Specialist presentation

1. Chris Baliga
April 15, 2019

2.  75 y/o male with NHL on chemo through a portacath,
splenectomy, presents to the ER with pain, reddness,
swelling around port site, as well as f/c/AMS, cough
 He recently travelled to Arizona and raised chickens.
Has dogs and cats at home. Daughter recently
returned from Sierra Leone, transited through Jedah,
and has a febrile URI acquired during travel.
 What would you do, what do you think?

5.  How to Diagnose? What would you do if you suspect
this?
 Blood Cultures from line and peripherally
 Quantitative Blood Cultures
 Culture from Catheter tip
 Culture from Catheter exit site
 Subcuetaneous segement of line

6.  Differential Growth:
Line + and peripheral –
Time to positivity: 2 hours difference
Quantitative Cultures: 3 fold difference

7.  Culture the tip, not the subcuetaneous segment for
short term lines (IJ, subclavian, Femoral, etc)
 Growth of >15 CFU from 5 cm segment by roll-plate
method or >100 CFU by sonication
 From long term catheter, culture both hub/SQ
segment, as well as tip
 Culture Port reservoir contents as well as line

8.  Draw cultures as early as you can, and prior to abx if
possible
 If multiple ports, culture them all!

13.  CAP=?
 HCAP=?
 Hospitalization within 90 days, attending HD centers, IV
therapy, wound care, chemotherapy, residents of NH/SNF
 HAP=?
 pneumonia 48 hours or more after admit
 VAP=?
 pneumonia more than 48-72 hrs after intubation
 Why do we care?
 Different bugs!

14.  CAP=?
 HCAP=?
 Hospitalization within 90 days, attending HD centers, IV
therapy, wound care, chemotherapy, residents of NH/SNF
 HAP=?
 pneumonia 48 hours or more after admit
 VAP=?
 pneumonia more than 48-72 hrs after intubation
 Why do we care?
 Different bugs!

15.  Why do we care?
Different bugs!
 What bugs in VAP?

16.  History of MDR GNRs
 Severe co-morbid conditions (high risk of resistance:
IV abx in past 90 days), or high risk of mortality
(CRRT, ARDS)
 Immune compromised
 Septic Shock
 Recent (past 90 days) or current CCU stay greater than
2 days
 Bronchiectasis
 CF

17.  Non-invasive as good as invasive
 Semiquantitative Cx preferred
 Biomarkers like CRP, procalcitonin not recommended

18.  No longer recommended in most cases
 BAL with
>10,000 CFU
 Brush with
>1000 CFU
 Of note, a negative trach aspirate (by gram stain or
inflammatory cells) in someone without a recent (72
hrs) change in abx has a good NPV of 94%

20.  7 days in most cases
 Can use procalcitonin to decide if ok to stop, but utility
when using a 7 day stop date for antibiotics not known

21.  PCN resistance by?
penicillinase
 Anti-staph PCN resistance?
=MRSA
mecA which encodes PBP2a
 MRSA treatment options?
 MIC creep
 If MIC to vanc >2, then cannot achieve therapeutic
levels with troughs of 15-20
 If MIC=2 ???

22.  VISA=?
vancomycin intermediate S. aureus
MIC 4-16
Thought to be due to thickened cell wall
no change in activity just more targets for the abx to
bind to

23.  Heterovisa?
Subpopulations of staph
which have decreased
susceptibility within a
larger population of
fully susceptible
organisms

24.  Vancomycin resistant S. aureus
MIC>32
Why?
vanA gene from VRE
Instead of d-ala-d-ala chain, has d-ala-d-lac

25.  vanA gene
 How do you treat?
 E. faecalis?
 E. faceium?

26.  ESBL=?
extended spectrum beta-lactamase
classically in E. coli and Klebsiella
hydrolyzes cefotaxime, ceftriaxone, ceftazidime,
aztreonam
essentially get a profile where first or second generation
cephalosporins are susceptible but thirds are resistant
 inhibited in vitro by beta-lactamase inhibitors, so pip-tazo
susceptible
 Plasmid mediated
 Rx?
carbapenem

27.  Essentially a derepressed ampC mutant in a
population of bacteria, but more commonly called
inducible
 Plasmid mediated
 So culture with sensitivities which are good, improves
on therapy, and then worsens
 SPACE organsisms? Also SPICE organisms?
Serratia, Providencia, Pseudomonas, Proetus,
Acinetobacter, Citrobacter, Enterobacter
 Rx=?
carbapenem

28.  Originally described in Klebsiealla pneumoniae
 Now found in most enterics: E. coli, cirto, entero,
Salmonella
 Also in Pseudomonas and Acinetobacter
 Imipenem may appear susceptible but it is not
 Resistant to all beta-lactamses, cephalosporins,
carbapenems, and aztreonam
 Many genes, but for KPC=blakpc

29.  Usually associated with medical care in India or
Pakistan
 Now becoming more common in UK
 Found in USA as well
 All enterics can have this
 blaNDM1
 Resistant to all beta-lactams, cephalosporins,
carbapenems except aztreonam (although all US
isolates and many are resistant to that by other
mechanisms)

30.  Also ones which only target carbapenems but not
necessarily everything else (so not as bad)
 How to treat? Call me!
 Options limited.
 Non-betalactams if lucky: quinolones, aminoglycosides,
tertacyclines
 Tigecyline
 Polymixin (colistin) if you are really unlucky
 Newer beta-lactams/beta-lactamase inhibitors:
ceftazidime/avibactam, ceftolozane/tazobactam,
meropenem/vaborbactam
 Worse clinical outcomes