The pneumococcus is a member of the commensal microbiota of the human nasopharynx. However, it can also cause serious diseases such as meningitis and pneumonia, killing nearly a million people each year (O'Brien et al., Lancet 2009).
The 1980s marked the beginning of the era of pneumococcal multi-drug resistance, especially among risk populations who undergo multiple courses of antimicrobial therapy, such as adult patients with chronic respiratory diseases. In this population, multi-drug resistance in pneumococci continued to rise, reaching up to 33% in 2012 (Domenech et al., J. Antimicrob. Chemother. 2014).
The incidence of antibiotic resistant pneumococci in the human body can occur by several mechanisms such as the replacement of susceptible pneumococci by a resistant community-acquired strain, by spontaneous mutation, or by the acquisition of an antibiotic resistance marker from other Streptococci by the process of transformation. Transformation is controlled by a developmental process called competence. We and others have shown that certain antibiotics can induce competence and thus the spread of antibiotic resistance (Prudhomme et al., Science 2006; Slager et al., Cell 2014). In addition, competence induces active killing of neigboring bacteria enabling the acquisition of DNA (for a recent review see Veening and Blokesch, Nature Rev. Microbiol. 2017).
Our lab is trying to understand how antibiotic resistance is acquired and spread in pneumococcal populations. Another interest is understanding the mechanisms underlying non-genetic factors influencing antibiotic therapy such as collective resistance (Sorg et al. PLoS Biol. 2016) and heteroresistance (Sorg and Veening, Nature Commun. 2015). Typical techniques we use in this research are genomics (DNA/RNA seq), single cell analysis (microscopy/FACS), luciferase assays and genetic engineering.