Multi-Resistant Organisms (MROs)


List of multi-resistant bacteria species

  • Methicillin Resistant Staphylococcus aureus (community and hospital MRSA)
  • Vancomycin-Intermediate Resistant Staphylococcus aureus (VISA) and Heterogeneous Vancomycin-Intermediate-Resistant Staphylococcus aureus (hVISA)
  • Methicillin-Resistant Staphylococcus epidermidis (MRSE)
  • Vancomycin Resistant Enterococcus (VRE)
  • Vancomycin Resistant Staphylococcus aureus (VRSA) and Vancomycin Resistant Staphylococcus epidermidis (VRSE)
  • ESCAPPM organisms (Gram negative rods) – Enterobacter species, Serratia species, Citrobacter freundi, Aeromonas, Proteus vulgaris, Providencia, Morganella morganii
  • Extended Spectrum Beta-Lactamases (ESBLs) – E coli, Klebsiella, Enterobacteriae
  • Stenotrophomonas
  • Acinetobacter baumanii
  • Pseudomonas aeruginosa
  • Streptococcus pneumoniae
  • New Delhi metallo-β-lactamase 1 (NDM-1)
  • Multi-resistant Acinetobacter baumani


Risk factors for infection with multidrug-resistant Gram-negative organisms (e.g. ESBLs)

  • recent international travel to areas with a high prevalence of multidrug-resistant Gram-negative organisms (eg within 6 months)
  • prolonged hospitalisation
  • residence in a long-term care facility
  • previous colonisation or infection with a resistant Gram-negative organism

Hospital-acquired MRSA

  • penicillin-binding protein mutation coded by the mecA gene on a transposon
  • also produces to multiple other classes (tetracyclines, macrolides, sulphonamides, aminoglycosides)
  • treatment: vancomycin, tiecoplanin, rifampicin, fusidic acid, ciprofloxacin

Community-acquired MRSA

  • similar mechanism to Hospital-acquired MRSA + additional gene (PVL)
  • often seen in Pacific Island born patient and Indigenous communities
  • treatment: vancomycin, teicoplanin, clindamycin, sometimes rifampicin, fusidic acid, ciprofloxacin, co-trimoxazole, erythromycin


  • genes code for factors such as additional peptidoglycan synthesis and reduced need for peptidoglycan cross-linking
  • significance of hVISA is uncertain -> MIC is the same for MRSA but daughter strains have higher MIC
  • treatment: teicoplanin, linezolid, quinupristin-dalforpristin, cotrimoxazole


  • methicillin resistant staphylococcus epidermidis
  • penicillin-binding protein mutation coded by the mecA gene as per MRSA

Vancomycin Resistant Enterococcus (VRE)

  • Enterococcus faecium and Enterococcus faecalis
  • normally low virulence organisms -> but can become significant pathogens in debilitated, immunosuppressed patients receiving broad-spectrum antimicrobial treatment
  • in 1990’s in the US vancomycin resistance emerged
  • colonise GI tract -> spread by hand contamination by hospital staff
  • once established remains endemic
  • resistance is passed onto more pathogenic organisms such as Staph aureus
  • mechanisms of resistance:

(1) pencillin-binding protein mutations
(2) beta-lactamase production
(3) aminoglycoside-modifying enzymes
(4) antibiotic drug efflux pumps
(5) alterations in cell wall components coded by transposons (Van A to F phenotypes)


  • previous treatment with anti-microbials (especially vancomycin, cephalosporins, and broad spectrums antibiotics)
  • increased length of stay
  • renal insufficiency
  • enteral tube feeding
  • prevalence of VRE colonised patients in the unit
  • residents of long-term care facilities


  • potential transmission of resistance to Staph aureus
  • determined by presence of infection (UTI, bacteraemia, endocarditis, respiratory infections)
  • colonisation and subsequent transmission (requirement for isolation)
  • septaecaemia
  • intra-abdominal abscesses


  • specific antimicrobial therapy if patient develops active infection

Van A: resistant to vancomycin and teicoplanin
Van B: resistant to vancomycin, teicoplanin may be effective but resistance likely to emerge with prolonged use (use linezolid, tigecycline, dalfopristin-quinapristin, daptomycin)
Van C: partly resistant to vancomycin

  • treatment: ampicillin, tetracyclines, quinolones, linezolid, teicoplanin (some), quinupristin-dalfopristin (Enterococcus faecium only)
  • minimisation of cross contamination (isolation and infection control)
  • limitation of broad spectrum antibiotics
  • surveillance until patient clear


  • alterations in cell components coded by transposons – Van A gene transferred from VRE
  • treatment: linezolid, quinupristin-dalfopristin, cotrimoxazole, chloramphenicol


  • Gram negative rods
    • Enterobacter species
    • Serratia species
    • Citrobacter freundi
    • Aeromonas
    • Proteus vulgaris (non-mirabilus) + Pseudomonas
    • Providencia
    • Morganella morganii
  • rapidly inducible production of beta-lactamase during therapy with cephalosporins (especially third-generation agents)
  • treatment: carbapenems, fourth generation cephalosporins, ciprofloxacin, aminoglycosides


  • Klebsiella pneumoniae, Escherichia coli, other Enterbacteriaceae
  • genetically coded resistance to broad-spectrum beta-lactam antibiotics -> extended spectrum pencillins, third generation cephalsporins, aztreonam
  • co-resistant to co-trimoxazole, aminoglycosides and quinolones
  • in vitro appear to be sensitive to cephalsporins, but have resistance in vivo
  • treatment: carbapenems or fourth generation cephalsporins

Stenotrophomonas maltophilia

  • intrinsic resistance to many beta-lactam antibiotics, including carbapenems and aminoglycosides
  • treatment: co-trimoxazole (drug of choice), ticarcillin-clavulanate, ceftazidime and fluoroquinolones

Acinetobacter baumannii

  • intrinsic resistance to beta-lactam and aminoglycosides
  • found in soil and sand
  • treatment: carbapenems and aminoglycosides (two agents often successfully used even if in-vitro resistance demonstrated)

Pseudomonas aeruginosa

  • intrinsically resistance to many antibiotics through:

(1) efflux pumps
(2) loss of porins
(3) altered target enzymes
(4) beta-lactamases
(5) metllocarbapenemases
(6) aminoglycoside-modifying enzymes

  • treatment: dual therapy in severe infections -> ciprofloxacin, gentamicin, tobramycin, ceftazidime, piperacillin-tazobactam, ticarcillin disodium and clavulanate potassium, imipenem, meropenem, amikacin, nebulised colistin (chronic bronchiectasis)

Streptococcus pneumoniae

  • penicillin and cephalosporin intermediate resistance and some high level resistance
  • precise proportions are unknown
  • North American data: may be between 40-80%
  • normal resistance: penicillin MIC < 0.1microgram/mL
  • intermediate resistance: MIC 0.1-1microgram/mL (treat with high dose penicillin)
  • high resistance: MIC > 2.0micrograms/mL (treat with vancomycin and/or fluoroquinolones)

New Delhi metallo-Clactamase 1 (NDM-1)

  • an enzyme that produces resistance to a broad-range of beta-lactam antibiotics
  • produces a carbapenemase
  • bacteria involved: E. coli, Klebsiella pneumoniae, Acinetobacter baumannii
  • can spread to other bacteria through horizontal gene transfer (via plasmids)
  • treatment: tigecycline and colistin

Multi-resistant Acinetobacter baumani

  • Gram negative aerobic organism
  • inherently resistant, low virulence, opportunistic
  • unless risk factors (see below) usually is a colonsier
  • risk factors: immunosuppressed, prosthetic material (catheters, lines, tubes, devices)
  • resistance via beta-lactamases, metalloproteases, reduced membrane permeability, enhanced efflux
  • outbreaks associated with: high use of cephalosporins, quinolones and carbapenems
  • difficult to clear because of wide spread colonisation
  • treatment:
    — colistimethate sodium (adult and child) 2.5 mg/kg up to 150 mg IV, 12-hourly,or
    — tigecycline 100 mg IV, for the first dose, then 50 mg IV, 12-hourly (in adults)
    — generally 14 to 21 days but requires individual assessment

References and Links

Journal articles

  • Dhillon RH, Clark J. ESBLs: A Clear and Present Danger? Crit Care Res Pract. 2012;2012:625170. doi: 10.1155/2012/625170. Epub 2011 Jun 6. PubMed PMID: 21766013; PubMed Central PMCID: PMC3135063.
  • Pillai DR, McGeer A, Low DE. New Delhi metallo-β-lactamase-1 in Enterobacteriaceae: emerging resistance. CMAJ. 2011 Jan 11;183(1):59-64. doi: 10.1503/cmaj.101487. Review. PubMed PMID: 21220461; PubMed Central PMCID: PMC3017254.

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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