Abstract
Haemophilus influenzae has become increasingly resistant to beta-lactam antibiotics. Three major mechanisms, both enzymatic and non-enzymatic, are involved. Enzymatic resistance is mainly due to production of a TEM-1 plasmid-mediated beta-lactamase, and in some cases to a new enzyme ROB-1. Of the non-enzymatic mechanisms, decreased permeability due to alteration of outer membrane proteins seems to be rare in comparison to decreased affinity of penicillin-binding proteins for beta-lactam antibiotics. Enzymatic resistance is present in about 10-20% of clinical isolates, while non-enzymatic resistance is present only in 2-4%.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Anti-Bacterial Agents / metabolism
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Anti-Bacterial Agents / pharmacology*
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Bacterial Proteins*
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Carrier Proteins / metabolism
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Cell Membrane Permeability
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Drug Resistance, Microbial
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Haemophilus influenzae / drug effects*
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Haemophilus influenzae / enzymology
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Hexosyltransferases*
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Humans
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Muramoylpentapeptide Carboxypeptidase / metabolism
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Penicillin-Binding Proteins
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Peptidyl Transferases*
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beta-Lactamases / metabolism
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beta-Lactams
Substances
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Anti-Bacterial Agents
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Bacterial Proteins
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Carrier Proteins
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Penicillin-Binding Proteins
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beta-Lactams
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Peptidyl Transferases
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Hexosyltransferases
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Muramoylpentapeptide Carboxypeptidase
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beta-Lactamases