The Eradication of Infectious Diseases

Did you know that “Guinea worm disease,” also called dracunculiasis, is about to become the second infectious disease of humans to be fully eradicated by a disease control program? Humans become infected by the nematode that causes the disease when they drink unfiltered water that contains the intermediate host for the nematode: copepods. To reduce human infection rates, the Carter Center’s Guinea Worm Eradication Program has led an international effort to educate people about the importance of filtering their water. For instance, a simple straw containing a filter can prevent people from ingesting the copepods that transmit the nematode larvae. The control program has been very successful! Since 1986, the yearly number of reported Guinea worm cases has dropped by 99.99%! Just 126 cases were reported in 2014. We’re so close!

The first human disease to be fully eradicated was smallpox. If you don’t know much about smallpox, here’s the quick version: having smallpox was awful, and the disease was often fatal. But we couldn’t prevent smallpox transmission by giving people special straws with filters. The smallpox virus was transmitted directly between people, and the best way to stop transmission was to vaccinate a sufficient proportion of the population so that they would no longer be susceptible to the disease. In the late 1970s, the whole world hit that vaccination target, and smallpox was eradicated.

Also, here’s an interesting tidbit: recent work coming out of the Democratic Republic of the Congo suggests that during the time of the mass vaccination campaigns, the smallpox virus was actually working double duty by protecting people from the monkeypox virus. Since the 1980s, the incidence of monkeypox has increased dramatically in that region. People who live in forested regions are the most likely to become infected by monkeypox, because the virus is typically hosted by (you guessed it) monkeys (Rimoin et al. 2010). But it turns out that prior vaccination with the smallpox vaccine also reduces monkeypox infection risk. That means that people who weren’t born during the years of mass vaccination (i.e., young people) have a higher risk of becoming infected (Rimoin et al. 2010).

Finally, let’s talk about one more incredible eradication program, but this time let’s focus on a pathogen that didn’t infect humans. Rinderpest, or cattle plague, was a viral disease that infected both wildlife (e.g., wildebeest, buffalo) and cattle. The disease often caused high cattle mortality rates, which resulted in huge economic losses for humans. But after a massive vaccination program, rinderpest was officially declared as eradicated in 2011.

So, there you have it. We have almost eradicated Guinea worms via a long-term education program. And we have successfully eradicated two important viral diseases (smallpox and rinderpest) via massive vaccination programs. Next stop – HIV vaccine?


Predator vs. Parasite vs. Parasitoid vs. Mutualist– A Simple Classification Scheme

One of the most frequently accessed posts on this blog defines the terms “predator,” “micropredator,” “parasite,” and “parasitoid” and then presents a classification scheme for differentiating among those natural enemies (Lafferty and Kuris 2002). If you haven’t read that post yet, I recommend taking a look before you read this one. I obviously fancy the dichotomous key presented in the previous post quite a bit. However, it is not be the best classification scheme for all situations. For example:

  1. Check out Britt Koskella’s comments on the previous post – it is difficult to classify the bacteriophages that she studies using that classification scheme.
  2. The previous key may be difficult to use for educational purposes. For instance, it requires explaining castration and trophic transmission, which are concepts that might be unnecessarily complicated for explaining the distinction between parasites and predators to non-specialists.
  3. The previous key only deals with natural enemies, so we can’t use it to explain how mutualists and commensalists fit into this group of trophic relationships.
  4. The previous key doesn’t show how relationships can vary with life stages, ecological conditions, and environmental conditions.
  5. The previous key doesn’t have any pictures of snails on it. (Priorities.)

Therefore, having an additional classification scheme that specializes in some of the aforementioned areas would be useful. And – you guessed it – one was recently(ish) published (Parmentier and Michel 2013)! This classification scheme uses two continuous variables to designate relationships: the relative duration of the association (RDA) and the fitness effects on the ‘host.’

The relative duration of association ranges from 0 to 1, where 0 means that the ‘symbiont’ (including predators) spends none of its lifetime associated with the ‘host’ (or prey), and 1 means that the symbiont spends all of its lifetime associated with the host. For instance, predators and micropredators have RDA’s close to zero – a lion spends only a small portion of its life with a single zebra prey. Conversely, an adult trematode parasite (the worm in the orange section of the figure) will spend that entire life stage in association with a single host. The RDA is the Y axis on the figure below.

In recent months, we’ve talked a lot about the fitness effects that symbionts have on their hosts. Briefly, symbionts may have both negative and positive effects on hosts, and it is the net effect that determines how we classify the relationship. However, the net effect can vary with ecological and environmental conditions (see here, here, and here). Therefore, whenever we place a point on this graph, we need to remember that it might slide left or right as conditions vary.


Parasitoid wasps spend the entirety of their larval life stage in the host, and they ultimately kill the host. In this figure, parasitic castrators – like the trematodes that castrate snails – end up in the same region as the parasitoids. And this is where bacteriophages and Cordyceps fungi would fall out, too. However, like we discuss in the previous post, the term “parasitoid” is probably not a good one for this group, because that term is usually used to refer specifically to the unique life cycles of parasitoid wasps. In this figure, it means any parasite that reduces host fitness to zero.

Predators like lions, frogs, and crayfish also reduce prey fitness to zero. However, micropredators and herbivores (e.g., mosquitoes and cows) are special classes of predators that do not kill their prey. Then there is a group of animals that consume plants, but are probably more appropriately classified as parasites because they spend the majority of their life span (or a single life stage) on a single host plant. Therefore, things that eat plants will typically fall out somewhere between the aphids and the micropredators. (I should note that herbivores can have more than minimal impacts on host plant fitness, but many grazers have small impacts.) Similarly, Mark Siddall – the man who went on a quest for the hippo ass leech – doesn’t like classifying leeches as micropredators, because some spend most of their time on a single host. Therefore, most leeches would also fall out somewhere along that line between aphids and mosquitoes. Except, yaknow, the ones that are actually predators, and fall out near the lions.

On the mutualism side of things, we have symbionts like pollinators, which are only very briefly associated with each host; they’re like micropredators, but with positive fitness effects on their hosts. And then there are symbionts that are associated with single hosts for most of their lifespans, like ants on Acacia trees or guard crabs on corals. But again, remember that those relationships might shift left on the X axis as conditions vary.

Speaking of which, finding an example of a commensalist is hard. I used the example of epibionts on hermit crab shells, which help protect the hermit crabs from some predators but make the hermit crabs more susceptible to other predators. The net effect is unclear, but the positive and negative effects might balance out to a zero net effect.

So, there you have it. I think this figure should be really useful, especially as a general framework.


Lafferty, K.D., and A.M. Kuris. 2002. Trophic strategies, animal diversity and body size.  TREE 17(11): 507-513. (Direct link to PDF download)

Parmentier, E., and L. Michel. 2013. Boundary lines in symbiosis forms. Symbiosis 60: 1-5.

Mad Cow Disease

Last week, I discussed the One Health Concept, which suggests that the health of humans, livestock, wildlife, and environment are all interconnected. Our food production systems are an important component linking humans, livestock, wildlife, and the environment, and I explained some ways that human food production systems influence pathogen emergence. Today, I’m going to briefly expand on this idea and encourage you to become as informed as possible about how the food that you consume is created, processed, and prepared.

There are MANY humans on the planet. It would be unrealistic to expect that feeding that many people can be accomplished without unintended consequences, such as disease outbreaks and environmental alteration. However, it would be unethical for humans to ignore these negative consequences when they occur. It would also be self-destructive in the long term, because as the One Health Concept explains, human health cannot flourish unless we make sure that our livestock, wildlife, and ecosystems are also flourishing. Therefore, when these problems arise, we should turn to scientists and social scientists for innovations in the ways that we create, process, and prepare our food.

Here’s an example. Bovine spongiform encephalopathy (BSE) is a disease that occurs in cattle around the world. BSE is caused by prions, which are misfolded proteins that cause deterioration of neurological tissues (i.e., the brain). These prions aren’t destroyed by high temperatures, so consumption of infected tissues – even after cooking – can transmit the prions to new hosts. If humans consume the tissues, the disease is called new variant Creutzfeldt-Jakob disease. And if cows consume the tissues, the disease is called bovine spongiform encephalopathy – or, more commonly, mad cow disease.

You might be wondering why cows would ever eat infected cow brains. That seems like a pretty unlikely scenario, because cows are vegetarians. However, cattle farming operations used to include these tissues as meat and bone meal that went into cattle feed. When the transmission route for BSE was discovered, legislation was passed in many countries that prohibited using those high risk tissues as feed for cattle or as food for humans. Additionally, countries have adopted various testing strategies, which at minimum require the removal of any visibly sick animals from the food chain.

In hindsight, feeding cows to other cows on a huge scale seems like a bad idea – if not for ethical reasons, than for pathogen transmission reasons. But of course, you can also see how using those materials in the feed also represented a way to reduce waste products (really important for environmental health) and to cut costs associated with producing beef on such a massive scale. The important thing is that we address the problem to reduce the risks to animal, human, and environmental health. However, while some measures have been taken and BSE incidence is declining, others argue that some practices – such as feeding calves on cow blood as a milk substitute – continue to cause risks to animal and human health. But of course, with money and health on the line, controversy can explode when topics like this hit mainstream media.

So, what are some solutions? Well, that is very complicated and goes far beyond the realm of ecology and into the realm of socioeconomics. In other words, outside my realm of expertise. :P But that’s a total cop out, so here is my two cents worth: (1) Transparency in food production systems can reduce the mistrust that citizens feel when problems like this arise (there is no question that things like this will happen). (2) Citizens should be as informed as possible about how their food is grown/raised and processed. This will allow them to vote with their forks, and with many eyes on these complex systems, we will hopefully be more likely to nip problems like this in the bud.

And finally, a sad cartoon of a cow in a straight jacket:


The Disease Triangle and the One Health Concept

Two important frameworks in disease ecology are the Disease Triangle and the One Health Concept. Today I want to describe these two paradigms and how they fit together.

The Disease Triangle represents a simple concept: in order for a parasite to cause pathology – that is, for “disease” to occur – the parasite must be present, a susceptible host must be present, and environmental conditions must be sufficient to result in pathology. If you chop off one side of the triangle, there will be no disease. For instance, if you inject a parasite into an immune host, the pathogen will not be able to establish, and there will be no disease. Or, if you inject a pathogen into a susceptible host, but the host is living fat and happy in a high-resource, low-stress environment, the ‘parasite’ may not affect the host’s fitness even after successfully establishing. I’ve covered the context-dependent nature of symbiosis in several recent posts (here, here, here, here), so check those out to see other examples of how the fitness consequences of harboring symbionts can vary with environmental/ecological conditions.


Let’s talk about humans as our focal hosts now. In order for pathogens to cause disease in humans, we again need susceptible human hosts and environmental conditions that lead to pathology. But we should specify exactly what we mean by “environment.” For instance, where does ecology fit in the environment? The One Health Concept explicitly recognizes the role of wildlife and livestock in human health, and distinguishes this from other environmental factors. The idea is that the health of the environment, wildlife, livestock, and humans are all intricately tied together, and when the health of one component declines, the health of the other components also declines. Usually, people draw this concept as a triangle or a venn diagram with the three vertexes/circles as humans, animals, and the environment, like this:

One Health V1.2

Today, I’m going to present the idea somewhat differently. First, I want to continue to have the pathogens as an explicit component in the One Health Concept. Second, I like to think about the environmental component in a more dynamic way, so I’ve shifted things around a bit:

OneHealth V2


The majority (61%) of human pathogens are zoonotic, meaning that they are transmitted between animals and humans (Taylor et al. 2001). And if we limit our concerns to just emerging infectious diseases (EID) of humans, 75% of those are zoonotic!  (If you aren’t sure what an EID is, check out last week’s post.) Here are some examples of major human pathogens that either spillover from animals or are vectored by animals:

Ebola Virus – primates, bats, etc.

Rabies – dogs, bats, etc.

Influenza – pigs, chickens, etc.

Schistosomiasis – snails as intermediate hosts

HIV – originally spilled over from primates

Hanta Virus – rats

Bubonic Plague – vectored by fleas (and lice?), spilled over from rats

Lyme Disease – vectored by ticks, spills over from mammals

Malaria – vectored by mosquitoes

Hendra virus – bats, horses

Clearly, understanding how pathogens are transmitted among wildlife and livestock and how these pathogens then spillover into human populations is a vital step in understanding how and when these pathogens will emerge in human populations. And when pathogens do not just jump hosts into human once, but are maintained in animal populations and repeatedly transmitted to humans (e.g., Lyme Disease), community ecology may be an important determinant of human infection risk (i.e., dilution and amplification effects).


As I mentioned previously, susceptible humans need to be present in order for disease to occur. There are also many socioeconomic considerations that can influence whether an epidemic occurs, the magnitude or duration of the epidemic, and/or the degree of pathology (e.g., morbidity, mortality) that individuals experience. I can’t describe all of those factors in one post, but here are a few:

Trust of government and health officials: This is a huge consideration. For instance, in the United States, there are currently outbreaks of pathogens that are entirely preventable by readily available vaccinations, but distrust of vaccinations has led citizens to refuse to vaccinate their children. Similarly, hygienic practices are vital for containing the spread of Ebola virus in the affected African countries. However, citizens mistrust health workers, and they may not follow advice for reducing virus transmission, such as going to the hospital as soon as they experience symptoms and avoiding kissing the deceased and going to the hospital as soon as they experience symptoms (Gross 2014).

Population Size: Population density can play a big role in determining the probability that a pathogen will successfully invade a human population, as well as determining whether the pathogen will persist or fade out after the initial epidemic.

Globalization: By connecting populations of humans that otherwise would not be connected, global travel makes it possible for pandemics to occur when there would otherwise be contained, regional epidemics after spillover of a pathogen from animals into humans.

Food: Where we acquire our food and how we prepare it can also have important implications for the spread of infectious diseases. For instance, if we allow farmers to grind up cows and put that protein into the feed of other cows, we increase the risk of mad cow disease (bovine spongiform encephalopathy) in our livestock and new variant Creutzfeldt-Jakob disease in humans. If we raise livestock in dense populations, we increase the probability of pathogen epidemics in our livestock, and these pathogens may then spillover into human populations when humans interact with or consume infected animals. Similarly, if hunters come into close contact with wild animals in the process of acquiring, cooking, and selling bushmeat, they increase their personal risks of contracting wildlife pathogens, which may then spread through human populations. And if we use antibiotics on a massive-scale in our farming practices, we may inadvertently select for highly resistant bacteria that we can no longer combat with existing medical resources.

Hygiene/Sanitation/Social Norms: Are sick people encouraged to stay home from work, and do they feel like they can afford to miss work or school? Do people use condoms to reduce the probably of contracting STIs? Do people typically kiss or shake hands when they greet?


In addition to the presence of the focal pathogen, it is important to consider other symbionts that hosts may harbor. For instance, infection with one pathogen may increase susceptibility to other pathogens, or co-infection may turn hosts into pathogen superspreaders.


Finally, just like we discussed with the Disease Triangle concept, even if pathogens, animals, and humans are all present, we won’t necessarily see an emerging infectious disease. Environmental conditions can tip the scale in one direction or the other, as indicated by the green and white arrows illustrating the transition from the disease-free to disease-present venn diagrams. Here are a few environmental factors that may be important:

Pollution: Pollution can stress animal and human populations, making them more susceptible to disease.

Deforestation/Agriculture: When we clear forest land for agriculture, we often bring humans, their livestock, and wildlife into closer contact than they would be otherwise, and this can increase the risk of pathogen spillover from wildlife to humans. For instance, when we raise pigs near fruit trees visited by bats, we increase the risk of virus transmission from bats to pigs and then to humans. Additionally, deforestation, urbanization, pollution, and other types of environmental change may result in changes in animal communities, which may in turn affect pathogen transmission.

Not all anthropogenic changes to the environment will result in increased transmission risk. For instance, by draining wetlands in massive regions of the United States, citizens eradicated much mosquito habitat, and therefore eliminated malaria as a major pathogen in the United States. Similarly, climate change has the potential to tip the scale favorably for some pathogens in some locations, but not all pathogens in all locations will be positively affected by climate change. Therefore, the environmental conditions that are “favorable” for some diseases won’t necessarily be the same for other diseases.


Gross, M. 2014. Our shared burden of diseases. Current Biology 24(24): pR1139–R1141.

Taylor, L.H., S.M. Latham, M.E. Woolhouse. 2001. Risk factors for human disease emergence. Philos Trans R Soc Lond B Biol Sci. 356(1411):983-9.

Emerging Infectious Diseases

Next week, I’m going to talk about the role of livestock, wildlife, and the environment in emerging infectious diseases (EIDs) of humans. This week, I want to talk more generally about emerging infectious diseases.

Let’s start with the most straightforward part: “infectious.” EIDs are caused by some kind of transmissible pathogen. Therefore, heart disease and obesity are not EIDs, even though there are major epidemics of these diseases in some countries. (As a side note, there are some cool papers that relate the spread of non-infectious diseases, like obesity, through social networks to the spread of memes.) And “disease” means that there is pathology or fitness decreases experienced by the hosts as the result of a pathogen.

There are two ways that infectious diseases can be “emergent.” First, an emerging pathogen can be novel to a naïve or highly susceptible host population, meaning that it never existed in that population or species before. For instance, the newest emerging fungal pathogen of salamanders in Europe (Batrachochytrium salamandrivorans) exists in populations of relatively resistant salamanders in Asia, but has not previously existed in European salamanders (Martel et al. 2014). B. salamandrivorans was likely introduced into Europe via the pet trade, and European salamanders are highly susceptible to the pathogen.

Pathogens can also be considered emergent when they have existed in a population previously (i.e., endemic pathogens), but the pathogens weren’t noticed by humans until recently and/or infection rates or mortality rates recently increased due to some change in ecological or environmental conditions (e.g., changing amounts of forest fragmentation and the re-emergence of Lyme disease).  Next week, I’ll go into much more detail about how disease emergence depends on ecological and environmental conditions.

Finally, why should we care if a pathogen causing an EID is novel to the focal host population or endemic to the population? Because the control measures that we use will depend on whether the pathogen is novel or endemic. For instance, targeting the trade of salamanders originating in Asia appears to be the best option to stop the spread of B. salamandrivorans, and that would not be the case if B. salamandrivorans were endemic to salamanders all over the world.

WrongWorm References:

Martel, A., et al. 2014. Recent introduction of a chytrid fungus endangers Western Palearctic salamanders. Science 346(6209): 630-631.

Spartants on Epiphytes: Species Assembly Rules

On Monday night, I read an amazing paper. It was so amazing that I knew I’d need to save it for my post on Parasite Ecology’s second birthday…which I then realized was less than two days away. So, in the past 24 hours, I have fallen hopelessly in love with ants (again!), reorganized two months worth of queued posts, and made a symbiont cartoon incorporating the phrase, “This is Sparta!” – something that I’ve been waiting for the right moment to do for TWO YEARS. The moment has arrived. Happy Birthday, Parasite Ecology! 

As we’ve talked about previously, some ants live on plants in special hollow chambers that the plants provide called domatia. But ants can also live on plants that don’t provide domatia, such as the epiphytic birds’ nest ferns that trap leaf litter in the canopies of tropical forests. Amazingly, up to 12 ant species can be found living together on just one of these epiphytes! But what determines exactly which species can be found living together?

Ant competition might be a major structuring force that determines which ant species live together in a given epiphyte community, and ant species that are most similar in size may be more likely to compete. And in fact, in a survey of 86 epiphytes, ant species that were similar in size were less likely to co-occur than one would predict based on a null model (Fayle et al. 2015). But that doesn’t prove that competition is driving the observed pattern, so Fayle et al. (2015) conducted an experiment where they inoculated epiphytes with single or multi-host communities of ants, and then two days later, they inoculated the same epiphytes with an “invader” species. There was strong competition between similarly sized ants, but not between ants of disparate sizes. Furthermore, the threshold size ratio between the invading and resident ants that determined whether there was strong competition or not was roughly the same in both the observational study and the invasion experiments.  And get this:

“In each replicate, an invading colony was introduced into a fern, which was supported on a fluon-coated cylinder above a fluon- coated container, and left for 24 h with ants ejected from the fern falling into the container. Competition manifested as direct attacks between workers of different colonies, with ants sometimes being thrown from the edge of the fern (Appendix S3).”  


Ok, but we’re not done! Fayle et al. (2015) took things a step further and ran simulations with different sets of species assembly rules to see which set of rules, if any, could re-create the community diversity patterns that they observed in the field. Their null model was that size-based competition didn’t matter, so that every species had the same probability of invading a community, regardless of the sizes of the resident species. They compared this to four other sets of rules (1a, 1b, 2a, 2b), where the relationship between the invader-resident size difference and the strength of competition was described as a (1) threshold assembly rule or a (2) saturating assembly rule and competition between ants was assumed to be (a) between the invader and the resident of the most similar size (nearest neighbor competition) or (b) between the invader and all resident species (diffuse competition).  The rules that resulted in the best fit to the observed diversity patterns were the combination of the saturating relationship between the invader-resident size difference and the strength of competition and nearest neighbor competition (2a). SO. COOL.

Go check out the paper! It’s open access.


Fayle, TM, P Eggleton, A Manica, KM Yusah, and WA Foster. 2015. Experimentally testing and assessing the predictive power of species assembly rules for tropical canopy ants. Ecology Letters 18: 254–262.

Koala Chlamydia

Happy Valentine’s Day!!

Koalas are adorable. (Seriously, go google image search koalas.) Koalas are also a threatened species, where population sizes in Australia are declining rapidly. Part of this decline is due to human encroachment into koala habitat: we cut down their trees, run them over with our cars, and let our dogs attack them. Another major cause of koala population declines is disease.

What pathogen is wiping out koalas? Well, it’s one that you probably wouldn’t guess: chlamydia. The bacteria is transmitted between males and females during sex and between mothers and their joeys, and the disease can be very, very unpleasant for infected koalas. The range of symptoms includes lesions, urinary incontinence, secondary yeast infections, sterilization due to infection in the reproductive tract, conjunctivitis and even blindness when infection occurs in the eyes, and death in the worst cases.

For koala populations as a whole, chlamydia-induced infertility is a huge problem. The prevalence of infection can be very high in koala populations, which leaves very few reproductively functional individuals. The good news is that there’s also a huge effort underway to treat and rehabilitate sick and injured koalas. Additionally, a vaccine has been developed to prevent koala chlamydia, and early trials with the vaccine have been successful.  Let’s hope that in the near future, a typical koala conversation will look like this:    

Koalifications Koalas aren’t the only animals that have STDs, of course. For instance, you might rekoal a post (I’m so sorry, really) that I wrote last Valentine’s Day about insect STDs. Go check it out!