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Drew Bridges

Assistant Professor

  • Pittsburgh PA

Bridges's lab uncovers signals bacteria use to coordinate their behaviors, aiming to turn those signals into new ways to treat infections.

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Biography

Drew Bridges studies how bacteria make developmental decisions based on extracellular sensory information. His lab focuses on is the formation and disassembly of multicellular bacterial communities called biofilms. Previously, the Bridges Lab pioneered the use of new imaging approaches to investigate the full biofilm lifecycle in the global pathogen, Vibrio cholerae, from initial cell attachment to biofilm growth, to biofilm disassembly. They combine imaging approaches with techniques including genetics, biochemistry, and biophysics theory to discover and characterize the molecular mechanisms controlling biofilm dispersal.

In the long term, the research program will expand to other microorganisms and their unique lifestyles to learn what principles are general and which are species-specific. These discoveries will be relevant to infection and could inform the development of approaches to manipulate bacterial behavior, potentially leading to new strategies for controlling disease.

Areas of Expertise

Microbiology
Microscopy
Signal Transduction
High Throughput
Image Analysis‎

Media Appearances

CMU Study Uncovers How Dangerous Bacteria Build and Break Down Biofilms

Mellon College of Science News  online

2026-06-29

“Our platform can be used to inform researchers of the genes that underlie the biofilm regulation of diverse species and could be used to identify new biofilm-disrupting drugs,” Bridges said. “Simultaneously, this paper really lays out the fundamental genetics underlying the specific pathogen S. pneumoniae.”

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Researchers Identify New Target To Fight Antibiotic Resistance

Mellon College of Science News  online

2025-12-18

Drew Bridges, an assistant professor in Carnegie Mellon University’s Mellon College of Science, said the research could be an important tool in fighting a growing threat.

“Traditional antibiotics work in a simple way — they kill bacteria,” Bridges said. “It's the same problem as with chemotherapy — the survivors cause problems. When you apply a bunch of antibiotics, a subpopulation of cells survives, they repopulate the population, and they're all resistant.”

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We’re Outta Here | Novel imaging technique tracks individual bacterial cells as they leave their biofilm community

Mellon College of Science News  online

2025-04-29

“Being able to transition in and out of the biofilms is critical for bacteria to be able to spread between niches. It could be between some environmental locations or, more relevantly, it could be between hosts or infection sites,” said Drew Bridges, assistant professor in the Department of Biological Sciences.

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Media

Education

Princeton University:

Postdoctoral Fellowship

2022

Dartmouth College

Ph.D.

Biological Sciences

2016

Appalachian State University

B.S.

Chemistry

2011

Articles

A branching cell-fate decision in biofilm dispersal enables long-term surface persistence

bioRxiv

Kasivisweswaran, S., Prentice, J.A., Bridges, A.A.

2026

Biofilms are the most ancient multicellular communities on Earth, representing a primitive developmental system that protects microbes from threats. Biofilm dispersal, whereby bacteria exit biofilms, is critical for the spread of pathogens to new infection sites. Here, using Vibrio cholerae, we show that dispersal events are accompanied by a branching cell-fate decision. While ~90% of cells disperse, a viable subpopulation remains within a residual matrix. This post-dispersal biofilm community (PDBC) is established by the matrix protein RbmA and adopts a specialized anabolic program that enhances tolerance to antibiotics and bacteriophages. Our findings reveal that PDBCs act as a resilient "seed-bank" capable of rapidly re-populating the niche without requiring de novo matrix biosynthesis, providing a mechanistic basis for the recurrence and spread of chronic infections.

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Label-free microscopy enables high-throughput identification of genes controlling biofilm development

mBio

MR, P., Prentice, J.A., Eutsey, R.A., Mikheyeva, I., Hiller, N.L., Bridges, A.A.

2026

The biofilm mode of growth plays a critical role in microbial ecology and in the persistence of human pathogens. Yet, much remains unknown regarding the molecular determinants of biofilms in human pathogens. In this study, we present label-free analysis of biofilms (LFAB), an imaging approach that combines time-lapse, low-magnification brightfield microscopy with regional optical density measurements to quantify biofilm biomass. Unlike other approaches to biofilm biomass quantification, LFAB enables real-time, non-perturbative, and high-throughput monitoring of biofilms. We validated LFAB in diverse microbes and found that our measurements strongly correlate with traditional biofilm assays. We then used LFAB to identify and characterize critical factors mediating biofilm formation in Streptococcus pneumoniae, a major human pathogen whose biofilm lifecycle is known to be intimately related to colonization and infection.

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A small periplasmic protein governs broad physiological adaptations in Vibrio cholerae via regulation of the DbfRS two-component system

Nature Communications

Nguyen, E., Agbavor, C., Steenhaut, A., Pratyush M. R., Hiller, N. L., Cahoon, L. A., Mikheyeva, I. V., Ng, W.L., Bridges, A. A.

2025

Two-component signaling pathways allow bacteria to sense and respond to environmental changes, yet the sensory mechanisms of many remain poorly understood. In the pathogen Vibrio cholerae, the DbfRS two-component system controls the biofilm lifecycle, a critical process for environmental persistence and host colonization. Here, we identified DbfQ, a small periplasmic protein encoded adjacent to dbfRS, as a direct modulator of pathway activity. DbfQ directly binds the sensory domain of the histidine kinase DbfS, shifting it toward phosphatase activity and promoting biofilm dispersal. In contrast, outer membrane perturbations, caused by mutations in lipopolysaccharide biosynthesis genes or membrane-damaging antimicrobials, activate phosphorylation of the response regulator DbfR.

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