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:
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:
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:
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.