HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Schaber, J. A. Articles by Hamood, A. N. Search for Related Content PubMed PubMed Citation Articles by Schaber, J. A. Articles by Hamood, A. N. Agricola Articles by Schaber, J. A. Articles by Hamood, A. N.

Analysis of quorum sensing-deficient clinical isolates of Pseudomonas aeruginosa

Departments of Microbiology and Immunology,¹ and Surgery,² Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA

Correspondence Abdul N. Hamood abdul.hamood{at}ttuhsc.edu

Received January 26, 2004
Accepted May 27, 2004

Pseudomonas aeruginosa produces multiple virulence factors and causes different types of infections. Previous clinical studies identified P. aeruginosa isolates that lack individual virulence factors. However, the impact of losing several virulence factors simultaneously on the in vivo virulence of P. aeruginosa is not completely understood. The P. aeruginosa cell-to-cell communication system, or quorum sensing (QS), controls the production of several virulence factors. Animal studies using constructed QS mutants indicated that loss of the QS system severely impacts the virulence of P. aeruginosa. In this study, we tried to determine if deficiency within the QS system compromises the ability of P. aeruginosa to establish infections in humans. We have identified five QS-deficient strains through screening 200 isolates from patients with urinary tract, lower respiratory tract and wound infections. These strains lacked LasB and LasA activities and produced either no or very low levels of the autoinducers N-(3-oxododecanoyl) homoserine lactone and N-butyryl homoserine lactone. PCR analysis revealed that three isolates contained all four QS genes (lasI, lasR, rhlI and rhlR) while two isolates lacked both the lasR and rhlR genes. We also examined the five isolates for other virulence factors. The isolates produced variable levels of exotoxin A and, with one exception, were deficient in pyocyanin production. One isolate produced the type III secretion system (TTSS) effector proteins ExoS and ExoT, two isolates produced ExoT only and two isolates produced no TTSS proteins. The isolates produced weak to moderate biofilms on abiotic surfaces. Analysis of the patients’ data revealed that two of the isolates represented a single strain that was isolated twice from the same patient within a 1 month interval. One QS-deficient clinical isolate (CI-1) lacked all tested virulence factors and produced a weak biofilm. These results suggest that naturally occurring QS-deficient strains of P. aeruginosa do occur and are capable of causing infections; and, that besides the known virulence factors, additional factors may contribute to the ability of certain strains such as CI-1 to establish an infection.

This article has been cited by other articles:

				D. Jaklic, A. Lapanje, K. Zupancic, D. Smrke, and N. Gunde-Cimerman Selective antimicrobial activity of maggots against pathogenic bacteria J. Med. Microbiol., May 1, 2008; 57(5): 617 - 625. [Abstract] [Full Text] [PDF]

				E. Ferrell, N. L. Carty, J. A. Colmer-Hamood, A. N. Hamood, and S. E. H. West Regulation of Pseudomonas aeruginosa ptxR by Vfr Microbiology, February 1, 2008; 154(2): 431 - 439. [Abstract] [Full Text] [PDF]

				J. A. Schaber, A. Hammond, N. L. Carty, S. C. Williams, J. A. Colmer-Hamood, B. H. Burrowes, V. Dhevan, J. A. Griswold, and A. N. Hamood Diversity of biofilms produced by quorum-sensing-deficient clinical isolates of Pseudomonas aeruginosa J. Med. Microbiol., June 1, 2007; 56(6): 738 - 748. [Abstract] [Full Text] [PDF]

				P. O. Jensen, T. Bjarnsholt, R. Phipps, T. B. Rasmussen, H. Calum, L. Christoffersen, C. Moser, P. Williams, T. Pressler, M. Givskov, et al. Rapid necrotic killing of polymorphonuclear leukocytes is caused by quorum-sensing-controlled production of rhamnolipid by Pseudomonas aeruginosa Microbiology, May 1, 2007; 153(5): 1329 - 1338. [Abstract] [Full Text] [PDF]

				A. M. Lujan, A. J. Moyano, I. Segura, C. E. Argarana, and A. M. Smania Quorum-sensing-deficient (lasR) mutants emerge at high frequency from a Pseudomonas aeruginosa mutS strain Microbiology, January 1, 2007; 153(1): 225 - 237. [Abstract] [Full Text] [PDF]

				S. Furukawa, S. L. Kuchma, and G. A. O'Toole Keeping Their Options Open: Acute versus Persistent Infections J. Bacteriol., February 15, 2006; 188(4): 1211 - 1217. [Full Text] [PDF]

				R. Garcia-Medina, W. M. Dunne, P. K. Singh, and S. L. Brody Pseudomonas aeruginosa Acquires Biofilm-Like Properties within Airway Epithelial Cells Infect. Immun., December 1, 2005; 73(12): 8298 - 8305. [Abstract] [Full Text] [PDF]

				P. Salunkhe, C. H. M. Smart, J. A. W. Morgan, S. Panagea, M. J. Walshaw, C. A. Hart, R. Geffers, B. Tummler, and C. Winstanley A Cystic Fibrosis Epidemic Strain of Pseudomonas aeruginosa Displays Enhanced Virulence and Antimicrobial Resistance J. Bacteriol., July 15, 2005; 187(14): 4908 - 4920. [Abstract] [Full Text] [PDF]