the population would go extinct due to a fluctuation in the birth and death events the reservoir in the quiescence buffer population can bring the population back from the brink of extinction. The efficiency of this mechanism for escape is sensitive to the entry and exit rates to and from the quiescent state, respectively. The main difference between our mechanism for escape and the one proposed in [1, 2] is the following. Iwasa and co-workers propose a mechanism based on random search of the state of types of individuals for one that is fitter than the others in the presence of a given selection prossure (drug, etc.). In contrast we have demonstrated here that the overall survival probability of a population may increase by introducing a dormant type. Since this type is unable to reproduce its reproductive fitness is zero, nevertheless the existence of this drug resistant stage is able to improve the fitness of the entire population in as much as the population obtains a higher probability for survival. The mechanism proposed here shares a number of features in common with the phe- nomenon of bacterial persistence [22–25]. Persistence is a form of resistance to antibiotics exhibited by bacterial colonies where resistance is not acquired by a gene mutation which allows the bacteria to grow exponentially fast in the presence of a particular drug. Instead, as schematically shown in Fig. 9, killing of bacteria goes through a fast phase where the population decreases exponentially until the killing rate slows down leaving behind a rem- nant of cells which differ from the sensitive ones in that they are in a dormant state but are otherwise genetically identical to their sensitive counterparts. In fact, when the drug is removed, a colony of “normal” bacteria is regrown from the persistent cells. The mechanism for persistence appears to involve a phenotypic switch [22] where cells switch from a rapidly growing, but drug-sensitive phenotype to a dormant but drug-resistant phenotype, although there has recently been the suggestion that persistence might be a social trait [24]. According to [22], there exist two types of persisters. Type I persisters, according to their terminology, are only produced during the exponential growth phase and therefore their numbers are fixed at the time of innoculation and determined by the size of the innocolum. Type II persisters, on the contrary, divide and grow continuously, but an order of magnitude slower than their non-persistent counterparts, and their numbers are determined by the total population numbers. The quiescence mechanism put forward here is therefore distinct from type I persisters, but very similar to the behaviour exhibited by type II persisters, which means that the analysis methods, in particular, the evolutionary formalism used to study 14