Intestinal helminth co-infection is an unrecognised risk factor for increased pneumococcal carriage density and invasive disease

Alice E Law,Richard K Grencis,Daniel R Neill,Philip J Cooper,Andrea A Lopez Rodas,Rebecca K Shears,Aras Kadioglu

doi:10.1038/s41598-021-86508-4

Abstract

Infection with Streptococcus pneumoniae is the leading cause of death in children and burden of disease is greatest where helminth infections are also common. We investigated the impact of intestinal helminth co-infection on pneumococcal carriage; a risk factor for invasive disease. We used a mouse co-infection model and clinical data to assess the impact of co-infection on carriage density. Co-infection in mice was associated with increased pneumococcal carriage density and dissemination into lungs. Helminth-infected children also exhibited increased carriage density as compared to uninfected children. Anthelmintic treatment may be a cost-effective method of reducing pneumococcal disease burden in lower-income countries.

Highlights

Infection with Streptococcus pneumoniae is the leading cause of death in children and burden of disease is greatest where helminth infections are common
We established a T. muris and S. pneumoniae co-infection model to determine whether soil-transmitted helminth (STH) infection altered pneumococcal carriage density, and/ or dissemination into the lower airways
Mice were infected with T. muris, and 28 days later, when the worms had matured into adults, mice were infected with a carriage-inducing dose of S. pneumoniae

Summary

Introduction

Infection with Streptococcus pneumoniae is the leading cause of death in children and burden of disease is greatest where helminth infections are common. A pathogen’s disease potential can be magnified by their relationship with other pathogens and co-infections involving intestinal helminths are of particular interest due to their ability to modulate systemic host immunity[2,3,4]. This modulation ensures chronicity of infection from childhood through to adult life and influences immune homeostasis and inflammatory responses to microbial p athogens[3,4]. Detailed studies to define the incidence of pneumococcalSTH co-infection in human populations have yet to be performed

Methods

Results

Conclusion