Lady Beetles and Parasites as “Weapons”

Everyone knows that lady beetles are awesome.  But if you have somehow missed out on the lady beetle fan club until now, here’s your chance to get in on the lady beetle love.  Asian lady beetles use “biological weapons” – parasite weapons [Relevant]  This is awesome enough that it made it into the May issue of Science.  The story goes like this:

Asian lady beetles, aka Harlequin lady beetles, are the ones that you see all the time.  They’re not native; we introduced them to control our agricultural pests.  The problem is that the Asian lady beetle then turned into a pest, mostly because the arrival of this species caused declines in populations of native species of lady beetle.  That’s sad, because there are some really, really cool lady beetles out there, and we don’t want them to go away.

What is it about these Asian lady beetles that causes the declines in the native species?  One reason is that ALBs have symbiotic fungi.  These are actually microspordian parasites, but it turns out that ALBs aren’t affected by the parasites (probably because ALBs have tons of antimicrobial peptides).  However, the parasites are quite deadly to other, native lady beetle species.     

If science doesn’t work out, I think I’ve got a career in lady beetle art?

How do the ALBs use their killer fungi on native species?  BAZOOKAS.  Ok, not really.  It turns out that these fungi end up in the ALB eggs, and it just so happens that lady beetles tend to eat the eggs of competing species.  So, a native lady beetle comes along, tries to wipe out some future ALB babies while simultaneously having an afternoon snack, and ends up getting infected by the fungus.  Awe-some.  Well, ok, not awesome, but you gotta hand it to the ALBs and their parasites.

Should we try taking antimicrobial peptides from ALBs and injecting them into native lady beetle species?  


Vilcinskas, A., K. Stoecker, H. Schmidtberg, C. Rohrich, and H. Vogel. 2013. Invasive Harlequin ladybird carries biological weapons against native predators. Science 340(6134): 862-863.

Zombie Ants

Instead of talking about a specific paper today, I’m going to talk about ZOMBIE ANTS <cue horror music>.  Parts of this will count as self-plagiarism, because I’ve blogged about this in other places.  Let the post cannibalism begin!

I attended the annual meeting of the American Society of Parasitologists last summer, and it was awesome.  David Hughes gave a really awesome talk called “Zombie Ants: The Precise Manipulation of Social Insect Behavior by a Fungal Parasite.”  I’m sure you’re totally hooked already, but just in case you’re not seeing how cool this is, let me reel you in with some photos.  (These aren’t ants, but you’ll see those later.)

Photo from here.

Photo from here.   For more cool fungus pics, just google “Cordyceps fungus.”

Parasites often manipulate their host’s behavior in order to increase the probability that they (the parasites) will be successfully transmitted to their next host.  In the case of the parasitic fungus of these ants, the fungus wants the ant to go hang out somewhere that will result in the fungus being able to rain spores down on other ants.  It does this by making the ants climb up to a leaf above an area of a high ant traffic (areas that Hughes calls “killing fields”). The ant is then “forced” to bite down on the main vein of that leaf, and then its mandibles get stuck that way, so that the ant is attached to the underside of the leaf forever.  Then the fungus sprouts out of the ant’s head and does its whole raining spores of death thing.

Since David Attenborough explains things better than I do, I’m going to link you to David Hughes’ website, where he has more info and some sexy videos (including Attenborough).

As a final note, Hughes is looking into using this parasitic fungus as a form of biocontrol for pest ants, like on farms.  In other words, YOU TOO could have your very own ZOMBIE ANTS.

How do you feel about using parasites as biocontrols?  That’s a huge can of worms, I know, but I’d like to hear your opinions.

Foraging Competition Reduces Disease Transmission

I just read a neat 2013 Ecology Letters paper.  Here’s the question:  how does host density affect disease transmission? 

Civitello et al. (2013) studied a simple aquatic disease system.  Daphnia dentifera consume fungal spores (Metschnikowia bicuspidate) as they forage on algae, the fungus reproduces in the Daphnia host, and when the host dies, more spores are released into the environment. 

Daphnia infected with fungal spores. Credit.

Typically, we might predict that as the density of Daphnia increases, we might see increased disease transmission.  There are more hosts eating more spores and thus more spores are being produced, so an increase in transmission seems to make sense.  However, Civitello et al. (2013) proposed two ways that increased host density might decrease transmission.  First, increasing the number of foraging Daphnia should increase the number of spores being taken out of the environment.  So, perhaps higher Daphnia densities actually deplete spore densities, making susceptible hosts less likely to consume spores.  Second, Daphnia are known for their intraspecific interference competition.  The more Daphnia you have, the lower their foraging rates, and perhaps the lower the encounter rates between susceptible hosts and spores.

To figure out how Daphnia density affects fungus transmission, Civitello et al. (2012) did four things.  First, they built submodels of disease transmission that just looked at Daphnia’s consumption of spores.  Then they did an experiment where they varied Daphnia and spore densities.  They used that infection and spore consumption data to parameterize their submodels, and to see which submodel performed the best.  Next, they stuck their submodels into a full epidemiological model of the system and determined how Ro and infection prevalence changed with host density.  Finally, they compared the results of the overall model (with each submodel) to field data.

Here’s what they found.  In the experiment, transmission increased with spore density, but decreased with host density.  The submodels that included interference competition among the Daphnia best described those results.  When they put that submodel into the full epidemiological model, they found something surprising:  the model predicted that infection prevalence and Ro should have unimodal relationships with host density.  Guess what?  That’s exactly what they saw in the field!  Infection doesn’t occur until you have some minimum density, it increases to some optimum, and then declines until the prevalence is 0 at host densities where interference competition reduces foraging on spores below levels that can maintain the parasite population.  NEAT! 

Do you remember my recent posts about how the vital rates of malaria and mosquitoes (and Ro) have unimodal relationships with temperature?  Now here’s a paper saying that Ro has a unimodal relationship with host density, instead of a positive, linear relationship.  Are you sensing a trend?  It looks like transmission rates don’t just increase linearly to infinity. 

Here’s my favorite line of the paper:  “The linear interference model statistically crushed the standard and phenomenological alternatives.”  I hope to be cool enough someday to say that my hypothesis CRUSHED the status quo.  I’ve added that goal to my bucket list.

What do you think?  Were you surprised that competition can regulate parasite transmission?


Civitello, D.J., S. Pearsall, M.A. Duffy, and S.R. Hall.  2013.  Parasite consumption and host interference can inhibit disease spread in dense populations.  Ecology Letters.