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About the Authors:
Justin M. Calabrese
* E-mail: [email protected]
Affiliations Smithsonian Conservation Biology Institute, Front Royal, Virginia, United States of America, Helmholtz Centre for Environmental Research-UFZ, Leipzig, Germany
Jesse L. Brunner
Affiliations Cary Institute of Ecosystem Studies, Millbrook, New York, United States of America, School of Biological Sciences, Washington State University, Pullman, Washington, United States of America
Richard S. Ostfeld
Affiliation: Cary Institute of Ecosystem Studies, Millbrook, New York, United States of America
Introduction
Parasites, from nematodes and trematodes to lice and ticks, are typically highly aggregated on their hosts with relatively few individuals hosting the large majority parasites [1]–[3]. Indeed, parasite burdens among hosts are usually described by a negative binomial distribution (NBD) with its characteristic long right tail representing those few highly infected hosts [1], [3]. While many explanations for macroparasite (e.g., helminthes, cestodes, nematodes) aggregation exist, most involve small differences among host in terms of behavior, innate susceptibility, or acquired immune responses being magnified throughout the infection and/or lifetime of the host [1], [4]–[8]. Life-long infections and parasite replication on or in the host tend to increase aggregation, while density-dependent parasite mortality and parasite-induced host mortality work to reduce aggregation [4]. Most arthropod vectors, however, spend only a short time on their hosts and reproduce elsewhere, so these feedbacks have little time to manifest. While variation in extrinsic factors has historically been discussed as a potential cause of aggregation [1], [9], [10], recent studies have focused mainly on identifying the intrinsic host characteristics (e.g., sex, age, activity rates) presumably associated with large parasite burdens [11]–[14].
Understanding the cause(s) vector aggregation on hosts is important because this aggregation can inflate the potential rate of spread of an infection [15], [16]. One widely-cited example is tick-borne encephalitis (TBE), which is caused by a virus transmitted between Ixodes ricinus ticks when they co-feed on hosts such as yellow-necked mice, Apodemus flavicollis [17], [18]. Most TBE transmission occurs on the hosts with the greatest tick burdens [11]. If public health interventions could target the most infested 20% of hosts, transmission of TBE to humans could be effectively reduced by 75% [11], but similar interventions targeted at random hosts could be expected to have only negligible impact [15], [16]. Thus identifying those hosts responsible for feeding and...