Staphylococcus Aureus

Reviewed and revised 3 September 2015

OVERVIEW

  • aerobic gram positive cocci
  • has developed beta-lactamase activity thus is not susceptible to penicillin (use flucloxacillin at doses of 2g 4-6 hrly)
  • because of increasing MRSA in the community, empiric treatment should be vancomycin in many settings
  • prevalence of hospital acquired MRSA varies from unit to unit
  • if no obvious source consider occult sources:
    — epidural abscess
    — psoas abscess
    — endocarditis

PATHOPHYSIOLOGY

  • commensal bacterium that colonizes the nares (its primary reservoir), axillae, vagina, pharynx, and/or damaged skin surfaces
  • S. aureus is unique in its ability to invade and cause disease in previously normal tissue at virtually all sites

Staphylococcus aureus is intrinsically to penicillin by 3 mechanisms:

  • hyperproduction of β-lactamases
  • modification of the normal penicillin-binding proteins (PBPs), and
  • presence of an acquired penicillin-binding protein (PBP2a)

CLINICAL MANIFESTATIONS

  • local and systemic features of infection

Common sites

  • skin and soft-tissue, e.g. cellulitis, pyomyositis, abscess and necrotizing fasciitis
  • respiratory, e.g. necrotizing pneumonia, lung abscess and empyema
  • bone and joint, e.g. osteomyelitis and septic arthritis
  • endovascular infections, e.g. endocarditis, septicaemia
  • infected prosthesis, e.g. joint replacements, valve replacements

Toxin mediated syndromes

  • Toxic shock syndrome
  • Staphylococcus scalded skin syndrome

INVESTIGATIONS AND MANAGEMENT

  • all patients with staphylococcal bacteremia should have echocardiography
  • consider pan-scan CT to identify occult source (e.g psoas abscess)
  • consider MRI to rule out epidural abscess

ANTIBIOTIC CHOICE, DOSE AND FREQUENCY

Choice of antibiotic consideration

  • ensure Staphyloccocus coverage
  • actual Staph (aureus vs coag –ve)
  • hospital or Community Acquired
  • site of infection and ability of drug to penetrate infected area
  • endemic resistance patterns (MRSA, VISA, hVISA, VRSA, VRSE)
  • presence of Toxic Shock Syndrome (addition of Clindamycin for endotoxin activity)
  • allergies
  • previous treatment with antibiotics with treatment failure and previous sensitivity patterns

Dosing Regimen

  • high dose for life threatening infections
  • give IV
  • loading dose
  • appropriate interval dosing
  • reduce if renal impairment
  • reduced if develop side effects
  • dose reduced if Na+ load unacceptable to patient

MSSA (METHICILLIN SENSITIVE)

Sensitive to:

  • flucloxaciliin 100mg/kg/day in divided doses
  • clindamycin 4mg/kg Q6hrly
  • co-trimoxazole 80-100mg/kg of sulphamethoxazole
  • erythromycin 20mg/kg/day in divided doses
  • fusidic acid 1g Q8hrly
  • gentamicin 3-5mg/kg LD -(titrate to trough)
  • tetracycline 500mg Q12hrly

Also treated by:

  • vancomycin 10mg/kg LD -> dose as per trough level
  • linezolid 600mg Q12hrly (adult)
  • meropenem 1g Q8hrly (adult)
  • quinpristin-dalfopristin 7.5mg/kg Q8hrly
  • rifampicin 20mg/kg /day
  • teicoplanin 400mg LD, 400mg @ 12 hrs, 400mg Q24hrly
  • tigecycline 100mg LD, 50mg Q12hrly

MRSA (METHICILLIN RESISTANT)

Hospital Acquired Methicillin Resistant (HA-MRSA)

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

Community Acquired Methicillin Resistant (CA-MRSA)

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

VISA (VANCOMYCIN INTERMEDIATE RESISTANT)

Heterogenous Vancomycin Intermediate Resistant (h-VISA)

  • significance of hVISA is uncertain as the MIC is the same for MRSA but daughter strains have higher MIC
  • MIC range of 1-4mcg/mL
  • continued stress from vancomycin leads to VISA

Vancomycin Intermediate Resistant (VISA) or Glycopeptide Intermediate Resistant (GISA)

  • genes code for factors such as additional peptidoglycan synthesis and reduced need for peptidoglycan cross-linking
  • CDC definition:
    (1) MIC between 8-16mcg/mL with a broth micro-dilution test
    (2) MIC > 6mcg/mL with E-testing
    (3) growth within 24 hours on commercially prepared brain-heart infusion agar containing 6mcg/mL of vancomycin
  • can’t use disc diffusion for VISA detection
  • treatment: teicoplanin, linezolid, quinupristin-dalforpristin, or cotrimoxazole

VRSA (VANCOMYCIN RESISTANT)

  • MIC > 32 mcg/mL
  • first reported in US in 2002
  • contains vanA determinant that mediates the high level of vancomycin resistance seen in VRE (MIC was > 1024 mcg/mL)
  • treatment: linezolid

References and Links

Journal articles

  • Boucher H, Miller LG, Razonable RR. Serious infections caused by methicillin-resistant Staphylococcus aureus. Clin Infect Dis. 2010 Sep 15;51 Suppl 2:S183-97. [pubmed]
  • Rehm SJ. Staphylococcus aureus: the new adventures of a legendary pathogen. Cleve Clin J Med. 2008 Mar;75(3):177-80, 183-6, 190-2. .[pubmed]
  • Rehm SJ, Tice A. Staphylococcus aureus: methicillin-susceptible S. aureus to methicillin-resistant S. aureus and vancomycin-resistant S. aureus. Clin Infect Dis. 2010 Sep 15;51 Suppl 2:S176-82. [pubmed]

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and 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 two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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