Date Published: April 20, 2012
Publisher: Public Library of Science
Author(s): Simon M. Firestone, Naomi Cogger, Michael P. Ward, Jenny-Ann L. M. L. Toribio, Barbara J. Moloney, Navneet K. Dhand, Alex R. Cook. http://doi.org/10.1371/journal.pone.0035284
The influences of relative humidity and ambient temperature on the transmission of influenza A viruses have recently been established under controlled laboratory conditions. The interplay of meteorological factors during an actual influenza epidemic is less clear, and research into the contribution of wind to epidemic spread is scarce. By applying geostatistics and survival analysis to data from a large outbreak of equine influenza (A/H3N8), we quantified the association between hazard of infection and air temperature, relative humidity, rainfall, and wind velocity, whilst controlling for premises-level covariates. The pattern of disease spread in space and time was described using extraction mapping and instantaneous hazard curves. Meteorological conditions at each premises location were estimated by kriging daily meteorological data and analysed as time-lagged time-varying predictors using generalised Cox regression. Meteorological covariates time-lagged by three days were strongly associated with hazard of influenza infection, corresponding closely with the incubation period of equine influenza. Hazard of equine influenza infection was higher when relative humidity was <60% and lowest on days when daily maximum air temperature was 20–25°C. Wind speeds >30 km hour−1 from the direction of nearby infected premises were associated with increased hazard of infection. Through combining detailed influenza outbreak and meteorological data, we provide empirical evidence for the underlying environmental mechanisms that influenced the local spread of an outbreak of influenza A. Our analysis supports, and extends, the findings of studies into influenza A transmission conducted under laboratory conditions. The relationships described are of direct importance for managing disease risk during influenza outbreaks in horses, and more generally, advance our understanding of the transmission of influenza A viruses under field conditions.
Influenza A viruses are enveloped RNA viruses of the family Orthomyxoviridae, and a major cause of morbidity and mortality in both humans and livestock, worldwide , , . Spread may be via direct contact, over short distances on large ‘cough’ droplets (diameter >10 µm), over longer distances in aerosols of small droplet nuclei (diameter <10 µm) and on fomites , . Meteorological variables such as air temperature, relative humidity, rainfall and wind have been suggested as important drivers of the spread and seasonality of influenza in both human , , ,  and animal populations . Recently, Lowen et al. described, under laboratory conditions, how relative humidity and ambient temperature combine to influence the transmission of both seasonal (A/H3N2) and pandemic (A/H1N1) human influenza A , , . The effects of several other environmental variables (soil pH, sunlight and surface permeability) on the survivability of influenza A viruses were established in earlier laboratory-based experimentation , . Analyses of the contribution of wind to the spread of epidemics of influenza, and indeed other infectious diseases, are more limited. Most studies present either circumstantial evidence that the mean direction of epidemic spread coincides with prevailing wind conditions at the time of an outbreak , , analyses of data aggregated to a low temporal or spatial resolution , , or associate spread from a small number of sources with atmospheric dispersal modelling outputs . Such research must also overcome the added complexity of movement of individuals within the population at risk. To our knowledge, this empirical analysis provides the first estimates of the contribution of humidity, air temperature and wind to the spread of an actual outbreak of influenza (‘in the field’). We have demonstrated that it is possible to detect an association between wind velocity and disease spread, and directly estimate the strength of such an association. This advances our understanding of the windborne spread of influenza from purely circumstantial association to a hypothesis statistically-tested with empirical data. Source: http://doi.org/10.1371/journal.pone.0035284