Enterobacter species


  • Gram-negative, aerobic, motile bacilli of the Enterobacteriaceae family. Ferments lactose and forms mucoid colonies. Commonly found in water, sewage, and soil.[8]
  • Opportunistic human pathogen includes E. cloacae (most common), E. aerogenes (renamed Klebsiella aerogenes), E. gergoviae[17] and Pantoea agglomerans.
  • High levels of drug resistance often seen and due to:
    • AmpC β-lactamases - Ambler class C
      • Chromosomal AmpC can be constitutive (always active) or inducible (variably active) and are not inhibited by β-lactam β-lactamase inhibitors.[19]
        • β-lactams must be present for activation of inducible β-lactamases, so initial susceptibility reports may not detect resistance that can emerge during therapy.
      • Plasmid-mediated[9]
        • Phenotypic assays are unable to distinguish between AmpC β-lactamase production due to derepression of chromosomal versus plasmid-associated ampC gene.
    • Plasmid-encoded extended-spectrum β-lactamases (ESBLs)
      • ESBL genes include blaCTX-M, blaSHV, and blaTEM. Commercially available molecular platforms limited to detection blaCTX-M.
      • Most often such organisms demonstrate elevated MICs to cefepime.
      • ESBLs inactivate most penicillins, cephalosporins, and aztreonam.[1]
    • Carbapenemases[14]
      • Ambler class A - Most common are Klebsiella pneumoniae carbapenemases (KPC) that can be produced by any Enterobactrerales.
      • Ambler class B - Metallo-β-lactamases include: New Delhi (NDMs), Verona integron-encoded (VIM), and imipenem-hydrolyzing (IMPs)
      • Ambler class D - Oxacillinase (OXA-48-like) carbapenemases
  • Ceftriaxone MIC ≥ 2 is used as a proxy for ESBL production.
  • Other resistance mechanisms
    • Alterations in the active site of penicillin-binding protein
    • Defects in outer membrane permeability that reduce diffusion of β-lactams into the cell
    • Presence of efflux pumps that move β-lactams out of the cell

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Last updated: February 16, 2023