Analyses of contact-tracing data on the spread of infectious disease, combined with mathematical models, show that control measures require better knowledge of variability in individual infectiousness. The SARS epidemic was notable for the existence of'superspreaders' who infected dozens of people, whereas other infectious individuals infected few or none. Were SARS super-spreaders anomalies, or are superspreaders characteristic of most infectious diseases? What effects does heterogeneity in infectious-ness have on disease emergence and control? On page 355 of this issue, Lloyd-Smith et al. provide insight into such questions, and more. The first question any ecologist asks about an invasive species is: what is the invader's intrinsic capacity for population increase? To answer this, the species' basic reproductive number, R_0, is measured by the average number of offspring per capita that survive to reproductive age. For a directly transmitted infectious disease, be it polio, smallpox, SARS, HIV/AIDS or some newly emerging pathogen, R_0 is the average number of infections produced by an infected individual in a susceptible population. If R_0 is less than one, a self-sustaining epidemic is not possible (at least without further pathogen evolution). If R_0 exceeds one, then although early stochastic fluctuations may extinguish the invader, an epidemic is possible. If R_0 is large, an epidemic is virtually certain.
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