Group B Streptococcus (GBS) is an opportunistic pathogen that causes sepsis, meningitis, pneumonia, and skin and soft tissue infections in neonates and adults. GBS is well-adapted to survive in humans due to a plethora of virulence mechanisms that afford responses to support bacterial survival in host environments.
Phagocytosed bacteria encounter a range of reactive species, including reactive oxygen species (ROS) such as H2O2 that are generated as part of the host defence. ROS can damage essential bacterial proteins and cell components, consequently impairing bacterial metabolism and cell growth/survival. GBS does not express catalase, an enzyme that decomposes H2O2 to H2O and O2; nonetheless it can tolerate high levels of oxidative stress and survive exposure to high levels of H2O2.
Here, we combined the use of a high-density mutant library with high-throughput, transposon-directed insertion site sequencing (TraDIS) and identified a suite of genes that are essential for GBS survival in H2O2 stress. These genes encode for a variety of factors involved in regulation, metabolism, transport and signal transduction. Interestingly, an o-acetyltransferase (oafA) we identified as essential for survival in H2O2 stress is also required for GBS survival in whole blood and copper stress. Further analyses revealed that deletion of oafA in GBS affects biofilm formation, cell wall integrity and intracellular survival. Overall, this study provides novel insights into factors like oafA that affects cell biology, ultimately providing a better understanding on how GBS resists H2O2 stress and the host immune system.