From the jump, Pranita Tamma gave her fellow infectious disease doctors a wake-up call at IDWeek 2026, and it was not subtle. She titled her plenary lecture, “Antimicrobial Resistance: The Next Pandemic is Already Here.” In her lecture, Tamma relayed a harrowing case study of a nine-year-old boy whose bloodstream was infected with one of the toughest superbugs known. The boy was in a modern hospital, and his doctors did everything right. Yet his doctors struggled to save him.
Within an hour of admission, doctors obtained blood and urine cultures. The boy was immediately given cefepime, a broad-spectrum cephalosporin used to treat moderate to severe bacterial infections.
Knowing how serious the infection was, the doctors added a second powerful antibiotic 12 hours later: meropenem, used to treat serious bacterial infections.
Within an hour, the lab results came in, identifying E. coli as the culprit. An hour later, PCR-based lab tests on a cross-section of resistance genes identified the bacterial gene encoding New Delhi metallo-beta-lactamase (NDM-1), an enzyme that inactivates three classes of antibiotics widely used to treat tough infections: penicillins, cephalosporins, and carbapenems.1
A Dangerous Enzyme Spreads
Scientists first identified NDM-1 in 2008 in New Delhi, India, and it has since spread globally in E. coli and several other gram-negative bacteria that are priority pathogens. In the process, the enzyme has evolved several ways to protect itself from even powerful antibiotics. These include becoming more stable to degradation, learning to function without the trace mineral zinc it previously required, and hiding in membrane sacs called vesicles just beneath the bacteria’s surface.2,
Making the problem tougher, Tamma said, is that the gene for NDM-1 sits on a mobile genetic element that lets it move easily among bacteria, including across different bacterial species. The genetic element, called a transposon, inserts itself into a plasmid that many bacteria carry. “It’s as if NDM has a designated parking spot versus driving around looking for a place to go,” Tamma explained.
A New Antibiotic Falters
An antibiotic called cefiderocol, first approved in 2019, had been proving effective against a number of WHO priority bacterial pathogens. But the bacteria in the nine-year-old boy had a gene that let it resist even cefiderocol, and two other genes that helped it evade a combination therapy called aztreonam and avibactam that is also used to treat resistant infections.
Sadly, the boy died of his infection. But a combination of cefepime and zidebactam, an antibiotic approved just last May, which was not available to treat the boy, still manages to knock down the type of battle-hardened microbes that killed him.2
Despite relaying this harrowing tale from the clinical trenches, Tamma ended on an optimistic note, pointing not to new-generation antibiotics, but more than half a dozen promising non-antibiotic options to prevent or treat resistant infections, including vaccines, monoclonal antibodies, CRISPR-Cas precision antimicrobials, and bacteriophage therapies.4
“What’s really exciting are all these non-antibiotic options on the horizon,” she said.
