Infectious Disease Updates

  • Fungal infections – dx and tx
  • CAPNA – dx and tx
  • Testing for C diff
  • GN resistance
  • PPD v Quantiferon Gold
  • MRSA – mgmt, tx
  • The host is the most important factor:
    • Hematopoietic stem cell transplant recipients:  molds >> yeast (ie, Candida)
    • Malignancy:  molds = yeast (less risk with non-leukemic heme malignancies (eg, multiple myeloma) and with solid tumors) – the chemo is the main contributor.
    • Solid organ transplant:  molds = yeasts
    • Critical care patients: yeast >> molds (not common in critical care unless they’re one of the above groups)
    • Concomitant lung disease and critical care:  yeast > molds
    • General surgical patients: yeast >> molds
  • Clues to fungal infection:  immunosuppression, lack of response to antibiotics, “halo sign” on CT (lighter, hazy infiltrate surrounding the main goomba; often “hazy, patchy, ground-glass appearance” – if unilateral, VERY suggestive of fungal).
  • Causes:
    • Endemic:  Crypto, Coccidio (AZ, NM, CA – and can be carried by winds…) – ask where they’ve been, where they get care!
    • Molds:  Aspergillus (most common), Mucormycosis (this is bread and fruit mold – think about this in uncontrolled diabetics), Fusarium (this is a flower/plant mold – why fresh flowers are not allowed on the transplant unit!), Scedosporium (also a plant/environmental mold).  Mucor, fusarium and Scedosporium are all surgical diseases – not adequately treated with meds alone.
    • Yeast: Candida
  • Diagnosis:
    • Yeast:  blood cultures: negative in 50%.  57.8% positive with 2+ organs involved at autopsy.  If high suspicion, have to order specific fungal isolate tests.  Biopsies and other source cultures.  CHECK THE FUNDI!  Candida endophthalmitis occurs in 4-25% of candidemia cases.  If they have endophthalmitis, it lengthens the therapy signficantly.
    • Endemic fungi:  Specific serologies – crypto Ag, histo urine Ag, Coccidio Ab & complement fixation.
    • Molds:  definitive dx requires histopathology and culture, but…Gomori methamine silver stain and PAS stains are valuable tissue stains.  Histopath cannot distinguish between Aspergillus and Fusarium.
  • Treatment:
    • When is fluconazole still first-line therapy for fungemia?
      • mild-to-mod illness, no recent azole exposure
      • DO NOT ASSUME that (+) Candidal blood cultures are contaminants!  Pt can be febrile but look good.
      • Candida in the bladder has a higher resistance rate – may have to push the dose up, or get sensitivity testing.
    • When can we step down from IV regimen to PO azole?
      • transition to fluconazole once Candida spp. is known and pt is stable.
    • Is there a role for combination therapy?
      • Limited data – mainly in endocarditis and CNS infections – amphotericin B and 5-flucytosine.
      • Utility of immunotherapy (efungumab) combined with other agents is being researched, some research into interferon-gamma therapy, too.
    • C. glabrata and C. krusei – often resistant to fluconazole and itraconazole.  C krusei is completely resistant to fluconazole, but otherwise may be dose-dependent.
  • Mandell L, et al. Clin Infect Dis 2007; 44:S27-72.
  • What tests should we order in a patient ADMITTED with community-acquired PNA?
    • ICU:  BCx, SCx, Legionella UAT, Pneumococcal UAT, endotracheal aspirate if intubated, consider BAL.
    • Failure of outpatient abx:  sputum Cx, Legionella UAT, Pneumococcal UAT.
    • Active EtOH abuse:  BCx, SCx, Legionella, Penumococcal.
    • Severe COPD:  Sputum Cx
  • How long should we treat a patient diagnosed with community-acquired PNA?
    • Minimum of 5 days
    • Before stopping therapy, pt should be:
      • afebrile for 48-72h
      • no supplemental O2 (unless pre-existing O2 requirement)
      • no more than one “clinical instability factor”:  HR > 100, RR > 24, SBP < 90
    • Hayashi, et al. Clin Infect Dis 2011; 52(10): 1232ff. – longer duration of therapy if:  initial therapy not active against identified pathogen; if extrapulmonary infx identified; P aeruginosa, S aureus, Legionella or other less common pathogens; or if pt has necrotizing pneumonia, empyema or abscess.
  • ESBL (extended-spectrum beta-lactamase producing) organism
  • What GN organisms prone to ESBL resistance do we need to consider?
    • Pseudomonas
    • Acinetobacter baumanni
    • Enterobacteriaceae (cloacae or aerogenes), Klebsiella pneumoniae, E. coli (more often in LTCFs)
  • Several mechanisms of resistance are inducible – that is, they do not show up until we add the antibiotic to the mix!  The culture will show “susceptible,” but then treatment won’t work!
  • Carbapenemases exist!  “ESBL on steroids.”  Found in S maltophilia, sometimes Enterobacter, Bacteroides, K pneumoniae and E coli.  Fortunately, these are carbapenem-specific, so others may still work.
    • Gupta N et al.  Clin Infect Dis 2011; 53(1): 60-67.  – risks for CRE – health-care exposure, mechanical ventilation, recent stem-cell or organ transplantation, ICU stay…
  • Risks for ESBL:  healthcare-associated infections, indwelling catheters, sicker patients.  Also UTI with K pneumoniae, age >60, DM, prior abx use.
  • Treatment options if ESBL suspected:  imipenem, meropenem, doripenem.
  • Do blood cultures need to be checked to ensure clearance?  We don’t know, no good data.  Probably a good idea if source unknown or patient is not improving.
  • Not everyone is from N America!  Ask where people were born.  Africa, India, China, parts of SE Asia have the higher endemic rates.
  • What is the best way to test for prior exposure to MTb?
    • AFB – best for active MTb
    • PPD – risk for active TB in pt’s with TST+ is 5-10%; interval between infection and (+) TST is 2-12 weeks.  Fair amount of false (+) and false (-) tests.
    • Quantiferon Gold – ELISA test detects IgG in whole blood when incubated with synthetic peptides similar to those on MTb.  Definitely superior in pts who have received BCG vaccine.
    • TST is preferred in children < 5 yo.
  • Don’t repeat C diff testing if the patient is improving on treatment.
  • Bagdasarian N, et al.  JAMA 2015 – Sens and Spec of different C diff tests
  • Potage CR, JAMA Intern Med 2015 – we are probably overdiagnosing patients with C diff because we test for the toxin, not for the bacteria (or the clinical disease)!
  • Treat for a MINIMUM of 14 days as long as it is uncomplicated bacteremia
  • Everyone else gets 4 weeks (prosthetic valves, etc.)
  • Endocarditis gets 6 weeks
  • If no MRSA, use a cephalosporin or extended spectrum PCN.  Nafcillin if CNS involvement.
  • If using Vanco for MRSA, continue with vanco if MIC < 2.
 From Rocky Mountain Hospital Medicine conference, 2016, Barron

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