Analysis of quorum sensing-deficient clinical isolates of Pseudomonas aeruginosa

• Published in: Journal of medical microbiology Vol. 53; no. 9; pp. 841 - 853
• Main Authors: Schaber, J. Andy, Carty, Nancy L, McDonald, Naomi A, Graham, Eric D, Cheluvappa, Rajkumar, Griswold, John A, Hamood, Abdul N
• Format: Journal Article
• Language: English
• Published: Reading Soc General Microbiol 01-09-2004; Society for General Microbiology
• Subjects: 4-Butyrolactone - analogs & derivatives; 4-Butyrolactone - metabolism; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacteriology; Biofilms - growth & development; Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Bacterial; Humans; Infectious diseases; Medical sciences; Metalloendopeptidases - genetics; Metalloendopeptidases - metabolism; Microbiology; Miscellaneous; Mutation; Pseudomonas aeruginosa; Pseudomonas aeruginosa - genetics; Pseudomonas aeruginosa - growth & development; Pseudomonas aeruginosa - pathogenicity; Pseudomonas aeruginosa - physiology; Pseudomonas Infections - microbiology; Transcription, Genetic; Virulence; Pseudomonadales; Microbiology; Bacteria; Pseudomonadaceae; Pseudomonas aeruginosa; Quorum sensing; Clinical isolate
• ISSN: 0022-2615; 1473-5644
• DOI: 10.1099/jmm.0.45617-0

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.
Abbreviations: 3OC 12 -HSL, N-(3-oxododecanoyl) homoserine lactone; C 4 -HSL, N-butyryl homoserine lactone; CF, cystic fibrosis; CI, clinical isolate; QS, quorum sensing; TTSS, type III secretion system.