# Host heterogeneity and unpredictability in parasite outbreaks

## TL;DR

This study shows that host differences in susceptibility and infectiousness don't change parasite spread but make it harder to predict, using beetles and a parasite in experiments and models.

## Contribution

The study provides a rare experimental test of how host heterogeneity affects parasite transmission and predictability using a lab-based system and agent-based modeling.

## Key findings

- Host heterogeneity in susceptibility and infectiousness does not affect parasite spread but increases unpredictability in transmission measures.
- Population mean susceptibility and infectiousness, not heterogeneity, explain differences in parasite transmission.
- High heterogeneity leads to high variability in epidemiological outcomes even with identical starting conditions.

## Abstract

Individuals can differ in how likely they are to acquire parasites (susceptibility) and to pass them on to others (infectiousness). Questions of how those differences affect the spread of parasites are often addressed using mathematical models, and there is little experimental work which has directly tested those predictions. Using a laboratory-based host–parasite system, we experimentally tested how parasite spread is affected by different levels of variation between individuals in susceptibility and infectiousness. We combined our experiments with modeling to show that variation among hosts did not affect parasite spread but did affect the predictability of measures of parasite spread. Future work must test how differences between hosts affect this predictability in more detail.

Experimental tests of the effects of host heterogeneities on parasite transmission are rare; previous studies focus on a single host trait over one generation of transmission. Thus, the long-term epidemiological consequences of interacting host heterogeneities remain unclear. We used a laboratory-based experimental system comprising the red flour beetle (Tribolium castaneum) infected with the eugregarine parasite, Gregarina cloptoni, to show, firstly, that two colonies of the beetle are heterogeneous in their susceptibility and infectiousness to the eugregarine. We then constructed experimental populations that differed in population-level heterogeneity in susceptibility and infectiousness by varying proportions of the colonies in the populations and tracked parasite transmission over eight weeks. We found that differences in parasite transmission among populations were explained by population mean susceptibility and infectiousness, rather than heterogeneity. Finally, to test the effects of heterogeneity on equilibrium parasite transmission we developed an agent-based model (ABM) for our host–parasite system. Results from our model showed that populations with the highest level of heterogeneity had the highest between-simulation variability in epidemiological measures. This demonstrated that even with the same starting conditions, host heterogeneities can drive high levels of uncertainty in epidemiological predictability. Our work presents a rare experimental assessment of how heterogeneities in susceptibility and infectiousness affect parasite transmission, showing that while these heterogeneities may not affect transmission directly, they can still affect epidemic variability, and hence predictability. This variability has considerable consequences for outbreak management strategies yet remains understudied, so further tests of the effects of host heterogeneity on epidemic variability will be important.