Thus the existence of population density-dependent thresholds for disease emergence is particularly relevant (26, 27) . This explains the abrupt transitions of urban diseases between non-persistence to endemic and endemic to epidemic behavior as population densities of susceptible humans, hosts, and vectors reach critical densities. The classic illustration is that of measles which, given its particular transmission rate, requires human settlements with population sizes in excess (>250,000) of what historically existed in most pre-industrial states and geographically isolated populations even today (28). Thus, for example, many infectious diseases endemic on continents have not become established on islands despite their occasional introduction and the occurrence of local outbreaks. The same mathematical ecology that explains why measles and virtually all diseases have threshold densities, explains the much lower thresholds existing for vector-borne diseases such as arboviruses (29) . Particularly noteworthy is the theoretical demonstration that the pathogen 'reproductive rate' increases with the square of vector population density. This indicates threshold densities can fast be breached as domestic and peridomestic hosts and vectors expand (or re-expand) their geographic ranges (once they are introduced or re-introduced) and increase their densities. This helps explain the explosive re-emergence of dengue and dengue hemorrhagic fever in the American Tropics as vector populations responded to relaxed controls and new breeding habitats associated with urbanization (30) . This phenomenon can be likened to the gradual build-up of 'dead and down' wood across a forested landscape with a history of fire suppression. The build-up of fuel, like that of host or vector populations, becomes an 'accident waiting to happen' when a single ignition event in one locality, similar to a single infection event, spreads to the entire region.