Scott J. Weissman, MD

Since the initiation of intrapartum antimicrobial prophylaxis for group B streptococcus during pregnancy, E. coli has become the leading bacterial cause of early-onset sepsis (EOS) in newborns. Now, with ampicillin-resistant rates >80% among E. coli isolates, it remains unclear whether contemporary EOS isolates represent antibiotic-resistant derivatives of the traditional K1-encapsulated clones described in the 1970’s (which would facilitate rapid point-of-care screening tests) or a more diverse array of novel antibiotic-resistant clones like those that have complicated empiric treatment of community-acquired UTI (e.g., Bactrim-resistant “clonal group A”). My lab uses PCR- and sequence-based molecular typing techniques to characterize clinical isolate collections gathered through active and passive surveillance by the NICHD Neonatal Research Network and the Minnesota Department of Health.

With the appearance of EOS-associated clones resistant to standard ampicillin/gentamicin combination therapy, this project will inform guidelines for the empiric treatment of early-onset sepsis. My lab is also using molecular techniques to characterize the spread of plasmid-borne extended-spectrum beta-lactamase (ESBL) enzymes among Enterobacteriaceae. Since 2000, we have witnessed the worldwide emergence of Gram-negative “superbugs” such as E. coli ST131 and Klebsiella pneumoniae ST258—which not only encode multiple virulence factors associated with extraintestinal disease, but also Class A enzymes that hydrolyze third-generation cephalosporins and carbapenem antibiotics (CTX-M-15 and KPC, respectively). Our molecular typing methods will characterize the dynamics of antibiotic resistance, to distinguish epidemics of resistance genes that spread between plasmids, plasmids that spread between strains, and strains that spread across continents.