Abstract
Super-shedders are infectious individuals that contribute a disproportionate amount of infectious pathogen load to the environment. A super-shedder host may produce up to 10 000 times more pathogens than other infectious hosts. Super-shedders have been reported for multiple human and animal diseases. If their contribution to infection dynamics was linear to the pathogen load, they would dominate infection dynamics. We here focus on quantifying the effect of super-shedders on the spread of infection in natural environments to test if such an effect actually occurs in Mycobacteriumavium subspecies paratuberculosis (MAP). We study a case where the infection dynamics and the bacterial load shed by each host at every point in time are known. Using a maximum likelihood approach, we estimate the parameters of a model with multiple transmission routes, including direct contact, indirect contact and a background infection risk. We use longitudinal data from persistent infections (MAP), where infectious individuals have a wide distribution of infectious loads, ranging upward of three orders of magnitude. We show based on these parameters that the effect of super-shedders for MAP is limited and that the effect of the individual bacterial load is limited and the relationship between bacterial load and the infectiousness is highly concave. A 1000-fold increase in the bacterial contribution is equivalent to up to a 2–3 fold increase in infectiousness.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-016-0323-3) contains supplementary material, which is available to authorized users.
Highlights
The phenomenon of super-shedding, where a small fraction of individuals contributes a disproportionate load of infectious pathogens to the exposure experience of susceptible individuals, has received much attention in the past several years with respect to human disease [1] and selected livestock pathogens, as well as the virtual spread of viruses [2,3,4,5]
If infection is driven by indirect contacts where susceptible individuals are exposed to infectious organisms present in a well-mixed environment, and the contribution of an individual scales linearly with the amount of pathogen shed, individuals shedding pathogens several orders of magnitude higher than the average infectious individual would drive infection dynamics by increasing the total force of infection by a similar order
We have here developed a theoretical basis for the limited effect of the super-shedder paradox in Mycobacterium avium subspecies paratuberculosis (MAP)
Summary
The phenomenon of super-shedding, where a small fraction of individuals contributes a disproportionate load of infectious pathogens to the exposure experience of susceptible individuals, has received much attention in the past several years with respect to human disease [1] and selected livestock pathogens, as well as the virtual spread of viruses [2,3,4,5]. This 10-fold larger force of infection would result in very large outbreaks Such an increase in infection prevalence is generally not observed or expected [13, 14], leading to the so-called super-shedder paradox: an observed high amount of shedding that results in relatively little impact on infection dynamics. This unexpected limited correlation between infectious burden and force of infection may be hypothesized to be due to transmission models where the force of infection is a concave function of the pathogen load rather than a linear function. We show using this model that at least in the case studied here, super-shedding does not induce super-spreading
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