NIH funds study on drug-resistant bacteria that causes gonorrhea

Christopher Davies, Ph.D., associate dean for research at the Whiddon College of Medicine, was awarded a five-year, $3.5 million grant from the National Institutes of Health to determine the molecular mechanisms that confer antibiotic resistance to Neisseria gonorrhoeae.

Neisseria gonorrhoeae is the bacterial species that causes gonorrhea, a sexually transmitted illness responsible for more than 800,000 infections annually in the United States and some 78 million cases worldwide. Untreated or untreatable infections, Davies said, can lead to pelvic inflammatory disease and infertility in women, gonococcal arthritis in both sexes, and an increased risk of contracting and transmitting HIV. There is

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In recent decades, resistance of Neisseria gonorrhoeae toward multiple classes of antibiotics has increased steadily, leaving only extended-spectrum cephalosporins as recommended treatments. The cephalosporin-resistant strains have spread globally, making the need for new treatments more urgent.

The emergence of cephalosporin-resistance in N. gonorrhoeae is due to mutations in a protein called penicillin-binding protein 2 (PBP2), an enzyme that is essential for bacterial cell-wall synthesis. The project aims to understand how mutations in PBP2 lower reactivity with cephalosporins while preserving its essential enzymatic function.

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“This is a delicate balancing act that must be negotiated by the bacteria,” Davies said. “If the mutations compromise enzyme function, the bacteria cannot grow, but if the effect of mutations on resistance is too small, then the bacteria will be killed by cephalosporins. The strains we are seeing have solved this conundrum.” a nationwide multicenter study funded by the National Institutes of Health. The Neonatal Intensive Care Unit (NICU) Antibiotics and Outcomes Trial will study routine antibiotic usage in extremely premature infants and gain insight into the long-term impacts. The study began in 2020 and will conclude in 2024. It was designed to determine whether routine antibiotic usage in extremely premature infants (fewer than 29 weeks of gestation) is linked to gut microbiota changes and results in higher adverse outcomes, such as sepsis, necrotizing enterocolitis or death.

Davies’ team will work to determine the molecular structures of PBP2 from cephalosporin-resistant strains of N. gonorrhoeae and also examine their properties biochemically. Early indications are that mutations act by restricting the protein dynamics of PBP2 in a way that selectively discriminates against cephalosporins.