In This Article Expand or collapse the "in this article" section Disease Ecology

  • Introduction
  • Historical Developments
  • Overviews
  • Journals
  • Defining Disease Ecology
  • Basic Epidemiological Models
  • The Basic Reproductive Number and Population Threshold
  • Frequency-Dependent Models, Individual Heterogeneities, and Superspreaders
  • Extending to Multihost Pathogens
  • Expanding to Multiple Pathogens in Hosts
  • Impacts of Pathogens on Ecosystems
  • Heterogeneity in Space/Landscape Epidemiology
  • Impacts on Hosts
  • Impacts of Climate and Climate Change
  • Applications

Ecology Disease Ecology
Richard S. Ostfeld
  • LAST REVIEWED: 22 February 2018
  • LAST MODIFIED: 22 February 2018
  • DOI: 10.1093/obo/9780199830060-0128


Disease ecology is a rapidly developing subdiscipline of ecology concerned with how species interactions and abiotic components of the environment affect patterns and processes of disease. To date, disease ecology has focused largely on infectious disease. The scientific study of infectious disease has a long history dominated by specialists on the taxa of infectious agents (e.g., bacteriologists, virologists), mechanisms of host defense (e.g., immunologists), effects of infection on individual hosts (e.g., pathologists), effects on host populations (epidemiologists), and treatment (e.g., practicing physicians and veterinarians). Disease ecology arose as scientists increasingly recognized that the interactions between pathogen and host could be conceptually united with other interspecific interactions, such as those between predator and prey, competitors, or mutualists. At its simplest, an infectious disease consists of an interaction between one species of pathogen and one species of host. The evolution of disease ecology since the late 20th century has incorporated additional layers of complexity, including recognition that most pathogens infect multiple species of host, that hosts are infected with multiple pathogens, and that abiotic conditions (e.g., temperature, moisture) interact with biotic conditions to affect transmission and disease. As a consequence, a framework broader than the simplest host-pathogen system is often required to understand disease dynamics. Disease ecologists are interested both in the ecological causes of disease patterns (for instance, how the population density of a host influences transmission rates), and the ecological consequences of disease (for instance, how the population dynamics of a host species change as an epidemic progresses). Consequently, disease ecology today often integrates across several levels of biological organization, from molecular mechanisms of pathology and immunity; to individual-organism changes in health, survival, and reproduction; to population dynamics of hosts and pathogens; to community dynamics of hosts and pathogens; to impacts of disease on ecosystem processes; to ecosystem-level effects of climate change and landscape change on disease.

Historical Developments

The emergence of disease ecology has involved the gradual integration of several distinct lines of inquiry. One foundational development was the creation of a mathematical model of malaria shortly after the initial description of the life cycle of the malaria parasite, Plasmodium, in Anopheles mosquitoes by Sir Ronald Ross (Ross 1915). Ross’s model distinguished subpopulations of mosquitoes and humans that were susceptible from those that were infected, and it tracked the latency to infection both in vector and host. The Ross model was later generalized in models in Kermack and McKendrick 1927, which classified individuals in a host population into the following epidemiological compartments: susceptible (S), exposed (E), infectious (I), or recovered (R), and it tracked the rate at which they transitioned from one class to another. These models were tailored for specific types of diseases according to, for example, whether there is latency from exposure to infectiousness, whether hosts recover, or whether recovered hosts regain susceptibility. Tracking the numbers of individuals in each compartment and rates of transition allowed researchers to quantitatively describe and predict epidemics. Another foundational development was the incorporation of parasites into early experimental ecology. Thomas Park’s observation (Park 1948) that infection by a sporozoan parasite converted a dominant competitor into an inferior one, reversing the outcome of competition between two species of flour beetle (Tribolium spp), strongly influenced population and community ecologists. A third key development was recognition of the profound importance of infectious diseases on host populations, communities, and ecosystems. Examples include descriptions of diseases shaping human history in Diamond 1997 and Dobson and Carper 1996, a study of rinderpest shaping African wildlife communities in Plowright 1982, and Daszak, et al. 1999, which is an exploration of the association of the chytrid fungus Batrachochytrium dendrobatidis with amphibian declines worldwide. Together, these developments allowed epidemics to be understood through models and impressed upon ecologists their importance in affecting population and community dynamics.

  • Daszak, P., L. Berger, A. A. Cunningham, A. D. Hyatt, D. E. Green, and R. Speare. 1999. Emerging infectious diseases and amphibian population declines. Emerging Infectious Diseases 5.6: 735–748.

    DOI: 10.3201/eid0506.990601

    This paper was among the first to describe the effect of pathogen invasions, particularly the chytrid fungus Batrachochytrium dendrobatidis, on amphibian populations and the conservation consequences of emerging diseases of wildlife.

  • Diamond, J. 1997. Guns, germs, and steel: The fates of human societies. New York: W. W. Norton.

    This influential popular book argues that infectious diseases have profoundly affected the course of human civilization. The advent of agriculture in Eurasia caused crowding and the domestication of wild ungulates, which in turn led to zoonotic transmission of animal pathogens that adapted to human hosts (including smallpox, measles, and influenza viruses). Later dispersal of these pathogens with their human hosts transformed the course of history. Revised edition published as recently as 2011.

  • Dobson, A. P., and E. R. Carper. 1996. Infectious diseases and human population history. BioScience 46.2: 115–126.

    DOI: 10.2307/1312814

    These authors describe the effects of human population density, aggregation, age structure, and other demographic variables on disease transmission, linking historical human population dynamics to the history of some major infectious diseases.

  • Kermack, W. O., and A. G. McKendrick. 1927. Contribution to the mathematical theory of epidemics. Proceedings of the Royal Society of London A 115.772: 700–721.

    DOI: 10.1098/rspa.1927.0118

    This foundational paper describes the first models of pathogen transmission in which the host population is divided into an exhaustive set of compartments indicating their infection status: susceptible, exposed, infectious, and recovered. This paper provided the basis for many subsequent models of many infectious diseases.

  • Park, T. 1948. Experimental studies of interspecies competition 1: Competition between populations of the flour beetles, Tribolium confusum Duval and Tribolium castaneum Herbst. Ecological Monographs 18.2: 265–307.

    DOI: 10.2307/1948641

    A classic paper in competition theory, this was highly influential in experimentally demonstrating how parasites could fundamentally alter the outcome of competition between closely related species. Park showed how a competitively dominant species of flour beetle became competitively subordinate when it was infected.

  • Plowright, W. 1982. The effects of rinderpest and rinderpest control on wildlife in Africa. Symposia of the Zoological Society of London 50:1–28.

    A foundational description of the history of rinderpest introduction, via cattle, into populations of wild ungulates in sub-Saharan Africa, this paper describes the consequences of wildlife mortality for African ecosystems, and the effects of livestock vaccination programs on the dynamics of this disease.

  • Ross, R. 1915. Some a priori pathometric equations. British Medical Journal 1.2830: 546–547.

    DOI: 10.1136/bmj.1.2830.546

    After having discovered the life cycle of the malaria parasite (Plasmodium) in mosquitoes in the 1890s, Sir Ronald Ross devised a simple model to describe the relationship among mosquito abundance, Plasmodium infection, and human cases of malaria. This foundational model has influenced malaria models throughout the subsequent century.

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