scholarly journals 154* Assessing the role of lysogenic bacteriophages in a cystic fibrosis epidemic strain of Pseudomonas aeruginosa

2011 ◽  
Vol 10 ◽  
pp. S39
Author(s):  
J.L. Fothergill ◽  
A.-A. Lemieux ◽  
C.E. James ◽  
I. Kukavica-Ibrulj ◽  
G. Filion ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Epidemic Strain

PCR-Based Detection of a Cystic Fibrosis Epidemic Strain of Pseudomonas Aeruginosa

2003 ◽  
Vol 7 (3) ◽  
pp. 195-200 ◽  
Author(s):  
Stavroula Panagea ◽  
Craig Winstanley ◽  
Yasmin N Parsons ◽  
Martin J Walshaw ◽  
Martin J Ledson ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Epidemic Strain

scholarly journals Role of quorum sensing by Pseudomonas aeruginosa in microbial keratitis and cystic fibrosis

Microbiology ◽  
2008 ◽  
Vol 154 (8) ◽  
pp. 2184-2194 ◽  
Author(s):  
M. D. P. Willcox ◽  
H. Zhu ◽  
T. C. R. Conibear ◽  
E. B. H. Hume ◽  
M. Givskov ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Microbial Keratitis

Characterization by pyocine typing and serotyping of oral and sputum strains of Pseudomonas aeruginosa isolated from cystic fibrosis patients

1987 ◽  
Vol 33 (3) ◽  
pp. 221-225 ◽  
Author(s):  
Kunio Komiyama ◽  
Brian F. Habbick ◽  
Tom Martin ◽  
Satwant K. Tumber
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Oral Cavity ◽  
Buccal Mucosa ◽  
Single Strain ◽  
Ecological Sites ◽  
Dental Plaques ◽  
Different Strains

Oral and sputum isolates of Pseudomonas aeruginosa in patients with cystic fibrosis were investigated. Of the 17 patients studied, 12 patients (71%) yielded both mucoid and nonmucoid variants of Pseudomonas aeruginosa from sputum and (or) various oral ecological sites, such as buccal mucosa, tongue dorsum, dental plaques, and saliva. A total of 51 strains of mucoid and nonmucoid Pseudomonas aeruginosa were isolated from these patients and were phenotypically characterized by both pyocine typing and serotyping. Five patients (42%) were colonized or infected by a single strain of Pseudomonas aeruginosa, whereas 7 patients (58%) were cocolonized or coinfected by two or more phenotypically different strains of Pseudomonas aeruginosa. To understand the mechanisms involved in Pseudomonas aeruginosa colonization, it may be necessary to identify multiple isolates of Pseudomonas aeruginosa not only from the sputum but also from the various oral ecological sites and to further explore the role of the oral cavity in this colonization.

Epidemiology of Pseudomonas aeruginosa in cystic fibrosis and the possible role of contamination by dental equipment

1997 ◽  
Vol 36 (2) ◽  
pp. 117-122 ◽  
Author(s):  
E.T. Jensen ◽  
B. Giwercman ◽  
B. Ojeniyi ◽  
J.M. Bangsborg ◽  
A. Hansen ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Dental Equipment

scholarly journals PmrB Mutations Promote Polymyxin Resistance of Pseudomonas aeruginosa Isolated from Colistin-Treated Cystic Fibrosis Patients

2011 ◽  
Vol 56 (2) ◽  
pp. 1019-1030 ◽  
Author(s):  
Samuel M. Moskowitz ◽  
Mark K. Brannon ◽  
Nandini Dasgupta ◽  
Miyuki Pier ◽  
Nicole Sgambati ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Lipid A ◽  
Clinical Isolates ◽  
Gain Of Function ◽  
Content Type ◽  
Regulatory Systems ◽  
Repeated Passage ◽  
High Level

ABSTRACTPseudomonas aeruginosacan develop resistance to polymyxin and other cationic antimicrobial peptides. Previous work has shown that mutations in the PmrAB and PhoPQ regulatory systems can confer low to moderate levels of colistin (polymyxin E) resistance in laboratory strains and clinical isolates of this organism (MICs of 8 to 64 mg/liter). To explore the role of PmrAB in high-level clinical polymyxin resistance,P. aeruginosaisolates from chronically colistin-treated cystic fibrosis patients, most with colistin MICs of >512 mg/liter, were analyzed. These cystic fibrosis isolates contained probable gain-of-functionpmrBalleles that conferred polymyxin resistance to strains with a wild-type orpmrABdeletion background. Double mutantpmrBalleles that contained mutations in both the periplasmic and dimerization-phosphotransferase domains markedly augmented polymyxin resistance. Expression of mutantpmrBalleles induced transcription from the promoter of thearnBoperon and stimulated addition of 4-amino-l-arabinose to lipid A, consistent with the known role of this lipid A modification in polymyxin resistance. For some highly polymyxin-resistant clinical isolates, repeated passage without antibiotic selection pressure resulted in loss of resistance, suggesting that secondary suppressors occur at a relatively high frequency and account for the instability of this phenotype. These results indicate thatpmrBgain-of-function mutations can contribute to high-level polymyxin resistance in clinical strains ofP. aeruginosa.

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