A survey and analysis is presented of the population biology of the badger (Meles meles) and the epidemiology of bovine tuberculosis (Mycobacterium bovis) within badger populations. Simple mathematical models are used to further our understanding of the processes that control the dynamics of badger abundance and disease transmission. Special attention is given to the identification of areas in which current knowledge is inadequate, and to future research needs. The badger is shown to have a low intrinsic population growth rate, a not insignificant maturation delay to first breeding, to produce small litters of cubs which experience high rates of mortality in their first year of life but low rates thereafter, and to exhibit limited powers of dispersal. Population abundance is largely determined by habitat type and long term stability appears to arise primarily as a consequence of density-dependent constraints on fecundity. Such constraints are thought to only operate at densities close to the carrying capacity of the habitat. Cyclic fluctuations in abundance, with a period of between six and eight years, may occur in areas of moderate to poor habitat. Such fluctuations will be most apparent with respect to cub abundance as opposed to adult density. Bovine tuberculosis is endemic within many badger populations throughout regions of Britain but is particularly prevalent in areas of good badger habitat in the southwest of England. Current evidence suggests that badgers play a significant role in disease transmission to cattle. It is argued that the infection is able to persist in high, moderate and low density badger populations. The observed stability of the disease appears to be a consequence of `pseudo-vertical' transmission (from parent to new born offspring), the long duration of infectiousness of infected animals (low disease-induced mortality rate), the presence of carriers and inactive cases and the social organization and behaviour of the host species. Disease prevalence is likely to be related to badger density although in a nonlinear manner. Control measures based on the removal of infected social groups of badgers in the southwest of England appear to have reduced the force of infection within badger populations by approximately 50%. The disease, however, remains endemic but at low levels of prevalence. The reduction in the force of infection has reduced the frequency of disease transmission to cattle herds. Eradication of the infection within badger populations may not be necessary for the short-term control of the infection in cattle. The persistence of low levels of infection in low density badger populations (suppressed by control measures), in areas of intensive cattle farming activity, however, presents a continual threat to cattle health in the long term. The ability of badger populations to recover from substantive reductions in density is poor, with a return time (to the pre-control state) of approximately five years. Small reductions in abundance, however, are likely to enhance net population growth rates as a consequence of the relaxation of density-dependent constraints on fecundity (the natural population regulatory mechanism). As such, rapid population growth to precontrol levels is predicted, following small reductions in density. As a consequence of the requirement for continual and substantive suppression of badger abundance (a renewable resource) in areas of intensive cattle farming it is suggested that alternative methods of disease control should be actively sought with a view to the design of more effective long-term control policies.