Amy Mathers
University of Virginia, VA·Microbiology & Immunology
Antibiotic resistance contributes to nearly five million deaths a year, and a big reason it spreads so fast is that resistance genes are portable. They ride on mobile genetic elements such as plasmids, small circles of DNA that bacteria can pass to each other, and transposons, DNA segments that jump from one location to another.
- Fields
Microbiology & Immunology
Public Health & Epidemiology
Medicine & Clinical Research
- Topics
antimicrobial resistance
antibiotic resistance
carbapenemase
- Grants
- 1 known grant, through Mar 2031
What they work on
- Determine which transposons, DNA segments that jump between locations, dominate movement of a carbapenemase resistance gene inside bacterial cells, by combining whole-genome sequencing of patient and environmental isolates with new mathematical analyses.
- Identify the plasmids that carry the carbapenemase gene between bacterial species and the biological factors that govern transfer, using laboratory experiments in a sink-drain model system that simulates hospital premise plumbing alongside mathematical modeling.
- Build predictive models of resistance gene spread across bacterial communities by integrating genomic and epidemiological data from more than 15 years of hospital surveillance.
- Test whether the superspreader framework generalizes by applying it to a different, emerging class of antimicrobial resistance genes.
More about the research
This means a resistance gene can hop between bacterial species rather than staying confined to one dangerous strain. Hospitals are a particularly hard setting: for over 15 years, this hospital has tracked many different bacterial species and strains that all carry one shared resistance gene, a carbapenemase, which destroys carbapenem antibiotics, often considered drugs of last resort. The gene has persisted in wastewater plumbing, especially sink drains, despite repeated disinfection. The project's premise is that killing bacteria with disinfectants and antibiotics has largely failed and may even select for resistance, so the better target is the mobile DNA itself, and in particular the "superspreaders": the specific bacterial hosts and genetic elements that do most of the transferring.
Why it matters
Hospital infection control currently aims at individual pathogens and relies on disinfection that has not stopped carbapenem-resistant bacteria from persisting in plumbing. Pinpointing the plasmids, transposons and bacterial hosts that drive resistance gene transfer could let hospitals and public health agencies target the sources rather than chasing single organisms, potentially reducing drug-resistant infections and slowing the emergence of harder-to-treat bacteria.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Michael Baym
Harvard University, MA·Microbiology & Immunology
Test whether the standard model of resistance evolution is incomplete by measuring the direct and indirect fitness costs of resistance and of specialization in evolving bacterial populations under tunable antibiotic selection.
Emile Gluck-Thaler
University of Wisconsin-Madison, WI·Genetics
Determine how rates of horizontal Starship transfer between fungi change in response to different environmental cues, using a newly developed laboratory transfer assay.
Catherine Wakeman
Texas Tech University, TX·Microbiology & Immunology
Identify vulnerability tradeoffs, weaknesses that appear when antibiotic-resistant bacteria reshape their physiology to survive drug exposure, and test whether targeting them clears infection in a mouse chronic wound model.
The school
University of Virginia: 43 labs on PI Pages, $814M a year on research, 413 research doctorates a year.
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