Are the majority of human EIDs really zoonotic?

 In 2001, Taylor et al. reviewed more than 1415 pathogens that infect humans. They found that 61% of those pathogens were zoonotic, meaning that they are transmitted between animals and humans. Furthermore, 75% of the pathogens classified as causative agents of emerging infectious diseases of humans were considered zoonotic. Clearly, if we want to understand pathogen transmission in human populations, we need to understand how these pathogens are spilling over from wildlife populations. But here’s a sensational question for you: are the statistics that I just summarized accurate?

Before I speculate further, I need to introduce a category of pathogens that may be commonly overlooked: sapronoses. Unlike ‘typical’ pathogens (whatever that means), sapronoses do not need a host to survive. While sapronoses might replicate in a host or even be transmitted among hosts, they can also reproduce and flourish in the environment outside of the host indefinitely. In contrast, pathogens with free-living stages eventually need a host to complete their life cycle.

Brain eating amoebas are one example of a sapronosis. These amoebas typically live in the environment, but they can accidentally enter the human body through the nose. For instance, this might occur when a human is swimming in water containing the amoebas. From there, the protist feeds on nervous tissue, and the human host almost always dies due to infection. Because the amoebas don’t really need a host for reproduction or transmission among environments, there is no selection pressure for the amoebas to keep their hosts healthy for longer periods by evolving reduced virulence. And because the amoebas aren’t transmitted directly among hosts, treating or quarantining infected people won’t reduce the probability that other humans become infected. Instead, limiting human contact with contaminated environments or treating contaminated environments to eradicate the sapronotic agent are the only ways to reduce transmission to other hosts.  Some other examples of sapronoses are anthrax, cholera, and tetanus.

Ok, back to my sensational question:

Kuris et al. (2014) reviewed a subsample of the human pathogens that Taylor et al. (2001) reviewed previously, and Kuris et al. (2014) found that one third of the subsampled pathogens were sapronoses. Cool! When they broke down the percentages by taxa, almost 100% of the fungi that they examined were sapronotic/saprophytic, as well as ~29% of the bacteria and ~13% of the protists. When Taylor et al. (2001) classified the pathogens, they found 113 zoonotic fungi. But Kuris et al. (2014) argue that their subsample suggests that almost all of the fungi should be saprophytic, not zoonotic. It may be that Taylor et al. (2001) classified saprophytic pathogens as zoonotic pathogens, leading to an overestimate of the proportion of human pathogens that are zoonotic.

I think it’s still safe to say that most human pathogens have an environmental and/or animal reservoir. Additionally, even though the proportion of human pathogens that are zoonotic might be less than “the majority” (i.e., <50%), a large proportion of the human pathogens would still be classified as zoonotic, even after reclassifying the potentially sapronotic pathogens. But Kuris et al. (2014) bring up a subtle point that deserves more attention: just because animals can be infected by a human pathogen doesn’t mean that there is transmission of the pathogen between animals and humans. Neat stuff!


Kuris, A.M., K.D. Lafferty, and S.H. Sokolow. 2014. Sapronosis: a distinctive type of infectious agent. Trends in Parasitology 30(8): 386-393.

Taylor, L.H, S.M. Latham, and M.E. Woolhouse. 2001. Risk factors for human disease emergence. Philos. Trans. R. Soc. Lond. B: Biol. Sci. 356: 983–989.

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.

Bats and Emerging Infectious Diseases

Bats are amazing.  It’s easy to forget about bats because we don’t usually see them, but they’re out there, performing important ecosystem services that we often take for granted.  If you don’t believe me, you can read this review by Kunz et al. (2011), which outlines some important services that bats provide for humans:

  1. Pollination
  2. Seed dispersal
  3. Arthropod suppression
  4. Guano for fertilizer
  5. Tourism – caving, etc.
  6. “Witches and sorcerers used bats in ancient magic to induce desire and drive away sleep.”  (Seriously, without bats, there would be no ancient magic.)
  7. Bats are frickin’ cute (I added this.)

Bats are also reservoirs for many viruses that cause serious human illnesses.  These include viruses like SARS, Ebola, 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.  Specifically, two major questions arise:

  1. Are bats hosts for more zoonotic viruses than other wildlife?
  2. If yes, what characteristics make bats such good reservoirs for these emerging zoonotic viruses?

In a recent meta-analysis of viruses of bats and rodents, Luis et al. (2013) found that on average, bat species host more zoonotic viruses than rodent species.  So, perhaps there is something special about bats that make them particularly good reservoirs!  Of course, comparing bats and rodents doesn’t fully answer Question 1, but it is a start to say that if we look at bats and another taxonomic group that shares many life history characteristics with bats, bat species host more viruses, on average. However, because there are more rodent species than bat species in the world, rodents host more total zoonotic viruses than bats.  Therefore, in terms of global human risk, bats don’t contribute more than rodents.

So, given that bats may be somewhat unique in their ability to host zoonotic viruses, what causes them to be such good hosts?  Good question!  At this point, no one can really say, but it’s probably a combination of some of these unique bat characteristics:

  1. Bats have unique feeding ecology, where they tend to spit out their food. They suck on the fruit/flower of choice and swallow the nectar/juice, but then spit out the remaining material.  If another animal comes along and eats the pulp off the ground, it might ingest virus particles from the bat, and the virus will have the opportunity to jump/spillover into a novel host species.
  2. Bats and humans tend to overlap in habitat, which provides opportunities for bat viruses to spillover into human populations.  This is particularly likely in places where humans are altering landscapes so that livestock operations and bat habitat get mixed together.  For instances, in places where livestock pigs have access to fruit that bats have spit out.
  3. Bats can be gregarious, where they may roost in extremely high densities.  Furthermore, multiple bat species may share the same roost.  High densities of susceptible individuals provide a virus’ dream population.
  4. Some bats migrate, and their long-distance travel may help them to spread viruses.
  5. Some bats hibernate, and that reduced metabolic activity may be important for some viruses, like rabies.
  6. Because bats are evolutionarily ancient, their viruses may have highly conserved cell-receptor proteins that are good at invading the cells of many mammal species.

The take home message is that we need to study bats and emerging infectious diseases more.  We know very little about how and why and when viruses spillover from reservoir hosts to novel species, but in this era of global change, understanding those spillovers is becoming crucial for human health.  And as Luis et al. (2013) found, the more we study a given host species, the more viruses we find that infect that species.  So, if we want to know which viruses bats currently harbor in order to asses which viruses might be most likely to spillover into human populations, we should invest in more bat research!

That brown thing is a tree.


Kunz, T. H., E. Braun de Torrez, D. Bauer, T. Lobova, and T. H. Fleming. 2011. Ecosystem services provided by bats. Annals of the New York Academy of Sciences 1223: 1–38. (PDF link)

Luis, A. D., D. T. S. Hayman, T. J. O’Shea, P. M. Cryan, A. T. Gilbert, J. R. C. Pulliam, J. N. Mills, M. E. Timonin, C. K. R. Willis, A. a Cunningham, A. R. Fooks, C. E. Rupprecht, J. L. N. Wood, and C. T. Webb. 2013. A comparison of bats and rodents as reservoirs of zoonotic viruses: are bats special? Proceedings of the Royal Society B 280: 20122753. (PDF link)