Nosocomial Pneumonia Dr Suruchi
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Tracking NI has becomedifficult
Shorter inpatient stays (averagepostoperative stay, now
approximately 5 days, is usuallyshorter than the 5- to 7-dayincubation period for S. aureussurgical wound infections)
Surveillance systems are optional tohospitals with infection-controlprograms
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Prevention ofVentilator
AssociatedPneumonia
(VAP)
AACN VAP Practice Alert
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Lecture Content
Epidemiology ofVAP
Preventionstrategies
HOB elevation
Ventilatorequipment changes
Continuous removalof subglottic
secretions Handwashing
AACN VAP Practice Alert
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Epidemiology of Ventilator Associated
Pneumonia (VAP)
AACN VAP Practice Alert
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Nosocomial Pneumonias
Account for 15% of all hospitalassociated infections
Account for 27% of all MICUacquired infections
Primary risk factor is mechanicalventilation (risk 6 to 21 times therate for nonventilated patients)
CDC Guideline for Prevention of Healthcare AssociatedPneumonias 2003Cook et al, Ann Intern Med 1998;129:433
AACN VAP Practice Alert
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Critical Care Interventions Increase Susceptibility
to Nosocomial Pneumonias
TrachealColonization
AlteredHost
Defenses
IncreasedNosocomialPneumonias
Intubation
AACN VAP Practice Alert
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VAP Etiology Most are bacterial pathogens, with
Gram negative bacilli common:
Pseudomonas aeruginosa
Proteus spp Acinetobacter spp
Staphlococcus aureus
Early VAP associated with non-multi-antibiotic-resistant organisms
Late VAP associated with antibiotic-resistant organism
AACN VAP Practice Alert
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Significance of NosocomialPneumonias
Mortality ranges from 20 to 41%,depending on infecting organism,
antecedent antimicrobial therapy, andunderlying disease(s)
Leading cause of mortality fromnosocomial infections in hospitals
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003Heyland et al, Am J Respir Crit Care Med 1999;159:1249Bercault et al, Crit Care Med 2001;29:2303
AACN VAP Practice Alert
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Significance of NosocomialPneumonias
Increases ventilatory supportrequirements and ICU stay by 4.3
days Increases hospital LOS by 4 to 9
days
Increases cost -
Heyland et al, Am J Respir Crit Care Med1999;159:1249Craven D. Chest 2000;117:186-187S
Rello et al, Chest 2002;122:2115
AACN VAP Practice Alert
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VAP Prevention
AACN VAP Practice Alert
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Continuous Removal ofSubglottic Secretions
Use an ET tube with
continuous suctionthrough a dorsal lumenabove the cuff toprevent drainageaccumulation
CDC Guideline for Prevention of Healthcare Associated Pneumonias
2003Kollef et al, Chest 1999;116;1339
AACN VAP Practice Alert
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HOB Elevation
HOB at 30-45o
CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003Drakulovic et al, Lancet 1999;354:1851
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Frequency of EquipmentChanges
VentilatorTubing
InnerCannulasof Trachs
AmbuBags
No RoutineChanges
Not Enough
DataBetweenPatients
CDC Guideline forPrevention of Healthcare Associated Pneumonias
AACN VAP Practice Alert
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Handwashing
What role does handwashing play innosocomial pneumonias?
Albert, NEJM 1981; Preston, AJM 1981; Tablan, 1994AACN VAP Practice Alert
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VAP Prevention
All recommendations are level IA
CDC Guideline for Prevention of Healthcare Associated
Pneumonias 2003AACN Practice Alert for VAP, 2004
Wash hands before and
after suctioning, touchingventilator equipment,and/or coming intocontact with respiratorysecretions.
AACN VAP Practice Alert
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Use a continuous subglotticsuction ET tube for intubationsexpected to be > 24 hours
Keep the HOB elevated to atleast 30 degrees unlessmedically contraindicated
VAP Prevention
All recommendations are level II
CDC Guideline for
Prevention of Healthcare Associated Pneumonias2003
AACN VAP Practice Alert
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No Data to Support TheseStrategies
Use of small bore versus large boregastric tubes
Continuous versus bolus feeding Gastric versus small intestine tubes
Closed versus open suctioningmethods
Kinetic beds
CDC Guideline forPrevention of Healthcare Associated
AACN VAP Practice Alert
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Potential consequences ofinappropriate antibiotic therapy
Inappropriate empiric antibiotictherapy can lead to increases in:
mortality
morbidity
length of hospital stay
cost burden
resistance selection
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Inappropriate antibiotictherapy
Inappropriate antibiotic therapy canbe defined as one or more of the
following: ineffective empiric treatment of
bacterial infectionat the time of its identification
the wrong choice, dose or duration oftherapy
use of an antibiotic to which thepathogen
is resistant
Evidence of improved clinical
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Evidence of improved clinicaloutcomes with appropriateempiric antibiotic therapy
A number of studies havedemonstrated the
benefits of early use ofappropriate empiricantibiotic therapy for patientswith nosocomial infections
Several key clinical studies arereviewed in the followingslides
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Inappropriate antibiotic therapy is a riskfactor for mortality among patients in theintensive care unit (ICU)
Infection-related mortality rates were assessedin a prospective cohort, single-centre study of2000 patients admitted to medical/surgical ICUs
655 patients had a clinically recognisedinfection:
442 (67.5%) had a community-acquiredinfection
286 (43.7%) developed a nosocomial
infection 73 (11.1%) had both community-acquired
and nosocomial infections
169 (25.8%) patients received inappropriate
initial antimicrobial treatment Kollef et al. Chest 1999;115:462474
Inappropriate antibiotic therapy is
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Inappropriate antibiotic therapy isa risk factor for mortality amongpatients in the ICU
Kollef et al. Chest 1999;115:462474
Hospital mortality (%)
0
20
50
60
Appropriate therapyInappropriate therapy
40
30
10
All causes Infectious disease-related
p
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Appropriate antibiotic therapy reducesmortality and complications in patientswith nosocomial pneumonia
The frequency of and reasons for changing empiricantibiotics during the treatment of hospital-acquiredpneumonia were assessed in a prospectivemulticentre study across
30 Spanish hospitals Of the 16 872 patients initially enrolled, 530
developed565 episodes of pneumonia after ICU admission
Empiric antibiotics (administered in 490 [86.7%] of
episodes) were modified in 214 (43.7%) casesbecause of:
isolation of micro-organism not covered by treatment(62.1%)
lack of clinical response (36.0%)
development of resistance (6.6%)Alvarez-Lerma et al. Intensive Care Med 1996;22:387394
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Alvarez-Lerma et al. Intensive Care Med 1996;22:387394
Appropriate antibiotic therapy reducesmortality and complications in patientswith nosocomial pneumonia
Appropriatetherapy
(n=284)
Attributable mortality
No. complications/patient
Shock
Gastrointestinal bleeding
Respiratory failure
Multiple organ failure
Extrapulmonary infection
Inappropriatetherapy
(n=146) p-value
16.2%
1.73 1.82
17.1%
10.7%
24.9%
12.5%
13.2%
24.7%
2.25 1.98
28.8%
21.2%
32.2%
21.2%
17.1%
0.04
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Appropriate early antibiotic therapy reducesmortality rates in patients with suspectedventilator-associated pneumonia (VAP) (Study1)
A prospective observation and bronchoscopy studyof patients with VAP assessed the impact ofbronchoalveolar lavage (BAL) data on the selectionof antibiotics and clinical outcomes in a
medical/surgical ICU 132 mechanically ventilated patients (hospitalised
>72 hours) with clinically confirmed VAP underwentBAL within 24 hours of diagnosis 107 patients received antibiotics prior to
bronchoscopy 25 patients received antibiotics immediately after
bronchoscopy Mortality rates were assessed in relation to the
adequacy and time of initiation of antibiotic therapy
Luna et al. Chest 1997;111:676685
Appropriate early antibiotic therapy reduces
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Luna et al. Chest 1997;111:676685
Appropriate early antibiotic therapy reducesmortality rates in patients with suspectedVAP(Study 1)
Mortality (%)
Pre-BAL Post-BAL Post-cultureresult
0
60
100
20
40
80
p
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ppropr a e ear y an o c erapy re ucesmortality rates and length of hospital stayin patients with bloodstream infection(Study 1)
An observational prospective cohort study of patientswith bloodstream infection examined whetherappropriate antibiotic therapy improved survival rate
Of the 3413 evaluable patients, 2158 (63%) receivedearly appropriate antibiotics
defined as starting within 2 days of the firstpositive blood culture, and if the causativepathogen was susceptiblein vitro to the administered drug
Mortality rates and median duration of hospital stayfor surviving patients were determined
Leibovici et al. J Intern Med 1998;244:379386
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Appropriate early antibiotic therapy reducesmortality rates and length of hospital stay inpatients with bloodstream infection (Study 1)
Leibovici et al. J Intern Med 1998;244:379386
Appropriate
therapy
(n=2158)
Mortality rate
Median duration of
hospital stay
Inappropriate
therapy
(n=1255) p-value
20.2%
9 days
(range 0117)
34.4%
11 days
(range 0209)
0.0001
0.0001
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Summary
Clinical evidence suggests thatearly use of appropriate empiric
antibiotic therapy improvespatient outcomes in terms of:
reduced mortality
reduced morbidity
reduced duration of hospital stay
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Resistance to antibacterialagents
Antibiotic resistance either arises as a resultof innate consequences or is acquired fromother sources
Bacteria acquire resistance by:
mutation: spontaneous single or multiplechanges in bacterial DNA
addition of new DNA: usually via plasmids,which can transfer genes from onebacterium to another
transposons: short, specialised sequencesof DNA that can insert into plasmids orbacterial chromosomes
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Mechanisms of antibacterialresistance (1)
Structurally modified antibiotictarget site, resulting in:
reduced antibiotic binding
formation of a new metabolicpathway preventing metabolism of
the antibiotic
Structurally modified antibiotic
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Structurally modified antibiotictarget site
Interior of organism
Cell wall
Target siteBinding
Antibiotic
Antibiotics normally bind to specific binding
proteins on the bacterial cell surface
Structurally modified antibiotic
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Structurally modified antibiotictarget site
Interior of organism
Cell wall
Modified target site
Antibiotic
Changed site: blocked binding
Antibiotics are no longer able to bind to modified
binding proteins on the bacterial cell surface
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Mechanisms of antibacterialresistance (2)
Altered uptake of antibiotics,resulting in:
decreased permeability
increased efflux
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Altered uptake of antibiotics:decreased permeability
Interior of organism
Cell wall
Porin channel
into organism
Antibiotic
Antibiotics normally enter bacterial cells via
porin channels in the cell wall
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Altered uptake of antibiotics:decreased permeability
Interior of organism
Cell wall
New porin channel
into organism
Antibiotic
New porin channels in the bacterial cell wall do
not allow antibiotics to enter the cells
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Altered uptake of antibiotics:increased efflux
Interior of organism
Cell wall
Porin channel
through cell wall
Antibiotic
Entering Entering
Antibiotics enter bacterial cells via porin
channels in the cell wall
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Altered uptake of antibiotics:increased efflux
Interior of organism
Cell wall
Porin channel
through cell wall
Antibiotic
Entering Exiting
Active pump
Once antibiotics enter bacterial cells, they are
immediately excluded from the cells
via active pumps
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Mechanisms of antibacterialresistance (3)
Antibiotic inactivation
bacteria acquire genes encoding
enzymes that inactivate antibiotics Examples include:
-lactamases
aminoglycoside-modifying enzymes chloramphenicol acetyl transferase
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Antibiotic inactivation
Interior of organism
Cell wall
Antibiotic
Target siteBindingEnzyme
Inactivating enzymes target antibiotics
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Antibiotic inactivation
Interior of organism
Cell wall
Antibiotic
Target siteBindingEnzyme
Enzyme
binding
Enzymes bind to antibiotic molecules
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Antibiotic inactivation
Interior of organism
Cell wall
Antibiotic
Target siteEnzyme
Antibiotic
destroyedAntibiotic altered,
binding prevented
Enzymes destroy antibiotics or prevent binding to target sites
Many pathogens possess multiple
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Many pathogens possess multiplemechanisms of antibacterialresistance
+Quinolones++Trimethoprim++Sulphonamide
++Macrolide+Chloramphenicol
+Tetracycline +++Aminoglycoside+Glycopeptide
++++-lactam
Modified target Altered uptake Drug inactivation
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Focus on -lactam antibioticresistance mechanisms
Three mechanisms of-lactamantibiotic resistance are
recognised: reduced permeability
inactivation with -lactamase
enzymesaltered penicillin-binding proteins
(PBPs)
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Multiple antibiotic resistancemechanisms: the -lactams
l ibi i
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-lactam antibioticresistance
AmpC and extended-spectrum -lactamase (ESBL) production are themost important mechanisms of-lactam resistance in nosocomialinfections
The antimicrobial and clinicalfeatures of these resistancemechanisms are highlighted in thefollowing slides
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-lactam resistance:AmpC -lactamase production
Worldwide problem: incidence increased from 1723% between
1991 and 2001 in UK
Very common in Gram-negative bacilli AmpC gene is usually sited on
chromosomes, but can be present onplasmids
Enzyme production is either constitutive(occurring all the time) or inducible (onlyoccurring in the presence of theantibiotic)
Pfaller et al. Int J Antimicrob Agents 2002;19:383388
Sader et al. Braz J Infect Dis 1999;3:97110; Livermore et al. Int J Antimicrob Agents 2003;22:1427
l t i t ESBL
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-lactam resistance: ESBLproduction
An increasing global problem
Found in a small, expanding group of
Gram-negative bacilli, most commonlythe Enterobacteriaceae spp.
Usually associated with large plasmids
Enzymes are commonly mutants of TEM-andSHV-type -lactamases
Jones et al. Int J Antimicrob Agents 2002;20:426431
Sader et al. Diagn Microbiol Infect Dis 2002;44:273280
A ti i bi l f t f
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Antimicrobial features ofESBLs
Inhibited by -lactamase inhibitors
Usually confer resistance to:
first-, second- and third-generation cephalosporins(eg ceftazidime)
monobactams (eg aztreonam)
carboxypenicillins (eg carbenicillin)
Varied susceptibility to piperacillin/tazobactam
Typically susceptible to carbapenems and
cephamycins Often clinically and/or microbiologically
non-susceptible to fourth-generation cephalosporins
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Clinical features of ESBLs
Even if sensitive to fourth-generationcephalosporinsin vitro, treatment failures occur in clinicalpractice
Create clinical difficulties due to cross-resistancewith other antibiotic classes (egaminoglycosides)
Associated with nosocomial outbreaks of highmorbidity and mortality
Result in overuse of other broad-spectrum
agents
Cli i l f il i th
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Clinical failure in thepresence of ESBLs
Recent data show high clinical failure rates among patientstreated with cephalosporins for serious infections causedby ESBL-producing pathogens
susceptible to cephalosporins in vitro
4/32 patients received cephalosporins to whichpathogens showed intermediate susceptibility and allfailed treatment
15/28 remaining patients with cephalosporin-susceptible pathogens failed treatment and 4 died
11 patients required a change in antibiotic therapy
Paterson et al. J Clin Microbiol 2001;39:22062212
Patients who failed cephalosporin
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Patients who failed cephalosporintherapy for serious infections due toESBL-producing organisms
Paterson et al. J Clin Microbiol 2001;39:22062212
Clinical failure rate (%)
0
60
100
20
1
40
80
2 4 8
Cephalosporin MIC (g/mL)
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Features of methicillin-resistantStaphylococcus aureus (MRSA)
Introduction of methicillin in 1959 wasfollowed rapidly by reports of MRSAisolates
Recognised hospital pathogen since the1960s
Major cause of nosocomial infectionsworldwide contributes to 50% of infectious morbidity in
ICUs in Europe
surveillance studies suggest prevalence hasincreased worldwide, reaching 2550% in
1997 Jones. Chest 2001;119:397S404S
S i i f ti t ti iti f MRSA
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Serious infections testing positive for MRSAisolates among hospitalised patients(1997 SENTRY data)
Patients (%)
0
30
50
10
Pneumonia
20
40
UTI Wound Bloodstream
Infection type
Jones. Chest 2001;119:397S404S
UTI
UTI = urinary tract infection
F t f MRSA id i
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Features of MRSA: epidemicstrains
Problem escalated in the early 1980s withemergence of epidemic strains (EMRSA)
first recognised in the UK
17 EMRSAs identified to date
Impact on hospitals is variable
presence of EMRSA can account for >50%
ofS. aureus isolates
Aucken et al. J Antimicrob Chemother 2002;50:171175
k f f l
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Risk factors for colonisation or
infection with MRSA in hospitals
Chambers. Emerg Infect Dis 2001;7:178182
Admission to an ICU
Surgery
Prior antibiotic exposure
Exposure to an MRSA-colonised patient
E f MRSA i th
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Emergence of MRSA in thecommunity
MRSA in hospitals leads to an associated rise in incidencein the community
Community-acquired MRSA strains may be distinct fromthose in hospitals
In a hospital-based study, >40% of MRSA infections wereacquired prior to admission
Risk factors for community acquisition included:
recent hospitalisation
previous antibiotic therapy
residence in a long-term care facility intravenous drug use
Colonisation and transmission are also seen in individuals(including children) lacking these risk factors
Hiramatsu et al. Curr Opin Infect Dis 2002;15:407413Layton et al. Infect Control Hosp Epidemiol 1995;16:1217; Naimi et al. 2003;290:29762984
Antimicrobial features of
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Antimicrobial features ofMRSA (1)
Mechanism involves altered target site
new penicillin-binding protein PBP 2' (PBP 2a)
encoded by chromosomally located mecA gene
Confers resistance to all -lactams Gene carried on a mobile genetic element
staphylococcal cassette chromosome mec(SCCmec)
Laboratory detection requires care
Not all mecA-positive clones are resistant tomethicillin
Hiramatsu et al. Trends Microbiol 2001;9:486493Berger-Bachi & Rohrer. Arch Microbiol 2002;178:165171
Antimicrobial features of
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Antimicrobial features ofMRSA (2)
Cross-resistance common with many otherantibiotics
Ciprofloxacin resistance is a worldwide problemin MRSA:
involves 2 resistance mutations
usually involvesparC and gyrA genes
renders organism highly resistant tociprofloxacin, with cross-resistance to other
quinolones Intermediate resistance to glycopeptides
first reported in 1997
Hiramatsu et al. J Antimicrob Chemother 1997;40:135136Hooper. Lancet Infect Dis 2002;2:530538
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Clinical features of MRSA
Common associations include: underlying chronic disease, especially
repeated
hospital stays prolonged/repeated antibiotics, especially the-lactams
Usually susceptible to at least one other
antibiotic Not all MRSAs behave as EMRSAs
Methicillin resistance is not a marker ofvirulence
Clinical features of MRSA:
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Clinical features of MRSA:transmission
Occurs primarily from colonised or infected patientsvia the hands of healthcare workers
contact transmission to other patients or staff verycommon
Airborne transmission important in the acquisition ofnasal carriage
Infection control measures include:
screening and isolation of new patients suspectedof carrying MRSA or S. aureus with vancomycinresistance
implementing infection control programmes
establishing adequate antibiotic policy to minimisedevelopment of resistance
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Management of MRSA
Educate on risks and control measures
Adhere to strict control measures to prevent
transmission, especially through contact
Treat patient with appropriate empiricand targeted therapy
Consider clearing patient of MRSA carriage
Gl tid i t f
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Glycopeptide resistance: focuson vancomycin resistance
Vancomycin-resistant enterococci(VRE)
Vancomycin-resistant S. aureus(VRSA)
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Features of quinolone resistance:Gram-negative organisms
Resistance most common in organisms associatedwith nosocomial infections
Pseudomonas aeruginosa
Acinetobacterspp.
also increasing among ESBL-producing strains
Meropenem Yearly Susceptibility Test InformationCollection (MYSTIC) surveillance programme(19972000)
13.4% of Gram-negative strains resistant tociprofloxacin
P. aeruginosa andAcinetobacter baumanniiarethe most prevalent resistant strains
increasing prevalence of resistance during
surveillance period Masterton. J Antimicrob Chemother 2002;49:218220Thomson. J Antimicrob Chemother 1999;43(Suppl. A):3140
Gram-negative organisms with
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g gresistance to ciprofloxacin (1997SENTRY data)
Organisms (%)
0
30
50
10
Stenotrophomonasmaltophilia
20
40
Acinetobacterspp. P. aeruginosa Escherichiacoli
All patients (USA)Lower RTI (USA and Canada)
Organism typeJones. Chest 2001;119:397S404S
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Features of quinolone resistance:
Gram-positive organisms
MRSA
S. aureus occurred in 22.9% of pneumonias inhospitalised patients in USA and Canada (1997SENTRY data)
Enterococcus spp. resistance
has developed rapidly, especially among VRE
Streptococcus pneumoniae resistance
emerging in many countries, including
community-acquired resistance Hong Kong (12.1%), Spain (5.3%) and USA
(
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Summary
Antibiotic resistance in the hospitalsetting is increasing at an alarming
rateand is likely to have an importantimpact on infection management
Steps must be taken now to controlthe increase in antibiotic resistance
Cosgrove et al. Arch Intern Med 2002;162:185190
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Summary
The Academy for Infection Management supports theconcept of using appropriate antibiotics early innosocomial infections and proposes:
selecting the most appropriate antibiotic based on the
patient,risk factors, suspected infection and resistance
administering antibiotics at the right dose for theappropriate duration
changing antibiotic dosage or therapy based onresistance and pathogen information
recognising that prior antimicrobial administration is arisk factor for the presence of resistant pathogens
knowing the units antimicrobial resistance profile andchoosing antibiotics accordingly