Abstract

A major challenge in disease ecology is to understand the role of individual variation of infection load on disease transmission dynamics and how this influences the evolution of resistance or tolerance mechanisms. Such information will improve our capacity to understand, predict, and mitigate pathogen-associated disease in all organisms. In many host-pathogen systems, particularly macroparasites and sexually transmitted diseases, it has been found that approximately 20% of the population is responsible for approximately 80% of the transmission events. Although host contact rates can account for some of this pattern, pathogen transmission dynamics also depend upon host infectiousness, an area that has received relatively little attention. Therefore, we conducted a meta-analysis of pathogen shedding rates of 24 host (avian) – pathogen (RNA-virus) studies, including 17 bird species and five important zoonotic viruses. We determined that viral count data followed the Weibull distribution, the mean Gini coefficient (an index of inequality) was 0.687 (0.036 SEM), and that 22.0% (0.90 SEM) of the birds shed 80% of the virus across all studies, suggesting an adherence of viral shedding counts to the Pareto Principle. The relative position of a bird in a distribution of viral counts was affected by factors extrinsic to the host, such as exposure to corticosterone and to a lesser extent reduced food availability, but not to intrinsic host factors including age, sex, and migratory status. These data provide a quantitative view of heterogeneous virus shedding in birds that may be used to better parameterize epidemiological models and understand transmission dynamics.

Highlights

  • In the last century, there has been an unprecedented increase in the numbers of emerging infectious diseases (EIDs), which pose significant risks to wild and domestic animal and human populations [1]

  • We comprehensively evaluated the inequality of viral load and present a meta-analysis of 24 avianvirus experimental infection studies, which included 17 species of birds and five RNA viruses of three different families, Orthomyxoviridae, low and high pathogenic avian influenza virus (LP- and HPAIV); Flaviviridae, West Nile virus (WNV) and St

  • Experimental Viral Infection Studies We identified experimental infection studies from a variety of host-pathogen systems that satisfied the following criteria: (a) individuals in each experiment were infected with a known dose of a viral pathogen, (b) the experimental birds were wild-type or wild-caught, so as to represent natural genetic variation, (c) pathogen load in the avian host was monitored for the entire infectious period, and (d) host pathogen load was measured at an anatomic site most relevant to transmission for a given host-pathogen system

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Summary

Introduction

There has been an unprecedented increase in the numbers of emerging infectious diseases (EIDs), which pose significant risks to wild and domestic animal and human populations [1]. Predicting the spread of a disease and changes in the number of infected individuals within a population is typically performed using epidemiological models, [2,3] which track the number of susceptible, infected, and recovered individuals. These models frequently assume a homogeneous population in which the ‘infected’ are infectious. We know that populations are heterogeneous and that individuals vary in their ability to maintain pathogens, with some individuals exhibiting high pathogen loads Given the same exposure rate we know that individuals vary in the ultimate pathogen load that they develop [7,11,12]

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