Pathogen risk refers to the danger presented by microorganisms that cause disease.
There is a clear evolutionary opportunity for a pathogenic or parasitic existence, living at the expense of nutrient-rich, warm, renewable hosts. These advantages are reflected by the number and variety of infectious organisms that are pathogenic to humans alone, with a comprehensive literature review identifying 1415 species (Taylor et al. 2001). These pathogens can be divided into five major taxonomic divisions: 15% are viruses (including prions), 38% bacteria (including rickettsia), 22% are fungi, 5% are protozoa, and 20% are helminths (Taylor et al. 2001). To further illustrate the appeal of a host environment, nonpathogenic bacteria (distinguished from pathogens by lack of host-damage) far outnumber human cells within our bodies (Rohmer et al. 2011). While nonpathogenic bacteria are tolerated by hosts, pathogenic organisms are exploitative and so have to overcome host defenses. These include specific evolved mechanisms, such as toxic compounds, which can function defensively or offensively by manipulating or destroying rival microbes and host immune defenses (Rohmer et al. 2011; Rudkin et al. 2017). However, many of these mechanisms cause damage to and risk killing the host. This means there is an evolutionary trade off that every pathogen must contend with; just as there is no advantage to be unable to colonize or to be killed by the host’s defenses, it is of no advantage to be so lethal that you kill the host before you have a chance to benefit from the environment, replicate, and spread to other hosts. How each species contends with this trade-off is different, for example, lethality and host damage matter less for bacteria that are able to survive longer outside the host, or after the host has died, or can transmit to new hosts rapidly (Rudkin et al. 2017).
Just as there are clear evolutionary advantages for pathogens to live at our expense, it is equally advantageous for animals to develop systems to defend against pathogens. Communicable diseases caused by pathogens present a significant risk to human health and life and, despite deaths caused by certain communicable diseases having lessened in the past 100 years (recently, for example, death by diarrheal diseases decreased by one million between 2000 and 2016), they remained as 3 out of the top 10 global causes of deaths in 2016 (diarrhea, tuberculosis, and lower respiratory infections). To illustrate the scale of this risk: the deadliest communicable diseases – lower respiratory infections – caused three million deaths worldwide in 2016 (WHO 2018). Further to the risk from existing pathogenic microorganisms, there is an ever-present risk of newly emerging pathogens, as 335 new infectious diseases have been reported since 1940 (Fumagalli et al. 2011; Taylor et al. 2001). These emerging infections are almost always caused by an existing pathogen that adapts to a new host. For example, the HIV virus previously infected chimpanzees and Ebola was previously found in bats (Sironi et al. 2015). There is also an evolutionary asymmetry to consider; humans have both far longer life spans and smaller populations than pathogens, meaning we evolve at a slower rate (Sironi et al. 2015). So, humans are faced with the threat of a wide variety of fast-evolving pathogens which are able to emerge as new threats from different host species.
Physiological and Behavioral Immune Systems
We are thought to manage the risks presented by pathogens first with our internal, physiological, immune system and second with a psychological, behavioral defense system. First, our physiological immune system uses two branches of defense, the innate immune system and the adaptive immune system. These two branches are primarily differentiated by mode of activation; the quicker but more primitive innate immune system relies on predetermined pattern recognition of abnormal, foreign bodies whereas the slower but more flexible adaptive immune system requires prior exposure and thus relies on specific recognition and immunological memory (Rohmer et al. 2011). Both systems are required for an effective response; emerging or unfamiliar pathogens must be dealt with quickly using the innate immune system, which can expel or hold the pathogen at bay until the adaptive immune system can develop a more sophisticated, tailored response.
The second system for reducing pathogen risk, based around psychological and behavioral defenses, offers the advantageous outcome of avoiding infection completely. Aside from the obvious risk that our immune system could be bested by invaders, fighting off infection is debilitating (even if just temporarily) and metabolically costly (Schaller 2011). Therefore, it is thought that humans also possess what is termed the behavioral immune system, which was coined to capture the apparent unified functioning of specific behaviors and cognition that work to reduce the risk of infection (Schaller 2011). It is proposed that this system responds to various environmental cues, such as unpleasant odors, that tend to co-occur with pathogens, and triggers the disgust emotion. This disgust reaction encourages either withdrawal, for example, through feelings such as nausea, or pathogen-removal behaviors, such as vomiting, washing, and spitting. This helps us avoid objects, animals, and even people that may pose an infection risk. However, just as the physiological immune system has costs (such as metabolic expense) as well as benefits, as does the behavioral immune system. The avoidant responses of the behavioral immune system can stand in the way of other fitness relevant goals, for example, by encouraging avoidance of social or mating opportunities because of the possibility they carry some infection risk (Schaller 2011). As such, the individual sensitivity of our behavioral immune system is another trade off which we must contend with.
Psychological Consequences of Pathogen Risk
Although all humans are at risk from pathogens, it seems likely that there is variability in the sensitivity of the behavioral immune system between individuals, both at a trait level and dependent on current pathogen risk. First, we can infer trait level differences in an individual’s behavioral immune system from measures of disgust sensitivity (which measures our natural predisposition to feel disgusted). These individual differences can have far reaching consequences for our behavior, for example, those who are highly disgust sensitive are more likely to be politically conservative (Inbar et al. 2009), differ in mate choice (Gangestad et al. 2006), and display harsher moral judgments (Chapman and Anderson 2014). This pattern of behavior suggests that those who are more disgust sensitive are more avoidant of those who are perceived to be potentially infectious or harmful.
An interesting example of how disease burden has influenced our psychology is differences in disgust sensitivity and ingroup bias. Interpersonal contact with unknown others would expose an individual to unencountered, dangerous, pathogens. As such, it is clear that there is a connection between ingroup bias and disgust, for example, participants were less disgusted by clothing worn by a member of their University (Reicher et al. 2016) and disgust sensitivity predicts dehumanization of arbitrary outgroup (Buckels and Trapnell 2013). This effect can also be seen temporarily in those who are at greater risk of infection, for example, women in their third trimester of pregnancy displayed elevated levels of ethnocentrism (Navarrete et al. 2007).
We can also use the example of ingroup bias to show that some cultural differences could be linked to differences in disease burden between cultures. Pathogen risk varies across cultures, both historically and in the present day. When controlling for demography, selection pressures imposed by variation in pathogenic load explain much genetic variation between populations and is thus argued to be the primary driver of local adaptation (Fumagalli et al. 2011). Aside from genetic variation, it has also been demonstrated that countries with a historically high disease burden are more likely to be collectivist (Fincher et al. 2008). The reason for this difference is hypothesized to be due to collectivist cultures having a stronger ingroup-outgroup differentiation which, as discussed above, would limit exposure to new pathogens (Jetten et al. 2006). In further support of this, it seems that individualistic cultures were subjected to a higher number of infectious disease outbreaks between 1950 and 2008 than collectivist cultures (Morand and Walther 2018). So, it seems that historically high pathogen risk may influence the psychology of a culture as well as providing some protection from infection.
It is not surprising that pathogens wish to benefit from the human body as it is an attractive ecosystem which at any time is home to thousands of microbial species, most of which rarely (if ever) cause us illness. Access to the rich diversity of nutrients within animal tissues is worth competing for, and as such dedicated pathogens have developed mechanisms that aid them in colonizing and replicating within host bodies. This is no easy task as humans have both psychological and immune defenses which exist to avoid, destroy, or expel viruses and infected somatic host cells. This competition to invade and avoid invasion exerts selection pressures on both organisms. As such, pathogen risk has far-reaching consequences for the virulence of the pathogens themselves, human biology, and both individual and cultural psychology.
- Fincher, C. L., Thornhill, R., Murray, D. R., & Schaller, M. (2008). Pathogen prevalence predicts human cross-cultural variability in individualism/collectivism. Proceedings of the Royal Society of London B: Biological Sciences, 275(1640), 1279–1285. https://doi.org/10.1098/rspb.2008.0094.CrossRefGoogle Scholar
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- WHO fact sheet. (2018). Top 10 causes of death. Geneva: World Health Organisation. http://www.who.int/en/news-room/fact-sheets/detail/the-top-10-causes-of-death