A microbiological analysis of 102 patients suffering from cystic fibrosis was conducted over a 22 month period. 20 microbial species with the following incidence were identified: Pseudomonas aeruginosa: 83.4%; Candida albicans: 29.4%; Staphylococcus aureus: 24.5%; Staphylococcus epidermidis: 11.8%; Haemophilus influenzae: 11.8%; Streptococcus pneumoniae; 6.9%; Pseudomonas maltophilia: 6.8%; Aspergillus fumigatus: 5.9%. Other species were present in less than 5% of the patients. In the majority of specimens with P. aeruginosa, more than one type (up to six) was detectable. These strains were identical in colony appearance, O-serotype and pyocin-type. Quantitative analysis revealed concentrations of colony-forming units of 10(7) to 10(9) for P. aeruginosa, 10(6) to 10(8) for P. maltophilia, 10(4) to 10(7) for S. aureus, 10(4) to 10(6) for S. epidermidis and 10(4) to 10(7) for C. albicans in the majority of specimens. Significant differences were observed in the time periods during which the pathogens persisted in the patients. Maximum persistence was observed for P. aeruginosa. P. maltophilia and A. fumigatus had about similar persistence rates, which were lower than those for P. aeruginosa but above those for S. aureus and H. influenzae. S. epidermidis was eliminated within shorter periods than S. aureus. C. albicans, although the second most frequent microorganism identified, showed a very low persistence rate. The microbiological analysis confirms results from other research centers (high incidence of P. aeruginosa), but reveals significant regional differences as well (Pseudomonas cepacia not detectable, higher incidence of P. maltophilia and C. albicans). This underlines the necessity for detailed qualitative and quantitative microbiological analysis of sputa from cystic fibrosis patients as a prerequisite for rational analysis of etiological, epidemiological and therapeutical aspects of cystic fibrosis.

Summary. In chronic Pseudomonas aeruginosa pulmonary infection of patients with cystic fibrosis (CF), antibiotic therapy generally fails to eradicate the bacterial pathogen. The mucoid bacterial phenotype, high sputum production by the host, and low airway levels of antibiotics seem to be responsible for the observed decrease in antibiotic efficacy. We hypothesized that early antibiotic treatment by inhalation in CF patients may be able to prevent or at least delay airway infection. In a prospective placebo-controlled, double-blind, randomized multicenter study, 22 CF patients received either 80 mg b.i.d. of aerosolized tobramycin or placebo for a period of 12 months shortly after the onset of P. aeruginosa pulmonary colonization.Two patients in the tobramycin and six patients in the placebo group stopped inhalation before the 12 month treatment period. Using life table analysis, the time to conversion from a P. aeruginosa-positive to a P. aeruginosa-negative respiratory culture was significantly shorter in the tobramycin-treated group than in the placebo group (P < 0.05, log rank test). Lung function parameters and markers of inflammation did not change in either group during treatment. The results of this study suggest that early tobramycin inhalation may prevent and/or delay P. aeruginosa pulmonary infection in CF patients. Pediatr. Pulmonol. 1998; 25:88-92.

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An epidemiological analysis of Staphylococcus aureus was conducted in a study group of 157 cystic fibrosis patients cultured over a 30-month period. The resulting S. aureus isolates were categorized by bacteriophage type, plasmid profile, and (in some instances) chromosomal restriction fragment pattern of the culture-positive patients with S. aureus (34 of 157) 44% only were sporadically infected while 68% shared identical strains with one or more other patients. Six patients exhibited persistent infection (for up to ten months) which, in three individuals, occurred as cycles of carriage and reappearance. By contributing toward our understanding of the persistence and spread of S. aureus in cystic fibrosis patients these data should aid in clarifying the role this organism may play in the course of the disease.

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