# Co‐Infection, but Not Infection Intensity, Increases Shedding in a Gastrointestinal Helminth of Gamebirds

## TL;DR

Co-infection with other parasites increases shedding of a gastrointestinal worm in gamebirds, more than the worm's infection intensity alone.

## Contribution

This study shows co-infection, not infection intensity, drives increased shedding of Heterakis gallinarum in gamebirds.

## Key findings

- Infection intensity was a poor predictor of Heterakis gallinarum shedding.
- Co-infection with Syngamus trachea, Capillaria spp., and/or Eimeria spp. increased shedding intensity.
- Each additional co-infection further increased H. gallinarum shedding.

## Abstract

Host heterogeneity in disease transmission is commonly seen across host‐pathogen systems, and identifying individuals who contribute disproportionately to pathogen transmission (i.e., superspreaders) is key to understanding disease dynamics and managing outbreaks. It is often assumed that shedding intensity is directly proportional to infection intensity. However, theory predicts that co‐infection might modulate the relationship between infection intensity and shedding, promoting increased onward transmission. Here, we quantify the relative importance of infection intensity and co‐infection on shedding in Heterakis gallinarum, a gastrointestinal helminth of gamebirds, in a population of ring‐necked pheasants during the shooting season of 2023. We found that infection intensity was a poor predictor of shedding intensity. Instead, increased shedding was linked to co‐infections with other endoparasites. Hosts co‐infected with Syngamus trachea, Capillaria spp. and/or Eimeria spp. exhibited higher shedding intensity of H. gallinarum than those infected with H. gallinarum alone. This effect was additive, with each additional co‐infection further increasing H. gallinarum shedding. There were no sex differences in shedding, but male hosts had higher H. gallinarum infection intensities. Our results show that shedding intensity is not simply explained by infection intensity, but rather is the result of complex host–parasite and parasite–parasite interactions. This highlights the importance of considering such interactions in understanding disease emergence and persistence in natural populations.

Host heterogeneity in disease transmission is influential in shaping disease dynamics, but its drivers remain poorly understood. Shedding intensity is often assumed to be directly proportional to infection intensity; however, we found that infection intensity was a poor predictor of shedding intensity in Heterakis gallinarum, a gastrointestinal helminth of gamebirds. Instead, increased shedding was linked to co‐infections with other endoparasites, highlighting the importance of complex host–parasite and parasite–parasite interactions for disease transmission dynamics.