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.