Lung and pharyngeal abscess caused by enterotoxin G- and I-producing Staphylococcus aureus.

We report a particularly serious case of extensive meticillin sensitive Staphylococcal lung and pharyngeal abscess. Our patient had no significant risk factors for severe infection. The detection of enterotoxin G and I here suggest that when present together, these toxins work synergistically to produce a more virulent strain of Staphylococcus aureus.

Bronchial mucosal dendritic cells in smokers and ex-smokers with COPD: an electron microscopic study.

BACKGROUND: Bronchial mucosal dendritic cells (DCs) initiate and regulate immune responses to inhaled antigens, viruses and bacteria. Currently, little is known of their numbers in patients with chronic obstructive pulmonary disease (COPD). While reductions in their numbers have been reported recently in smokers with asthma, nothing is known of the effects of cigarette smoking on bronchial DCs in COPD. The present study compares DC numbers in smokers and ex-smokers with COPD. METHODS: Endobronchial biopsies were obtained from 15 patients with moderate to severe COPD (10 current smokers with median forced expiratory volume in 1 s (FEV1) 45.5% predicted (range 23-68) and 5 ex-smokers with median FEV1 30% predicted (range 21-52)), 11 non-smokers with asthma (median FEV1 102% predicted (range 89-116)) and 11 non-smoker healthy controls (median FEV1 110% predicted (range 92-135)). Transmission electron microscopy (TEM) was used to identify the total population of DCs by their ultrastructure and their number in the epithelium and subepithelium was counted. RESULTS: Median (range) DC numbers were significantly lower in current smokers with COPD in the epithelium (0.0 (0.0-156.8) cells/mm2) and the subepithelium (4.5 (0.0-63.6) cells/mm2) compared with ex-smokers with COPD (97.9 (93.5-170.3) cells/mm2 in the epithelium (p<0.05); 91.8 (38.2-283.3) cells/mm2 in the subepithelium (p<0.01)). DC numbers in ex-smokers with COPD were similar to those in subjects with atopic asthma and healthy controls (131.6 (33.3-235.5) cells/mm2 in the epithelium and 64.4 (0.0-182.4) cells/mm2 in the subepithelium for the latter). CONCLUSIONS: In COPD, bronchial mucosal DC numbers are lower in current smokers while, in those who quit, numbers are similar to non-smoking subjects with asthma and non-smoking healthy controls. The functional consequences of the reduction in mucosal DC numbers in smokers with COPD have yet to be determined.

Airway mucosal inflammation in COPD is similar in smokers and ex-smokers: a pooled analysis.

Bronchial biopsy specimens from chronic obstructive pulmonary disease (COPD) patients demonstrate increased numbers of CD8+ T-lymphocytes, macrophages and, in some studies, neutrophils and eosinophils. Smoking cessation affects the rate of forced expiratory volume in one second (FEV(1)) decline in COPD, but the effect on inflammation is uncertain. Bronchial biopsy inflammatory cell counts were compared in current and ex-smokers with COPD. A pooled analysis of subepithelial inflammatory cell count data from three bronchial biopsy studies that included COPD patients who were either current or ex-smokers was performed. Cell count data from 101 subjects, 65 current smokers and 36 ex-smokers, were analysed for the following cell types: CD4+ and CD8+ T-lymphocytes, CD68+ (monocytes/macrophages), neutrophil elastase+ (neutrophils), EG2+ (eosinophils), mast cell tryptase+ and cells mRNA-positive for tumour necrosis factor-alpha. Current smokers and ex-smokers were similar in terms of lung function, as measured by FEV(1) (% predicted), forced vital capacity (FVC) and FEV(1)/FVC. The results demonstrate that there were no significant differences between smokers and ex-smokers in the numbers of any of the inflammatory cell types or markers analysed. It is concluded that, in established chronic obstructive pulmonary disease, the bronchial mucosal inflammatory cell infiltrate is similar in ex-smokers and those that continue to smoke.

Effects of fluticasone propionate on inflammatory cells in COPD: an ultrastructural examination of endobronchial biopsy tissue.

BACKGROUND: Inhaled corticosteroids (ICS) markedly reduce bronchial mucosal inflammation in asthma but whether they have an anti-inflammatory effect in airway tissue in chronic obstructive pulmonary disease (COPD) is unknown. METHODS: A study of endobronchial biopsy samples was conducted as part of a double blind, placebo controlled, randomised trial of parallel design. Patients had mild to moderately severe COPD (FEV(1) 25-80% of predicted) and were given 3 months treatment with ICS, fluticasone propionate (FP; 500 micro g twice daily, n=14) or placebo (n=10). Biopsy tissue taken at baseline and after treatment was examined by transmission electron microscopy to count the numbers of all ultrastructurally distinct inflammatory cells. RESULTS: Compared with their baseline values, FP resulted in a significant decrease (on average 65%) in the numbers of mucosal mast cells (median 7.8 (range 1-33) v 2.8 (1-14), p<0.05). The reductive effect of FP held true when the post-treatment values of the placebo and FP groups were compared: 8.8 (1-24) v 2.8 (1-14) (p<0.05). Unexpectedly, there were significantly more neutrophils in the FP than in the placebo group: 4.0 (0-23) v 1.7 (0-8), respectively (p<0.05). There were no alterations to other cell types including mononuclear cells. Symptoms markedly improved in the patients treated with FP for 3 months. CONCLUSION: Fluticasone propionate given for 3 months to patients with COPD has selective effects on the inflammatory cells in the bronchial mucosa: the reduction in mast cell numbers may account for the improvement in symptoms over this time.

Pneumococcal vaccine.

Streptococcus pneumoniae is a frequent cause of pneumonia and meningitis. This article looks at the pneumococcal vaccine, its uses, efficacy, and adverse effects and how vaccination may be improved. We also look at the role of the new conjugate vaccines.