116 cystic fibrosis patients were observed, by monthly examinations over an eight-month period, to investigate the importance of non-bacterial respiratory infections (NBI) in exacerbations of the respiratory disease. Sputum was examined for bacteria, and serum investigated for antibody response against virus, mycoplasma and chlamydia and for antibodies against Pseudomonas aeruginosa. During this period each patient had, on an average, 2.9 exacerbations of which 76% were associated with bacteria, most frequently P. aeruginosa (51%), and 20% with NBI, although bacteria were also present in most of these cases. No etiology was established in 18% of the exacerbations. The NBI were caused by respiratory syncytial virus (RSV) (9%), parainfluenza virus (5%), influenza virus (3.6%), adenovirus (2.4%), mycoplasma (0.6%) and chlamydia (0.6%). The incidence of exacerbations was higher in patients with chronic P. aeruginosa infections. RSV infections were more common in patients who developed chronic P. aeruginosa infection during the study period, and RSV infections were frequently associated with a rise of P. aeruginosa antibodies in patients who harboured these bacteria. The important role of NBI as mediators of onset of chronic P. aeruginosa infections in cystic fibrosis patients is suggested.
The annual mortality rate of cystic fibrosis patients with chronic Pseudomonas aeruginosa lung infection at the Danish CF-centre ranged from 10 to 20% in the years 1970-1975. In this period the patients received antipseudomonal chemotherapy only during acute exacerbations of infection. From 1976 99 patients acquired chronic P. aeruginosa infection and were given regular and intensive antipseudomonal treatment 3-4 times per year. The patients were followed for 612 patient-years; 7 died and the 10-year survival rate after onset of P. aeruginosa infection was 90% +/- 4%. The annual mortality rate is now 1-2%. Although precipitating antibodies against P. aeruginosa increased significantly, pulmonary function did not deteriorate with duration of infection. Cross-infection between patients caused an increased incidence of chronic P. aeruginosa infection which was reduced by hygienic measures.
During the period 1971-75, 51 cystic fibrosis (CF) patients who contracted chronic P. aeruginosa infection were treated at the Danish CF centre with anti-pseudomonas chemotherapy only when their clinical condition deteriorated considerably. During the period 1976-80, 58 CF patients who contracted chronic P. aeruginosa infection were treated at the Danish CF centre with anti-pseudomonas chemotherapy on a regular basis every 3 months. Each routine 24 day-course of chemotherapy consisted of tobramycin in combination with carbenicillin or other beta-lactam antibiotics with activity against P. aeruginosa. In case of allergy or resistant strains monotherapy with tobramycin was used. The 5-year survival of CF patients from the time of the onset of the chronic P. aeruginosa infection increased from 54% in the first period to 82% in the second period (p less than 0.05), and lung function (peak expiratory flow rate) also improved significantly. It is concluded that intensive "maintenance" chemotherapy against P. aeruginosa improves survival and quality of life of CF patients although permanent eradication of P. aeruginosa is not accomplished.
A double blind controlled trial of Becotide (beclomethasone diproprionate) inhalations was carried out for treating cystic fibrosis patients with chronic P. aeruginosa lung infection to determine its efficacy and safety. The aim of the treatment was to diminish the inflammatory response in the lungs of these patients, a response which is initiated by an allergic type III reaction. Pulmonary inflammation was evaluated by measurements of proteolytic activity, albumin concentration and immune complex activity in the sputum sol-phase before, during, and after the 16 weeks the trial lasted. 26 cystic fibrosis patients participated (13 received Becotide and 13 placebo) and the results showed that local steroids have no effect on the inflammatory response in the lungs of cystic fibrosis patients with chronic P. aeruginosa lung infection. No adverse effects were demonstrated. There was, however, a significant increase in the inflammatory parameters for all 26 cystic fibrosis patients when the trial period was over, compared to the insidious pulmonary destruction which takes place in the lungs of these patients, and it corresponded to a significant decrease (p less than 0.05) in forced vital capacity which took place at the same time. Therefore, chronic P. aeruginosa lung infection in these patients should be treated as efficiently as possible.
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