Divergent mechanisms for passive pneumococcal resistance to ?-lactam antibiotics in the presence of Haemophilus influenzae.
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ABSTRACT: Otitis media, for which antibiotic treatment failure is increasingly common, is a leading pediatric public health problem.In vitro and in vivo studies using the chinchilla model of otitis media were performed using a ?-lactamase-producing strain of nontypeable Haemophilus influenzae (NTHi 86-028NP) and an isogenic mutant deficient in ?-lactamase production (NTHi 86-028NP bla) to define the roles of biofilm formation and ?-lactamase production in antibiotic resistance. Coinfection studies were done with Streptococcus pneumoniae to determine if NTHi provides passive protection by means of ?-lactamase production, biofilm formation, or both.NTHi 86-028NP bla was resistant to amoxicillin killing in biofilm studies in vitro; however, it was cleared by amoxicillin treatment in vivo, whereas NTHi 86-028NP was unaffected in either system. NTHi 86-028NP protected pneumococcus in vivo in both the effusion fluid and bullar homogenate. NTHi 86-028NP bla and pneumococcus were both recovered from the surface-associated bacteria of amoxicillin-treated animals; only NTHi 86-028NP bla was recovered from effusion.Based on these studies, we conclude that NTHi provides passive protection for S. pneumoniae in vivo through 2 distinct mechanisms: production of ?-lactamase and formation of biofilm communities.
SUBMITTER: Weimer KE
PROVIDER: S-EPMC3071235 | biostudies-literature | 2011 Feb
REPOSITORIES: biostudies-literature
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