The epidemiology of chronic colonization of airways with Pseudomonas aeruginosa was monitored in 44 patients with cystic fibrosis (CF) by DraI/SpeI macrorestriction analyses of 489 isolates. Sequential P. aeruginosa isolates (144) that had been collected from 32 CF patients over < or = 2.5 years were investigated, and 12 patients were followed for 8 years after onset of colonization. Forty-eight different genotypes were uncovered from 481 typeable isolates. Ten genotypes were found in > 1 unrelated CF patient. The 6 most frequent clones were identified in 58% of isolates. Ten of the 12 patients monitored for 8 years were harboring their initially acquired P. aeruginosa clone at all times, with subtle shifts of fragment patterns indicating subclonal variation. During colonization, the bacteria gradually lost pyocin and phage typing responses, supporting the view that genotypically discordant P. aeruginosa strains develop a common phenotype.

Abstractlung transplant recipients in our clinic infected with Pseudomonas aeruginosa acquired new Background -The source of airway colonisation with Pseudomonas aeruginosa strains or retained their strains which they harboured before lung transplantation. Methods -Seventy four P aeruginosa isol-were different from those carried before the H von der HardtPreoperative isolates were retrieved from (Thorax 1997;52:318-321) sputum samples and postoperative isolates

We have conducted a comprehensive study of the molecular basis of cystic fibrosis (CF) in 350 German CF patients. A screening approach based on single-strand conformation analysis and direct sequencing of genomic polymerase chain reaction products has allowed us to detect the molecular defects on 95.4% of the CF chromosomes within the coding region and splice sites of the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The spectrum of sequence changes comprises 54 different mutations, including 17 missense mutations, 14 nonsense mutations, 11 frameshift mutations, 10 splice site variants and two amino acid deletions. Eleven of these mutations have not previously been described. Our results reflect the marked mutational heterogeneity of CF in a large sample of patients from a non-isolated population.