BACKGROUND: Colistin resistant Pseudomonas aeruginosa have rarely been reported in cystic fibrosis (CF) patients. METHODS: We performed a 17-year prospective study on colistin susceptibility and compared our findings with clinical variables. RESULTS: The first outbreak started in 1995 and lasted 5 years. It involved 27 CF patients who had inhaled colistin twice daily for a median of 10 years. Colistin resistant isolates persisted in individual patients for a median of 75 days after colistin was withdrawn. A second outbreak started in 2004. It involved 40 patients, 17 of whom were the same as in the first outbreak. Most resistant isolates belonged to two major clones that had similar genotypes in the two outbreaks. The P. aeruginosa isolates were all non-mucoid and they appeared in a group of chronically infected patients that had been admitted to the same ward for antibiotic treatment and had been followed at the same week-days in the outpatient clinic. Patients were individually isolated to avoid cross-infection and colistin inhalation was avoided in the CF outpatient clinic and in the ward after both outbreaks. Since 2004, no further spread has been observed. CONCLUSION: It is important that the colistin resistant clones do not spread to non-infected patients since colistin is an important antibiotic for eradication of initial and intermittent P. aeruginosa colonisation.
BACKGROUND: Colistin resistant Pseudomonas aeruginosa have rarely been reported in cystic fibrosis (CF) patients. METHODS: We performed a 17-year prospective study on colistin susceptibility and compared our findings with clinical variables. RESULTS: The first outbreak started in 1995 and lasted 5 years. It involved 27 CFpatients who had inhaled colistin twice daily for a median of 10 years. Colistin resistant isolates persisted in individual patients for a median of 75 days after colistin was withdrawn. A second outbreak started in 2004. It involved 40 patients, 17 of whom were the same as in the first outbreak. Most resistant isolates belonged to two major clones that had similar genotypes in the two outbreaks. The P. aeruginosa isolates were all non-mucoid and they appeared in a group of chronically infectedpatients that had been admitted to the same ward for antibiotic treatment and had been followed at the same week-days in the outpatient clinic. Patients were individually isolated to avoid cross-infection and colistin inhalation was avoided in the CFoutpatient clinic and in the ward after both outbreaks. Since 2004, no further spread has been observed. CONCLUSION: It is important that the colistin resistant clones do not spread to non-infectedpatients since colistin is an important antibiotic for eradication of initial and intermittent P. aeruginosa colonisation.
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Authors: V Waters; J E A Zlosnik; Y C W Yau; D P Speert; S D Aaron; D S Guttman Journal: Eur J Clin Microbiol Infect Dis Date: 2012-07-29 Impact factor: 3.267