Evolution of pathogens in a man-made world

Abstract

Human activities have resulted in substantial, large-scale environmental modifications, especially in the past century. Ecologists and evolutionary biologists are increasingly coming to realize that parasites and pathogens, like free-living organisms, evolve as the consequence of these anthropogenic changes. Although this area now commands the attention of a variety of researchers, a broad predictive framework is lacking, mainly because the links between human activities, the environment and parasite evolution are complex. From empirical and theoretical examples chosen in the literature, we give an overview of the ways in which humans can directly or indirectly influence the evolution of different traits in parasites (e.g. specificity, virulence, polymorphism). We discuss the role of direct and indirect factors as diverse as habitat fragmentation, pollution, biodiversity loss, climate change, introduction of species, use of vaccines and antibiotics, ageing of the population, etc. We also present challenging questions for further research. Understanding the links between anthropogenic changes and parasite evolution needs to become a cornerstone of public health planning, economic development and conservation biology.

Figure 1

US mortality rates (per 100 000) attributable to infectious diseases during the 20th Century. In 1900, approximately 1/3 of all deaths were due to infectious diseases (primarily pneumonia, TB and diarrhoea). Note the dramatic spike in mortality associated with the Influenza Pandemic of 1918 (highlights ongoing risk of novel pathogens). Also note definite rebound since 1980, attributable to AIDS and remerging (drug resistant) pathogens. Taken from Armstrong et al. (1999).

Figure 2

Links between human activities and evolutionary ecology of parasites.

Figure 3

Development of ‘travel man‐made ecosystems’ consequences: connection topology from a regular ring lattice to a random network. The intermediate connection is called small ‘world’ network, and infectious diseases spread more easily in small‐world networks that in regular lattices (modified from Watts & Strogatz 1998).