Divergent mechanisms for passive pneumococcal resistance to ýý-lactam antibiotics in the presence of Haemophilus influenzae.
Divergent mechanisms for passive pneumococcal resistance to ýý-lactam antibiotics in the presence of Haemophilus influenzae.
复制标题
在流感嗜血杆菌存在的情况下，肺炎球菌对α-内酰胺抗生素产生被动耐药的不同机制。
DOI：
10.1093/infdis/jiq087
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Swords,WEdward
中科院分区：
文献类型：
--
作者：
Weimer,KristinED;Juneau,RichardA;Murrah,KyleA;Pang,Bing;Armbruster,ChelsieE;Richardson,StephenH;Swords,WEdward
Background.Otitis media, for which antibiotic treatment failure is increasingly common, is a leading pediatric public health problem.Methods.In vitro and in vivo studies using the chinchilla model of otitis media were performed using a β-lactamase-producing strain of nontypeableHaemophilus influenzae(NTHi86-028NP) and an isogenic mutant deficient in β-lactamase production (NTHi86-028NPbla) to define the roles of biofilm formation and β-lactamase production in antibiotic resistance. Coinfection studies were done withStreptococcus pneumoniaeto determine if NTHiprovides passive protection by means of β-lactamase production, biofilm formation, or both.Results.NTHi86-028NPblawas resistant to amoxicillin killing in biofilm studies in vitro; however, it was cleared by amoxicillin treatment in vivo, whereas NTHi86-028NP was unaffected in either system. NTHi86-028NP protected pneumococcus in vivo in both the effusion fluid and bullar homogenate. NTHi86-028NPblaand pneumococcus were both recovered from the surface-associated bacteria of amoxicillin-treated animals; only NTHi86-028NPblawas recovered from effusion.Conclusions.Based on these studies, we conclude that NTHiprovides passive protection forS. pneumoniaein vivo through 2 distinct mechanisms: production of β-lactamase and formation of biofilm communities.
