George Drusano
University of Florida, FL·Pharmacology
Some bacteria have become so resistant that almost no antibiotic reliably works against them. Two of the worst are carbapenem-resistant Acinetobacter baumannii and carbapenem-resistant Klebsiella pneumoniae, bacteria the CDC labels "urgent threats" because carbapenems, a last-line antibiotic class, no longer kill them.
- Fields
Pharmacology
Microbiology & Immunology
Medicine & Clinical Research
- Topics
antimicrobial resistance
carbapenem-resistant Acinetobacter baumannii
carbapenem-resistant Klebsiella pneumoniae
- Grants
- 1 known grant, through May 2029
What they work on
- Determine dose-response and resistance-suppression targets for newer antibiotics that lack such data, using dose-ranging and dose-fractionation experiments in the hollow fiber infection model, which reproduces human drug concentration profiles over days.
- Test promising two- and three-drug combinations against carbapenem-resistant Acinetobacter baumannii and Klebsiella pneumoniae, pairing drugs that inactivate penicillin-binding proteins (cell-wall-building enzymes) with non-binding partners that counter-select the other drug's resistance route.
- Characterize synergistic killing and resistance suppression by applying transcriptomics, proteomics and genomics to bacteria sampled from the hollow fiber model during suboptimal versus therapeutic drug exposures.
- Examine how treatment timing affects penicillin-binding protein expression, β-lactamases, efflux pumps and porins, and quantify non-replicating persisters and morphologically altered survivors using flow cytometry with sorting of fluorescently labeled strains.
More about the research
Giving a single drug often fails: survivors in the population quickly become resistant and the infection returns. The central hypothesis here is that beating these organisms requires carefully designed drug combinations and dosing schedules that both kill bacteria fast and block resistance from emerging.
Why it matters
Infections with carbapenem-resistant Acinetobacter and Klebsiella leave clinicians with few options, and single-drug therapy frequently fails as resistance emerges mid-treatment. By defining which drug combinations and dosing schedules kill these organisms extensively while suppressing resistant subpopulations, this work could supply dosing regimens that are ready to test in patients and make better use of antibiotics already available.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sergei Vakulenko
University of Notre Dame, IN·Microbiology & Immunology
Measure the activity of novel carbapenems against A. baumannii strains producing major CHDLs (enzymes that destroy carbapenems) and other carbapenemases, and use enzyme kinetics and structural studies to explain how the compounds inhibit these enzymes.
Samithamby Jeyaseelan
Louisiana State University, LA·Microbiology & Immunology
Determine how the antioxidant regulator Nrf2 affects survival, bacterial clearance and neutrophil accumulation and function during carbapenem-resistant Klebsiella pneumoniae (CRKP) pneumonia in mice.
Gauri Rao
University of Pittsburgh, PA·Pharmacology
Identify which pharmacokinetic and pharmacodynamic (PK/PD) factors should guide phage selection against clinical Pseudomonas aeruginosa isolates, using static time-kill assays and hollow fiber infection models.
The school
University of Florida: 65 labs on PI Pages, $1.3B a year on research, 795 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.