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目的 :探讨生物被膜 (BF)克雷白杆菌耐药机制 ,为临床选用抗生素提供理论依据。方法 :用改良平板培养法建立克雷白杆菌BF模型。用银染法及扫描电镜对BF进行鉴定。分别检测浮游克雷白杆菌 (A组 )、BF菌(B组 )、亚胺培南诱导BF菌 (C组 )、头孢西丁诱导BF菌 (D组 )、氧哌嗪青霉素诱导BF菌 (E组 )产生β 内酰胺酶的活性。结果 :B组β 内酰胺酶活性 (0 .5 496± 0 .0 99)U/mg高于A组 (0 .3 3 3 4± 0 .0 2 9) ,是A组 1.65倍 (P <0 .0 1) ;C组 (0 .772 8± 0 .0 3 79)、D组 (0 .663 4± 0 .0 5 5 8)、E组 (0 .60 70± 0 .0 465 )U/mg均高于B组 (P <0 .0 1) ;C组高于D组和E组 (P <0 .0 1) ;D组高于E组 (P<0 .0 1)。结论 :BF克雷白杆菌产生大量 β 内酰胺酶是其耐药主要原因之一 ,抑酶剂或含抑酶剂抗生素治疗BF克雷白杆菌相关感染可能有效
Objective: To investigate the drug resistance mechanism of Klebsiella pneumoniae biofilm (BF) and provide a theoretical basis for clinical use of antibiotics. Methods: BF model of Klebsiella pneumoniae was established by modified plate culture method. BF was identified by silver staining and scanning electron microscopy. Bacterioflankton buildup (group A), BF (group B), imipenem-induced BF (group C), cefoxitin-induced BF (group D) Group E) produce beta-lactamase activity. Results: The β-lactamase activity in group B (0.5496 ± 0.099) U / mg was significantly higher than that in group A (0.333 ± 0.029), which was 1.65 times of that in group A (P < (0 .772 8 ± 0 .0 3 79), group D (0.663 4 ± 0 .0 5 5 8), group E (0 .60 70 ± 0 .0 465) U / mg were higher than those in group B (P <0.01); those in group C were higher than those in group D and E (P <0.01); those in group D were higher than those in group E (P <0.01). CONCLUSION: The large amount of β-lactamases produced by Klebsiella pneumoniae is one of the major causes of drug resistance. Suppressor agents or antibiotics with inhibitors may be effective in the treatment of BF Klebsiella infection