IDSA guidelines on resistant organisms

• Which course of action should be instituted if a patient is found to have resistance but treatment is working?

  If cystitis- no need to change.

  Otherwise- start course of treatment with first day as first sensitive antibiotic.
• When should oral switch occur?

  If appropriate susceptible oral agent, reasonable source control, sufficient intestinal absorption and haemodynamically stable.
• What are the 3 mechanisms by which Enterobacterales produce AmpC?

  Inducible chromosomal resistance, stable chromosomal de- repression or via plasmid- mediated ampC genes
• Which antibiotics induce increased AmpC enzyme production?

  Ceftriaxone and ceftazidime
• Which species tend to have stable chromosomal de- repression of ampC?

  E. coli and Shigella
• In which species are constitutive expression of plasmid- borne ampC genes most commonly observed?

  E. coli, Klebsiella pneumoniae and Salmonella
• What are examples of plasmid bornd ampC genes?

  bla CMY, bla FOX, bla DHA, bla ACT, bla MIR
• Which Enterobacterales are moderate to high risk for clinically significant inducible AmpC production?

  Enterobacter cloacae, Klebsiella aerogenes, Citrobacter freundii
• What is the rate of emergence of resistance ito cephalosporins in E. cloacae, K. aerogenes and C. freundii?

  Around 8 to 40 %
• Which agents should be avoided in treatment of E. cloacae, K. aerogenes and C. freundii?

  Ceftriaxone and ceftazidime, even if initially susceptible, due to inducible resistance
• In which Enterobacterales can sensitivity testing generally be trusted regarding cephalosporin sensitivity?

  Serratia marcescens, M. morganii and Providencia, as unlikely to overexpress ampC (occurs in <5% of these organisms)
• When should less commonly encountered Enterobacterales be managed with alternative agents?

  If high bacterial burden and limited source control (e.g. endocarditis, ventriculitis), then consider alternative treatment with cefepime rather than ceftriaxone, even if less commonly recovered pathogens or S. macescens, M. morganiii or Providencia.
• Which antibiotics induce ampC genes?

  All beta lactams are on a spectrum; aminopenicillins (e.g. amoxicillin), narrow spectrum (1st gen) cephalosporins and cephamycins (e.g. cefoxitin) are potent AmpC inducers
• Which beta lactams are lower risk AmpC inducers?

  Piperacillin, ceftriaxone, ceftazidime and aztreonam, however ceftriaxone and ceftazidime are susceptible to hydrolysis and are often avoided
• What is the role of carbapenems in treatment of AmpC inducers?

  Imipenem (and thus probably the others) is a potent AmpC inducer, but forms stable acyl enzyme complexes, and so is less vulnerable to hydrolysis
• Which antibiotic is ideal for treatment of organisms with high risk of AmpC (C. freundii, K. aerogenes and E. cloacae)?

  Cefepime, because it is a weak inducer and resists hydrolysis. If MIC >4mg/microlitre, a carbapenem should be used
• From which sites is carbapenem resistant Acinetobacter baumanii (CRAB) more frequently isolated?

  More from wounds and respiratory specimens
• Which sole agent may be sufficient for treatment of mild CRAB?

  Ampicillin- sulbactam
• Which agent is most helpful as part of combination therapy for CRAB?

  Ampicillin sulbactam
• What is CRAB has resistance to ampicillin sulbactam in vitro?


  Continue ampicillin sulbactam and add other things
• Which treatment is preferred for urine CRAB infection?

  Colistin