PERSISTENCE OF PSEUDOMONAS-AERUGINOSA STRAINS IN RESPIRATORY-INFECTION IN AIDS PATIENTS

Citation
D. Asboe et al., PERSISTENCE OF PSEUDOMONAS-AERUGINOSA STRAINS IN RESPIRATORY-INFECTION IN AIDS PATIENTS, AIDS, 12(14), 1998, pp. 1771-1775
Citations number
19
Categorie Soggetti
Immunology,"Infectious Diseases",Virology
Journal title
AIDSACNP
ISSN journal
02699370
Volume
12
Issue
14
Year of publication
1998
Pages
1771 - 1775
Database
ISI
SICI code
0269-9370(1998)12:14<1771:POPSIR>2.0.ZU;2-1
Abstract
Objectives: To establish the clinical pattern of Pseudomonas aeruginos a respiratory infections in HIV-seropositive patients and to determine whether repeated isolation of the organism represents reinfection or recurrence and to assess whether common source, nosocomial infection o ccurred. Design and methods: Evaluation of the clinical pattern of P. aeruginosa respiratory infections by case note review and epidemioiogi cal characterization of P. aeruginosa by serotype determination and Xb al DNA macrorestriction analysis. Serum sensitivity testing of strains was performed to further define phenotypic characteristics of the iso lated organisms. Results: Seventy-three per cent (29 out of 40) of ind ividuals had P. aeruginosa isolated on two or more occasions in the se tting of clinical respiratory infection. Overall, 85% had evidence of P. aeruginosa to within 2 months of study completion or death. Epidemi ological characterization revealed persistence of unique single strain s in 93% of individuals where multiple isolates were available for tes ting, whereas only two patients harboured a common strain. The serotyp e distribution of strains was similar to that reported from non-HIV-po sitive patients. Conclusions: Once established, eradication of P. aeru ginosa from the respiratory tract of HIV-seropositive individuals with advanced immunosuppression is problematic and a chronic infective sta te appears common. There was no evidence of nosocomial transmission. S erotype loss and development of sensitivity to normal human serum were both observed and were highly correlated. This represents truncation of Q-antigenic lipopolysaccharide on the cell surface of P. aeruginosa and may reflect progression to phenotypes commonly associated with ch ronic infection in other clinical settings such as cystic fibrosis. (C ) 1998 Lippincott Williams & Wilkins.