A fast-rising strep bacterium has become increasingly notorious for causing serious infections in humans, including complications that can lead to muscle damage and patient death. New Houston Methodist research sheds light on how Streptococcus Dysgalactiae Subspecies Equisimilis (SDSE) causes disease and may provide important insights to aid in vaccine development.
Led by James Musser, M.D., Ph.D., chair of the Department of Pathology and Genomic Medicine and director of the Center for Infectious Diseases at Houston Methodist, the study appears in the American Journal of Pathology.
To better understand how SDSE causes disease compared to its better-known close relative, Strep A, Houston Methodist scientists used a genomic screening method known as TraDIS, to test gene function in SDSE. The study examined two closely related SDSE strains, which helped detect subtle strain‑specific differences that influence infection behavior.
"We identified several genes that were essential for bacterial survival in both laboratory and infection conditions," Musser said. "The study also identified various genes in each strain that influenced the bacteria's ability to grow and persist during muscle infection."
Unexpectedly, several genes traditionally associated with Strep A infection were found to reduce the survival and growth in SDSE when active, suggesting fundamental differences in how the two closely related bacteria cause disease.
"By defining which genes are truly required for growth and survival of the bacteria during infection, this work provides a foundation for understanding how SDSE causes severe disease and provides important information that may help in creating a SDSE vaccine," Musser said.
The researchers said as SDSE continues to be a threat, the findings provide a critical resource for future studies aimed at developing novel strategies to prevent and treat invasive SDSE infections.
Other collaborators on the study include Nayeemul Bari, Jesus Eraso, Randall Olsen and Luchang Zhu from Houston Methodist.
The study was supported by the Fondren Foundation.
