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J Infect Dis. 2011 Feb 15;203(4):549-55. doi: 10.1093/infdis/jiq087. Epub 2011 Jan 10.

Divergent mechanisms for passive pneumococcal resistance to β-lactam antibiotics in the presence of Haemophilus influenzae.

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Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.



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 β-lactamase-producing strain of nontypeable Haemophilus influenzae (NTHi 86-028NP) and an isogenic mutant deficient in β-lactamase production (NTHi 86-028NP bla) to define the roles of biofilm formation and β-lactamase production in antibiotic resistance. Coinfection studies were done with Streptococcus pneumoniae to determine if NTHi provides passive protection by means of β-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 β-lactamase and formation of biofilm communities.

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