Heterogeneity in host populations and communities can have large effects on the transmission and control of a pathogen. In extreme cases, a few individuals give rise to the majority of secondary infections, which have been termed super spreading events. Here, we show that transmission of West Nile virus (WNV) is dominated by extreme heterogeneity in the host community, resulting in highly inflated reproductive ratios. A single relatively uncommon avian species, American robin (Turdus migratorius), appeared to be responsible for the majority of WNV-infectious mosquitoes and acted as the species equivalent of a super spreader for this multi-host pathogen. Crows were also highly preferred by mosquitoes at some sites, while house sparrows were significantly avoided. Nonetheless, due to their relative rarity, corvids (crows and jays) were relatively unimportant in WNV amplification. These results challenge current beliefs about the role of certain avian species in WNV amplification and demonstrate the importance of determining contact rates between vectors and host species to understand pathogen transmission dynamics.
Disease has caused striking declines in wildlife and threatens numerous species with extinction. Theory suggests that the ecology and density-dependence of transmission dynamics can determine the probability of disease-caused extinction, but few empirical studies have simultaneously examined multiple factors influencing disease impact. We show, in hibernating bats infected with Geomyces destructans, that impacts of disease on solitary species were lower in smaller populations, whereas in socially gregarious species declines were equally severe in populations spanning four orders of magnitude. However, as these gregarious species declined, we observed decreases in social group size that reduced the likelihood of extinction. In addition, disease impacts in these species increased with humidity and temperature such that the coldest and driest roosts provided initial refuge from disease. These results expand our theoretical framework and provide an empirical basis for determining which host species are likely to be driven extinct while management action is still possible.
West Nile virus (WNV) has caused repeated large-scale human epidemics in North America since it was first detected in 1999 and is now the dominant vector-borne disease in this continent. Understanding the factors that determine the intensity of the spillover of this zoonotic pathogen from birds to humans (via mosquitoes) is a prerequisite for predicting and preventing human epidemics. We integrated mosquito feeding behavior with data on the population dynamics and WNV epidemiology of mosquitoes, birds, and humans. We show that
Culex pipiens, the dominant enzootic (bird-to-bird) and bridge (bird-to-human) vector of WNV in urbanized areas in the northeast and north-central United States, shifted its feeding preferences from birds to humans by 7-fold during late summer and early fall, coinciding with the dispersal of its preferred host (American robins,
Turdus migratorius) and the rise in human WNV infections. We also show that feeding shifts in
Cx. tarsalis amplify human WNV epidemics in Colorado and California and occur during periods of robin dispersal and migration. Our results provide a direct explanation for the timing and intensity of human WNV epidemics. Shifts in feeding from competent avian hosts early in an epidemic to incompetent humans after mosquito infection prevalences are high result in synergistic effects that greatly amplify the number of human infections of this and other pathogens. Our results underscore the dramatic effects of vector behavior in driving the transmission of zoonotic pathogens to humans.
Emerging vector-borne diseases represent an important issue for global health. Many vector-borne pathogens have appeared in new regions in the past two decades, and many endemic diseases have increased in incidence. Although introductions and local emergence are frequently considered distinct processes, many emerging endemic pathogens are in fact invading at a local scale coincident with habitat change. We highlight key differences in the dynamics and disease burden that result from increased pathogen transmission following habitat change compared with the introduction of pathogens to new regions. Truly in situ emergence is commonly driven by changes in human factors as much as by enhanced enzootic cycles whereas pathogen invasion results from anthropogenic trade and travel and suitable conditions for a pathogen, including hosts, vectors, and climate. Once established, ecological factors related to vector characteristics shape the evolutionary selective pressure on pathogens that may result in increased use of humans as transmission hosts. We describe challenges inherent in the control of vector-borne zoonotic diseases and some emerging non-traditional strategies that may be more effective in the long term.
Sea stars inhabiting the Northeast Pacific Coast have recently experienced an extensive outbreak of wasting disease, leading to their degradation and disappearance from many coastal areas. In this paper, we present evidence that the cause of the disease is transmissible from disease-affected animals to apparently healthy individuals, that the disease-causing agent is a virus-sized microorganism, and that the best candidate viral taxon, the sea star-associated densovirus (SSaDV), is in greater abundance in diseased than in healthy sea stars.
The distribution and intensity of transmission of vector-borne pathogens can be strongly influenced by the competence of vectors. Vector competence, in turn, can be influenced by temperature and viral genetics. West Nile virus (WNV) was introduced into the United States of America in 1999 and subsequently spread throughout much of the Americas. Previously, we have shown that a novel genotype of WNV, WN02, first detected in 2001, spread across the US and was more efficient than the introduced genotype, NY99, at infecting, disseminating, and being transmitted by Culex mosquitoes. In the current study, we determined the relationship between temperature and time since feeding on the probability of transmitting each genotype of WNV. We found that the advantage of the WN02 genotype increases with the product of time and temperature. Thus, warmer temperatures would have facilitated the invasion of the WN02 genotype. In addition, we found that transmission of WNV accelerated sharply with increasing temperature, T, (best fit by a function of T4) showing that traditional degree-day models underestimate the impact of temperature on WNV transmission. This laboratory study suggests that both viral evolution and temperature help shape the distribution and intensity of transmission of WNV, and provides a model for predicting the impact of temperature and global warming on WNV transmission.
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