[Microbiology of chronic rhinosinusitis with different clinical phenotypes].

Objective

To observe the microbiological characteristics and clinical correlation of chronic rhinosinusitis with different clinical phenotypes. Method:One hundred and ninety-six patients with chronic rhinosinusitis（CRS） underwent nasal endoscopic surgery, including 126 patients with Chronic rhinosinusitis with nasal polyps（CRSwNP） and 70 patients with chronic rhinosinusitis without nasal polyps（CRSsNP）; 78 patients with nasal septum deviation（control group） were enrolled. The nasal discharge samples were collected before operation, and the bacteria were isolated and identified by the traditional culture method. The bacteria were compared between the two groups by Pearson chi-square test or Fisher exact test, and the bacteria were compared between groups by Kruskal-Wallis rank sum test. Out statistically significant variables（P<0.05）. Result:The total bacterial detection rate was 73.0% in the three groups, 76.2% in the CRSwNP group, 68.6% in the CRSsNP group and 71.8% in the control group, respectively（P=0.579）. The detection rate of the bacteria was mainly Gram-positive bacteria. The higher detection rate included: Staphylococcus epidermidis, Pseudodiphtheria, Staphylococcus aureus, Haemophilus influenzaemola, Haemella influenzaemola. The detection rate of Haemophilus influenzae in the CRSwNP group and the control group（13.5% vs 2.6%, P=0.009）, but there were statistical differences CRSsNP.There was no statistically significant difference in the detection rate of the bacteria（8.6% vs 2.6%, P=0.15） between the CRSsNP group and the control group; The difference of staphylococcus aureus detection rate between NonECRSwNP group and ECRSwNP group was statistically significant （9.6% vs 28.1%,P=0.017）.There was no significant difference in staphylococcus aureus detection rate between NonECRSsNP group and ECRSsNP group （9.4% vs 16.7%, P=0.482）.

Conclusion

Haemophilus influenzae may be a potential cause of CRSwNP; S. aureus may promote the eosinophilic granulocyte inflammatory response to CRSwNP.