apic annual conference – june 10, 2009
TRANSCRIPT
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MDROsIt’s not just about MRSA
Titus L. Daniels, MD MPHAssistant Professor of Medicine (Infectious Diseases) – VUSMAssociate Hospital Epidemiologist – Vanderbilt Medical Center
Hospital Epidemiologist – Williamson Medical Center
APIC Annual Conference – June 10, 2009
Disclosers
Acknowledgements
• Vicki Brinsko • Amy Dziewior• Tracy Hann• Lorrie Ingram
• Jan Szychowski• Kathie Wilkerson• Vicki Sweeney
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MDROs
•MRSA = Methicillin – resistant Staphylococcus aureus
• VRE = Vancomycin – resistant enterococcus
• CDAD = C. difficile associated diarrhea
•MDRGN = Multi‐drug resistant Gram‐negatives
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An example
77 y/o male
Hospitalized much of the prior 90 days
Slowly recovering
Now extubated
Sitting up, working with physical therapy
Eating well, gaining weight
Family reporting “best he’s looked in a year”
Plans for rehab transfer in 2‐3 days
Then…
Diarrhea develops
Intubated again as sepsis develops
C. difficile test is positive
Toxic megacolon develops
Patients dies 48 hours later
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Why did this happen?
3 days before diarrhea started…
–Patient in adjacent room diagnosed with C. difficile diarrhea
–Staff repeatedly observed not adhering to hand hygiene or isolation practices
–Shared staff documented
CDAD
• Clostridium difficile–Gram positive spore forming organism
• Known pathogen since 1978
•Many consider a strict iatrogenic pathogen
• Previously easily recognized and treated
“New” strain
• Increased toxin production – as much as 20x
• Toxin appears more virulent
• Toxin is less likely to be “turned” off
• Resistant to fluoroquinolone antibiotics
• Organism associated with hypersporulation
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Rates of CDAD – United States
Diagnosis
• Relatively straight‐forward– Use of enzyme based tests most common
– Detection of toxin is important
– False negative results occur up to 20%
• Clinical suspicion and probabilities should not be swayed substantially by negative testing
Treatment
• Optimal treatment options are evolving
•Most experts recommend:– Vancomycin orally + metronidazole IV for severe disease
–Metronidazole for mild‐moderate disease•Oral is most effective
• IV is an alternative
• Use of probiotics?
STOPother antimicrobials
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VRE
•Gram positive bacteria
•Related to the Streptococci
•Long considered of “low”virulence
•Widely recognized cause of healthcare‐associated infections
VRE Epidemiology
Does VRE matter?
Chance of death with VRE is
2.5 times greaterthan with non‐VRE
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True MDROs
Gram‐negative bacteria–Klebsiella pneumoniae
–Pseudomonas aeruginosa
–Acinetobacter baumanniiTroops in Iraq Bring Resistant Bacteria Home
Sciences and MedicineMilitary Chases Mystery Infection
Drug resistant bacteria
≠NEW
A quick primer
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Resistance among “key” pathogens
Am J Infect Control 2004;32(8):470–485.
Imipenem resistance
Livermore. Ann Med 2003;35:226-234
Intermediate resistance Fully resistantThe Surveillance Network. >250 hospitals in US; >2000 reported infections annually
Resistance in U.S. ICUs
• 1994 ‐ 2004• > 300 intensive care units• 8537 isolates
– ~ 3600 resistant to at least one principal agent
• Fluoroquinolone resistance: 49.5 ‐ 73%• β‐lactam resistance: 39 ‐ 66%• Aminoglycoside resistance: 19 ‐ 30.5%• Carbapenem resistance: 9 ‐ 38.5%
Carey, et al. Abstract K-1495. 46th ICAAC; Sept. 2006
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Even more concerning…
•Emergence of carbapenemases–KPC = Klebsiella pneumoniaecarbapenemase
–CRE = carbapenem resistant Enterobacteriacae
Deaths associated with bacteria
PathogenBSIs per
10,000 adm% Total BSI n=20,978
% ICU BSI n=10,515
% Non‐ICU BSI n=10,442
% Total Crude Mortality
% ICU Crude Mortality
% Non‐ICU Mortality
CNS 15.8 31.3 35.9 26.6 20.7 25.7 13.8
S. aureus 10.3 20.2 16.8 23.7 25.4 34.4 18.9
Enterococcus 4.8 9.4 9.8 9 33.9 43 24
Ps. aeruginosa 2.1 4.3 4.7 3.8 38.7 47.9 27.6
Enterobacter 1.9 3.9 4.7 3.1 26.7 32.5 18
Klebsiella 2.4 4.8 4 5.5 27.6 37.4 20.3
E. coli 2.8 5.6 3.7 7.6 22.4 33.9 16.9
Serratia 0.9 1.7 2.1 1.3 27.4 33.9 17.1
A. baumannii 0.6 1.3 1.6 0.9 34.0 43.4 16.3
Wisplinghoff, et al. Clin Infect Dis 2004;39:309-17
24,179 BSIs from SCOPE Project
38.7% Pseudomonas aeruginosa34.0% Acinetobacter baumannii33.9% Enterococcus
Another example…
22 y/o male
75% burns from explosion
Hospitalized in burn unit 47 days
Fever develops
Cultures obtained
Empiric antibiotics started
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Blood cultures return positive for A. baumannii
• Amikacin = R
• Gentamicin = R
• Tobramycin = R
• Cefepime = R
• Imipenem = R
• Meropenem = R
• Amp/Sulbactam = R
• Pip/tazobactam = R
• Levofloxacin = R
• Tigecycline = R
Colistin = R
Now what do we do
Prevention
•Hand hygiene
• Isolation practices– Isolation based on syndromes or diagnoses
–When to stop
–Visitors
• Environmental cleaning
Antimicrobial Stewardship
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What is stewardship?
A practice that ensures the optimal selection, dose, and duration of an antimicrobial therapy that leads to the best clinical outcome for the treatment or prevention of infection while producing the fewest toxic effects and the lowest risk for subsequent resistance. (Gerding, 2001)
Use drives resistance
Relationship of use to resistance
Paul, et al. J Hosp Infect 2005;60:256-60
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There are NO antibiotics in development with novel mechanisms of action
Why is stewardship important?
Are we returning to the pre‐antibiotic era?
Does this matter to the IP?
Infection Prevention
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• Decrease in C. difficile infections
• Decrease in resistant Enterobacteriacae
• Trend toward reduced VRE infections
• No impact on MRSA infections
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Why aren’t we ALL doing this?
• Physician automony
• Perceived financial costs
• Institutional infrastructure– Administrative “buy‐in”
– Computerized vs. paper charting/orders
– Pharmacy staff/time
– Infectious Diseases/Epidemiologist availability
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Competing Interests
50% did NOT have CAP30% of these died
Summary
•MDROs increasing
•Mortality with resistance greater?
• Prevention is becoming the only option for many pathogens (i.e. Gram‐negatives)
• Antimicrobial stewardship and infection prevention are linked
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EVERYPatient.
EVERYTime.
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