When does a supershedder become a superspreader?: The impact of individual-level heterogeneities on population-level transmission and spread

Individuals vary greatly in both their susceptibility to infection and their likelihood of transmitting infections to others. Evidence from various disease outbreaks suggests that typically a minority of individuals (~20%) cause the majority of new cases (~80%) - these are the so-called "superspreaders". However, it is not clear what characteristics make someone a superspreader.

As we are only too aware from the COVID-19 pandemic, an individual's infection risk depends on how close and for how long they spend near infected individuals, such that some infected individuals may contact a disproportionately high number of susceptible individuals, acting as 'supercontactors'. Hence, supercontactors may indeed be superspreaders and drive transmission for many infectious diseases.

However, it is also possible that some individuals release many more infectious stages than others, acting as 'supershedders', which can also lead to disproportionately greater transmission potential. To complicate matters, these two processes, supershedding and supercontacting, can interact together - either exacerbating transmission (generally, if supershedders also tend to be supercontactors) or diminishing transmission (if supershedders tend to have few contacts, and vice versa).

These processes, whether driven by individuals having large numbers of contacts or being highly infectious, then scale up to determine how fast the parasite spreads through the host population, and the spatial distribution of infection 'hotspots'. As such, understanding the individual characteristics that determine supershedders and supercontactors, and how they are coupled to give rise to superspreaders, are crucial to predicting disease spread and for devising effective control measures.

So far, research on what host characteristics make a superspreader has focussed almost exclusively on pathogenic viral or bacterial outbreaks in humans. While clearly essential from a public health perspective, this narrow focus on certain human pathogens limits our ability to explicitly test the mechanisms underlying superspreading. Furthermore, it is far from clear how ideas of supercontacting and supershedding apply to the vast range of parasites with very different transmission modes and biologies from the pathogens that cause epidemics (or pandemics) in humans.

In particular, parasitic worms (helminths) are a ubiquitous and integral component of all natural ecosystems, playing a vital role in structuring ecological communities and having significant health and economic consequences for wildlife, humans and domestic animals. These helminths typically infect new hosts through long-lived infective stages that reside in the environment, thereby blurring the definition of 'contacts', and making it virtually impossible to determine the number of new infections arising from each initially infected individual.

Hence, established concepts relating supershedding, supercontacting, and superspreading do not apply directly to this important groups of parasites.

Here we will move this field forward through a comprehensive study that uses novel population-level field experiments in a highly tractable yet natural host-parasite system, wood mice and their parasitic worms, in which we can specifically reduce infections in either supershedding or supercontacting individuals. We will pair these field experiments with new theory and robust analytical methods to develop an in-depth understanding of how between-individual variation in infectiousness, movement patterns, and parasite transmission mode interact to drive parasite spread in natural communities.