Highly Pathogenic Avian Influenza virus (HPAI), Classical Swine Fever Virus (CSFV), and Foot-and-Mouth Disease Virus (FMDV) are highly contagious viruses affecting livestock and are among the World Organisation for Animal Health (OIE) listed diseases. The consequences of their recent epidemics in the Netherlands
[1]–
[3] have been enormous and include high mortality rates, economic losses incurred in implementing control strategies and reduced exports, and for HPAI, a risk of spread to humans
[1],
[4]. During the 2003 HPAI epidemic in the Netherlands, following detection of the first outbreaks in late February, movement bans were implemented followed by other control measures. Nevertheless, more farms became infected and therefore in the second week of March the measure of preventively culling contiguous flocks was adopted. In the end, 255 flocks were affected over the course of the epidemic and close to 30 million birds were culled; in addition, the virus was transmitted to 89 people causing one fatality
[4]. Between 80% and 90% of the outbreaks occurred through untraced routes, with the farm infection hazard increasing in the vicinity of earlier infected (but as yet undetected) farms
[5],
[6]. The sustained between-farm transmission despite extensive control measures demonstrated the difficulty of controlling HPAI spread in poultry-dense areas.
The mechanisms underlying the between-farm spread of HPAI are not clearly understood, especially those of indirect transmission (involving vectors or fomites and possibly wind-borne transfer), as opposed to direct transmission (transportation of live animals between farms)
[1],
[5],
[6]. Indirect transmission has played a major role in large epidemics involving viruses such as CSFV
[7],
[8] and FMDV
[9]. In the analysis of the Dutch 2003 HPAI epidemic data, Boender et al.
[5] used statistical spatial-temporal modelling techniques and identified high risk areas for epidemic spread. The same technique of using a spatial transmission kernel was used by
[9],
[10] in studies on the between-farm spread of FMDV in Great Britain. Although important insights, helpful for the development of control strategies laid out in contingency plans, were gained from these analyses, a lack of mechanistic (as opposed to statistical) understanding of the between-farm spread currently impedes the further improvement of these strategies. For example, the extent to which biosecurity measures on farms contribute to limiting indirect transmission is unclear, as is how these measures can be improved.
With stringent control measures put in place during epidemics including bans on the movement of animals, the direct spread of the virus is reduced. Therefore, indirect routes such as contamination of personnel and fomites do become the only pathway of virus spread. Indirect transmission could arise from human vectors transferring infective excreta such as manure from infected to recipient animals
[11]–
[13], mechanical transfer of excreta
[6],
[13],
[14] or a possible combination of these mechanisms.
The need to determine whether wind-borne transportation of the virus is one of the untraced routes of HPAI spread between farms is apparent. The simplest way possible is that where the virus is transported by wind from an infected farm directly to an uninfected farm as has been considered in plume models for FMDV spread
[15]–
[19]. Otherwise, the dispersal may be through a multi-stage process. In such a process, the virus may be transported from infected animals to recipient animals by wind during certain parts of the route and by other means (for example humans and vehicles) on other parts. Both scenarios require quantitative insight into the deposition pattern of (contaminated) farm dust.
Davis et al.
[20] conducted a study on the spread of Equine Influenza in Australia in 2007. They concluded that virus was spread over 1–2 km via wind-borne aerosols. However, the significance of wind-borne spread of HPAI is subject to divergent opinion. This lack of consensus was mentioned by Power
[21], who also noted the absence of any testing to support or refute a wind-borne theory of HPAI spread during the epidemics in Italy and the Netherlands. This route is often considered insignificant, but with no serious underpinning based on quantitative evidence. For example, Swayne and Suarez
[11] suggest that although aerosols and wind-borne contamination may have caused some secondary spread during the New South Wales HPAI H7N4 epidemic in 1997, they should not be regarded as important in the spread of infection. Yet in the analysis by Power
[21] of the 2004 H7N3 AI epidemic in Abbotsford, BC Canada, air samples taken around the infected poultry houses confirmed the circulation of HPAI in the air outside the barns. This motivates our aim to quantitatively assess whether, and to what extent, this route may have played a role in the Dutch 2003 HPAI epidemic.
We do this by developing a model for wind-borne transmission of HPAI between farms, and comparing its predictions for the distance-dependent wind-borne transmission risk with the observed transmission risk in the Dutch 2003 H7N7 epidemic
[5]. In our analysis, where possible, we use the Dutch 2003 H7N7 HPAI strain to quantify HPAI-specific parameters such as the within-flock basic reproduction ratio
. In our model, we consider the wind-borne dispersal and deposition of farm dust contaminated with HPAI. Our way of including deposition (that is, particle settling and accumulation on the ground) is in contrast to the existing plume models for wind-borne spread of FMDV and allows us to consider infection risks from inhalation by poultry of the originally deposited dust that becomes air-borne due to chicken activity instead of direct inhalation of air-borne dust arriving at ground level. We also include virus decay, as this influences the infection risks arising from deposited dust. Our model framework also allowed us to investigate dust deposition patterns between farms, which is relevant as a possible component of multi-stage indirect transmission mechanisms.
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