What percent of species extinctions are caused by parasites?

Next week, I’m going to talk about parasite-driven species extinctions. But first I thought it’d be fun to take a little poll. In our current mass extinction, what percentage of species extinctions do you think have been caused (i.e., extinct species) or nearly-caused (i.e., endangered species) by parasites, pathogens, or viruses? Round your answer to the nearest 10%.

This would be a good disease ecology prelims question.

White nose syndrome: control and prevention

I have been listening to a lot of webinars lately. Last week I posted about Ecohealth’s Zika virus webinar, and this week I want to talk about a White Nose Syndrome webinar that was hosted by the U.S. Forest Service and the Association of Fish and Wildlife Agencies. [I’ve already introduced the fungus (Pseudogymnoascus destructans, or Pd for short) that causes white nose syndrome in several North American bat species in some previous posts; you might want to read those before reading this.] The speakers were Drs. Sybill Amelon, Christopher Cornelison, Dan Linder, and SarahHooper. Note that this post is not organized in the way that the webinar was.

Government agencies have two major goals when it comes it to WNS: (1) help affected bat populations to recover, and (2) protect bat populations that have not yet been affected by WNS.

How can we help affected bat populations to recover?

Eliminating the causative agent of a population decline is an important first step in helping a species to recover – in this case, Pd is the causative agent. Therefore, many people are working on many different possible ways to reduce the prevalence of Pd-infection in affected colonies or to reduce Pd-infection intensities in infected bats. The goal here is to have an integrated disease management system, where many complimentary methods are used in tandem. These methods fall into two categories: those that directly tackle the pathogen, and those that try to make the environment less suitable for Pd (or more suitable for bat survival). Promising methods include the potential application of probiotic bacteria that produce anti-Pd volatile compounds to bats or the environment, using gene silencing to control Pd, and using UV light to kill the very UV-sensitive Pd spores.

When bats are infected with Pd, they have abnormal hibernation behaviors, including rousing from torpor more frequently than uninfected bats. Arousal from torpor burns fat reserves, and this ends up being the main cause of mortality in Pd-infected bats – they run out of fat stores before the end of the winter. So, to help bat populations recover in areas affected by WNS, we should avoid disturbing hibernating bats. We should also work to conserve important bat foraging habitats, so that bats can get big and fat before they start hibernating in the fall.

How can we protect bat populations that have not yet been infected by WNS?

As I posted about a few weeks ago, we’ve recently had some very bad WNS news: Pd reached the West Coast already, and way before we expected it to. Hopefully that’s some kind of crazy fluke and WNS hasn’t established on the West Coast. Regardless, we can play a big role in protecting WNS-free populations by delaying the spread of Pd to those colonies and practicing good early detection and eradication procedures when Pd turns up in new areas, whether we talking about the East or West Coasts. Scientists and cavers play particularly important roles here. We can’t really prevent infected bats from visiting uninfected hibernacula, but we can use good decontamination procedures to ensure that humans aren’t tracking Pd spores from uninfected to infected caves.

One big, looming question:

On the West Coast, bats don’t tend to huddle together in huge hibernacula during the winter, like they do on the East Coast. This complicates monitoring for WNS on the West Coast immensely, because it’s hard to find a lot of hibernating bats to check on them. It’s also unclear how the different hibernation strategies used by West Coast bats will affect the spread of Pd. There’s a lot of important data that needs to be collected here – and fast.

Zika virus: prevention and control

On 4 May, The International Association of Ecology and Health (IAEH) and Ecohealth Alliance hosted a Zika virus webinar. The speakers were Dr. Felipe Naveca, Deputy Director of research at FIOCRUZ ILMD Amazon institute in Manaus, and Dr. Jay Varma, Deputy Director of Infectious Disease at the New York City Department of Health. You should be able to get the recorded webinar from the Ecohealth website, if you’re interested, but I wanted to post a quick summary for you here.

What is Zika virus?

Zika virus is an arbovirus (arthropod borne virus) named after the Zika Forest where the virus was first documented. Zika virus isn’t new globally – it was first documented in 1947 – but it recently reached the Americas, where it has quickly spread. In Brazil, where other arboviruses are also highly prevalent, the incidence of Zika virus falls between that of Chikungunya and Dengue. Zika virus is particularly concerning because infected pregnant women are more likely to have spontaneous abortions and infants carried full term have a high risk of microcephaly.

How is Zika virus transmitted?

Zika virus is predominantly transmitted among humans by Aedes mosquitoes. However, it can also be sexually transmitted from an infected man to his sexual partners. (I don’t know if it can go the other direction.) Blood transfusions from infected individuals also lead to transmission.

How can individuals and governments control the spread of Zika virus?  

In countries/states/provinces that do not yet have a Zika epidemic, the best form of control is prevention and monitoring. The CDC recommends avoiding travel to regions with Zika virus and practicing strict mosquito avoidance (e.g., long sleeves, repellent) if you must travel to those areas. That’s especially important if you’re pregnant. Men traveling to Zika-infected areas should use condoms for months after returning to avoid transmitting Zika to their partners. Also, anyone traveling to infected areas should avoid denoting blood and avoid being bitten by mosquitoes after returning home. Infection can be asymptomatic (you don’t know you’re infected), so these precautions should be taken even if you don’t think you’re sick.

There is no vaccine for Zika virus, so the best ways to control the spread in epidemic areas are safe sex, mosquito avoidance, and vector control. There are many methods for vector control, and using a collection of methods will likely be more effective in the long run than using a single method (=a strong unidirectional selection pressure). Promising and effective methods include eliminating standing water where mosquitoes can breed, infecting mosquitoes with Wolbachia, selectively applying pesticides to reduce mosquito populations, and using female mosquitoes to spread pyriproxyfen among oviposition sites.

Could Zika virus establish in the Northeastern US?

At this point, it’s unclear. The CDC updated its potential distribution map for Aedes aegypti in the US to include regions much further north than the previous estimated distribution, but there aren’t necessarily any Aedes aegypti mosquitoes in those areas. There are other Aedes spp. mosquitoes in the Northeastern US, but at this point we don’t know if they would be competent Zika virus vectors or not. There’s also some question as to whether Culex mosquitoes can serve as vectors.

Does Zika virus infect any animals besides humans and mosquitoes?

Yes, Zika virus has been found in monkeys. But we still have very little information regarding zoonotic reservoirs for Zika virus.

Social spiders and hilarious field equipment

Before I even explain the topic of today’s post, I have to tell you that the papers that I’m blogging about today use the best and most hilarious piece of field equipment that I have ever seen. Project budgets may never be the same. I may even need to change study systems. Read on, if you dare.

The literature on parasites and animal personalities is ever-growing, perhaps because personalities have palpable consequences for transmission dynamics: the likelihood of direct transmission between infected and susceptible hosts often depends on host behavioral tendencies and their impacts on social interactions. I’ve blogged about this in the past: aggressive Tasmanian devils are more likely to transmit facial tumor disease to non-aggressive conspecifics and house finches that dominate the use of artificial feeders are more likely to acquire and transmit conjunctivitis. Similarly, in a world (er, Africa) where spiders live together in a shared web and cooperatively capture and share prey, bold spiders are more likely to transmit cuticular bacteria to shy spiders than shy spiders are to bold spiders (Keiser et al. 2016a). And what’s more, spider social networks are behaviorally disassortative, where bold spiders were more likely to rest in contact with shy spiders than they are with their own personality types. Thus, it appears that this system might be poised for rapid transmission of microbes, depending on the personality composition of the susceptible spiders in the colony.

These South African social spiders (Stegodyphus dumicola) live in colonies of a few dozen to over a thousand individuals. The ability to capture a large amount of large prey items is key to a colonies’ success, and colonies attack faster when they contain a mixture of bold and shy personality types in the group (Keiser et al. 2014). Furthermore, the execution of this important collective behavior is often based on the behaviors of one or a few important “keystone individuals” or leader spiders (Pruitt & Keiser 2014). These keystone individuals are so important in this system – and probably in many other systems, too – that we have to wonder: what happens when the keystone individuals take a sick day or even die from infection?

It turns out that increased bacterial load on colonies’ keystone individuals can impair the collective behavior of their entire society (Keiser et al. 2016b). Specifically, groups whose keystone individual are exposed to bacteria attack prey stimuli more slowly, and fewer individuals participate in the attack. Interestingly, the keystone’s participation in the task is not altered, suggesting that increased bacterial load alters the way keystones influence their colony-mates’ behavior.

Perhaps you find yourself wondering how, exactly, one might measure a spider group’s response to prey stimuli. Do you sit around and wait all night for some prey to get caught in the web? Boring. Do you try to throw a moth into the web and watch what happens? Rude. No, what you do is you attach a “hand-held vibrator” (Model: Flamenco Purple no. 4, Golden Triangle; do not Google if you’re at work) to a wire and then attach a piece of paper to the other end of that wire, and you use that vibrating piece of paper as your simulated prey. This is brilliant, and I HAVE SO MANY QUESTIONS. Why that model? How awkward is international travel for field work? I must know!


Anyways, social spiders are awesome, their personalities influence pathogen transmission, and their pathogens influence the role that individuals’ personalities play in colony behavior. Cool stuff!


Keiser, C.N., Jones, D.K., Modlmeier, A.P. & Pruitt, J.N. (2014) Exploring the effects of individual traits and within-colony variation on task differentiation and collective behavior in a desert social spider. Behavioral Ecology and Sociobiology, 68, 839-850.

Keiser, C.N., Pinter-Wollman, N., Agustine, D.A., Ziemba, M.J., LingranHao, J.G.L., and Pruitt, J.N. (2016a). Individual differences in boldness influence patterns of social interactions and the transmission of cuticular bacteria among group-mates. Proceedings of the Royal Society B, 283, 20160457.

Keiser, C.N., Wright, C.M. & Pruitt, J.N. (2016b) Increased bacterial load can reduce or negate the effects of keystone individuals on group collective behaviour. Animal Behaviour, 114, 211-218.

Pruitt, J.N. & Keiser, C.N. (2014) The personality types of key catalytic individuals shape colonies’ collective behaviour and success. Animal Behaviour, 93, 87-95.

Slugs ruin everything

Mutualisms are important; we’re sure about that. Here’s something we don’t know as much about: are mutualisms resilient? As species go extinct or species appear in new places, as nutrient cycles change, and/or as the global climate changes, will the mutualisms that ecological systems rely on keep functioning?

Errbody knows that I like ant-plant mutualisms, including seed dispersal mutualisms where ants take seeds with juicy eliaosomes back to their nests, eat off the eliaosomes, and then dump the seeds. I also loooove snails and their close relatives: SLUGS. Today, we shall combine them, and see what happens to ant-plant dispersal mutualisms when invasive slugs get thrown into the mix. Below is the short version, and you can read all of the details in Meadley Dunphy et al. (2016).

Slugs eat elaiosomes, just like ants. But unlike ants, slugs eat the elaiosomes without moving the seeds, so the seeds aren’t dispersed. Furthermore, when slugs eat the elaiosomes off seeds, ants won’t disperse the seeds anymore, so the mutualism is disrupted. Moral of this story: Slugs. Ruin. Everything.



Meadley Dunphy, S.A., K.M. Prior, and M.E. Frederickson. 2016. An invasive slug exploits an ant‑seed dispersal mutualism. Oecologia 181:149–159.

Food provisioning and wildlife disease dynamics

Humans change environments in many different ways, including accidentally or purposefully provisioning wildlife with novel food resources. For example, bird feeders, salt licks, ecotourism feeding stations, and dumpsters all provide concentrated food resources for wildlife. Does this food provisioning influence disease dynamics?

First, let’s consider how food provisioning might influence disease dynamics for parasites with any given transmission mode. The big rates that we care about here are the transmission rate (a function of contact rate and transmission success), birth and death rates, and immigration and emigration rates. If resource provisioning increases host population density via increased aggregation of individuals, increased birth rates or decreased death rates, and/or increased immigration or decreased emigration rates, then transmission rates for pathogens with direct contact density-dependent transmission should increase. In the same scenarios, pathogens with frequency-dependent transmission may not be affected by provisioning, or transmission rates may even decline if high birth rates dilute the prevalence of infection in the population. For pathogens that are transmitted via environmental stages, environmental stages may build up at resource provisioning sites when high densities of animals hang out there for long periods, increasing transmission. For pathogens that are transmitted via intermediate hosts, transmission may be reduced if hosts switch from foraging on intermediate hosts to foraging on human-provided resources.

Factors besides transmission mode might also be important. For instance, regardless of transmission mode, if resource provisioning increases host resistance – for instance, by increasing body condition – then transmission rates should decrease. Conversely, if resource provisioning decreases host resistance – for instance, if the provisioned food is nutritionally poor or there is high competition at sites with provisioning and body condition is reduced – then transmission rates should increase. Resource provisioning might also alter host tolerance to infection, so that hosts aren’t as sick but continue shedding infectious agents longer than they would if they didn’t have supplemental resources.

Ok, I think that covers most of the possibilities. Back to our question: does food provisioning influence disease dynamics? Yes, sometimes. Most of the mechanisms listed above were supported by at least one study in a recent review by Becker et al. (2015). Based on the long, messy list above, you can probably guess that sometimes food provisioning increases transmission, sometimes it decreases transmission, and sometimes nothing notable happens. The big take-home message is that there isn’t just one universal outcome when we provision wildlife with supplemental resources, and it’s important that we conduct more and better studies aimed at elucidating the epidemiological mechanisms underlying the observed relationships. Cool stuff!

Have you read this post about house finch conjunctivitis yet?



Becker, D.J., D.G. Streicker, and S. Altizer. 2015. Linking anthropogenic resources to wildlife–pathogen dynamics: a review and meta-analysis. Ecology Letters 18: 483–495.

My new favorite symbiosis: boxer crabs!

I can’t believe that I only just learned about the glorious symbiosis between boxer crabs and anemones. The crabs hold one tiny anemone in each claw, and they use the anemones to defend themselves from predators. The anemones benefit from increased access to food because they’re constantly being waved about.



And look at these dance moves!

That tiny cheerleader’s got game.

I’m in love.