Superspreading and the impact of individual variation on disease emergence

Supplementary Table 1 A summary of results from our statistical analysis of uncontrolled outbreaks, corresponding to the results shown in Figure 1a-c of the main article. Supplementary Table 2 Detailed results from our statistical analysis of uncontrolled outbreaks (elaborating on the summary shown in Supplementary Table 1), and from the analysis of data from four outbreaks before and after control measures were applied. Supplementary Figures Supplementary Figure 1. Prediction of SSE frequency. Supplementary Figure 2. Branching process results for Z~NegB(R 0 ,k). Supplementary Figure 3. Impact of control measures. Supplementary Figure 4. Estimation of the negative binomial dispersion parameter k from full datasets and from mean and proportion of zeroes. Here we summarize some of the known factors that contribute to differences in infectiousness among individuals, gathered from primary reports (including the SSE reports collected in Section 3.2.1, below) and from insightful discussions in the literature 1-8. This is a broad and complex topic and we do not intend this section as a complete review—we intend simply to delineate important issues and spur further research, which will be required to make practical use of the findings presented in the main text, particularly with regard to targeting more-infectious individuals for control. Variation in individual reproductive number arises due to a combination of host, pathogen and environmental effects. At the host level, distributions of contact rates are often skewed 9-13 and index cases in SSEs are often noted to have high numbers of occupational or social contacts 7,10,14. Increased transmission is correlated with host activities that facilitate pathogen dispersion, such as food handling 15 and singing 16,17. Transmission rates can exhibit strong age-dependence 10,18 , and previously vaccinated hosts often are less infectious 19,20. A recent experimental study documented substantial variation among human hosts in the amount of 'exhaled bioaerosols' (small droplets of airway-lining fluid) generated during normal breathing, suggesting a mechanism for variation in infectiousness for droplet-or aerosol-transmitted pathogens 21. (This study also demonstrated a potential means to reduce infectiousness by altering airway surface properties using inhaled saline solution.) Other relevant host factors may include hygiene habits, immunocompetence, norms regarding bodily contact, and tendency to seek treatment or comply with control measures. Host-pathogen interactions affect transmission rates via variation in pathogen load or shedding 15,20 and in symptom severity (which may increase transmission via greater shedding or decrease transmission due to reduced contact rate 10,15,19,20). Severe coughing, due either to pulmonary …