antimicrobial steward call february 11, 2019

Antimicrobial Steward Call February 11, 2019

Tennessee Department of Health Healthcare Associated Infections and Antimicrobial Resistance Program

Welcome

Adobe Connect Housekeeping

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Announcements

C. auris Tabletop Exercises

• PARTICIPANTS WILL LEARN HOW TO: – Define plans for C. auris containment across the continuum of care – Access resources for response – Engage stakeholders and promote collaboration between lab scientists, epidemiologists,

healthcare facility staff and other key players – Understand how C. auris is misidentified in clinical laboratories

Containment of Candida auris

Save the Date for the 2019 Tabletop Exercise!

• Columbia - Wednesday, January 9th

• Brentwood - Thursday, January 10th

• Jackson - Wednesday, January 23rd

• Memphis - Thursday, January 24th

• Bristol - Wednesday, February 6th

• Knoxville - Thursday, February 7th, 2019

• Chattanooga - Thursday, February 21st

• Cookeville - Friday, February 22nd

Tentative Run Time: 9:00am – 2:30pm

2017 SAAR Rebaseline

Standardized Antimicrobial Administration Ration (SAAR)

• Expresses observed to predicted antibiotic use – Predicted use based on data being submitted to produce models using facility

characteristics • SAARs for different groups of antibiotics • SAARs for adult and pediatric locations • SAARs for ICU and non-ICU locations • Can be calculated at the unit or hospital wide level

SAAR Evolution

• 2014 baseline SAAR models were developed using AU Option data from: – 77 acute care hospitals (350 adult and 33 pediatric locations)

• 2017 baseline SAAR models were developed using AU Option data from:

– Adult models: 449 acute care hospitals, 2156 locations – Pediatric models 109 acute care hospitals, 170 locations

• Larger sample size enabled:

– Inclusion of new location types – Adult and pediatric patient populations modeled separately – Increased precision of estimates of predicted use

Changes from 2014 baseline

• Added SAARs for two new adult locations: stepdown and oncology • Added SAAR for antifungals • Added SAAR for agents posing high risk for CDI • Added azithromycin SAAR for pediatrics • Added rate distribution for agents commonly used to treat highly

resistant pathogens

Adult SAARs

Pediatric SAARs

New Antimicrobial Therapies

Whitney J. Nesbitt, PharmD, BCPS, BCIDP Antimicrobial Stewardship Clinical Specialist

Vanderbilt University Medical Center

When Bugs Go Bad: Antimicrobial Stewardship Practices for Multidrug-

Resistant Gram-Negatives

• None

DISCLOSURES

OBJECTIVES

• Identify the newer antibiotics able to treat multidrug-resistant gram-negative pathogens

• Determine potential applications of the recently introduced antibiotics

• Discuss stewardship principles applied to antibiotic selection

Antimicrobial Resistance

CDC Threat Report 2013 > 2 million illnesses

23,000 deaths Urgent threat level

Carbapenem-resistant Enterobacteriaceae (CRE) Serious threat level

Multidrug-resistant (MDR) Acinetobacter Extended spectrum β-lactamase (ESBL) producing

Enterobacteriaceae MDR P. aeruginosa

Attributable Costs Excess direct healthcare costs up to $20

billion Loss of productivity up to $35 billion per year Leading cause of death by 2050

ANTIBIOTIC RESISTANCE THREATS, UNITED STATES 2013

CDC. Antimicrobial resistance threats in the US, 2013.

CAUSATIVE PATHOGENS IN HEALTHCARE-ASSOCIATED INFECTIONS

NEJM 2014;370:1198-208.

GRAM-NEGATIVE RESISTANCE MECHANISMS

NEJM 2010 May 13;362(19):1804-13

Presenter

Presentation Notes

Many different mechanisms by which bacterial exhibit resistance. This slide, while detailed, becomes increasingly important as we talk about how to position novel agents later in the talk. Beta lactamases are one of the most frequently encountered GNR resistance mechanisms, and also one of the most confusing. More on this later. Porin loss Bacteria can develop resistance to antibiotics by mutating existing genes (vertical evolution),[6,7] or by acquiring new genes from other strains or species (horizontal gene transfer).[8,9] The sharing of genes between bacteria by horizontal gene transfer occurs by many different mechanisms. Mobile genetic elements, including phages, plasmids and transposons mediate this transfer, and in some circumstances the presence of low levels of the antibiotic in the environment is the key signal that promotes gene transfer,[10]

• >1000 β-Lactamases described • Increasing prevalence

ΒETA-LACTAMASES

Antimicrob Agents Chemother 2010:969. http://www.lahey.org/Studies/

Ambler Class Mechanism Enzyme Substrates

A (ESBL, carbapenemases)

Serine residue at active site

TEM-1 TEM-2 SHV-1 CTX-M KPC-2

Penicillins, cephalosporins, +/- carbapenems

B Zinc cofactor (metallo-enzyme)

IMP-1 VIM-1 NDM-1

Most beta-lactams, including carbapenems

C (amp-C)

Serine AmpC CMY-2 ACT-1

Cephalosporins

D (OXA) oxacillinases

Serine OXA-1 OXA-10 OXA-48

Pencillins, cephalosporins, carbapenems

Presenter

Presentation Notes

Bush, K, and G.A. Jacoby. 2010. Updated functional classification of ß-lactamases. Antimicrob. Agents. Chemother. 54:969-976.

Antibiotic Enterobacteriaceae CR

P. aeruginosa

CR Acinetobacter

spp. ESBLs

AmpC KPC NDM-1 OXA-48 TEM SHV CTX-M

Ceftolozane-tazobactam

Partial Partial Partial Variable None None None Yes None

Ceftazidime- avibactam

Yes Yes Yes Yes Yes None Yes Variable None

Meropenem-vaborbactam

Yes Yes Yes Yes Yes None None

None None

Plazomicin Yes Yes Yes Yes Yes None Yes Variable Variable

MDR GRAM-NEGATIVE TREATMENT

Intl J Infect Dis 2017; 62:39. Clin Infect Dis 2018; 68:519.

CR = Carbapenem-resistant

Presenter

Presentation Notes

Before we discuss where these new drugs fit in to current treatment, we will review treatment of MDR bugs

EXTENDED SPECTRUM BETA-LACTAMASE (ESBL)

ESBL TREATMENT

• Resistant to: • Penicillins • 3rd generation cephalosporins • Monobactam (aztreonam)

• When susceptibilities are known • Fluoroquinolones due to different resistance mechanisms • Cefepime has mixed data

• Higher treatment failures when MIC >2

Antimicrob Agents Chemother 2016; epub Clin Infect Dis 2013:488-95. Antimicrob Agents Chemother 2015: 7558-63 J Agents Chemother 2014:871-880 Lancet Infect Dis 2015:475-85 OFID 2016, 20;3(3) OFID. 2017. 4(2):ofx099

Presenter

Presentation Notes

Check MICs (just started releasing these last year) For example: pip/tazo for treatment of ESBL 16/4 reported as “sensitive” But….depends on site of infection 16 probably not great for anything, 8 may be ok in urine, worse outcomes in bacteremia, 4 reasonable for most METHODS: We performed a retrospective study of monomicrobial bacteremia caused by ESBL producers at 2 medical centers between May 2002 and August 2007. The patients definitively treated with in vitro active cefepime (cases) were compared with those treated with a carbapenem (controls) in a propensity score-matched analysis to assess therapeutic effectiveness. The 30-day crude mortality is the primary endpoint. RESULTS: A total of 178 patients were eligible for the study. Patients who received cefepime (n = 17) as definitive therapy were more likely to have a clinical failure (odds ratio [OR] 6.2; 95% confidence interval [CI], 1.7-22.5; P = .002), microbiological failure (OR 5.5; 95% CI, 1.3-25.6; P = .04), and 30-day mortality (OR 7.1; 95% CI, 2.5-20.3; P < .001) than those who received carbapenem therapy (n = 161). Multivariate regression revealed that a critical illness with a Pitt bacteremia score ≥ 4 points (OR 5.4; 95% CI, 1.4-20.9; P = .016), a rapidly fatal underlying disease (OR 4.4; 95% CI, 1.5-12.6; P = .006), and definitive cefepime therapy (OR 9.9; 95% CI, 2.8-31.9; P < .001) were independently associated with 30-day crude mortality. There were 17 case-control pairs in the propensity scores matched analysis. The survival analysis consistently found that individuals who received cefepime therapy had a lower survival rate (log-rank test, P = .016). CONCLUSIONS: Based on the current Clinical and Laboratory Standards Institute susceptible breakpoint of cefepime (minimum inhibitory concentration ≤ 8 μg/mL), cefepime definitive therapy is inferior to carbapenem therapy in treating patients with so-called cefepime-susceptible ESBL-producer bacteremia. Wang et al: The role of cefepime for extended-spectrum β-lactamase (ESBL) bacteremia is unclear if susceptible in vitro. In a propensity score-matched study of patients with ESBL bacteremia, risk of death was 2.87 times higher for patients receiving cefepime compared with carbapenems (95% confidence interval [CI], .88-9.41). We compared 14-day mortality of patients with ESBL bacteremia receiving empiric cefepime versus empiric carbapenem therapy in a propensity score-matched cohort. There was a trend towards increased mortality in the cefepime group (hazard ratio, 2.87; 95% CI, .88-9.41), which enhances the existing literature suggesting that cefepime may be suboptimal for invasive ESBL infections. Open Forum Infect Dis. 2017 May 16;4(2):ofx099. doi: 10.1093/ofid/ofx099. eCollection 2017 Spring. Comparison Between Carbapenems and β-Lactam/β-Lactamase Inhibitors in the Treatment for Bloodstream Infections Caused by Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae: A Systematic Review and Meta-Analysis. Muhammed M1, Flokas ME1, Detsis M1, Alevizakos M1, Mylonakis E1. Author information Abstract BACKGROUND: Carbapenems are widely used for the management of bloodstream infections (BSIs) caused by extended-spectrum β-lactamase-producing Enterobacteriaceae (ESBL-PE). However, the wide use of carbapenems has been associated with carbapenem-resistant Enterobacteriaceae development. METHODS: We searched the PubMed and Scopus databases (last search date was on June 1, 2016) looking for studies that reported mortality in adult patients with ESBL-PE BSIs that were treated with carbapenems or β-lactam/β-lactamase inhibitors (BL/BLIs). RESULTS: Fourteen studies reported mortality data in adult patients with ESBL-PE BSI that were treated with carbapenems or BL/BLIs. Among them, 13 studies reported extractable data on empiric therapy, with no statistically significant difference in mortality of patients with ESBL-PE BSI that were treated empirically with carbapenems (22.1%; 121 of 547), compared with those that received empiric BL/BLIs (20.5%; 109 of 531; relative risk [RR], 1.05; 95% confidence interval [CI], 0.83-1.37; I2 = 20.7%; P = .241). In addition, 7 studies reported data on definitive therapy. In total, 767 patients (79.3%) received carbapenems and 199 patients (20.6%) received BL/BLIs as definitive therapy, and there was again no statistically significant difference (RR, 0.62; 95% CI, 0.25-1.52; I2 = 84.6%; P < .001). Regarding specific pathogens, the use of empiric BL/BLIs in patients with BSI due to ESBL-Escherichia coli was not associated with a statistically significant difference in mortality (RR, 1.014; 95% CI, 0.491-2.095; I2 = 62.5%; P = .046), compared with the use of empiric carbapenems. CONCLUSIONS: These data do not support the wide use of carbapenems as empiric therapy, and BL/BLIs might be effective agents for initial/empiric therapy for patients with BSI caused by likely ESBL-PE, and especially ESBL-E coli.

PIPERACILLIN-TAZOBACTAM FOR TREATMENT OF ESBLS • MIC matters for site of infection

• Piperacillin-tazobactam versus meropenem for treatment of ESBL-producers (MERINO Trial) • Mortality at 30 days

• 12.3% piperacillin-tazobactam versus 3.7% meropenem (p=0.002)

Clin Infect Dis 2012;15:167-74.

TREATMENT OF ESBLS

• “Low inoculum” infections • Urinary, biliary, and intra-abdominal infections • Piperacillin-tazobactam MIC < 8 mg/L

• Severe infections carbapenems JAMA 2018.320:984-94.

CARBAPENEM-RESISTANT ENTEROBACTERIACEAE (CRE)

• Aminoglycosides • Bactericidal • Nephrotoxicity, ototoxicity • Worse outcomes with monotherapy

• Tigecycline

• Bacteriostatic • Large volume of distribution poor for bacteremia (and maybe pneumonia)

• Polymixins (colistimethate, polymixin B)

• Nephrotoxicity, neurotoxicity, hepatotoxicity • Multiple formulations dose confusion/potential for error

• Combination therapy with polymixin + carbapenem

CRE TREATMENT HISTORY

Diagn Microbiol Infect Dis. 2013 February ; 75(2): 115–120.

• 89% isolates resistant to meropenem with MIC ≥ 4

• 30-day mortality • Monotherapy 54.3% • Combination 34.1% P=0.02

COMBINATION THERAPY FOR CRE

Presenter

Presentation Notes

Adequate therapy defined as if at least 1 drug displaying in vitro activity against the isolate All the patients in this study were treated with combination therapy with active drugs Synergy suggested from animal studies showing that meropenem still has activity with mic < or = to 4 and activity enhanced with colistin Despite meropenem MIC, it seems that patients still had better outcomes when carbapenem was used

CEFTAZIDIME-AVIBACTAM

• Avibactam • First non beta-lactam beta-

lactamase inhibitor • Inhibits class A and C ESBLs (some D)

• Greater activity against KPC and ampC than others

• No activity against class B (MBL)

• Avibactam reduces MIC against Enterobacteriaceae 4-1024 fold

• 4-fold against Pseudomonas

• Lacks adequate anaerobic coverage

Drugs 2013; 73:159.

CEFTAZIDIME-AVIBACTAM VERSUS BEST AVAILABLE THERAPY

Lancet Infect Dis 2016; 16: 661–73

REPRISE

• Complicated intra-abdominal infections and UTIs

• Pathogens − Enterobacteriaceae (94%) − Pseudomonas (7%)

• Median treatment duration: 10 days

• No difference in clinical cure at TOC

visit: 91% vs. 91%

CEFTAZIDIME-AVIBACTAM VERSUS BEST AVAILABLE THERAPY FOR CRE K. PNEUMONIAE BACTEREMIA

Antimicrob Agents Chemother 2017; 61:e00883-17

Presenter

Presentation Notes

Clinical success was defined at 30 days as survival, resolution of signs and symptoms of infection, sterilization of blood cultures within 7 days of treatment initiation, and absence of recurrent infections.

CEFTAZIDIME-AVIBACTAM VERSUS CEFTOLOZANE-TAZOBACTAM FOR MULTIDRUG-RESISTANT GRAM-NEGATIVES

• Comparison of activity against 120 MDR bacterial strains

Int J Infect Dis. 2017; 62: 39–43

96.5

10

97 100

45

94

0

10

20

30

40

50

60

70

80

90

100

ESBL (n=29) CRE (n=60) Pseudomonas (n=31)

Sens

itivi

ty (%

)

C/TC/A

P=0.00002

Presenter

Presentation Notes

In vitro Overall small numbers

CEFTAZIDIME-AVIBACTAM SUMMARY

• Potent activity against CRE • Avibactam reduces MIC 4-1024 fold in

Enterobacteriaceae • ESBL class A, C, D • Better outcomes than best available

therapy

• Not active against metallo-beta-lactamases

• Class B ESBLs: NDM, IMP, VIM

• Need metronidazole to cover anaerobes

• First in class, cyclic boronic acid beta-lactamase inhibitor • Lacks in vitro antibacterial activity • Potent inhibitor of:

• Class A (KPC, CTX-M, SHV, TEM) • Class C (P99, MIR, FOX)

• Most effective in inhibiting KPC when combined with meropenem

MEROPENEM-VABORBACTAM

Antimicrob Agents Chemother. 2017 Oct 24;61(11). Antimicrob Agents Chemother. 2016 Aug 22;60(9):5454-8

Presenter

Presentation Notes

First in its class No activity against Class B (metallobetalactamses) Class D (OXA ) – but you don’t really need it to have activity here because meropenem is typically stable

MEROPENEM-VABORBACTAM AND KPC ENTEROBACTERIACEAE

Antimicrob Agents Chemother. 2016 Aug 22;60(9):5454-8 Antimicrob Agents Chemother. 2017 Dec 21;62(1)

MEROPENEM-VABORBACTAM VERSUS BEST AVAILABLE THERAPY

TANGO-II

M/V BAT HAP/VAP or bacteremia

All-cause mortality 4/16(25%)

4/9 (44.4%)

Bacteremia EOT Overall Success 6/12

(50%) 3/8

(37.5%) TOC Overall Success 6/12

(50%) 2/8

(25%) cUTI/AP

EOT Overall Success 8/11 (73%)

2/4 (50%)

TOC Overall Success 3/7 (43%)

2/4 (50%)

Infect Dis Ther 2018; 7:439–455

Presenter

Presentation Notes

All cause mortality lower in vabomere group and death related to sepsis greated in the BAT group compared to that of vabomere Regardless of various medications used in combination therapy or monotherapy, vabomere had higher rates of clinical cure at EOT or TOC (18/28 [64.3%] and 16/28 [57.1%] respectively) except when compared to cetazidime/avibactam (although there was only 1 patient treated with this agent).

MEROPENEM-VABORBACTAM SUMMARY

• First in class carbapenem + BLI with novel MOA

• Potent activity against CRE with significant reduction of meropenem MIC

• ESBL Class A, C

• Not active against metallo-beta-lactamases

• Class B ESBLs: NDM, IMP, VIM

• Given over 3 hours every 8 hours and renal dosing

• Semisynthetic aminoglycoside derived from sisomicin

• Aminoglycoside modifying enzymes (AMEs) can exist concurrently with carbapenemases

• Plazomicin not inhibited by most AMEs

PLAZOMICIN

CARE STUDY

PLAZOMICIN SUMMARY

• Not inhibited by most AMEs

• Did not receiving FDA approval for treatment of bacteremia

• Synergy with meropenem

Omadacycline • FDA approved for ABSSSI and

and CABP • More active than doxycycline and

minocycline against Enterobacteriaceae and Acinetobacter

• Less active against ESBL and CRE-producing Enterobacteriaceae

Ervacycline • Also classified as a fluorocycline

• FDA approved for complicated

intra-abdominal infections • Did not gain approval for UTIs

• Improved activity against

carbapenem-resistant Acinetobacter and Stenotrophomonas

NEWLY APPROVED TETRACYCLINES

New Engl J Med 2019;380:588.

MDR PSEUDOMONAS

• Plethora of resistance mechanisms

PSEUDOMONAS RESISTANCE

CID. 2002;34(5),: 634–640

Presenter

Presentation Notes

Clin Microbiol Rev. 2009 Oct; 22(4): 582–610.

THE RISE OF MDR PSEUDOMONAS

Clin Microbiol Rev. 2009 Oct; 22(4): 582–610

Presenter

Presentation Notes

Defined as resistance to three or more drug classes

• Aminoglycosides • Bactericidal • Nephrotoxicity, ototoxicity • Worse outcomes with monotherapy

• Polymixins (colistimethate, polymixin B)

• Nephrotoxicity, neurotoxicity, hepatotoxicity • Multiple formulations dose confusion/potential for error

• Combination therapy with polymixin + carbapenem

PSEUDOMONAL TREATMENT HISTORY

Diagn Microbiol Infect Dis. 2013 February ; 75(2): 115–120.

• Potent anti-pseudomonal activity • Improved outer membrane permeability and stability against ampCs • Retains activity against Pseudomonas with efflux pump upregulation or loss of

OMP

• Enterobacteriaceae coverage similar to 3rd generation cephalosporins

• Lacks some coverage against • ESBL • Meropenem-resistant

• No metallo-beta-lactamase

CEFTOLOZANE-TAZOBACTAM

Antimicrob Agents Chemother. 2010 Sep;54(9):3933-7 Antimicrob Agents Chemother. 2007 Mar;51(3):826-30

Presenter

Presentation Notes

Antimicrob Agents Chemother. 2010 Sep;54(9):3933-7 Antimicrob Agents Chemother. 2007 Mar;51(3):826-30 Essential PBP for pseudomonas includes 1b, 1c, 2, 3 – ceftolozane has high affinity Not affected by efflux pumps or deficiency of OprD decreased activity Ceftolozane not active by itself against straings that exhibit TEM, OXA , CTX-M beta-lactamases (ESBL) when we add tazobactam

CEFTAZIDIME-AVIBACTAM VERSUS CEFTOLOZANE-TAZOBACTAM FOR MULTIDRUG-RESISTANT GRAM-NEGATIVES

• Comparison of activity against 120 MDR bacterial strains

Int J Infect Dis. 2017; 62: 39–43

96.5

10

97 100

45

94

0

10

20

30

40

50

60

70

80

90

100

ESBL (n=29) CRE (n=60) Pseudomonas (n=31)

Sens

itivi

ty (%

)

C/TC/A

Presenter

Presentation Notes

In vitro Overall small numbers

• 290 Pseudomonas isolates resistant to meropenem

• MIC at breakpoint: • 9% Ceftolozane-tazobactam • 30% Ceftazidime-avibactam • P > 0.0001

CEFTOLOZANE-TAZOBACTAM VERSUS CEFTAZIDIME-AVIBACTAM FOR PSEUDOMONAS

Beta-lactam susceptibility profile Cefepime 42%

Ceftazidime 46

Piperacillin-tazobactam 36%

Aztreonam 37%

Ceftolozane-tazobactam 91%

Ceftazidime-avibactam 81%

Antimicrob Agents Chemother 61:e00875-17.

Presenter

Presentation Notes

In vitro Avycaz inhibitory activity significantly lower than zerbaxa when more than 1 betalactam was nonsusceptible 12 drugs that were resistant to both: VIM was genotypic From respiratory tract (195) Blood (35) Wound (60)

• Ceftolozane-tazobactam • Increased activity

• Ceftazidime-avibactam

• May not be much benefit in Pseudomonal infections (MIC reduction only 4-fold) when compared to ceftolozane-tazobactam

• Meropenem-vaborbactam • Unclear benefit over ceftolozane-tazobatam

• Plazomicin

• Variable activity

SUMMARY OF PSEUDOMONAL THERAPIES

49

• Fosfomycin IV • Higher rates of cure and eradication compared to piperacillin-tazobactam

• ESBLs, aminoglycoside –resistant, and carbapenem-resistant Enterobacteriaceae, Pseudomonas, and Acinetobacter

• Cefiderocol

• “Trojan horse” mimicking natural siderophore iron complexes • Broad spectrum activity against MDR gram-negatives • Phase III trials for treatment of carbapenem-resistant gram-negatives underway

• Imipenem/cilastatin-relebactam

• Overcomes Pseudomonal resistance due to porin loss and ampC overexpression • Enterobacteriaceae activity (ESBLs, KPCs, and ampCs)

EMERGING ANTIBIOTICS

• Institutional pathogen prevalence and rates of resistance

• Causes of infection

• Formulary needs

• Creation of pathogen-specific algorithms

ANTIMICROBIAL STEWARDSHIP EVALUATION

REGIONAL CRE PREVALENCE

Antimicrob Agents Chemother. 2017 Jul 25;61(8)

Presenter

Presentation Notes

Lod Premier hospital database includes data from approximately 80 million admissions (>5 million added per year since 2011). Admissions data are provided by >500 participating acute care hospitals from across the United States and account for approximately 20% of all inpatient discharges in the nation (Premier Healthcare Database: Data that Informs and Performs, Premier, Inc., Charlotte, NC). ise et al. Prevalence of Invasive Infections Due to Carbepenem0Resistant Enterobacteriaceae among Adult Patients in US Hospitals. August 2017 vol. 61 no. 8e00228-17. January 2011 and 31 December 2014; positive culture for an Enterobacteriaceae strain obtained from a site consistent with the infection type Carbapenem resistance rates were stratified by U.S. geographic region (9 CDC regions), hospital type and characteristics (teaching versus nonteaching, urban versus rural), hospital unit (intensive care unit [ICU] versus non-ICU), infection type (cUTI, cIAI, HAP, or BSI), and pathogen (Klebsiella spp., Enterobacterspp., Escherichia coli, or other. A total of 60,551 infective episodes met the study criteria. Overall resistance to carbapenem was 2.3% with substantial variation by geographic region

REGIONAL CRE PREVALENCE

NE Central ICU Klebsiella: 12% CRE SE Central (TN) non-ICU E.coli: 0.2%

Take home: Need local data (hospital/unit>regional>national)

Account for patient population (ICU vs not), infection type (HAP vs other) Need decision support tools/risk stratification

Antimicrob Agents Chemother. 2017 Jul 25;61(8)

Presenter

Presentation Notes

Take home East North Central ICU Klebsiella infection=12.2% CRE East South Central (ie us) Non-ICU E.coli = 0.2% cUTI not in ICU = 0.2% CRE HAP 2/2 Klebsiella in ICU= 8.7% CRE Take home= must take your local data (hospital/unit>regional>national) Must account for patient population (ICU vs not), infection type (HAP vs other) Need decision support tools/risk stratification

• Institutional pathogen prevalence and rates of resistance

• Causes of infection

• Formulary needs

• Creation of pathogen-specific algorithms

ANTIMICROBIAL STEWARDSHIP EVALUATION

Whitney J. Nesbitt, PharmD, BCPS, BCIDP Antimicrobial Stewardship Clinical Specialist

Vanderbilt University Medical Center

When Bugs Go Bad: Antimicrobial Stewardship Practices for Multidrug-

Resistant Gram-Negatives

Final Announcements

• TDH AU PP Survey • Q4 2018 Packets are complete and ready to be disseminated

• Next Call

• April 9 at 2pm Eastern/1pm Central Time • Effects of Data Suppression for Antibiotic Susceptibility Testing

• Opportunities for involvement

• Speaker or Topic for future call • Antibiotic Use Reporting into NHSN and TDH AU Point Prevalence Survey

• Feedback always appreciated

• [email protected]

mailto:[email protected]

antimicrobial steward call february 11, 2019

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