that lives symbiotically on the snail and eats both miracidia and cercariae. People often suggest that these parasite predators could control trematode transmission, including the transmission of the trematode species that cause schistosomiasis and the related trematodes that cause Swimmer’s Itch. Cool stuff!


(Added to the list of things I cannot draw: motorcycles.)


Duval D, Galinier R, Mouahid G, Toulza E, Allienne JF, et al. (2015) A Novel Bacterial Pathogen of Biomphalaria glabrata: A Potential Weapon for Schistosomiasis Control? PLoS Negl Trop Dis 9(2): e0003489.

Sokolow, S.H., K.D. Lafferty, and A.M. Kuris. 2014. Regulation of laboratory populations of snails (Biomphalaria and Bulinus spp.) by river prawns, Macrobrachium spp. (Decapoda, Palaemonidae): Implications for control of schistosomiasis. Acta Tropica 132: 64–74.

Pitcher Plants Are Poop-Eating Toilets

Lots of plants eat poop (via roots), but pitcher plants acquire their fertilizer in a bizarre way: by becoming toilets. Check out these sweet examples:

Pitcher plants are well known for their carnivory: they live in soils with low nitrogen content, and they have spectacular adaptations for catching and digesting arthropods as an alternative means of nitrogen acquisition. But in Borneo, there are some pitchers that aren’t so great at catching arthropods. For instance, the Nepenthes lowii pitcher plant produces two kinds of pitchers: when the plants are immature, their pitchers are close to the ground, and they are proficient at catching and digesting arthropods. But when the plants are mature, they produce aerial pitchers with different shapes, open lids, no slippery wax, and rough inner surfaces. In other words, the aerial pitchers are missing many of the important adaptations for trapping arthropods. The aerial pitchers also have specialized nectar glands on the underside of the lid, and a super cute mammal called a tree shrew visits those nectar glands. And get this: the nectar glands are positioned in such a way that the tree shrew sits in the mouth of the pitcher plant while feeding, and that ensures that if the tree shrew defecates, it will fall into the pitcher plant. (You might need a visual of how shrews loo by sitting on the toilet backwards.) Clarke et al. (2009) estimated that 57-100% of the adult pitcher plants’ foliar nitrogen comes from tree shrew poo. Isn’t that wild?!

So, are tree shrews the only mammals that use pitchers as toilets? Nope. A different species of pitcher plant in the same genus (Nepenthes rafflesiana elongata) is also quite bad at catching arthropods. That was puzzling until Ulmar Grafe et al. (2011) found Hardwicke’s woolly bats (Kerivoula hardwickii hardwickii) roosting inside the pitcher plants during the day. In fact, the Hardwicke’s woolly bats that Ulmar Grafe et al. (2011) followed during their study roosted exclusively in pitcher plants! And the plants with bat visitors received ~34% of their foliar nitrogen from the bats. So, yeah, this interaction is kind of like paying for your room at a motel by leaving the toilet unflushed.



Clarke, CM, U Bauer, CC Lee, AA Tuen, K Rembold, and JA Moran. 2009. Tree shrew lavatories: a novel nitrogen sequestration strategy in a tropical pitcher plant. Biology Letters 5: 632–635.

Ulmar Grafe, T, CR Schoner, G Kerth, A Junaidi, and MG Schoner. 2011. A novel resource–service mutualism between bats and pitcher plants. Biology Letters 7: 436–439.

Plague: many European epidemics and many introductions from Central Asia

A few years ago, I stumbled across a paper whose very title blew my mind. Using archeological evidence, the authors claimed that, “Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe.” (You can see more about their awesome work here.) That paper was the first one to really pique my interest in the medieval plague epidemics, but it wasn’t the last:

Most people only know about the most famous plague epidemic in Europe – the Black Death – but there were actually many European plague epidemics. We know that plague didn’t originate in Europe, though. The first introduction is thought to have come from Asia. After that initial introduction, the plague might have hung out in reservoir hosts in between outbreaks in Europe. That’s what people used to think, anyways. But the reservoir host that was typically implicated was the black rat (see my previous post), and recent evidence suggests that the black rat couldn’t be responsible for many of the epidemics that occurred. So, where the heck did the plague come from in all of those epidemics?

Schmid et al. (2015) combed thousands of records of plague outbreaks in medieval towns that were near areas for which climate proxies (e.g., tree ring records) exist. The vast majority of those outbreaks occurred shortly after a neighboring town had an outbreak, which might suggest that town-to-town transmission by people is a more reasonable cause for most outbreaks than a rodent reservoir. However, some out the outbreaks didn’t follow outbreaks in neighboring towns, and they occurred in maritime towns. In those cases, plague might have been introduced into towns via ships.

But where was the plague coming from? Well, there are really only two options. The ships could be bringing in the plague from other European towns, or they could be bringing the plague from someplace else, like Asia. And interestingly, Schmid et al. (2015) found a relationship between a climate proxy in Asia (tree ring growth in juniper trees in the Karakorum mountains) and plague outbreaks that occurred ~15 years later in Europe.

Here’s what Schmid et al. (2015) hypothesize was happening in a typical plague cycle: in years that were climatically favorable, rodent populations in Central Asia boomed. Gerbils were living fast and loose, making babies and spreading fleas and plague amongst themselves. The flea populations responded to the sudden spike in host density by making lots of flea babies. So, there were lots of gerbils and lots of fleas. Then the climate shifted to something less favorable, there wasn’t enough food to go around, and the giant gerbil population crashed. That was no good for the fleas, who suddenly found themselves homeless. The fleas then had to go find different hosts – such as camels or humans – and they took the plague with them to their new hosts. (By the way, a similar thing might happen with Lyme Disease: acorn mast years might cause large mouse and tick populations, and after subsequent declines in the mouse populations, hungry ticks go looking for other hosts, including humans.)

So, you’re thinking, “Uh, yeah, so a few years after Central Asia is the Land of Plenty for gerbils, a billion hungry, plague-y fleas and go looking for other hosts in Central Asia. How does the plague repeatedly travel 4000km from Central Asia to the Black Sea to hop on a boat to Europe?” Uhhhh… good question. One hypothesis is that the plague traveled the Silk Road along with the caravans via humans and camels for ~10-12 years, eventually reaching the Black Sea. This is an area of study that people are focusing on now.

So, when the mainstream media picked this story up, they had all these witty lines about how people are all prejudiced against black rats, when really it’s the innocent-looking gerbils who are to blame for the plague. (Have you ever seen a black rat being wrongly interrogated by the authorities? It’s terrifying.)  I can’t think of anything wittier to say, but I made a cartoon of a gerbil wearing a blonde wig. You’re welcome.



Schmid, BV, U Buntgen, WR Easterday, C Ginzler, L Walloe, B Bramanti, and NC Stenseth. 2015. Climate-driven introduction of the Black Death and successive plague reintroductions into Europe. PNAS.

Plague in prairie dogs

Black-tailed prairie dogs are ground squirrels that live in the North American grasslands. Prairie dogs are important parts of grassland ecosystems because (1) their burrows are habitats for other species and (2) they are important prey for a variety of predators, including the endangered black-footed ferret. Prairie dogs are highly susceptible to sylvatic plague (caused by the Yersinia pestis bacteria), which causes nearly 100% mortality in infected prairie dogs. When epidemics wipe out entire prairie dog colonies, it is bad news for predators that rely on prairie dog prey. Therefore, there has been a lot research on sylvatic plague transmission, where the hope is that one day we will be able to fully understand and control prairie dog plague epidemics. I think this research tells a really cool story about the role of vectors and alternative hosts in parasite transmission, so I’m going to blog about some of that work today.


For a long time, plague transmission to prairie dogs was assumed to occur primarily through “blocked” fleas. Fleas infected by the Y. pestis bacteria develop a blockage in their digestive system that prevents them from feeding. Afterwards, when they’re trying and failing to feed on their hosts, they repeatedly attempt to regurgitate the blockage, and this injects the Y. pestis bacteria into the host. (Mmm.) But there’s a problem with this story: the fleas that live on prairie dogs (Oropsylla hirsuta) only occasionally become blocked, and it takes a long time for this blockage to occur. Therefore, it didn’t seem like fully blocked fleas could be responsible for the very rapid epidemics and die offs that often occur in prairie dog populations (Webb et al. 2006).

The Y. pestis bacteria might also be transmitted by other routes. For instance, direct contact with infectious droplets (i.e., airborne transmission), consumption of infectious tissue/cadavers, and bites from unblocked fleas might transmit Y. pestis to susceptible prairie dogs. To evaluate the plausibility of those possibilities, Webb et al. (2006) did a really cool modeling study. They found that transmission from blocked fleas and airborne transmission couldn’t be the sole cause of epidemics in prairie dogs, unless the rates of transmission were increased several orders of magnitude above the rates that people have observed in the field. Instead, Webb et al. (2006) suggested that some kind of short term reservoir must be playing a role in transmission – such as unblocked fleas, consumption of infectious cadavers, or alternative rodent hosts (e.g., grasshopper mice).

Shortly after, Eisen et al. (2006) found that transmission of Y. pestis from unblocked Oropsylla hirsuta is possible. In fact, transmission by unblocked fleas can occur very soon after infection – resulting in faster transmission – and infected fleas survive for a long time when unblocked, allowing them to continue to transmit the bacteria for longer than blocked fleas. Neat!

But what about the role of alternative rodent hosts in transmission of plague to prairie dogs? One long-standing hypothesis is that less susceptible rodent species maintain the Y. pestis bacteria enzootically (=without big epidemics) all the time, and then epidemics occur in prairie dog populations when the Y. pestis spills over from the reservoir host into prairie dog populations.  For instance, Jones and Britten (2010) found that when prairie dogs populations are genetically structured among regions, their fleas did not have genetically distinct populations, which suggests that other rodent species might disperse fleas (and Y. pestis) among prairie dog colonies. (See last week’s post for more examples where people used host and parasite population genetic structure to infer intra and interspecific transmission rates.)

But that only explains how alternative reservoir hosts, such as grasshopper mice, play a role in causing the start of prairie dog epidemics. Do grasshopper mice play any role in transmission among prairie dogs during plague epidemics?  Stapp et al. (2009) found that the number of prairie dog fleas increases on grasshopper mice during plague epidemics, probably because the fleas are forced to find new hosts when their prairie dog hosts die. Therefore, grasshopper mice can be short term hosts for infected prairie dog fleas. Additionally, grasshopper mice frequently go into prairie dog burrows, and their ranges can include burrows from 12-23 different prairie dog coteries, which are distinct social units that prairie dogs interact within (Kraft and Stapp 2013). Therefore, while the plague might remain enzootic in prairie dog colonies with very few or no grasshopper mice because the plague would rarely have opportunities to spread among coteries, grasshopper mice can greatly increase the rate of transmission in prairie dog colonies by spreading fleas and Y.pestis into multiple coteries (Kraft and Stapp 2013, Salkeld et al. 2010).

So, we have a bacteria that is vectored by fleas and alternative rodent hosts that can spread the fleas within and among prairie dog populations, thereby causing and exacerbating plague epidemics in prairie dogs. How do we control a pathogen like this? Two methods are currently being used. The first is treating the entrances to prairie dog burrows with insecticides in order to kill off the flea vectors. The second is a vaccine that provides prairie dogs with immunity to Y. pestis. However, dusting burrow entrances and catching and vaccinating individual animals takes a lot of time and money. Fortunately, people are working on an oral vaccine that can be put out in bait, like the oral vaccine for fox rabies that is air-dropped in bait by planes. The oral vaccine for prairie dogs will hopefully be more effective and cheaper than existing control strategies.


Eisen, R.J., Bearden, S.W., Wilder, A.P., Montenieri, J.A., Antolin, M.F. & Gage, K.L. (2006). Early-phase transmission of Yersinia pestis by unblocked fleas as a mechanism explaining rapidly spreading plague epizootics. PNAS 103:15380–15385.

Jones, P.H., and H.B. Britten. 2010. The absence of concordant population genetic structure in the black-tailed prairie dog and the flea, Oropsylla hirsuta, with implications for the spread of Yersinia pestis. Molecular Ecology 19: 2038–2049.

Kraft, J.P., and P. Stapp. 2013. Movements and burrow use by northern grasshopper mice as a possible mechanism of plague spread in prairie dog colonies. Journal of Mammalogy 94(5):1087–1093.

Salkeld, D.J., M. Salathe, P. Strapp, and J.H. Jones. 2010. Plague outbreaks in prairie dog populations explained by percolation thresholds of alternate host abundance. PNAS 107(32): 14247-14250.

Stapp, P., D.J. Salkeld, H.A. Franklin, J.P. Kraft, D.W. Tripp, M.F. Antolin, and K.L. Gage. 2009. Evidence for the involvement of an alternate rodent host in the dynamics of introduced plague in prairie dogs. Journal of Animal Ecology 78(4): 807-817.

Webb, C.T., C.P. Brooks, K.L. Gage, and M.F. Antolin. 2006. Classic flea-borne transmission does not drive plague epizootics in prairie dogs. PNAS 103(16): 6236-6241.

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.)


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.

Cheaters in Mutualisms

Ants are involved in an astounding diversity of symbiotic relationships: they pollinate flowers, they disperse seeds, they farm fungi, they defend trees and insects from natural enemies, etc. Those are some very diverse services! But of course, even when the ants are dutifully performing those services, the ants don’t necessarily benefit their partners. For instance, ants may also sterilize their host plants or eat some of the aphids that they are tending for honeydew. Furthermore, the net outcome for the ants’ partners may be context specific, where the costs and benefits of interacting with ants vary with ecological and environmental conditions. For instance, if you’re an Acacia tree, having ants around to protect you from elephants may be very beneficial, but only if you live in an area that actually has elephants.

Here’s a different question: do ants always benefit from their relationships with their partners? Ants appear to be the decision makers in many of these relationships, where trees and aphids and scale insects and fungi seem less capable of making active decisions to participate (or not) in the relationship. But it turns out that ant partners aren’t as passive as they seem, because they can often use “rewards” and/or “sanctions” to control ants. For example, trees can ‘decide’ how many domatia to produce or whether to produce extrafloral nectar, which in turn determines whether ants will be attracted to the tree. (For an example of a cool sanction, check out this system, where hosts eat their symbionts when the symbionts aren’t beneficial!)

Ants can also experience negative effects of symbiotic interactions when they are tricked by mimic species or individuals called “cheaters.” In fact, there are many neat insect species that trick ants. I really want to go crazy and devote a six page blog post to all of my favorite ones, but here are just two:

1) The lacewing larva that wears aphids: Yes, for real. Lacewing larvae eat aphids, but that can be hard to do when the aphids are protected by ants. So, these lacewing larvae have evolved to wear aphid carcasses (or the cottony-fluff that aphids create) like the proverbial sheep suit worn by the wolf. The ant defenders can’t detect the difference between the aphids and the lacewings in aphid clothing, so the lacewings get to sneak onto the aphid farm to feast without being chased off.

2) Aphids that aggressively mimic ants: A single species of aphid can often have several distinct phenotypes. For instance, there are phenotypes with wings that disperse across relatively long distances and wingless phenotypes that don’t disperse very far. In some aphid species, there are phenotypes that reproduce, and other soldier phenotypes that never reproduce and protect the colony from natural enemies. Finally, in the species Paracletus cimiciformis, there is a green, pot-bellied aphid phenotype that has a typical symbiotic relationship with ants, where the ants protect and clean the root-dwelling aphids in return for honeydew. There is also a second phenotype that is flatter and yellow-ish, with hydrocarbons in the cuticle that are similar to the hydrocarbons in ant larvae (Salazar et al. 2015). When adult ants find aphids with the flat phenotype, the ants carry the aphids back to the ant nest, and plop the aphids onto the piles of ant larvae. From there, the aphids feed on the hemolymph of the ant larvae using their piercing/sucking mouthparts! So, the aphids get to hang out in the protective environment provided by the ant nest while sucking on baby ant juices, and they don’t have to do anything in return. Awesome.



Salazar, A., B. Furstenaub, C. Quero, N. Perez-Hidalgo, P. Carazo, E. Font, D. Mantinez-Torres. 2015. Aggressive mimicry coexists with mutualism in an aphid. PNAS 112(4): 1101-1106.

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!



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