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Host manipulation by parasites: a spooky Halloween post

Happy Halloween! Turn on some spooky music, grab a handful of candy, and settle in for a spooky post about host manipulation by parasites! But do be careful eating; you never know when a parasite might be sneaking into your diet.

Cartoon of snails that look like Halloween candy because they have been manipulated by parasites.

What is adaptive manipulation?

If you’re a parasite enthusiast, you’ve probably heard about parasites that manipulate host behavior. But what, exactly, is host manipulation? We expect that infected hosts will often act “sick”; they might try to fight off their infections by raising their body temperature (fever) or eating medicinal plants, or they might be suffering from so much pathology from their parasites or immune responses that they lose their appetites, act lethargic, etc. But none of those sickness behaviors are adaptive manipulation. To be adaptive for the parasite, the changes to the host’s phenotype (coloration, morphology, and/or behavior) must produce a fitness benefit for the parasite, usually by increasing parasite transmission from one host to the next. Following this definition, the host’s phenotype is actually the parasite’s extended phenotype: the parasite’s genes control how the host looks or behaves.

To show that a host’s phenotype is an example of adaptive manipulation, we need to show that that the phenotype actually increases parasite transmission. This can be tricky! But here’s an example. Last week, we talked about the life cycle of Euhaplorchis californiensis, a trematode with a complex life cycle. The trematode infects killifish as the second intermediate host; specifically, it infects the hosts’ BRAINS. Infected killifish are more likely to do flashy swimming behaviors, like dashing up to the surface. This seems like an adaptive manipulation that would make infected fish more likely to get eaten by their definitive bird hosts; but how would you prove that? If you’re Kevin Lafferty, you’d put a bunch of killifish in two cages in the salt marsh, leaving one open to birds and one closed to birds. You can hear Kevin describe the experiment in this TED talk. At the end of the experiment, the cage that was open to birds had fewer infected fish than the cage closed to birds, because the infected fish with the flashy behaviors were more likely to be eaten than uninfected fish. The manipulated behavior increased transmission by increasing predation.

Most parasites that manipulate host behavior are not as well studied as Euhaplorchis californiensis. Therefore, we should be careful not to overstate adaptive benefits where they do not exist or have not been demonstrated, or to overdramatize demonstrated adaptive behaviors. For example, we often say that crickets infected with nematomorphs commit suicide by jumping into water, but not all crickets die or even lose the ability to reproduce after being infected. Furthermore, infected crickets aren’t so water-fixated that they hop in a straight line to the nearest waterbody; they’re just more likely to end up in water than uninfected crickets. It’s important to remember that many details tend to be glossed over when telling exciting and spooky stories, including those about parasites that manipulate host behavior.    

What kinds of manipulation exist?

We’ve mentioned a few examples, but how common is adaptive manipulation among parasites? We don’t know exactly how many parasites have evolved to manipulate their hosts, but we do know of a few hundred examples spread across many parasite groups (platyhelminths, acanthocephalans, nematodes, nematomorphs, arthropods, bacteria, fungi, protozoa, and even viruses). In fact, host manipulation mechanisms seem to have evolved independently many times within and between parasite groups. From this, we can conclude that adaptive manipulation is common, despite seeming so biologically bizarre.

But of course, there is spectacular variation among parasites in the ways that they manipulate their hosts. We can divide these methods into roughly five manipulation targets: predator avoidance, habitat choice, feeding or foraging, bodyguard behavior, and contact rates. I’ll explain each below.

Predator avoidance. Host manipulation seems especially common for parasites with complex life cycles that involve trophic transmission, where an intermediate host is consumed by a definitive host. In these systems, parasite transmission may be increased whenever the intermediate host becomes more conspicuous or less defended from the definitive host. Euhaplorchis californiensis is a good example of a parasite the manipulates how prey behave in the presence of predators.

Habitat choice. Sometimes parasites with complex life cycles have host species that do not share the same habitats or propagules (environmental stages) that require different habitats than the hosts, making it tricky for the parasite to make it from one host to the next. For example, larval nematomorphs infect terrestrial crickets and other arthropods, adults are free swimming in aquatic environments, and then larvae need to make it back to terrestrial environments to infect more arthropods. Nematomorphs manipulate cricket behavior to make them more likely to jump into water bodies—habitats that they would not usually choose. The story for how nematomorphs make it back to terrestrial environments might be even weirder, but the details are still being studied.

Host feeding behavior. Many parasites are consumed and/or transmitted during feeding, like those that are transmitted by blood-feeding insect vectors. If a vector only ever takes one blood meal, it cannot move parasites from one host to the next. To increase transmission opportunities, several parasites are known to affect vector feeding behavior, causing vectors to feed on more hosts and/or change their feeding behavior to increase the likelihood that a given feeding event will lead to transmission. A very different example might be trematodes that castrate their first intermediate snail hosts; snails reduce the time and energy that they spend reproducing when they are castrated, and instead spend that time eating, growing larger, and making more tissues available for the parasites to turn into more parasites. You can more read about parasitic castrators and gigantism in this blog post, including whether gigantism is truly adaptive for parasites.

Bodyguard behavior. Some parasites cause their hosts to co-opt normal behaviors or use abnormal behaviors to protect their parasites. For example, parasitoid wasp larvae cause orb weaving spiders to construct a protective web, and after eating the spider, the wasp larvae use the protective web as a safe hide out while they pupate. If you don’t go Google parasite bodyguards after reading this, you aren’t doing Halloween right.

Contact rates. Finally, although parasites with complex life cycles are usually the focus of adaptative manipulation research, parasites with direct life cycles and direct transmission might also benefit from manipulating host behavior. For example, if sexually transmitted parasites can cause their hosts to be more promiscuous, the parasites will be more likely to make it to a new host. It is unclear if there are few examples of this type of manipulation because it is understudied or because it is uncommon among directly transmitted parasites.

Now that you know what adaptive manipulation is and isn’t and what types of manipulation exist, you’re ready to go explore the many amazing examples that scientists have discovered or maybe to go discover a new example of your own! If you’re looking for good places to start, I recommend this TED talk by Ed Yong and this cartoon by The Oatmeal.


Moore, J. Parasites and the Behavior of Animals. (Oxford University Press, 2002).

Poulin, R. Chapter 5 – Parasite Manipulation of Host Behavior: An Update and Frequently Asked Questions. in Advances in the Study of Behavior (eds. Brockmann, H. J. et al.) vol. 41 151–186 (Academic Press, 2010).

Simple versus Complex Life Cycles

When you first start learning about parasite ecology—and even decades later, when you’re an expert—parasite life cycles can be confusing! Parasite life stages have a plethora of fancy names, like L3 larva and miracidium, which can be difficult to remember. Furthermore, every parasite’s trajectory from immature to adult stages seems different than the last, and we don’t even know all the life cycle details for most parasite species. So, if you’re feeling confused by parasite life cycles, you’re in good company! You might never memorize all the complex life cycles that exist, but you can understand the general ecology and evolution of complex life cycles. We’ll cover the basics in this post.

Simple versus Complex Life Cycles:

Let’s start with simple life cycles, which are sometimes called direct life cycles or one-host life cycles. Monoxenic or homoxenous parasite species with simple life cycles only use a single host species in their life. The single host species is entered by infective stages of the parasite, and then the parasite grows and develops in the host before switching to reproducing within the host.

Direct life cycle parasites include parasites with fecal-oral transmission, like Ascaris lumbricoides, a roundworm that infects humans. Adult male or female roundworms live in the small intestine, where the female releases fertilized eggs into the environment through human feces. Eggs are ingested by people when they (usually accidentally) consume fecal matter. The parasite grows and develops in a series of larval stages in multiple tissues. The larvae eventually make their way to the respiratory system, where they are then coughed up and swallowed, which allows them to find their way to the small intestine to mature. This entire life cycle uses just a single host (humans), even as the parasite goes through many developmental stages inside and outside host.

This life cycle diagram for a simple life cycle parasite, Ascaris lumbricoides, depicts the parasite moving through several life stages from egg to larvae to adult, where the eggs exist in the external environment and the other life stages occur in the human host.

Now let’s move on to complex life cycles, which are sometimes called indirect life cycles or multi-host life cycles. Parasites with complex life cycles are indirectly transmitted from one host species to the next. These heteroxenic parasites need to use multiple host species in sequence to successfully develop and reproduce. Reproduction occurs in the final host in the life cycle, which is called the definitive host. The one or more hosts where parasite growth or development occur (but no reproduction occurs) are called intermediate hosts. Sometimes a parasite will not complete any life stages within a host, and instead only use the host for transportation; those transportation hosts are called paratenic hosts. The number of hosts needed to complete a life cycle is the life cycle length, and it must be at least two hosts long.

Ready for some examples? Schistosomiasis is caused by a parasite with a two-host life cycle, which uses humans as the definitive human host and snails as the intermediate host. Euhaplorchis californiensis is an example of a parasite with a three-host life cycle, which uses birds like herons as the definitive host, snails as the first intermediate host, and killifish as the second intermediate host. Life cycle lengths appear to have an upward limit, because most life cycles require four or fewer host species. Why do you think that is?

The life cycle of Euhaplorchis californiensis, a trematode that must sequentially infect three host species to complete its life cycle. This life cycle diagram came from The Ethogram Blog.

To get from one host to the next, parasites with complex life cycles can use a few different modes of horizontal transmission. Passive transmission occurs when the parasite just waits around for the next host, like when E. californiensis eggs in heron feces wait to be consumed by a salt marsh snail. Active transmission occurs when the parasite is free-living in the environment and moves around to seek out the next host, like when E. californiensis cercariae leave their snail host and swim around looking for a killifish to infect. And finally, complex life cycles often involve trophic transmission, where the parasite is consumed along with its intermediate host by the next host in the life cycle. Trophic transmission is used by all cestodes and acanthocephalans and many nematode and trematode species. Trophic transmission is probably so common in complex life cycles because predator–prey interactions are one of the most common ways that two (host) species might interact.  

Three ways to add hosts to a life cycle

You might have noticed that we need to make an important distinction between whether a parasite uses multiple host species in sequence, in parallel, or both. For example, E. californiensis does both: it must infect birds, snails, and killifish in that order to complete its life cycle, so it uses multiple host species in sequence. But it can also use multiple host species at a given life stage; in particular, E. californiensis can successfully infect and reproduce in more than one bird species. The number of host species that a parasite can successfully use for any given life stage is quantified as host specificity. Many complex life cycle parasites have high host specificity for some parts of their life cycle (e.g., they can only infect a single snail species as a first intermediate host) and low specificity for other parts of their life cycle (e.g., they can infect many bird species as definitive hosts).

This brings up an important question: how do host species get “added” to a parasite’s life cycle? We assume that parasite species start by infecting just one host species and then complex life cycles evolve from those simple life cycles. There are two ways that a host species is thought to be added in sequence, thereby increasing the life cycle length: upward incorporation and downward incorporation.

In upward incorporation, a new definitive host that is a predator of the original definitive host is added to the life cycle. Parasites that can infect the new predator without being digested are selected for because they have avoided a source of mortality. They also likely have higher adult body sizes, life spans, and fecundity inside the new definitive host, because the new definitive host species should be larger and longer-lived, on average, than the old definitive host species. After the new definitive host species is added to the life cycle, the parasite then represses reproduction in the old definitive host species, which is now used as an intermediate host. There is an upper limit to how long the life cycle can be made using upward incorporation, because there are only so many trophic levels in a given food web.

In downward incorporation, a new intermediate host that consumes free-living stages of the parasite and is consumed by the definitive host is added to the life cycle. (Yes, parasites are often eaten by predators!) This again reduces parasite mortality, because the parasites can now infect the new intermediate host instead of being digested. Since fewer parasite stages are lost to mortality and more make it to the definitive host via trophic transmission, overall transmission rates increase. Both downward incorporation and upward incorporation are thought to have led to the evolution of complex life cycles for some parasite species.  

This diagram from Parker et al. (2015) shows how a host is added to higher trophic level in upper incorporation and a lower trophic level in downward incorporation.

There is also lateral incorporation, where host species are added in parallel, making the parasite species less host specific (more of a generalist) for a given life stage. Parasites can benefit from infecting more host species in a given life stage whenever that makes them more likely to be able to find a host that they can successfully infect that can continue their life cycle. However, there are also some likely costs associated with being a generalist, instead of specializing on just one host resource.

Final thoughts

In summary, some parasite species have complex life cycles and some have simple life cycles. Some parasite species are highly host specific at every life stage and others are host generalists that seem to infect nearly everything. There’s a lot of variability in parasite life cycles, but in general, they can be described by their life cycle length and the transmission modes that parasites use to get from one host to the next. Beyond that, each life cycle diagram is just a bunch of fancy terminology.

If you’re new to parasite ecology and thinking about life cycles for the first time, I have a question to leave you with: how do you think scientists have figured out all these life cycles? If you found a new species of larval trematode in a fish, how would you figure out its life cycle?


Parker, G.A., Ball, M.A. & Chubb, J.C. (2015). Evolution of complex life cycles in trophically transmitted helminths. I. Host incorporation and trophic ascent. J. Evol. Biol., 28, 267–291.

Panamanian snake community toadally changes due to chytrid

 We should conserve general parasite biodiversity, because parasites play important roles in ecosystems. However, we should also do our best to control invasive or emerging parasite species that have large, negative impacts on species and ecosystems. One such parasite is Batrachochytrium dendrobatidis, a fungal parasite that causes chytridiomycosis in amphibians. There is some debate regarding how many amphibian species have been impacted by the global spread of the chytrid fungus. But no matter how you slice it, chytrid fungus has devastated amphibian communities globally, causing many declines and many extinctions. As amphibians disappeared, what happened to ecosystems?

In a recent paper, Zipkin et al. (2020) found that snake communities in Panama shifted after chyrid spread through the amphibian community. Comparing hundreds of transect surveys before and after chytrid invaded, they found that after chytrid invasion, there were fewer snake species and the snake community was more homogenous. Several snake species also had reduced body condition, on average. All of this makes sense, because many tropical snakes eat adult amphibians or amphibian eggs, and thus amphibian declines might have decreased prey availability. As a person who enjoys canned soup and using toilet paper, I feel a strong affinity for these tropical snakes and their pandemic-induced resource shortages.

We often focus on the key results of projects, without taking the time to truly appreciate the methods that yielded these results. So I just want to take a moment to appreciate the hard work and careful analyses in this study by Zipkin et al. (2020). Ecologists rarely have enough data from before parasite invasion to document how ecosystems change from before to after invasion, so the hundreds of before surveys in this project are especially valuable. Zipkin et al. (2020) also dealt with a tricky problem in their analyses; many snake species are very rare and hard to detect. For example, 12 out of 36 snake species that they observed were only observed a single time! Knowing that this uncertainty was important to incorporate, Zipkin et al. (2020) used a great Bayesian analysis to quantify not just how much the snake community changed, but also how confident they could be in their results, given snake rarity. If you want to read all about it, check out their paper, which is available as a PDF on researchgate!      


E. F. Zipkin, G. V. DiRenzo, J. M. Ray, S. Rossman, K. R. Lips, Tropical snake diversity collapses after widespread amphibian loss. Science. 367, 814–816 (2020).

A Global Plan for Parasite Conservation

Why should we conserve parasites?

If you’re a long-time follower, you probably already know why we should conserve parasites. But for those of you who are new, welcome, and please enjoy this short journey into posts from the past!

Parasitism is a common consumer strategy in the natural world; so much so that 40-50% of all animals might be parasites! That’s perhaps millions of parasitic animal species spread across 15 phyla, including animals as diverse as ticks, intestinal worms, and bot flies. There are also parasitic plants and fungi. Parasites might have especially high extinction risks, because they are at risk from both primary extinction pressures, like the direct effects of climate change, and secondary extinction, or co-extinction, when their host species decline or disappear. If conservation efforts are supposed to conserve all species based on their intrinsic value, then parasite species should be a large target for conservation activities.

But maybe you’re more of a utilitarian, and you want to know what parasites do for ecosystems and for us. The short answer? A lot, and probably a lot more than we know. We know the most about parasite species that harm people, harm our domestic species, and threaten wildlife species, but those parasite species are just drop in the bucket of global parasite biodiversity. We haven’t discovered and described most of those other, relatively benign parasite species, even in groups that we know provide important ecosystem services, like the parasitoid wasps that provide pest control. And some parasite species have already gone extinct due to human activities—science didn’t even give them a name before we didn’t have them any moa. All of this is to say that we do not know everything about parasites, so we do not know exactly what a world without parasites would look like.

But we do know that parasites play important roles in ecosystems. For example, parasite biomass is a large and important part of food webs. Within food webs, parasites link many species together in ways that we might not even expect, like the nematomorphs that cause crickets to jump into streams, where the crickets are eaten by endangered Japanese trout. Every non-parasitic species that you can think of evolved with parasites and interacts with parasites, which is why sex and immune systems evolved. In humans, immune systems might totally freak out in the absence of parasites, leading to auto-immune disorders. While no one wants to conserve detrimental human parasites, a few relatively benign parasites might be good for people and other species, too. Parasites are so central to the biology and ecology of non-parasitic species that some question whether we can even conserve hosts without their parasites: if we brought back mammoths from extinction, but couldn’t bring back mammoth parasites, would we really have brought back mammoths?      

What steps do we need to take to conserve parasites?

There are strong arguments for conserving parasites, but unfortunately, we are not conserving parasites yet. In fact, in some cases, we are driving parasites to extinction when we try to conserve other species, like when we delouse or deworm host species brought into captivity. Given how little we know about most parasite species and how little we are currently doing to conserve them, what immediate steps can we take to conserve parasite biodiversity?

We suggest that 12 steps should be taken in the next decade to conserve parasite biodiversity. Some of these steps will appeal most to researchers interested in fundamental science and people who want to participate in community science programs, because they involve data collection and synthesis. For instance, we need more research about how parasite biodiversity responds to changes in host biodiversity. Other steps are geared more towards practitioners, because they involve risk assessment and prioritization and conservation practice, like creating ways to assess parasites’ extinction risks and building red lists of threatened parasite species. And everyone can enjoy and be involved with the steps related to education and outreach, like including parasite-themed lessons in K-12 and college education.

If you’re interested in learning more about the 12 steps in The Global Parasite Conservation Plan, check out our recently published paper! This was a wonderful group effort from an international team of researchers, many of whom you might have seen at our ESA Organized Oral Session in 2018. And for a bunch of new papers about parasite conservation, check out our whole “Parasite Conservation in a Changing World” special issue that was just published in Biological Conservation!

This was, of course, a shameless plug for my own research, but it was for a good cause. Let’s save the parasites.

Parasite Ecology Papers to Read While Stuck at Home During the Pandemic

Many people are having a hard time being productive right now, and that’s OK! If you do not have the time, quiet, or mental fortitude to keep up with the scientific literature, that is completely understandable. But sometimes reading papers can be a productive distraction from other, big work tasks that are especially difficult to tackle when you’re not 100% on your game. And when they’re good, reading papers can be fun and inspiring! So I’ve started curating a list of disease ecology, parasite ecology, and parasitology papers that were published thus far in 2020. If I’ve missed any great papers, please let me know, and I’ll add them!


Clonemate cotransmission supports a role for kin selection in a puppeteer parasite (This is AMAZING and I need to blog it.)

Recovery from infection is more likely to favour the evolution of migration than social escape from infection

Ecosystem-level papers:

Parasitism in ecosystem engineer species: a key factor controlling marine ecosystem functioning

Does deforestation increase malaria prevalence? Evidence from satellite data and health surveys

An Empirical Test of the Role of Small-Scale Transmission in Large-Scale Disease Dynamics

Towards common ground in the biodiversity-disease debate

Community- and population-level papers:  

Urbanization and translocation disrupt the relationship between host density and parasite abundance

Viral zoonotic risk is homogenous among taxonomic orders of mammalian and avian reservoir hosts

Ecological and evolutionary drivers of hemoplasma infection and bacterial genotype sharing in a Neotropical bat community

The Road Not Taken: Host Infection Status Influences Parasite Host-Choice

Environmental reservoir dynamics predict global infection patterns and population impacts for the fungal disease white-nose syndrome

Tracking the assembly of nested parasite communities: Using beta-diversity to understand variation in parasite richness and composition over time and scale

It’s a wormy world: Meta-analysis reveals several decades of change in the global abundance of the parasitic nematodes Anisakis spp. and Pseudoterranova spp. in marine fishes and invertebrates

Ecological consequences of parasite host shifts under changing environments: More than a change of partner

Systematic review of modelling assumptions and empirical evidence: Does parasite transmission increase nonlinearly with host density? (Are shameless plugs allowed?)

Deer, wolves, and people: costs, benefits and challenges of living together

Within-host processes or organism-level papers:

Concomitant Immunity and Worm Senescence May Drive Schistosomiasis Epidemiological Patterns: An Eco-Evolutionary Perspective

Parasite Infection Leads to Widespread Glucocorticoid Hormone Increases in Vertebrate Hosts: A Meta-Analysis

Characterization of viruses in a tapeworm: phylogenetic position, vertical transmission, and transmission to the parasitized host

Robot Contact Rate Activity for K-12 Students to do at Home

Since schools have closed across the country and world, parents and teachers are looking for learning activities that students can do at home. So I’m posting an easy experiment for Grades 3-6 that uses HEXBUGs, popular robot toys, to explore why we’re doing social distancing during the coronavirus pandemic. This activity could be modified for other grade levels. For instance, you could add in more replicates of each “treatment group” (number of robots), and then have students calculate and plot the means of each treatment group. Or you could have them use a line to predict how many contacts would occur for 10 or 20 robots—more than they probably own. Have fun!

ContactRateLab_K-12 <-PDF link



Bat Conservation and COVID-19

In the past week, my social media feeds – which encompass many people who love bats and support conservation – have been increasingly full of pleas and demands for the media to stop villainizing bats for the 2019-nCov outbreak. I can understand this sentiment; I certainly do not want mobs of people with torches and pitchforks to go out and cull bat colonies to try to protect human health. In fact, even in cases where the transmission of a deadly virus to people is ongoing, like transmission of rabies from vampire bats to people in Peru, killing a bunch of bats doesn’t necessarily reduce human risk; it might even increase it, due to complex disease dynamics! So the sentiment to be careful with how we portray the threats that bat-borne viruses pose for public health in news articles is one that I can support.

HOWEVER, today these social media posts contain a new element: a blog post by a famous bat conservation biologist, Merlin Tuttle, who argues that we have no reason to implicate bats in the 2019-nCov outbreak, and that researchers who are trying to find this virus and other viruses in bats are just in it for the easy research and grant money, because virus spillover from bats to people is very rare and not worth studying:

“…Compared to snakes or other animals, they [bats] are by far the easiest to quickly capture and process, have few defenders, and are already widely feared. Associating bats with rare, little-known viruses provides tempting opportunities for quick publication, big grants, and career advancement14.

Nevertheless, history does not support this bias. The great pandemics have come from birds, rodents or primates, not bats15. In truth, bats have one of our planet’s finest records of living safely with humans2,14.”

If you have been a long-term follower of this blog, you’ll know that I have never once criticized a paper or focused on the negatives, because I generally find that to be unproductive. But this is not Merlin’s first wildly irresponsible post that pits the general public against researchers by misrepresenting the scientific literature, and I fear that this one could have real negative impacts. So in this space, I want to provide some resources to people interested in bat conservation to learn more about how viral spillover events (like this coronavirus epidemic) and bat conservation are related.

Let’s start with some general information about spillover of viruses from bats. There is no question that bats are reservoirs for many viruses that cause serious human illnesses.  These include viruses like SARS, rabies, and some paramyxoviruses like the Hendra and Nipah viruses.  Because these viruses are such a big deal, there has been a lot of recent attention to bats and their potential as reservoirs for high-impact emerging zoonotic viruses. This work has shown that bat species do seem to be reservoirs for a disproportionate number of viruses, on average, in comparison to species in other taxonomic groups, like rodents. And there might be several reasons why bats have so many viruses but can live with them without being sick. Bats are reservoirs for many coronaviruses and similar viruses (e.g., SARS), so it is highly like that the 2019-nCov has a bat reservoir.

Bats can infect people with these viruses in many different ways. For instance, people can become infected by the rabies virus when they are bitten by a bat or when they contact bodily fluids from bats. People could also become infected by batborne viruses by handling bats or consuming bats, or by consuming things that bats defecated on/in (as in the palm sap and Nipah example). And finally, bats can infect other wildlife or domesticated species, and people can become infected by contacting/consuming those other species. We do not know which transmission route led to spillover from bats to people for this coronavirus, but in general, wildlife markets (for consumption or pet trade) do bring together bats, other wildlife, and people in unnatural ways, and there is a lot of potential for spillover from bats to people in these settings.

Viral spillover from bats is a real threat to global human health and has serious impacts on global economies, so we should be doing everything we can to neutralize those threats. One of the best ways to do that is by advancing global bat conservation. In particular, if we can keep bats in their undisturbed, natural habitats, we can minimize the chances of bat to human transmission. This isn’t as easy as saying, “Stop eating bats!” The global community needs to make a real effort to ensure that in places with high bat diversity (and thus high bat virus diversity), people are empowered to conserve bat habitats and bats because they have enough to eat, don’t need to cut down forests for fuel, etc.

If you have helpful resources for learning more about spillover of viruses from bats and how to use these spillover events as opportunities to advance local and global support for bat conservation, please leave them in the comments!

Contact function lab for undergraduate or graduate courses

Hello, Educators! Contact rate functions are a central component in SIR models, but they can be difficult to cover in disease ecology courses, because things get “mathy”. So I developed a hands-on contact function lab that allows students to discover and explore the various contact functions using experiments with tiny robots, called HEXBUGs. HEXBUGs are so fun to use that other people have developed similar labs, and I borrowed the awesome SkyNet premise from one such lab designed by David Civitello. If you want to adapt and run a lab like this, you can buy the HEXBUGs online or in a toy store near you. I’m sharing the worksheet that that I used for this lab, which you are welcome to edit and share as you please. I’m also happy to send you the answer key and the final graph to help pick the best HEXBUG densities to use in your lab. Happy educating!

Lab Worksheet (Word doc)

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Extreme competence and extreme incompetence

The February reading group paper was “Extreme Competence: Keystone Hosts of Infections”. If you’ve been following the blog for awhile, you probably know that this is a topic near and dear to my heart; I’ve often mused about superspreaders, superreceivers (here and here), and other types of “super hosts”. In fact, I think about this so often that I’ve started to get a bit bored with wondering why some individuals in a host population or some host species are really good at passing on their parasites. As Martin et al. (2019) point out, the superspreader idea is pretty sexy and superspreaders might be especially conspicuous, so it seems like everyone is looking for them and talking about them. But not me. My new quest is to figure out what makes a host “bad”.

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In my hunt for bad boys (most of which cannot be discussed in a public venue), I worked on an idea that wasn’t brought up in the Martin et al. (2019) paper: other symbionts can make hosts super bad for parasites. That’s right, folks. Without a substantial Twitter discussion to guide this post, y’all are being subjected to a story from my dissertation. BRACE YOURSELVES.

On almost every continent on this planet, there are freshwater snails, and it seems like all of those snail species are at least sometimes infested by little ectosymbiotic oligochaete worms, called Chaetogaster limnaei. Chaetogaster are fascinating for several reasons, but their claim to fame in the literature is their diet: they’ll eat anything that fits in their mouths, including trematode parasites. From a snail’s perspective, this is awesome, because they gain at least some protection from being infected by trematode eggs, miracidia, and cercariae. In fact, after an absolutely abhorrent amount of pipetting – which caused by left thumb to grow a muscle as big as an egg – I found that the more Chaetogaster a snail had, the less likely the snail was to get infected by free-swimming trematode larvae. (And because Chaetogaster rapidly asexually reproduce, the more free-swimming trematode larvae a snail is exposed to, the more Chaetogaster it suddenly has, meaning that snails in risky waters get increased parasite defenses!)

Snails with many Chaetogaster are not a good target for trematodes, in the same way that a hotdog stand surrounded by hungry lions isn’t a good target restaurant for buying your lunch. But this probably isn’t particularly inconvenient for trematodes, because just just like most hotdog stands aren’t surrounded by hungry lions, most snails don’t have many Chaetogaster. As I’ve blogged about before, Chaetogaster are aggregately distributed amongst snail hosts, such that most snails have 0 or 1 worms, and just a few snails have many worms. Therefore, just a few snails are what we might call “super bad hosts”.

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As Martin et al. (2019) point out, we know that 20% of hosts are typically responsible for 80% of parasite transmission. That 20% contains the superspreaders that we’re all so excited about. But my dissertation work shows something else: ~20% of hosts are “super bad hosts” that might be acting as superdiluters, with Chaetogaster literally sucking up the trematode population. This is interesting because Chaetogaster is just one defensive symbiont species in a world full of hosts covered in symbionts that eat parasites. Defensive symbionts are probably affecting host competence in many, many systems, so these interactions might be a good place to look as we start carefully quantifying variation in host competence within populations.

Finally, since we’re talking about symbiosis today, I’ll leave you with some advice: this year’s March Mammal Madness has an ENTIRE LINEUP of symbioses, including ants + aphids and Bornean bats + pitcher plants. Obviously, one of these will be the 2019 champion. Go fill out your brackets accordingly!

What is a neglected tropical disease?

When I first sat down to write this post, I thought that I’d start with a quick definition of the term Neglected Tropical Disease (NTD). I thought I knew what an NTD was – I even study a few! – so I was surprised when a definition didn’t immediately pop into my head. And I wasn’t alone. Several people who read our January Parasite Ecology Reading Group Paper also wondered how we decide which human infectious diseases should be considered NTDs.

If you’re like us, you probably thought about Googling it; surely WHO, CDC, etc. have some sort of NTD definition? They sort of do. But while major health organizations all use generally similar verbiage on their websites and in their reports, none of them seem to have a particularly precise definition. It would be hard to use their definitions to decide whether a given human infectious disease was an NTD or not.

What we seem to have instead of a precise definition is the World Health Organization’s list of 18 NTDs. And what an ecologically interesting list it is! There are viruses, bacteria, protozoa, and helminths. There are parasites with vectorborne transmission, fecal-oral transmission, and environmental transmission. Such diversity! In fact, at first glance, the NTDs seem to have little in common. And at second glance, the list seems oddly short. For instance, this article shared by Valentin Greigert asks why hepatitis E, which kills 70,000 pregnant women a year, doesn’t make the list.

The crux of the issue seems to be deciding who is neglecting NTDs. Is it politicians? Is it researchers? Funding agencies? Drug developers? Rich nations? This is a difficult question to answer, because it requires quantifying how much attention different human infectious diseases are receiving.

To figure out which diseases are or are not neglected by research, Furuse (2018) counted the number of publications (i.e., one metric of research effort) for 52 human infectious diseases, to see if NTDs are studied less than non-NTDs. They found that relative to their disease burdens, only a few NTDs are understudied. The only NTDs that were considered understudied relative to their global burdens were lymphatic filariasis, trichuriasis, ascariasis, onchocerciasis, hookworm disease, and trematodiasis. And, as the above article suggested would be the case, some diseases that are not on the accepted list of 18 NTDs had relatively high burdens and relatively few published studies, like paratyphoid fever. (To see the full list, go check out the paper.)

Over on Twitter, there was some interesting discussion about why some diseases had relatively many or few research papers relative to their burdens. In general, it was hard to guess, and Furuse (2018) notes that the reasons are potentially unique to each disease. And thus our conversation kept circling back to whether and how this burden-adjusted research intensity method could be useful in identifying and controlling NTDs. My personal ponderings have been about which types of research papers could be most indicative of neglect vs. attention. For instance, many NTDs already have effective and relatively cheap control methods that are sufficiently deployed in rich nations but not in poor nations, like water sanitation, so we might not need much research on ways to interrupt transmission for those NTDs. Instead, we might need research on where/when those controllable NTDs exist or the best ways to deploy control operations. And thus only some types of research are highly relevant for any given NTD? Anyways, there is a lot to ponder about this neat analysis. You should give it a read and share your thoughts with us!

In closing, I’ll leave you with this description – not a definition – of NTDs. Maybe one day I’ll be able to amend this post with a precise definition. 

Neglected Tropical Diseases…

…are diseases that affect poor populations that lack basic requirements like clean water, sanitation, education opportunities, and access to affordable healthcare. If you don’t study infectious diseases and you aren’t poor, you probably haven’t heard of more than four of the 18 NTDs in the figure below, despite the fact that they affect billions of people.

…trap people in a disease–poverty cycle. No matter how hard they work or how much economic assistance they receive, populations afflicted by NTDs will remain impoverished without disease control efforts because their disease burdens continue to result in lost economic mobility.

…disproportionally affect tropical and subtropical nations because poverty (i.e., people making less than $1 USD per day) is prevalent in “the global south”. But NTDs aren’t restricted to the the tropics. For instance, it is difficult to estimate NTD burdens, but NTDs are thought to affect thousands to millions of people in the United States.

…tend to be chronic diseases that cause substantial human morbidity, rather than mortality, but several of NTDs do cause substantial mortality, especially in children.

…can often be prevented/controlled/treated using existing, effective, and relatively cheap methods, such as education and water sanitation, but not always. When control methods are lacking, NTDs are often neglected by drug research and development efforts, because it isn’t usually profitable to develop drugs for people who won’t be able to pay for them.

…lack public and political visibility and discourse because they affect people with limited economic and political power, they are associated with stigma/shame, and/or they don’t have high, news-worthy mortality rates like HIV/AIDs, tuberculosis, and malaria.

Figure taken from here:

NTD fig