kcnpnm 2014 conference. objectives compare and contrast the antimicrobial drug classes understand...
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BUGS AND DRUGS: UPDATE ON
ANTIMICROBIAL THERAPY
KCNPNM 2014 Conference
Objectives
Compare and contrast the antimicrobial drug classes
Understand the types of antimicrobial drug resistance that can occur
Create treatment plans for which antimicrobial therapy can be managed successfully
Related prudent use of antimicrobial therapy to quality metrics
Introduction
The modern age of antibiotic therapeutics was launched in the 1930s with sulfonamides and the 1940s with penicillin
Since then, many antibiotic drugs have been developed, most aimed at the treatment of bacterial infections
These drugs have played an important role in the dramatic decrease in morbidity and mortality due to infectious diseases
While the absolute number of antibiotic drugs is large, there are few unique antibiotic targets
Nine Factors to Consider When Selecting an Antibiotic1. Spectrum of coverage2. Patterns of resistance3. Evidence or track record for the specified
infection4. Achievable serum, tissue, or body fluid
concentration (e.g. cerebrospinal fluid, urine)
5. Allergy6. Toxicity7. Formulation (IV vs. PO); if PO assess
bioavailability8. Adherence/convenience (e.g. 2x/day vs.
6x/day)9. Cost
Principles of Antibiotic TherapyDirected Therapy (15%) Infection well defined Narrow spectrum One, seldom two
drugs Evidence usually
stronger Less adverse
reactions Less expensive
Empiric Therapy (85%) Infection not well defined
(“best guess”) Broad spectrum Multiple drugs Evidence usually only 2
randomized controlled trials
More adverse reactions More expensive
Why So Much Empiric Therapy?
Need for prompt therapy with certain infections Life or limb threatening infection Mortality increases with delay in these cases
Cultures difficult to do to provide microbiologic definition (i.e. pneumonia, sinusitis, cellulitis)
Negative cultures Provider Beliefs
Fear of error or missing something Not believing culture data available “Patient is really sick, they should have ‘more’ antibiotics” Myth of “double coverage” for gram-negatives e.g.
pseudomonas “They got better on drug X, Y, and Z so I will just continue
those”
To Increase Directed Therapy for Inpatients:
Define the infection 3 ways Anatomically, microbiologically, pathophysiologically
Obtain cultures before starting antibiotics Use imaging, rapid diagnostics and special
procedures early in the course of infection Have the courage to make a diagnosis Do not rely solely on “response to therapy” to
guide therapeutic decisions; follow recommended guidelines
If empiric therapy is started, reassess at 48-72 hoursMove to directed therapy (de-escalation or
streamlining)
To Increase use of Directed Therapy for Outpatients:
Define the infection 3 ways Anatomically, microbiologically, pathophysiologically
Obtain cultures before starting antibioticsOften difficult in outpatients (acute otitis media,
sinusitis, community-acquired pneumonia) Narrow therapy often with good supporting
evidenceAmoxicillin/clavulanate for AOM, sinusitis and CAPPenicillin for Group A Streptococcal pharyngitisClindamycin or trimethoprim/sulfamethoxazole for
simple cellulitisTrimethoprim/sulfamethoxazole or ciprofloxicin for
cystitis
IS AN INFECTION PRESENT?
Signs and Symptoms
Increase in WBCs and a “left shift” Fever Pain and Inflammation Hemodynamic changes Neurologic changes Gram stain
Overview Colonization
Where bacteria are supposed to resideBacteria are present but no signs and symptoms of
infection Infection
Where bacteria invadeBacteria are present and have often migrated to
different organs to cause systemic infectionMost likely to occur
○ The intrinsic virulence of the particular organism○ The immune status of the host○ The quantity or load of the initial innoculant
Treat Bacterial Infection, not Colonization
Many patients become colonized with potentially pathogenic bacteria but are not infectedAsymptomatic bacteriuria or foley catheter
colonizationTracheostomy colonization in chronic respiratory
failureChronic wounds and decubitiLower extremity stasis ulcersChronic bronchitis
Can be difficult to differentiatePresence of WBCs not always indicative of infectionFever may be due to another reason, not the positive
culture
Treat Bacterial Infection, not ColonizationExample: Asymptomatic Bacteriuria
≥105 colony forming units is often used as a diagnostic criteria for a positive urine culture
It does NOT prove infection; it is just a number to state that the culture is unlikely due to contamination
Pyuria also is not predictive on its own
It is the presence of symptoms AND pyuria AND bacteriuria that denotes infection
CAP: often a difficult diagnosis X-rays can be difficult to
interpret. Infiltrates may be due to non-infectious causes.
Examples:AtelectasisMalignancyHemorrhagePulmonary edema
Do Not Treat Sterile Inflammation or Abnormal Imaging Without InfectionExample: Community-Acquired Pneumonia (CAP)
Acute bronchitis Common colds Sinusitis with symptoms
less than 7 days Sinusitis not localized to
the maxillary sinuses Pharyngitis not due to
Group A Streptococcus spp.
Gonzales R, et al. Annals of Intern Med 2001;134:479Gonzales R, et al. Annals of Intern Med 2001;134:400Gonzales R, et al. Annals of Intern Med 2001;134:521
Do not Treat Viral Infections with Antibiotics
Culture and Sensitivity
Final identification of pathogen and effectiveness of antibiotics
May not give appropriate informationPatient previously taking antibioticsCulture not obtained properlyContaminationNot time sensitive
Key Terms
MIC = Minimal inhibitory concentration. Lowest concentration of antimicrobial that inhibits growth of bacteria. Commonly used in clinical lab
MBC = Minimal bactericidal concentration. Concentration of an antimicrobial that kills bacteria. Used clinically only in special circumstances
Breakpoint = The MIC that is used to designate between susceptible and resistant. Arbitrarily set by the laboratory
Breakpoint Susceptibility Susceptible – pathogens with the lowest
MICs and are most likely to be eradicated with antibiotic therapy
Intermediate - ?? – Treatment may be successful if the antibiotic is used in higher doses or if the antibiotic has good penetration into the infection site
Resistant – significantly higher MICs that will cause a less than optimal clinical outcome even if higher doses of the antibiotic are used
Concept of Breakpoint to Determine Susceptibility
Antibiotic MIC Breakpoint Susceptibility
Ampicillin >16 8 Resistant
Gentamicin 2 4 Susceptible
Cephalothin >16 N/A Resistant
Cefepime 8 32 Susceptible
Cefotaxime 16 16/32 Intermediate
Ceftazidime 2 32 Susceptible
Aztreonam 4 16 Susceptible
Ciprofloxacin 2 2 Resistant
Amp/Sulbactam >16 8 Resistant
Meropenem 4 4/8 Intermediate
Pip/tazo 8 32-64/128 Susceptible
EXAMPLE: Susceptibility testing for a single isolate of Pseudomonas aeruginosa
-Breakpoint for intermediate resistance for meropenem is 4 and for piperacillin/tazobactam (pip/tazo) 32
-Pip/tazo is the better choice between the two
-Ciprofloxacin is a poor choice even though the MIC is lowest of the three
Resistance
Introduction
Since the first use of antibiotics in the 1930s and 1940s, bacteria quickly adapted and developed mechanisms to escape their effects
Over the following decades, new antibiotics were developed to overcome resistance
Since the 1990s, new antibiotic development has fallen sharply while bacterial resistance continues to increase
Antibiotic resistance is responsible for countless human deaths and billions of dollars in healthcare expenses
70% of bacteria that cause healthcare-acquired infections are resistant to common antibiotics
Agriculture
Inpatient
Outpatient
Antibiotic Use Leads to Antibiotic Resistance
Clearing Up Misconceptions Misconception: Antibiotics are no longer
effective because people who have taken the medication have developed a tolerance to the drug
Truth: People do NOT develop a tolerance to drugs; the reason drugs no longer work is because the bacteria is no longer killed by the drug because they have become resistant to the effects
Factors that Promote Resistance Exposure to antibiotics
Prolonged courses Use of incorrect antibiotic Sub-therapeutic doses Treatment of viral infections
Introduction of resistant organisms from outside the population Transfers from outside facilities
○ Long-term care facilities are primary reservoirs of antimicrobial resistance
Food sources (BSE, VRE, Hepatitis A, GI bugs) Mobile society (SARS)
Tissue culture passage effect Spread from patient to patient (hand hygiene) Animal to human spread - agriculture
Reasons for Antibiotic Overuse : Conclusions from Eight Focus Groups
Patient Concerns Want clear
explanation Green nasal
discharge Need to return to
work
Physician Concerns Patient expects
antibiotic Diagnostic
uncertainty Time pressure
Barden L.S. Clin Pediatr 1998;37:665
Antibiotic Prescription
“As long as we expose bacteria to antibiotics, they will evolve resistance to them. The more exposure…the more rapidly resistance will occur”
(National Institute of Allergy and Infectious Diseases, 2014)
Antibiotic Use Leads to Antibiotic Resistance
Resistant bacteria or their genetic determinates are selected when colonizing or infecting bacteria are exposed to antibiotics
Resistant bacteria can then be transmitted between patients
Highest risk patients:ImmunocompromisedHospitalizedInvasive devices
(central venous catheters)
Antibiotic Mechanism of Action
Daptomycin
DaptomycinDaptomycinDaptomycinDaptomycinLinezolid
Daptomycin
Linezolid
Mechanisms Of Antibiotic Resistance Can be related back to how
the antibiotic works Bacteria are capable of
becoming resistant through several mechanisms
One or many mechanisms may exist in an organism
Multidrug-resistant bacteria often have multiple mechanisms
Genes encoding resistance may exist on plasmid or chromosome
Alteration in Target Molecule
Decreased Permeability
Mechanisms of ResistanceAntibiotic Degrading Enzymes
Sulfonation, phosphorylation, or esterifictation Especially a problem for aminoglycosides
β-lactamasesSimple, extended spectrum β-lactamases (ESBL),
cephalosporinases, carbapenemasesConfer resistance to some, many, or all beta-
lactam antibioticsMay be encoded on chromosome or plasmidMore potent in gram-negative bacteriaExamples: S. aureus, H. influenzae, N.
gonorrhoeae, E. coli, Klebsiella sp., Enterobacter sp., Serratia sp., other enteric bacteria, anaerobes
Extended Spectrum -lactamases
-lactamases capable of hydrolysing extended spectrum cephalosporins, penicillins, and aztreonam
Most often associated with E. coli and Klebsiella pneumoniae but spreading to other bacteria
Usually plasmid mediated Aminoglycoside, ciprofloxacin and
trimethoprim-sulfamethoxazole resistance often encoded on same plasmid
Has become a significant resistance determinate in acute and long-term care facility enteric pathogens
Class A Carbapenemases Most common in Klebsiella pneumoniae (KPC) Also seen in E. coli, Enterobacter, Citrobacter,
Salmonella, Serratia, Pseudomonas and Proteus spp.
Very often with multiple other drug resistance mechanisms, resistance profile similar to ESBL but also carbapenem resistant
Became problem in New York City first in 2002-2003 and is being increasingly recognized in Mid-Atlantic US.
Spreading across species to other gram-negatives and enterobacteriaceae
Emerging in long-term care facilities
Multidrug Resistant Gram-Negative Organisms Development of resistance to multiple antimicrobial
classes severely limits treatment options and the incidence of resistance is rising
Proportion of isolates resistant to three antibiotic classes ranged from 10 to 60% for different gram-negative bacteria, while some are resistant to four antibiotic classes
Resistant to 3 antibiotic classes
Resistant to 4 antibiotic classes
Pseudomonas aeruginosa 10% 2%
Acinetobacter baumannii 60% 34%
Klebsiella pneumoniae 15% 7%
Multidrug Resistant Gram-Negative Organisms Widespread use of cephalosporins and beta-lactam
combination antibiotics has led to extended-spectrum beta-lactamases (ESBLs), which are resistant to both classes Carbapenems have been the only effective agents for ESBLs
Emergence of carbapenemases, such as Klebsiella pneumoniae carbapenemase (KPCs) are threatening carbapenems as the antibiotics of last resort Significant issue for many military personnel due to the high
amount of Acinetobacter in the desert NO NEW ANTIBIOTICS ON THE HORIZON!!!
Mechanisms of ResistanceDecreased Permeability
Pseudomonas spp. Affects many antibiotics including
carbapenems
Efflux Pumps Pseudomonas spp. (multiple antibiotics) Tetracyclines Macrolides
Mechanisms of ResistanceTarget Alteration
DNA gyrase • Fluoroquinolones• Many gram-negatives, S. pneumoniae
Penicillin-binding protein• Methicillin-resistant S. aureus (MRSA)• Penicillin-resistant S. pneumoniae
Gram positive cell wall• Vancomycin• Enterococcus spp.
Mechanisms of ResistanceTarget Alteration (cont’d)
Ribosome • Tetracyclines• Macrolides
○ S. pneumoniae, Staphylococcus sp., N. gonorrhoeae, enteric gram-negative rods
Treatment Options for Common Infections
HA-MRSA
Patients have multiple risk factors Usually involves various types of infection
BacteremiaIntravenous linesPneumoniaSkin and soft tissue infections
Transmission is person to person Growth rate is slow Resistant to multiple antibiotics Need to make sure that patient has an infection
Antibiotic Therapy for HA-MRSA Usually resistant to multiple antibiotics
Resistant to penicillins and cephalosporinsMay be resistant to clindamycin and trimethoprim-
sulfamethoxazole Drugs of choice include vancomycin, linezolid
(Zyvox), daptomycin (Cubicin), or quinupristin-dalfopristin (Synercid)
CA-MRSA Risk factors not clearly identified other than more
likely in a younger patientDes seem to be a correlation between sharing of close
quarters Transmission is person to person Growth rate is fast The prevalence factor is PVL (panton-valentine
leukocidin) and two major clones have been identified - makes this strain more virulent
Resistant to beta-lactams, but sensitive to other agents
Antibiotic Therapy for CA-MRSA When the infection is skin/ soft tissue, incision
and drainage of area may be needed Usually resistant to the beta-lactams (penicillin
and cephalosporins) Usually sensitive to clindamycin, trimethoprim-
sulfamethoxazole, minocycline, doxycycline May be beneficial to add Rifampin for
synergistic effect Also sensitive to vancomycin, daptomycin, and
linezolid, although these agents are not first-line
Acute Pharyngitis One of the four most common
episodic clinic visit May be viral or bacterial
40% of children with pharyngitis have Group A Streptococcal pharyngitis○ Most commonly affected ages of 5
to 12 years○ Not usually seen in children under
age 3Only 5-15% of adult cases of
acute pharyngitis are caused by group A beta-hemolytic streptococcal (GABHS)
Acute Pharyngitis Treatment
No antibiotics when viral!Treatment with antibiotics usually last for 7 to 10 days
○ Penicillin○ Amoxicillin or amoxicillin/ clavulanate○ Second or third generation oral cephalosporin○ Macrolide
Penicillin is recommended for initial treatment of GABHS○ No resistance seen in the United States yet
Fluoroquinolones are NOT appropriate
Rhinosinusitis Most cases are viral
Less than 10% are bacterialResolves in about 7 days
Bacterial - often atypicalsDouble-sickening – symptoms last longer than 7 daysNasal congestionCough - often worse at night due to drainageFacial pain - above or below the eyes that worsens when
patient leans forwardToothache - if maxillary sinuses are involvedHeadachePurulent drainage, although nasal discharge alone is not a
good predictor of a bacterial infection○ Clear to yellow to green
High fever – 102 or higher
Pharmacologic Treatments
Regardless of whether the etiology is infectious, allergic, or irritant, treatment should focus on relieving obstruction and establishing drainage
Analgesics Decongestants Antihistamines Corticosteroids Mucolytics Antibiotics
Antibiotics Rhinosinusitis is the fifth most common
diagnosis for which an antibiotic is prescribed First need to be sure that the infection is
bacterial – most are viral and not bacterial Want to use antibiotics with good coverage of
atypicals and gram-positive organisms, as well as good penetration into the sinus cavity
Usually need to treat for 10 to 14 days If chronic sinusitis, may need to consider 3 to 4
weeks of antibiotics, especially if surgery may be required
Antibiotics For milder infections
Penicillins, such as amoxicillin/clavulanateDoxycycline
May not be as effective due to increasing resistance among pneumococciSecond or third generation cephalosporinsMacrolides
For more serious infectionsAmoxicillin/ clavulanate (high dose)Quinolone with antipneumococcal activity, such as
levofloxacin PQRS Measure
Treatment Options for OM
Studies have shown that the symptoms of OM spontaneously resolved in 80% of children at 2 to 7 days. (Otalgia – endpoint)More likely to be bacterial if child has siblings or attends
day care Ibuprofen or acetaminophen are the best options for
pain control Analgesic ear drops can also provide symptomatic
relief Some controversy over the use of decongestants,
although fluid accumulating behind the ear drum is often a contributing factor
Treatment Options for OM
Antibiotics Amoxicillin or Amoxicillin/ clavulanateSecond or third generation cephalosporinMacrolide
PQRS Measure
Pneumonia Common lower respiratory tract infection that
causes inflammation of the lung parencyma Pneumonia – sixth leading cause of death The defense mechanisms of the lung usually help
to prevent passage of foreign materialsDisease states, such as COPDAgeSmoking
Immunization!Pneumococcal vaccination will help to decrease
incidence and severity of susceptible strains of pneumonia
CAP vs HCAP HCAP - Healthcare-associated pneumonia
Acquired in an environment, such as a hospital, residing in a nursing home, receiving home health care, or dialysis
Usually caused by very different organisms○ MRSA○ Gram-negative organisms
CAP - Community-acquired pneumoniaStreptococcus pneumoniaeMore than 15% of S. pneumoniae are highly resistant to
penicillin and increasingly resistant to macrolides and cephalosporins
Hospital Core Measure
Macrolide-Resistant S. pneumoniaePrevalence is Increasing in US – 2000 to 2005
Jenkins S. et al Emerg Infect Dis. 2009;5:1260Hicks L et. Al. Emerg Infect Dis. 2010;16:896
Empiric Treatment - Outpatients
Macrolide (azithromycin, clarithromycin) Doxycyline If S. pneumoniae is thought to be the causative
organism, then a penicillin or cephalosporin would be the drug of choice provided there is no resistance
Also starting to see resistance to macrolidesIf resistance is an issue, may need to use a
quinolone
Empiric Treatment - Inpatients
Necessary to cover both typical and atypical pathogens Ampicillin/Sulbactam plus a Macrolide Newer Fluoroquinolone – high dose, short course Third-generation Cephalosporin plus a Macrolide s
With structural lung disease a regimen with activity against Pseudomonas should be considered, such as a Third or Fourth generation Cephalosporin plus a Fluoroquinolone
If aspiration pneumonia is suspected, Metronidazole or Clindamycin can be added
In treating pneumococcal pneumonia that is highly resistant, an IV fluoroquinolone, vancomycin, or linezolid may need to be added to the regimen.
Early gram-stain may be helpful for choosing antibiotics Core Measure
Treatment Options for Bronchitis No antibiotics! Increase hydration Expectorants/ Antitussives Antipyretics Albuterol ? If antibiotics are considered
Macrolides or doxycycline for atypical coverageSecond generation cephalosporinsAmoxicillin/clavulanate (high dose)Quinolones when compromised lung function
C. Diff Treatment Decreasing the use of antibiotics that most often
lead to C diff infections by 30% could lead to 26% fewer infectionsQuinolonesBeta-lactamsExtended spectrum cephalosporin
In 23% of patients, C difficile-associated disease will resolve within 2 to 3 days of antibiotic discontinuation
Avoid anti-motility agents Hospital HAC Measure
C. Diff Treatment Infection can be treated with either metronidazole
or oral vancomycin for 10 to 14 daysLikely to take 2 to 4 days before the diarrhea stopsVancomycin should only be used if treatment failure to
metronidazole, patient is pregnant, or known resistant strain
Oral agents preferred but may use IV metronidazole if patient cannot tolerate oral therapy
New Strain of C diff Increased rates of C diff-associated disease with more
severe symptoms and an increase in mortality has been seen
Meta-analysis showed a 23% annual increase in hospitalizations from C diff-associated disease from 2000 through 2005 along with a 35% increase in deaths
A new strain of C diff has been found that appears to be more virulent, produces greater quantities of toxin A and B, and is resistant to current therapies
Cause may be changes in antimicrobial usage Treatment – metronidazole or vancomycin Fidoxamicin Fecal transplant
Gaining more acceptance No standard administration approach
Most often enema/ colonoscopy although can be administered through NG tube
Stool slurry that needs to be used immediately from donor
Success is measured through resolution of symptoms and absence of relapse within 8 weeks
Fecal Transplant
UTI Organisms E. coli causes 80% of all community-acquired UTIs and
about half of UTIs in the hospitalE. coli has become increasingly resistant to TMP-SMX to
where it is no longer a first line agent for complicated UTI or pyelonephritis
Beta-lactams are associated with about a 40% resistance rate for E. coli
Other pathogens include gram-negative rods, such as Proteus, Klebsiella, and EnterobacterAlthough the quinolones are used for complicated UTIs, more
resistance is being seen with Enterococci Nitrofurantoin has low resistance, but has little use
beyond the urinary tract because of poor tissue perfusion
Summary of Asymptomatic Bacteriuria Treatment
Treat symptomatic patients with pyuria and bacteriuria Don’t treat asymptomatic patients with pyuria and/or
bacteriuria Define the symptomatic infection anatomically Dysuria and frequency without fever equals cystitis Dysuria and frequency with fever, flank pain, and/or
nausea and vomiting equals pyelonephritis Remember prostatitis in the male with cystitis
symptoms Remove catheters!!!
SCIP Measure PQRS Measure Hospital HAC Measure
Treatment Options for UTIs
Antibiotic Duration
Uncomplicated UTI TMP-SMX orNitrofurantoin
3 days
Uncomplicated UTI in Older Women TMP-SMX 7 days
Uncomplicated UTI with Suspected Resistant Organisms
Quinolone (ciprofloxacin)
3 – 7days
UTI in Pregnancy Amoxicillin/ clavulanate orSecond Generation Cephalosporin or Nitrofurantoin
7 – 10 days
Complicated UTI (Outpatient) Quinolone 10-14 days
Complicated UTI (Inpatient) Third Generation Cephalosporin orCarbapenem
10- 14 days
Treatment Options for UTIs
Antibiotic Duration
Pyelonephritis Quinolone plus Aminoglycoside orThird Generation Cephalosporin or Antipseudomonal Penicillin
7 – 14 days, up to 21 days
Hospital-Acquired UTI Quinolone orThird Generation Cephalosporin orCarbapenem orAntipseudomonal Penicillin
10-14 days
Pearls for Antibiotics
Key Points for Antibiotics Carbapenems
Not all agents are the same○ Ertapenem – not as broad spectrum○ Doripenem – concern about use in pneumonia
Use carefully due to the development of carbapenases Clindamycin
Good choice for CA-MRSAPsedomembraneous colitis
Daptomycin Should not be used for pneumoniaWatch for myositis
Key Points for Antibiotics Fluoroquinolones
Same effect either PO or IVStarting to see more issues with resistanceWatch for tendon issues Not indicated for children under the age of 16
LinezolidSame effect either PO or IVShould be reserved for when resistance to vancomycin
is presentThrombocytopenia – more common after 10 days of
therapyPotential serotonin syndrome?
Key Points for Antibiotics Metronidazole
Same effect either PO or IVPotential for several adverse reactions’
○ GI Watch for disulfiram-like reaction with alcohol
PenicillinsUse may be limited because of resistanceAddition of other agents to help combat resistance
RifampinShould not be used as monotherapy because quick
development of resistanceUsed in combination with other antibiotics in the treatment of
CA-MRSA for synergistic effectChange in secretions to red-orange
Key Points for Antibiotics Sulfa
Several potential drug-drug interactionsLots of potential adverse reactionsWatch for hypersensitivity reactions
TetracyclinesDrug-drug and drug-food interactionsContraindicated in pregnancy and in children under age 16
VancomycinIV for MRSA onlyPO for C diff onlyWatch renal function and monitor trough levels
Antimicrobial Stewardship
What Is Antimicrobial Stewardship? Antimicrobial stewardship is a
mutlidisciplinary approach for rational antibiotic therapyMust be based on evidence-based guidelinesMust be based on dataMust apply to all practitioners
Core Actions to Prevent Antibiotic Resistance
1. Preventing infections
2. Prevent the spread of resistance
3. Tracking and surveillance
4. Improve antibiotic prescribing through stewardship
5. Development of new antibiotics and new diagnostic tests for resistance bacteria
Principles of Antibiotic Stewardship• Re-evaluate, de-escalate or stop therapy at 48-72
hours based on diagnosis and microbiologic results• Re-evaluate, de-escalate or stop therapy with
transitions of care (e.g. ICU to step-down or ward)• Do not give antibiotic with overlapping activity• Do not “double-cover” gram-negative rods (i.e.
Pseudomonas sp.) with 2 drugs with overlapping activity
• Make sure that all prescriptions/orders for antibiotics have the appropriate dose, duration, and indication
Limit duration of surgical prophylaxis to <24 hours perioperatively
Use rapid diagnostics if available (e.g. respiratory viral PCR)
Prevent infectionUse good hand hygiene and infection control
practicesRemove catheters
Consult infectious disease
Principles of Antibiotic Stewardship
Conclusion Antibiotics clearly save lives Poor prescribing of antibiotics are putting patients at
unnecessary risk Adverse reactionsDevelopment of resistant organisms
Every time an antibiotic is prescribedIf at all possible, order recommended cultures before antibiotics
are givenMake sure an indication, dose, and expected duration are part
of the prescription orderReassess within 48 hours and adjust antibiotic or discontinue if
warranted Pay for performance indicators
