Bronchial hyperresponsiveness and bacterial respiratory infections.
Some studies suggest a potential role for bacterial respiratory tract infections in the development of bronchospasm and the progression of chronic obstructive pulmonary disease (COPD). Patients with bronchiectasis or cystic fibrosis have exaggerated airway reactivity; croup in children can also cause exaggerated upper and lower airway responsiveness. Bronchial obstruction after inhalation of Haemophilus influenzae and other bacteria has been reported. Between January 1989 and June 1990 we and two other centers studied 193 patients suffering from acute exacerbation of asthma. Fifty-two (27%) of these patients had bacteria in their sputum. Streptococcus pneumoniae, Streptococcus pyogenes, Staphylococcus aureus, Moraxella catarrhalis, and H influenzae were the most commonly isolated bacterial species. Antibiotics may be of value in the treatment of infective lung disease, not only by killing bacteria but also by preventing increases in bacterial histamine levels within the lung airways. Moreover, an antibiotic of proven efficacy can reduce airway reactivity in patients with bacterial exacerbations of COPD or bronchial asthma. In 12 patients with acute bacterial exacerbation of asthma and high airway reactivity to methacholine, a ten-day course of treatment with cefaclor and existing bronchodilators induced microbiologic cure and a slight but nonsignificant change in airway reactivity in nine patients. Antibiotic therapy has a minor but clear role in the control of acquired bronchial hyperreactivity during bacterial respiratory infections in asthmatic patients; however, because of airway inflammation, an antibiotic's efficacy is evident only when the inflammatory process subsides. Approaches designed to minimize airway reactivity may contribute to the prevention or reversal of respiratory failure during exacerbation of COPD and bronchial asthma.
Cazzola
M
M
Department of Pulmonary Medicine, A. Cardarelli Hospital, Naples, Italy.
Matera
M G
MG
Rossi
F
F
D001249:Asthma / Q000209:etiology* / Q000276:immunology; D001424:Bacterial Infections / Q000150:complications*; D001991:Bronchitis / Q000209:etiology / Q000276:immunology; D004731:Endotoxins / Q000276:immunology / Q000633:toxicity; D006636:Histamine Release / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D008173:Lung Diseases, Obstructive / Q000150:complications / Q000276:immunology*; D013183:Sputum / Q000382:microbiology
D004731:Endotoxins