The effective reproduction number R, which describes transmission once an epidemic is underway, declined during the course of the observed epidemics ( Figure 3C ). At the level of individuals, vaccination coverage reduced the number of secondary cases per rabid dog ( Figure 4B ). More than 300 vaccinated dogs were identified by contact tracing as having been bitten by rabid animals. Only ten of these animals showed any signs indicative of rabies, although in the absence of vaccination approximately 50% (P rabiesjbite ¼ 0.49) ( Table 1) of these would have been expected to succumb to the disease. Individual actions by dog owners such as tying or killing exposed or infectious animals also had an impact. By killing rabid dogs, villagers reduced the overall average infectious period by around 16% (3.7 d for rabid animals that died from the disease versus 3.1 d for all infected animals, including those that were killed). However, there were no consistent declines through time in the number of bites by rabid dogs ( Figure S3 ). Thus we consider vaccination to have been the overwhelming factor in curtailing the outbreaks ( Figure 4A ). From our estimates of R 0 , we calculate the deterministic critical vaccination threshold for rabies elimination in rural To calculate R 0 , we excluded dogs that were killed, tied, or those that disappeared before biting any other dogs. Variability in biting behaviour means that a small number of individuals disproportionately affect transmission and can potentially spark an epidemic, but since most individuals cause few, if any, infections, R 0 is low and most introductions quickly die out ( Figure 4C ). (B) Exponential epidemic growth in Serengeti (blue, R 0 ; 1.2) and Ngorongoro (red, R 0 ; 1.1) districts. The R 0 estimates from the epidemic trajectories were relatively insensitive to the period used for fitting the exponential curve. The inset shows the distribution of R 0 estimates based on fitting to different regions of the time series. (C) The effective reproductive number, R, (averaged over three-month intervals) for Serengeti (blue) and Ngorongoro (red) districts measured from reconstructed epidemic trees that incorporate prior knowledge on who infected whom. Dots indicate the number of secondary cases resulting from each primary case (inferred from the composite tree of most likely links, with random jitter to avoid superposition on the y-axis). R 0 estimated from these reconstructions (during the period of exponential epidemic growth) was ;1. The exponential growth rates of the epidemics were estimated by fitting exponential curves to monthly time series of rabies incidence and converted to estimates of R 0 using the serial interval distribution from the contact tracing data in Tanzania (see Materials and Methods). Estimates based on weekly data are shown in parentheses. The estimated period of exponential epidemic growth, the year of the epidemic onset, and a description of the epidemic setting (where available) are listed. For populations that were partially vaccinated, we corrected our R 0 estimates by dividing by the proportion of vaccinated animals at the onset of the outbreak. Our estimates show that R 0 for canine rabies is inherently low throughout its historic global range. doi:10.1371/journal.pbio.1000053.t002 We found no effect of age on the frequency of litters for female dogs older than 3 months. Domestic dog population growth was estimated from the demography data collected in Serengeti district (r dogs ) and confidence intervals generated from bootstrapping the data. Domestic dog population densities for 2004 were estimated from 2002 national census data (with projected human population growth rates of 2.6% and 3.8% per annum in Serengeti and Ngorongoro respectively) and human:dog ratios (generated from household questionnaires). Alternate estimates of domestic dog population growth rates were extrapolated for each district (r Serengeti and r Ngorongoro ) using these data. Overall domestic dog densities are presented despite considerable variation at the village level. doi:10.1371/journal.pbio.1000053.t003 Figure 4 . The Impact of Vaccination on Transmission (A) The size of village-level outbreaks (defined as at least two cases not separated by more than one month, isolated cases are assumed to be nonpersistent introductions) in Serengeti (blue, n ¼ 138) and Ngorongoro (red, n ¼ 20) districts plotted against village-specific vaccination coverage at the outbreak onset. Coverage was extrapolated from a demographic model initialized with village-specific dog population estimates and incorporating village-specific vaccination data. Gray shading and contours correspond to the probability of observing an outbreak of a particular size or less, generated from 10,000 stochastic simulations of rabies transmission for every initial vaccination coverage (contours were calculated conditional upon .1 secondary case occurring). The inset illustrates a village-level example of the susceptible reconstruction used to calculate instantaneous vaccination coverage plotted beside rabies cases in that village.