Chlamydia pneumoniae infection and acute exacerbation of chronic obstructive pulmonary disease (COPD)

Citation
D. Karnak et al., Chlamydia pneumoniae infection and acute exacerbation of chronic obstructive pulmonary disease (COPD), RESP MED, 95(10), 2001, pp. 811-816
Citations number
15
Categorie Soggetti
Cardiovascular & Respiratory Systems","da verificare
Journal title
RESPIRATORY MEDICINE
ISSN journal
09546111 → ACNP
Volume
95
Issue
10
Year of publication
2001
Pages
811 - 816
Database
ISI
SICI code
0954-6111(200110)95:10<811:CPIAAE>2.0.ZU;2-A
Abstract
The objective of the study was to investigate the possible association of C hlamydia pneumoniae (Cpn) in acute exacerbations of chronic obstructive pul monary disease (COPD) patients. Thirty-eight acutely exacerbated COPD patie nts and 17 healthy smokers were enrolled in the study, as the study and con trol groups respectively. Nasopharyngeal swabs and paired serum samples for antibody testing of Cpn (microimmunofluorescence-MIF) were obtained from a ll subjects. Sputum cultures of COPD patients were also performed. No patho genic bacteria were isolated from nasopharyngeal swabs in any subject. Sero logic evidence of recent Cpn infection was observed in 13 (34%) COPD patien ts and in one (5%) control subject. The prevalence of Cpn IgG and IgM antib odies representing acute infection were significantly higher in COPD patien ts than in control subjects (P < 0.05 and P < 0.01 respectively). Prevalenc e of IgA antibodies and IgG pre-existing antibodies did not show any differ ence (P > 0.05). Microbiologic culture of the sputa yielded potentially pat hogenic micro-organisms in 23 of 38 (60%) COPD patients. Alpha-haemolytic s treptococcus (35%), Niesseria spp. (31%) and Candida spp. (9.5%) were most prominent micro-organisms in positive cultures, Although a high prevalence of IgG antibodies against Cpn was detected, it was the sole causative agent in only four (10%) patients. We conclude that a remarkable number of COPD patients (34%) are acutely infected with Cpn and it may either be the sole causative agent or frequently a co-agent in acute exacerbations. (C) 2001 H arcourt Publishers Ltd.