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RESPIRATORY INFECTIONS IN CYSTIC FIBROSIS PATIENTS CAUSED BY VIRUS, CHLAMYDIA AND MYCOPLASMA–POSSIBLE SYNERGISM WITH PSEUDOMONAS AERUGINOSA
Author(s) -
PETERSEN N. T.,
HØIBY N.,
MORDHORST C. H.,
LIND K.,
FLENSBORG E. W.,
BRUUN B.
Publication year - 1981
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1981.tb05757.x
Subject(s) - pseudomonas aeruginosa , medicine , chlamydia , cystic fibrosis , mycoplasma , sputum , virus , immunology , respiratory system , respiratory disease , microbiology and biotechnology , antibody , virology , bacteria , lung , biology , pathology , tuberculosis , genetics
. Petersen, N. T., Høiby, N., Mordhorst, C. H., Lind, K., Flensborg, E. W. and Bruun, B. (Paediatric Department TG, Rigshospitalet, and Statens Seruminstitut, Copenhagen, Denmark). Respiratory infections in cystic fibrosis patients caused by virus, chlamydia and mycoplasma–possible synergism with Pseudomonas aeruginosa. Acta Paediatr Scand, 70: 623,.–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 infection. 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.