Infection With Pseudomonas Cepacia In Chronic Granulomatous Disease: Role Of Nonoxidative Killing By Neutrophils In Host Defense

Pseudomonas aeruginosa and Pseudomonas cepacia are catalase-producing bacteria, but only P. cepacia causes infections in patients with chronic granulomatous disease (CGO). The in vitro killing of P. aeruginosa and P. cepacia by polymorphonuclear leukocytes (PMNL) from patients with CGO and from heal...

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Bibliographic Details
Published in:The Journal of infectious diseases 1994-12, Vol.170 (6), p.1524-1531
Main Authors: Speert, David P., Bond, Mason, Woodman, Richard C., Curnutte, John T.
Format: Article
Language:English
Subjects:
Bacteria
Biological and medical sciences
Blood
Burkholderia cepacia
Burkholderia cepacia - immunology
Burkholderia cepacia - pathogenicity
Catalase
Child
Child, Preschool
Chronic granulomatous disease
Free Radical Scavengers
Granulomatous Disease, Chronic - complications
Granulomatous Disease, Chronic - immunology
Heterozygote
Humans
Infections
Major Articles
Male
Medical sciences
Neutrophils
Neutrophils - immunology
Neutrophils - metabolism
Pneumonia
Pseudomonas
Pseudomonas aeruginosa - immunology
Pseudomonas cepacia
Pseudomonas Infections - complications
Pseudomonas Infections - immunology
Reactive oxygen species
Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
Staphylococcus aureus - immunology
Superoxide Dismutase
Superoxides
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Description
Summary:Pseudomonas aeruginosa and Pseudomonas cepacia are catalase-producing bacteria, but only P. cepacia causes infections in patients with chronic granulomatous disease (CGO). The in vitro killing of P. aeruginosa and P. cepacia by polymorphonuclear leukocytes (PMNL) from patients with CGO and from healthy adults was assessed. Of 6 patients with CGO who developed severe infections with P. cepacia, 4 died. PMNL from the 2 survivors and 6 other patients with CGO killed P. aeruginosa strains efficiently and P. cepacia strains poorly. PMNL from 2 patients with autosomal recessive CGO and from 2 carriers for X-linked CGO killed P. cepacia intermediately between normal controls and patients with X-linked CGO. When superoxide anion and hydrogen peroxide were scavenged with superoxide dismutase and catalase, normal PMNL killed P. aeruginosa but not P. cepacia. Thus, P. cepacia, but not P. aeruginosa, is a pathogen in patients with CGO, because it resists neutrophil-mediated nonoxidative bactericidal effects.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/170.6.1524