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.

How fast can pathogen epidemics spread?

Everyone dreads the idea of a pathogen that can rapidly spread across vast distances, especially if that pathogen causes high host mortality or morbidity. For today, I’m going to ignore host mortality/morbidity part, and just focus on the first part: how fast can pathogens spread across space, and what affects their rate of spread?

To start answering this question, we need to dig backwards in the literature more than a decade to an Ecology Letters paper by McCallum et al. (2003). They searched the literature for estimates of the rate of pathogen spread across space in marine or terrestrial systems, while excluding any pathogens whose spread was mostly facilitated by human activities. The pathogen with the fastest rate of spread was a herpes virus that infected pilchards (fish) in Austrailia. The virus spread at rates of up to 11,000 km per year!!

In general, pathogens in marine environments tended to spread faster than pathogens in terrestrial environments. Pathogens might spread more quickly in marine environments because marine habitats tend to be more connected (or more “open”), with higher dispersal rates among patches than in terrestrial environments. However, there was a lot of variation in the rates of pathogen spread in both environments, where some terrestrial pathogens spread rapidly and some marine pathogens spread very slowly. Some of that variation can be explained by host mobility: pathogens that infect sessile (or at least very slow) host species spread more slowly than pathogens that infect highly mobile host species. Neat!

I want to see this analysis done again with the data that have accumulated since 2003. Someone get on that!



McCallum,H., D. Harvell, and A. Dobson. 2003. Rates of spread of marine pathogens. Ecology Letters 6(12): 1062-1067.

Will Tasmanian devils soon go extinct?

Last week, we talked about Tasmanian devil facial tumor disease, which is caused by an infectious cancer that is transmitted after a susceptible devil bites a tumor on an infected devil. After becoming infected, devils almost always die within several months. As the disease has spread through their range, devil populations have drastically declined, and there is great concern that the devils will go extinct in the near future. But not all infectious diseases that cause high host mortality will lead to host extinction, so what is special about Tasmanian devil facial tumor disease?

A while ago, I posted about the difference between pathogens with density dependent and frequency dependent transmission dynamics. To recap: when transmission is density dependent, the rate of host contacts (and thus pathogen transmission) increases with host density. When transmission is frequency dependent, the rate of host contacts (and thus pathogen transmission) does not change with host density. This means that as a host population crashes due to high mortality from an infectious disease, the transmission rates of pathogens with density dependent transmission will decline, but the transmission rates of pathogens with frequency dependent transmission will not change. Therefore, it isn’t possible for pathogens with density dependent transmission to be the cause of host extinction, because the pathogen will go extinct due to low transmission rates before the host goes extinct. (Note, however, that pathogens with density dependent transmission might cause declines in a host population that make the host population more susceptible to local extinctions due to stochastic events, like bad breeding years.)

Historically, only sexually transmitted pathogens and vector transmitted pathogens were thought to have frequency dependent transmission. And we know that Tasmanian devil facial tumor disease is not sexually transmitted or vector transmitted. However, McCallum et al. (2009) found that models with frequency dependent transmission fit mark-recapture data for devil disease dynamics better than models with density dependent transmission. How can that be? Well, it might that the number of aggressive encounters between individuals is not dependent on host density; for instance, if confrontations at carcasses continue to be likely to occur even as populations decline.

When pathogens utilize frequency dependent transmission, we know that unselective culling to reduce the number/density of susceptible hosts won’t stop a pathogen from invading a naïve host population. That’s because no matter how many individuals you cull, you won’t reduce the actual pathogen transmission rate, which is independent of host density. But what if instead of unselective culling, we try to stop the spread of Tasmanian devil facial tumor disease by selectively culling infected individuals? A culling program was undertaken to try this, but it was not effective (Lachish et al. 2010). Beeton and McCallum (2011) used epidemiological models to show that while selective culling might be effective, the rate of culling that would be necessary is just too high to be logistically possible given current resources.

Tasmanian devils have been the largest extant marsupial carnivore since the thylacine went extinct. What will happen if the Tasmanian devil goes extinct? Well, there are already documented changes in the animal communities in Tasmania that might be caused by devil declines, where the abundances of some species (e.g., feral cats) have increased and the abundances of other species (e.g., eastern quoll – so cute!) have decreased (Hollings et al. 2014). But the long term changes that will result from devil population declines (or full extinction) are hard to predict.

It’s a rough time to be a marsupial.


Beeton, N. and H. McCallum. 2011. Models predict that culling is not a feasible strategy to prevent extinction of Tasmanian devils from facial tumour disease. Journal of Applied Ecology, 48: 1315–1323.

Hollings, T., M. Jones, N. Mooney, and H. McCallum. 2014. Trophic cascades following the disease-induced decline of an apex predator, the Tasmanian devil. Conservation Biology 28(1): 63-75.

Lachish, S., H. McCallum, D. Mann, C.E. Pukk, and M.E. Jones. 2010. Evaluation of selective culling of infected individuals to control tasmanian devil facial tumor disease. Conservation Biology 24(3): 841-851.

McCallum, H., M. Jones, C. Hawkins, R. Hamede, S. Lachish, D. Sinn, N. Beeton, and B. Lazenby. 2009. Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction. Ecology 90(12): 3379–3392.

The evolution of virulence and ‘virulence management’

By definition, parasites/pathogens harm their hosts.  The degree to which parasites harm their hosts is called virulence.  The more virulent the parasite, the more it damages the host.  From an ecological perspective, we measure virulence in terms of reduced host survival and/or reproduction.

Why are some parasites/pathogens more virulent than others?  When should parasites evolve to be very virulent, and when should they evolve to be more benign?

Ewald (1993 and elsewhere) argued that a parasite’s virulence evolution should be related to the transmission mode of the parasite.  For instance, consider three types of transmission: direct transmission where the parasite cannot survive for long in the environment (e.g., the common cold – rhinovirus), direct transmission where the parasite can survive for a long time in the environment (e.g., smallpox), and vector transmission (e.g., malaria).  Virulence should be maladaptive if it hampers transmission – as in case 1.  If you’re so sick with a cold that you cannot leave your house, the virus is less likely to infect new hosts.  Virulence should be high whenever it increases transmission – as in 2 and 3.  If the virus can survive for a long time in the environment, why not go crazy replicating in the host (to the demise of the host) and then hang out in the environment until another host comes around?  And if the virus is vector-transmitted, why not replicate to a high density (to the detriment of the host) to insure that the vector gets a good dose of parasite with a blood meal?  Also, making the host lethargic might increase the likelihood that a vector gets a blood meal.

Ewald (1993) also suggested that by understanding how transmission can affect virulence evolution, medical scientists might be able to manipulate the evolution of virulence in important parasites/pathogens.  By reducing the probability of transmission, we could increase the cost of virulence (assuming that there is a trade-off between virulence and transmission).  Parasites should be more prudent when the probability of transmission is low.

Ewald (1993) gives several examples of pathogens that have evolved to become less virulent when the probability of transmission was reduced, but let’s just talk about HIV.  HIV is the sexually-transmitted retrovirus that causes AIDS.  HIV hangs out in white blood cells and can remain latent (=inactive) for long periods within the host, but the virus can also rapidly reproduce.  The longer the latent period, the less virulent the virus is, and the faster the reproduction rate, the more virulent the virus is.

How could we increase the probability of transmission of HIV?  If a human population were to change culturally from a monogamous, family-oriented culture to a more polygamous one, the rate of partner change and thus HIV transmission would increase.  Correspondingly, Ewald (1993) discussed some evidence that HIV can be more virulent in urban areas with many unmarried individuals than in rural areas that are more family-oriented.  (Of course, this is just one of many factors that affect the probability of HIV transmission, so please don’t go crazy on the cultural interpretations.)

How could we decrease the probability of transmission of HIV?  Condoms and safe sex education!  Ewald (1993) presented some evidence that the use of the drug AZT to treat HIV couldn’t completely explain the evolution of lower HIV virulence in homosexual males in urban areas in the 1980’s.  Increased use of safe sex practices might explain some of that decreased virulence.

Ewald (1993) is a bit old – there’s some great evidence for/against this idea of ‘virulence management’ in the literature now.  But the Ewald (1993) paper is a good read and a ‘popular’ article, so check it out!


Ewald, P.W. 1993. Evolution of virulence.  Scientific American.

Related 2001 interview with Dr. Ewald from PBS.