What is a vector?

Precise definitions are important in science, because I said so (and other better reasons). In parasite ecology, the tricky definitions that students often mix up are things like parasite versus parasitoid and microparasite versus macroparasite. In fact, at least 20 visitors per week happen upon this blog because they want look up one of those terms.

But it isn’t just students and the general public who struggle with tricky definitions in parasite ecology. Within the field, we can’t even agree on what to call our discipline! (Disease ecology? Parasitology? Epidemiology?) And it has recently come to my attention that a term that I thought had bullet-proof definition is somewhat controversial among parasite ecologists.

In an awesome special issue of the Philosophical Transactions of the Royal Society B that just came out this month, there was a thought-provoking article entitled, “What is a vector?” The idea for the article came from a working group of the British Ecological Society’s ‘Parasites & Pathogens’ Special Interest Group, where participants unexpectedly found that they did not all use the same definition of “vector.” The article contained a whole list of possible definitions that the authors found in the literature, including this subset, which I have re-numbered for my own purposes:

Definition 1A: “Any organism (vertebrate or invertebrate) that functions as a carrier of an infectious agent between organisms of a different species.”

Definition 1B: “Any organism (vertebrate or invertebrate) or inanimate object (i.e., fomite) that functions as a carrier of an infectious agent between organisms.”

Definition 2: “Any organism that can transmit infectious diseases between humans or from animals to humans.”

Definition 3A: “Hosts that transmit a pathogen while feeding non-lethally upon the internal fluids of another host.”

Definition 3B: “Blood-feeding arthropods such as mosquitoes, ticks, sandflies, tsetse flies and biting midges that transmit a pathogen while feeding non-lethally upon the internal fluids of another host.”

I couldn’t believe that parasite ecologists differed so much with their working definitions, so I put them into a poll, and then I asked you guys to tell me which definitions you use. (Thanks for your participation!) To my great surprise, your answers were all over the place! No one really used Definition 2 (the “anthropocentric” definition), but all of the other definitions received some support. As of 21 March, the most popular definition was 1A, and 1A+B were more popular than 3A+B.

Wilson et al. (2017) do a great job of discussing the pros and cons of each definition, and they also take a stab at a possible mathematical definition (the “sequential” definition), so I’d recommend giving their paper a read for a lot more coverage than you’re going to get here. I’m just going to cover two points that were surprising to me.

First surprise: I did not expect that so many people would prefer 1B over 1A, because I don’t like including fomites in the definition of a vector. My primary reason for preferring IA is that we already have a term for inanimate objects that transmit infectious agents (i.e., fomites). Wilson et al. (2017) provide a good discussion on the utility of thinking about some fomites (e.g., drug needles) in pseudo-biological terms that would normally apply to vectors. But I think that I’d still prefer to call things like needles “fomites,” even if it’s helpful to think of their parallels with living vectors.

Second surprise: I did not expect that so many people would prefer 1A+B to 3A+B. As Wilson et al. (2017) discuss, the 1A+B definitions are broad; for instance, the wording suggests that we include intermediate hosts (i.e., snails infected by trematodes) as vectors! It also suggests that any host capable of interspecific transmission could be a vector. 

In the end,Wilson et al. (2017) suggested that parasite ecologists think carefully about their definitions of the term “vector,” and then they scored a closing home run with, “all vector definitions are wrong, but some are (we hope) useful.” WOMP WOMP.

Give the paper a read, and share your thoughts in the comments!


Wilson, A. J., E. R. Morgan, M. Booth, R. Norman, S. E. Perkins, H. C. Hauffe, N. Mideo, J. Antonovics, H. McCallum, and A. Fenton. 2017. What is a vector? Phil. Trans. R. Soc. B 372:20160085.

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




Monty Python and the Holy Grail






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?


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?


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!





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.)


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.