Avian diversity and West Nile virus: testing associations between biodiversity and infectious disease risk

Abstract

The emergence of several high profile infectious diseases in recent years has focused attention on our need to understand the ecological factors contributing to the spread of infectious diseases. West Nile virus (WNV) is a mosquito-borne zoonotic disease that was first detected in the United States in 1999. The factors accounting for variation in the prevalence of WNV are poorly understood, but recentideas suggesting links between high biodiversity and reduced vector-borne disease risk may help account for distribution patterns of this disease. Since wild birds are the primary reservoir hosts for WNV, we tested associations between passerine (Passeriform) bird diversity, non-passerine (all other orders) bird diversity and virus infection rates in mosquitoes and humans to examine the extent to which bird diversity is associated with WNV infection risk. We found t h at non-passerine species richness (number of non-passerine species) was significantly negatively correlated with both mosquito and human infection rates, whereas there was no significant association between passerine species richness and any measure of infection risk. Our findings suggest that non-passerine diversity may play a role in dampening WNV amplification rates in mosquitoes, minimizing human disease risk.

Figure 1

Map of St Tammany Parish, Lousiana with the locations of study sites. On the false colour infrared image, vegetated areas appear in shades of red and brown, open water in blue and black, wetland areas in greenish grey to reddish blue, and developed land in light blue and white.

Figure 2

Associations between measures of avian diversity or abundance and mosquito infection rates; r²=coefficient of determination for linear regression tests with *p≤0.05 and **p≤0.01. (a) Non-passerine species richness versus Cx. species infection prevalence (MLE). (b) Non-passerine species richness versus Cx. nigripalpus MLE. (c) Non-passerine species richness versus density of infected Cx. species (DIM). (d) Non-passerine species richness versus Cx. nigripalpus DIM. (e) Passerine species richness versus Cx. species MLE. (f) Passerine species richness versus Cx. nigripalpus MLE. (g) Passerine species richness versus Cx. species DIM. (h) Passerine species richness versus Cx. nigripalpus DIM. (i) Non-passerine abundance versus Cx. species MLE. (j) Non-passerine abundance versus Cx. nigripalpus MLE. (k) Non-passerine abundance versus Cx. species DIM. (l) Non-passerine abundance versus Cx. nigripalpus DIM.

Figure 3

Relationship between human WNV disease incidence by county and non-passerine species richness in (a) 2002 and (b) 2003. In minimum adequate multiple regression models, non-passerine species richness was the sole predictor of disease incidence in 2002 (r=−0.52, t=−3.79, p<0.001), and one of two predictors of disease incidence in 2003 (r=−0.34, t=−2.49, p<0.05).