Mechanisms of beta-lactam resistance in Haemophilus influenzae

Eur J Clin Microbiol Infect Dis. 1988 Oct;7(5):610-5. doi: 10.1007/BF01964237.

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

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anti-Bacterial Agents / metabolism
  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins*
  • Carrier Proteins / metabolism
  • Cell Membrane Permeability
  • Drug Resistance, Microbial
  • Haemophilus influenzae / drug effects*
  • Haemophilus influenzae / enzymology
  • Hexosyltransferases*
  • Humans
  • Muramoylpentapeptide Carboxypeptidase / metabolism
  • Penicillin-Binding Proteins
  • Peptidyl Transferases*
  • beta-Lactamases / metabolism
  • beta-Lactams

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Carrier Proteins
  • Penicillin-Binding Proteins
  • beta-Lactams
  • Peptidyl Transferases
  • Hexosyltransferases
  • Muramoylpentapeptide Carboxypeptidase
  • beta-Lactamases