NiV emergence in Malaysia occurred in two phases, and our current understanding of the processes leading to its emergence is outlined in figure 5 . Phase I of emergence, the occurrence of human cases, required that only two criteria be met: circulation of the virus in a local bat population and the existence of a pathway for transmission from Pteropus bats to pigs. In phase I, early human cases were directly linked to the transmission of virus from bats to pigs, with all identified cases occurring in the immediate vicinity of the index farm where bat-to-pig transmission ignited rapid pig-to-pig transmission and produced a tight cluster of human cases on the index farm and an adjacent property. Phase II of emergence, incident human cases outside the area of transmission from flying foxes, required that the criteria for phase I be met but also mandated the existence of a pathway for transmission to humans that had become unlinked from the wildlife reservoir. In principle, several scenarios could have produced such a pathway, as illustrated in figure 5 ; however, the evidence amassed here indicates that the causal pathway realized (highlighted in dark blue). Alternative pathways that would have been sufficient to produce both phases of emergence-had they occurred-are indicated by dashed arrows. Specifically, introduction of Nipah virus into an area with extremely dense pigfarming activity (such as Port Dickson in Negeri Sembilan or Sabang Perai Utara in Pulau Penang) probably could have resulted in viral persistence without priming and reintroduction. However, these areas lacked factors further up the causal pathway: the absence of Pteropus bats in these areas prevented viral introduction prior to the establishment of an alternative source of infection (e.g. persistent viral circulation on the index farm in Kinta, Perak). Similarly, if Nipah virus in Malaysia had resulted in human-to-human transmission, an alternative causal pathway could have produced incident human cases outside the area of transmission from flying foxes, as was seen in the Faridpur outbreak in Bangladesh in 2004 [34] , but there is no evidence that such human-to-human transmission occurred in Malaysia [35] . The causal pathway that was realized in Malaysia most probably involved (i) the creation of a pathway for transmission from bats to pigs via agricultural intensification (i.e. dual-use agriculture, or the practice of planting fruit trees on land used for livestock production, and increased fruit production through time) and (ii) repeated introduction of the virus into a high-turnover commercial pig population in Perak that led to viral persistence and set the stage for phase II of the emergence process. FF, flying fox. some years after the maturation of the mango trees owing to chance events within the system, e.g. fruit bat population dynamics, migratory behaviour or the dynamics of NiV in bat populations. This is supported by our own work on Hendra virus which suggests that, when the virus is actively transmitted within a bat colony, there is a heightened chance of repeated spillover, but circulation of the virus in bats is unlikely at any given place and time [36] . On the other hand, we cannot rule out the possibility that specific local conditions in late 1996 and early to mid-1997 caused increased viral shedding among bats in the area surrounding the index farm, thereby increasing the risk of cross-species transmission to pigs. Given the high mobility of flying foxes and the seasonal fluctuation in colony sizes in peninsular Malaysia [33] , NiV is probably transmitted regularly between roost sites and throughout the region. Such dynamics explain the ubiquity of NiV antibodies, and our data suggest that flying foxes and possibly NiV were regularly present near the index farm in Perak prior to the 1998 -1999 outbreak. Thus, we propose that it is plausible that flying foxes repeatedly introduced the virus onto the index farm in 1997.