Beginning on January 1, 2002 the person-time at risk was divided into three-week time strata. Control periods were chosen by matching the hazard period by day of the week within the stratum, and could both precede, both follow, or straddle the hazard period [26, 27] . Random directionality of control selection was used in order to avoid biases that can occur with unidirectional or uniform bidirectional control selection [26] . The 1-3 day incubation period of S. pneumoniae was used to estimate the lag days between acute environmental occurrence and case onset, or plausible effect period [28] . We also evaluated effects during the period immediately preceding incubation (i.e., 4-6 day lags) to evaluate the possibility that environmental conditions might affect risk via enhanced transmission of S. pneumoniae. We evaluated the effects of both raw environmental exposures, and quantile ranks within time strata through construction of conditional logistic regression models [24] . Analyses were performed using SAS version 8.01 (SAS Institute, Cary, NC) and Stata version 9.1 (Stata Corporation, College Station, TX). Both spectral decomposition and construction of autocorrelograms identified annual periodicity of infection, with peak incidence in mid-February (phase = 6 weeks) (Figures 1 and 2) . Strong statistical evidence for seasonal oscillation was obtained from Poisson regression models (P for seasonal oscillation < 0.001). A significant annual increase in incidence was seen throughout the study period, though this was more marked prior to 2004 (IRR per year 1.34, 95% CI 1.08 to 1.66) than subsequently (IRR 1.22, per year 95% 1.16 to 1.34) (Figure 3 ). We found no clear trends in the incidence of IPD or case-fatality in individual age groups, and no significant heteroge-