Divergent Mechanisms for Passive Pneumococcal Resistance to [beta]-Lactam Antibiotics in the Presence of Haemophilus influenzae.
Weimer, Kristin E.D.; Juneau, Richard A.; Murrah, Kyle A.; Pang, Bing; Armbruster, Chelsie E.; Richardson, Stephen H.; Swords, Edward W.
[Article]
Journal of Infectious Diseases.
203(4):549-555, February 15, 2011.
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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 [beta]-lactamase-producing strain of nontypeable Haemophilus influenzae (NTHi 86-028NP) and an isogenic mutant deficient in [beta]-lactamase production (NTHi 86-028NP bla) to define the roles of biofilm formation and [beta]-lactamase production in antibiotic resistance. Coinfection studies were done with Streptococcus pneumoniae to determine if NTHi provides passive protection by means of [beta]-lactamase production, biofilm formation, or both.
Results. 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.
Conclusions. Based on these studies, we conclude that NTHi provides passive protection for S. pneumoniae in vivo through 2 distinct mechanisms: production of [beta]-lactamase and formation of biofilm communities.
(C) Copyright Oxford University Press 2011.