Several mechanisms have been previously proposed for the appearance of NiV in pig and human populations in 1998. One frequently cited explanation is that flying foxes harbouring NiV were new to the region where transmission to pigs occurred, driven there by climatic anomalies. In late 1997, an El Niñ o Southern Oscillation-related drought and burning of forested land in Sumatra and Kalimantan (Indonesia) created an atmospheric haze across Sumatra and peninsular Malaysia [18] . One of us (K.B.C., see group author list) hypothesized that this atmospheric haze caused atypical flying fox immigration from Sumatra across the Straits of Malacca into peninsular Malaysia and northward towards Perak [18] . This hypothesized movement of flying foxes into an area with large pig farms potentially outside the species' normal range was proposed to have precipitated transmission of the virus from bats to pigs. However, a retrospective diagnosis of human NiV encephalitis cases on the index farm in early 1997 indicates that bat-to-pig transmission did not result from these specific environmental conditions. In particular, seven of these cases occurred prior to the rise in airborne particulate matter that is diagnostic of the haze event, which peaked in September 1997 [18] . The recognition of cases prior to the haze event refutes the hypothesis that this event drove initial cross-species transmission (table 1) . Furthermore, at the time of the major outbreak in pigs and humans, NiV antibodies were found to be widespread in flying fox colonies within peninsular Malaysia [12] , suggesting that the outbreak was not the result of a (recent) point source introduction of the virus into the bat population, as previously suggested [18] .