John Farrow, PhD

Research Assistant Professor

Office: Biotechnologies Building Room 131
Phone: 252-744-2358
Fax: 252-744-3535


The spread of antibiotic-resistant bacteria is a major problem worldwide, and approximately 2.8 million antibiotic resistant infections occur each year in the United States. Our research is focused on two Gram-negative bacterial pathogens that are common causes of healthcare-associated infections: Acinetobacter baumannii and Pseudomonas aeruginosa. Both of these species are recognized for their extremely high rates of multi-drug resistance. Our goal is to learn more about how these bacteria survive, spread, and cause disease, in order to develop new interventions to control or treat infections by these organisms.

Acinetobacter baumannii

The majority of A. baumannii infections occur in hospitalized, critically ill individuals, and the spread of these bacteria in healthcare setting is a major concern. A. baumannii can survive on dry surfaces for weeks to months. This allows it to become a persistent contaminant, and it can rapidly colonize new patients who enter a contaminated hospital environment. We are working to learn more about the molecular mechanisms that allow A. baumannii to survive drying. We are also studying how A. baumannii manages the transition from the environment into the host, where it must rapidly adapt to new conditions to cause an infection.

Pseudomonas aeruginosa

P. aeruginosa is an opportunistic pathogen that can cause infections at many different body sites. P. aeruginosa infections are seen most commonly in healthcare settings, and these bacteria also cause chronic infections in individuals with cystic fibrosis. During infections, these bacteria communicate with each other using small molecules as signals to coordinate the expression of virulence factors. This communication is essential for these bacteria to be able to cause disease. We are studying the details of how these signaling molecules are controlled and produced, with the goal of finding new targets for therapeutics.


  1. Palethorpe S, Farrow, JM 3rd, Wells G, Milton ME, Cavanagh J, Actis LA, Pesci EC. 2022. Acinetobacter baumannii coordinates its stress responses via the BfmRS two-component regulatory system. Journal of Bacteriology. 204(2):e0049421.
  2. Farrow JM 3rd, Pesci EC, Slade, DJ. 2021. Genome sequences for two Acinetobacter baumannii strains obtained using the Unicycler hybrid assembly pipeline. Microbiology Resource Announcements. 10(10):e00017-21.
  3. Farrow JM 3rd, Wells G, Palethorpe S, Adams MD, Pesci EC. 2020. CsrA supports both environmental persistence and host-associated growth of Acinetobacter baumannii. Infection and Immunity. Sep 2020;IAI.00259-20.
  4. Farrow JM 3rd, Wells G, and Pesci EC. 2018. Desiccation tolerance in Acinetobacter baumannii is mediated by the two-component response regulator BfmR. PLOS One. 13(10):e0205638.
  5. Cole SJ, Hall CL, Schniederberend M, Farrow JM 3rd, Goodson JR, Pesci EC, Kazmierczak BI, Lee VT. 2018. Host suppression of quorum sensing during catheter-associated urinary tract infections. Nature Communications. 9(1):4436.
  6. Farrow JM 3rd and Pesci EC. 2017. Distal and proximal promoters co-regulate pqsR expression in Pseudomonas aeruginosa. Molecular Microbiology. 104(1):78-91.
  7. Farrow, JM 3rd, Hudson, LL, Wells, G, Coleman, JP, and Pesci, EC. 2015. CysB negatively affects the transcription of pqsR and Pseudomonas quinolone signal production in Pseudomonas aeruginosa. Journal of Bacteriology. 197(12):1988-2002.
  8. Ellison ML, Farrow JM 3rd, Parrish W, Danell AS, Pesci EC. 2013. The transcriptional regulator Np20 is the zinc uptake regulator in Pseudomonas aeruginosa. PLOS One. 8(9):e75389.
  9. Knoten, CA, Hudson LL, Coleman JP, Farrow JM 3rd, Pesci EC. 2011. KynR, a Lrp/AsnC-type transcriptional regulator, directly controls the kynurenine pathway in Pseudomonas aeruginosaJournal of Bacteriology. 193(23):6567-75.
  10. Farrow JM 3rd, Sund ZM, Ellison ML, Wade DS, Coleman JP, Pesci EC. 2008. PqsE functions independently of PqsR-Pseudomonas quinolone signal and enhances the rhl quorum-sensing system. Journal of Bacteriology. 190(21):7043-51.
  11. Rajamani S, Bauer WD, Robinson JB, Farrow JM 3rd, Pesci EC, Teplitski M, Gao M, Sayre RT, Phillips DA. 2008. The vitamin riboflavin and its derivative lumichrome activate the LasR bacterial quorum sensing regulator. Molecular Plant-Microbe Interactions. 21(9):1184-92.
  12. Oglesby AG, Farrow JM 3rd, Lee JH, Tomaras AP, Greenberg EP, Pesci EC, Vasil ML. 2008. The influence of iron on Pseudomonas aeruginosa physiology: a regulatory link between iron and quorum sensing. The Journal of Biological Chemistry. 283(23):15558-67.
  13. Coleman JP, Hudson LL, McKnight SL, Farrow JM 3rd, Calfee MW, Lindsey CA, Pesci EC. 2008. Pseudomonas aeruginosa PqsA is an anthranilate-coenzyme A ligase. Journal of Bacteriology. 190(4):1247-55.
  14. Cugini C, Calfee MW, Farrow JM 3rd, Morales DK, Pesci EC, Hogan DA. 2007. Farnesol, a common sesquiterpene, inhibits PQS production in Pseudomonas aeruginosa. Molecular Microbiology. 65(4):896-906.
  15. Farrow JM 3rd, Pesci EC. 2007. Two distinct pathways supply anthranilate as a precursor of the Pseudomonas quinolone signal. Journal of Bacteriology. 189(9):3425-33.
  16. Overman RG Jr, Enderle PJ, Farrow JM 3rd, Wiley JE, Farwell MA. 2003. The human mitochondrial translational initiation factor gene (MTIF2): transcriptional analysis and identification of a pseudogene. Biochimica et Biophysica Acta. 1628(3):195-205.