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New Issues in bacteria we thought we knew so well. Meet the new Staphylococcus aureus. Donna Holton, Infectious Diseases, CHR Oct 23, 2008. HARBOUR BRETON NEWFOUNDLAND. Who am I. ID specialist with training in epidemiology GP who worked in outport NFLD 1981-1983 - PowerPoint PPT Presentation
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New Issues in bacteria we thought we knew so well.
Meet the new Staphylococcus aureus
Donna Holton,
Infectious Diseases, CHR
Oct 23, 2008
HARBOUR BRETON NEWFOUNDLAND
Who am I ID specialist with training in epidemiology
GP who worked in outport NFLD 1981-1983 Worked in Kenya doing HIV in the late ’80s Worked for Health Canada as epidemiologist
(created the TB Guidelines for Canadian Hospitals) Self employed epidemiologist (organized the 1997
Canadian Antimicrobial Resistance Conference) Worked in Regina as Infectious Diseases doctor Work in Calgary as ID and do HIV and Infection
Control
Who am I I have done talks for all the companies re:
antibiotics and HIV Abbott, BMS, Wyeth-Ayerst, GSK
Interested in biofilm infections and hospital building design
HIV trials with a wide variety of companies Tibotec, GSK, Abbott, Boehringer-Ingelheim, NeurogesX, Argos Therapeutics, Gilead, Pzifer, Merck
I sit on three boards for new HIV drugs (Abbott, Kaletra: Merck, Raltegrevir: Pzifer, Maraviroc)
I am part of the committee writing Canadian HIV treatment guidelines
Learning ObjectivesMethicillin resistant Staphylococcus
aureusMRSA
1. How have Staphylococcus aureus infections changed?
2. What is the prevalence of MRSA in the CHR3. Infection vs colonization4. Treatment- who, what , and when?5. What will the future look like?
With Many Thanks
To all the IPCs who collect the bloodstream infections and to Stephanie who enters the data
To CLS and Provincial Lab especially Drs. Dan Gregson, Deirdre Church and Marie Louie
To all IPCs who took part in the Mark of Zoro study
Staphylococcus aureus
Very successful bacteria: can infect anyone bacteria
Ubiquitous
In the days before antibiotics whole wings of hospitals were filled with people who had chronic S. aureus infections
2% of lactating women died of S. aureus mastitis
S. aureus causes Soft tissue infections
Basically any, impetigo, cellulitis, muscle abscess
Joint infections Surgery site infections Endocarditis Osteomyelitis Prosthetic device infections Others: pneumonia, organ abscesses
Produces toxins that cause different diseases food poisoning, toxic shock
My Jan 28th caseWhy is my patient not
improving? 40 yr female with abscess in her left
thigh WBC 22 with 20 neutrophils Blood cultures negative Not toxic, just not getting better
Clinical issues the usual bacterial suspects that cause
uncomplicated soft tissue infection are Group A Streptococcus S. aureus
Cultures rarely done
Because this lady has a large abscess, the pathogen is more likely to be S. aureus rather than Group A Streptococcus
Staphylococcus aureus is a common cause of infection
Name five drugs from five different antibiotics classes
that area) Oral S. aureus antibiotics
b) IV S. aureus antibiotics
15 Classes of anti-S. aureus drugs Class Oral (n=9 ) IV (n=12)
Penicillin Cloxacillin Cloxacillin
Cephalosporin Keflex Ancef
Carbapenum Meropenum
Sulfa “septra” “septra”
Macrolides All Azithromycin
Lincomycins Clindamycin Clindamycin
Tetracyclines All
Glycopeptide Vancomycin
Quinolones Not cipro* Levo, Moxi
Others LinezolidFusidic AcidRifampin
Linezolid, Tigecycline, Daptomycin, Synercid
*CIPRO has an MIC that just works but that also means it often fails against S. aureus. Spain has a > 30% resistance rate
**Rifamycins work but not alone
My Jan 28th caseWhy is my patient not
improving? 40 yr female with abscess in her left
thigh WBC 22 with 20 neutrophils Blood cultures negative Nasal and rectal cultures negative for
MRSA Superficial wound (skin intact) swab
grew Cloxacillin susceptible S. aureus
In your practice, what kind of soft tissues infections are you
seeing?If you are aware of several patients have MRSA, do they have the same spectrum of disease?
In HPTP we are seeing a new spectrum of disease
90% are variations of soft tissue themes Story of the Spider bite Large often complex abscesses Multiple skin lesions Co-infection with Group A Streptococcus Patients have multiple infections despite
good treatment Patients come from the community
Courtesy Melissa Tobin-D’Angelo, Georgia DHR
Carbuncle
Furuncle (boil))
AbscessFolliculitisFolliculitis
We are seeing a new spectrum of disease
~10% infections creating critical illnesses Necrotizing pneumonia
-Vayalumkal (new ped ID staff) article CJEM 2007:9(4):300-3.. Pt died-CDC is investigating 2 deaths (11 yr old and 13 year children) who died when MRSA complicated a viral “flu” like illness (2008)
22/73 kids who died of influenza in 2006-7 had Staphylococcus 2nd bacterial infection
Rare cases where it caused necrotizing fasciitis, purpura fulmanans
This type of MRSA seems to have acquired new abilities to cause critically serious disease
Courtesy of M. Farley
BMJ 2006;332;838-841
My Jan 28th caseWhy is my patient not
improving? 40 yr female with abscess in her left thigh WBC 22 with 20 neutrophils Blood cultures negative Nasal and rectal cultures negative for MRSA Superficial wound swab grew Cloxacillin
susceptible S. aureus Smart hospitalists are concerned this
patient has an antibiotic resistant S. aureus
Hospitalist was concerned patient had Methicillin
resistant Staphylococcus aureus (MRSA)
Which of the 15 class(es) of Staphylococcal Drugs can not
be used if a patient has MRSA?
MRSA has developed resistance to ALL current
Beta Lactams
Name the three beta lactam classes
MRSA = resistance to all of current beta lactam antibiotics
All of the penicillin class regardless of generation or complexity i.e., can not use Cloxacillin, Clavulin or Tazocin
All of the current cephalosporins regardless of generation
All of the current carbapenum (meropenum, imipenum, ertapenum)
And MRSA usually comes with even MORE resistance than this!!!
12 non-Beta lactam S. aureus drugs Class Oral (n=9 ) IV (n=12)
Penicillin Cloxacillin Cloxacillin
Cephalosporin Keflex Ancef
Carbapenum Meropenum
Sulfa “septra” “septra”
Macrolides All Azithromycin
Lincomycins Clindamycin Clindamycin
Tetracyclines All
Glycopeptide Vancomycin
Quinolones Not cipro* Levo, Moxi
Others LinezolidFusidic AcidRifampin
Linezolid, Tigecycline, Daptomycin, Synercid
*CIPRO has an MIC that just works but that also means it often fails against S. aureus. Spain has a > 30% resistance rate
**Rifamycins work but not alone
Why is this resistance so important that the
Alberta Government has declared war on it?
Because the loss of the Betalactam = the loss of
bactercidal antibiotics
If the Betalactms are gone so are the Fluroquinolones
What is an Antibiotic Resistant Organism?
An organism that We can no longer use our first string (bactercidal) antibiotics
We still have antibiotics but we are sending in the second
string (bacteriostatic)
12 non-Beta lactam S. aureus drugs Class Oral (n=9 ) IV (n=12)
Penicillin Cloxacillin Cloxacillin
Cephalosporin Keflex Ancef
Carbapenum Meropenum
Sulfa “septra” “septra”
Macrolides All Azithromycin
Lincomycins Clindamycin Clindamycin
Tetracyclines All
Glycopeptide Vancomycin
Quinolones Not cipro* Levo, Moxi
Others LinezolidFusidic AcidRifampin
Linezolid, Tigecycline, Daptomycin, Synercid
**Rifamycins work but not alone
Betalactam antibiotics work by interfering with
the penicillin binding proteins (PBP).
This prevents the bacteria cell wall from being built
Think Cement Retaining Wall
S. aureus builds cross links in the bacteria cell wall that strengthen the wall (think rebar)
If beta lactams can bind to the cell wall, the beta lactams prevent the cross links
The cell wall has no “ribar” and collapses The bacteria dieMRSA means that S. aureus has worked out
how to prevent Beta lactams from binding
Mechanism of Staphylococcus aureus Methicillin Resistance
Beta lactam antibiotics bind to penicillin binding protein 2 (PBP 2)
When S. aureus changes PBP 2 to PBP 2’ (also called PBP 2a) all currently licensed for use in Alberta beta lactam antibiotics become useless. -Change occurs via the Mec A gene.
In the presence of the Mec A gene, the beta lactam antibiotics can not attach to the PBP and so the bacteria grow because the bacteria cells walls are cross linked and strong
A short history of S. aureus Resistance
Penicillin (the drug not the class)
1928 - Penicillin discovered
1939 - Penicillin first used as treatment
1945 - Resistance to penicillin identified
1980’s < 1% susceptible to penicillin
A short history of S. aureus Resistance:
Solving Penicillin Resistance 1959 Vancomycin created and looked like
drug of choice
1959 Methicillin introduced
followed by many “copycat” semi synthetic
penicillins (i.e., cloxacillin, oxacillin, nafcillin)
1964 first cephalosporins introduced (Ancef)
A Short History of S. aureus resistance:
Develops Resistance to Semi-synthetic penicillins and
cephalosporins 1961 - First identified MRSA (UK)
1981 - MRSA appears in Canada
1995 - MRSA begins to escalate in
Canada
1999 – 6% of S. aureus are MRSA in
Canada
Antimicrobial Resistance among NosocomialInfections with Gram-Positive Pathogens, Canada (yellow) & US (green) and by ICU
Status (pink)
Source: NNIS Data:Fridkin and Gaynes Clinics in Chest Medicine June ‘99 303-16CNISP 2000 (colonization/infection)
Canada
United States
Figure 1. Incidence and rate per 1,000 patient admissions for MRSA (infections and colonizations) from 1995 to 2006 in Canadian hospitals participating in CNISP
Rate is blue line
# of cases = red barsData from CNISP Jan 2008
To all organisms Resistance is not futile, Resistance is survival
S. aureus has 4 different alphabet soup names to
describe resistanceMRSA, hVISA,
GISA (not VISA), VRSA
Look up Staphylococcus aureus in Infection Control manual
S. Aureus resistance to “methicillin” and
Vancomycin
0
10
20
30
40
1940 1950 1960 1970 1975 1980 1985 1990 1995 2000 2003
Year
% R
esis
tan
ce
Methicillin
Vancomycin
1st use methicillin 1959
1st MRSA 1961
Europe, UK Aus, India
Vancomycin Resistance2002
1st MRSA US Outbreak
USA ,AusIreland Worldwide
Vancomycin intermediate resistance 1997
What is happening to S. aureus
Calgary?
MRSA isolates (in and out patients) ACH
1 15 5 3 4 5 4 6 8
11
24
38
59
05
101520253035404550556065
1986 1992 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008
Years
Nu
mb
er
S. aureus Bacteremias
0
20
40
60
80
100
120
140
160
2003 2004 2005 2006 2007 Year
Nu
mb
er
of
ca
se
s
MSSA
MRSA
10.6 13.4 16.7 23.9 34.3 %MRSA
Odd year
Calgary Health Region, Adult Nosocomial Blood Stream
Infections
Stable rate of BSI per 1000 patient days (0.8)
Total BSI
SA
Comparison of Organisms Having Multiple Drug Resistances 2004 to 2007 (Fiscal Year)
Organisms Having Mulitple Drug Resistances
MRSA
VREEscherichia
Klebsiella
PseudomonasMRSA
VRE
Escherichia
Klebsiella
Pseudomonas
Organisms Having Multiple Resistances
MRSA
VREoth Gram Negative
Escherichia
Klebsiella
Pseudomonas MRSA
VRE
oth Gram Negative
Escherichia
Klebsiella
Pseudomonas
Organisms Having Multiple Drug Resistances 2006
58%
0%
14%
5%
4%
7%
7%5%
MRSA
VRE
E. coli
Enterobacter
Klebsiella
Pseudo
Steno
Other GramNegative
Organisms Having Multiple Drug Reisistances 2007
59%
1%
15%
13%
1%
2%
4%
5%MRSA
VRE
E. coli
Enterobacter
Klebsiella
Pseudo
Steno
Other Gram Negative
2004 fiscal year (n=41)
2005 fiscal year (n=43)
2006 fiscal year (n=56)
2007 fiscal year (n=82)
S. aureus in CHR Emergency Room: prior to 2004 slow but steady increase
in per cent
0
1
2
3
4
5
6
% M
RSA in E
R iso
late
s
1985 1990 1995 2000 2005
Year
MRSA
0
5
10
15
20
25
30
% M
RSA
in E
R
isol
ates
1985 1990 1995 2000 2005 2007
Year
From 2004 to Dec 2007,From 2004 to Dec 2007, MRSA took offMRSA took off
MRSA seems to have changed
Before 2004, MRSA was acquired in
Acute Care Hospitals 75% of cases Specific clones
Long term care 10% of cases
Community 8%
As a resident at FMC I meet my first “Hospital MRSA”
This MRSA was the one in the journals Was associated with Thames, Australia, U.S.
Burn Units Only available antibiotic was Vancomycin Occurred in
elderly, frail hospital patients burn, ICU and dialysis units
Caused infection (bacteremias) but a lot of people just seemed to be colonized
This organism plus VRE were the basis of creating increased isolation in acute care settings Private room Standard + contact
After that first patient my MRSA experience changed
“Prairie” MRSA caused simple skin infections had an effective oral agents (TMP-SMX,
clindamycin) occurred in an isolated population (First Nations) was found on the Prairies Was not a research project, no one was able to
get any traction for research on this type of MRSA
So we treated the kids and young people with Septra and they got better.
2005
Until 2005, the majority of MRSA isolates came from the hospital environment
Since mid 2005, most of the MRSA isolates came from the community
Clinical Syndromes – Invasive MRSAEIP Active Bacterial Core(ABCs) MRSA
Surveillance2004 – 2005New%
(n=865)Old%
(n=5522)
Skin / soft tissue infection 33.8† 10.2
Pneumonia 16.3 14.1
Endocarditis (? New biofilm gene(s)) 11.5† 5.0
Internal / deep seated abscess 9.0† 4.4
Osteomyelitis 8.3 7.5
Septic arthritis, native joint 5.1† 2.3
Septic shock 4.3 4.4
Endocarditis and / or metastatic complications (? New biofilm gene(s))
21.3† 9.9
Bacteremia 80.5† 88.2
Bacteremia, uncomplicated (no source)^ 23.8† 47.4
†Difference tested by Chi Square with p value <0.0001 Ray SM et al. IDSA 2005
Type of MRSA causing bacteremia
Prior to 2006, most of the nosocomial bacteremias were caused by MRSA 2, 6, and 8 i.e, the “hospital” or “old” MRSAs
Since 2006, the “new” or Community or “10” MRSA is the major cause of the MRSA bacteremias
My previous antibiotic suspectibility patterns
persisted
Boyce JM (2003), Clin Updates ID
GISA
Since 2004 epidemiological questions
became important.
What are the five current CHR risk factors for MRSA?
I tell the clerks and residents in HPTP if they can not answer this question for each patient with soft tissue infections I will
fail them
MRSA Risk Factor Questions
“Old question” Do you a lot of contact with the hospital system
Do you volunteer, work or live atthe jail
the drop in center Do you smoke, inject, snort any
recreational drugs? Are you or anyone you know MRSA
positive? secondary questions “do you work on the rigs, in
construction, do you work out at a gym”
Who are the MRSA patients now?
Hospital (Old) Elderly or renal
patients
Many visits to hospital Lots of positive nasal
swabs
Not a lot of infection
Called “hospital” acquired MRSA
Community (New) Young people, jail,
drugs, homeless
Few visits to hospital <50% of nasal swabs
positive
Lots of infection
Called “community” acquired MRSA
Risk Factors for Neonatal MRSA Infection in a Well-infant
NurseryNguyen 2007 ACHE 28(4): 407-
411 Risk for newborn infants to have MRSA
Circumcision 2nd outbreak had multi-dose lidocaine vial Surgical instruments uncovered
Infections often looked like diaper rashes
Investigation of moms. No MRSA in nose
The lab has now worked some of my previous epi
questions
The Staphylococcal resistance is much more than “just” a MEC A
gene
Methicillin Resistance in Staphylococcus aureus
beta lactam antibiotics work by interfering with the penicillin binding proteins (PBP)
MRSA organism change the PBP2 i.e., PBP2 becomes PBP2’
Resistance comes on a cassette called staphylococcal chromosomal cassette Mec (SCCmec). Cassette has
Mec A Two regulatory genes (Mec I and Mec R1) Two site specific recombinases +/- other antibiotic resistances
The size of the cassette (SCC) suggests if resistance to other antibiotics might be
presentLarger cassettes have more
room to carry more than “just” beta lactam antibiotic
resistance
CLS M-PCR typing scheme for SCCmec
MW
MW
300
400
800600500
bp
200
1000
(613) (398) (280) (776) (493) (200) (880) (325)
I II III IVa IVb IVc IVd VSCCmec
100
mecA
AB12121 (5)Type 5 ccrClass C mecV
AB097677CommunityType 2 ccrClass B mecIVd
AB096217 (4)CommunityType 2 ccrClass B mecIVc
AB063173 (3)CommunityType 2 ccrClass B mecIVb
AB063172 (3)CommunityType 2 ccrClass B mecIVa
AB37671 (1)HospitalType 3 ccrClass A mecIII
D86934 (1)N315Type 2 ccrClass A mecII
AB033763 (1)HospitalType 1 ccrClass B mecI
GenBank No. and
Reference
Where found
ccr-complexc
mec-complexb
SCCmec types and subtypesa
Current SCCmec types and Type IV subtypes
Modified from Okuma et al J Clin Micro 2002Modified from Okuma et al J Clin Micro 2002
mec complex (A,
B, C, D)
ccr complex (1, 2, 3 & 5: ccrA1-4, ccrB1-4 & ccrC)
type 5 ccr (ccrC)Type V
Type IVcType IVd
ccrC: single copy of a new gene encoded cassette chromosome recombinase
SCCmec types:
J (Junkyard)
Other MRSA naming schemes
Simple CanadaNML
United States
Hospital Acquired
2, 6, 8 100, 200
Community acquired*
10, 7 300, 400
*Very complex wording ..
Hospital associated community acquired MRSA
National Lab has now changed to spa
Why is CA-MRSA 10 different?
No one is sure Some ideas have been put forward
PVL (presence increases from 1.6% to 18%) agr gene changes Enterotoxin H and 15 superantigens Combinations of changes
But from your practice point of view, it is different..
The U.S have very rapidly moved to 59% (Morgan 2006 NEJM) S. aureus infections are MRSA and the “risk” groups are not holding
My patient uses crack cocaine daily and
her partner is MRSA positive
and She says she had an MRSA buttock abscess last year in
Edmonton
My Jan 28th caseWhy is my patient not
improving Smart hospitalists: Start Cloxacillin,
Vancomycin
Why is she not getting better?
U/S show 15 cm!!!! Abscess. Culture grows MRSA. No source control. No control of infection
We will need to get smarter about treating abscess to avoid hVISA,
GISA Paper after paper is saying how
important it is to drain the abscesses.. This takes time
1. What PPE should we use? Should you wear a procedure mask to open an abscess
2. How do we clean the room?
Background MRSA infections can cause worse clinical
outcomes than MSSA infections CNISP reported increased rate of MRSA in
Canadian hospitals from 0.46 to 5.90 per 1000 admissions 1995-2004
Health care costs of MRSA in Canada estimated at $82 million in 2004
Patients with MRSA require prolonged hospitalization (average 26 days)
Goetghebeur M, Landry PA, Han D, Vicente C. (2007). Methicillin-resistant Staphylococcus aureus: A public health issue with economic consequences. Can J Infect Dis Med Microbiol. Vol. 18. No 1. January/February Alberta Government Guidelines 2007
MRSA changes face of oseomyelitis
Gever, June 30, 2008 290 kids with osteomylitis
1999-2001 22.6% MRSA2001-2003 31.1% MRSA
33/290 kids had MRSA osteomyelitis 69% of MRSA had bone abscesses vs 11-
39% of other cause (p < 0.05) Significantly longer median days with
fever, complications, days to normal CRP and Sed rate, days of hospitalization
In the Adult World
Some paper have shown that so long as you anticipate MRSA, that outcomes are similar. My concern is that the patient description makes me think MRSA 2, 6, 8 i.e, the “old” MRSA
Will come back to this in the future section
Strain specific rates (per 100,000), by Month for MRSA in Alberta
(Jan 1, 2006 -Dec 31, 2007)
0 . 0 0
1 . 0 0
2 . 0 0
3 . 0 0
4 . 0 0
5 . 0 0
6 . 0 0
7 . 0 0
8 . 0 0
J a n - 0 7 F e b - 0 7 M a r - 0 7 A p r - 0 7 M a y - 0 7 J u n - 0 7 J u l - 0 7 A u g - 0 7 S e p - 0 7 O c t - 0 7 N o v - 0 7 D e c - 0 7
Rate
(per
100
,000
)
C M R S A 2 ( n = 8 5 5 ) C M R S A 6 ( n = 1 5 8 ) C M R S A 7 ( n = 2 1 8 ) C M R S A 8 ( n = 3 1 ) C M R S A 1 0 ( n = 2 , 0 8 9 )
Alberta Government Guidelines
Strain specific rates (per 100,000), by Health Region for MRSA in Alberta (Jan 1, 2006 -Dec 31, 2007)
Health RegionCMRSA Strain Type
2 4 6 7 8 10
Chinook 53.0 0.0 0.3 14.4 0.6 25.2
Palliser 45.4 0.0 0.0 1.5 0.5 34.7
Calgary 32.0 0.1 0.4 5.8 1.5 59.9
DTHR 62.8 0.3 3.3 3.3 0.3 30.0
East Central 12.1 0.4 5.8 4.5 0.4 15.7
Capital 7.1 0.0 9.4 4.6 0.3 45.5
Aspen 7.0 0.6 8.5 9.0 1.1 32.1
Peace Country 5.4 0.0 2.9 1.8 0.0 59.0
Northern Lights 3.3 0.7 2.0 11.3 1.3 92.0
ALBERTA 24.7 0.1 4.2 5.5 0.8 48.0
Alberta Government Guidelines
MRSA has attracted a lot of government interest
Poster bug for adequacy of infection control
Demonstration project to show effectiveness of government oversight of health care
Much responsibility has been passed along
Limited resources provided
A Balancing Act Try to limit risk to others re transmission
Some would have us lock MRSA positive patients in their rooms
Admitted to take part in a program Day care, schools Rehabilitation Psych Elderly programs
Acute Care, Long Term Care schools have different goals for clients
AHW states
Primary mechanism for transmission of MRSA is via HCWs who are temporarily
colonized with MRSA
But infection control rarely has a single
action that effectively stops an event
Infectious agent
Reservoirs
Portal of exit
Portal of entry
Means of transmission
What is the ability of the host to stop invasion Chain of
Transmission
Framework for Intervention
AHW acknowledges these risk factors for Community
MRSA: the 5 C’s Cleanliness Crowding Contact Sharing Contaminated articles Compromised skin
These are “community risk factors”.
What do they look like as health care risk factors?
AHW acknowledges these risk factors for Community MRSA: the
5 C’s Cleanliness
Can not conduct study because asks pts to be bathed every day
Crowding Over capacity is hard We need 116-170 isolation beds per day in CHR
Contact The “old” MRSA was polite with few family
members ill. The “new” MRSA also affects family members.
Sharing Contaminated articles Staphylococcus is a ubiquitous organism. Toys,
computers, hand rails, pagers, cell phones etc etc Compromised skin
APEC 2006 study
One day prevalence study In 1237 sites or 21% of US healthcare
facilities Looking for all patients know to have
MRSA i.e., patient could be colonized or have an active infection
APEC study results
Rate 16-48 (avg 34) MRSA positive/ 1000 patients or 1.6 to 4.8% of patients (11 x higher than expected) (10-17% of colonized)
Gender 54% male, 46% female Identified by
81% detected by clinical culture19% by surveillance culture
Site 37% skin and soft tissue 63% other
CHR Prevalence studyOr did we have all the MRSA patients correctly isolated?
IPC did a quick study looking at 3 adult units. One unit per site
RGH medicine, FMC orthopedics, PLC palliative and “overflow” medicine
Did Nasal and “Mark of Zoro” on admission and at specified intervals
MRSA is already common in U.S.
MRSA is already here
PLC had the most positives by a long shot
? Exposure in hospital, health care We realized that PLC was different in that
we had 2 individual (Jan and Leah) doing the swabs on the prevalence days and they did GROIN “z” swabs (my fault, I said groin) while FMC and RGH ended “z” at belt level.
? If difference is difference in real life v.s. technique
ACH ER Study
Aug-Dec 2007 All children presenting to ER with
cellulitis or abscess 9/50 (18%) shown to be MRSA positive
If you culture MRSA someone’s skin do they
have an infection?
We all have bacteria on our skin Some bacteria stay on our skin for long time
periods Persistent 20% (range 12-30%) Intermittent 30% (range 16-70%) Non-carrier 50% (range 16-69%)
Some bacteria may be only transiently present and if we do proper hand hygiene (alcohol hand rubs or soap and water) these organisms will not become part of the “normal” organisms on skin-the bacteria are “bounced” off the skin like a rubber ball off a surface
Finding bacteria does not
necessarily mean there is an infection
Only temporarily on skin
“normal” flora, not invading
Local redness, pain, swelling, heat, pus
Systemically ill with fever, chills, rigors sometimes ICU serious
Colonization
Local infection
Systemic infection
Definitions of infectionInvasion and multiplication of micro-organisms
in body tissues associated with tissue destruction or host inflammatory response
Criteria1. Two local findings (redness, warmth,
purulent secretions, pain, tenderness) or2. Superficial soft tissue infection must have
cellulitis (redness of the surrounding skin) or3. Deep infection.. Presence of abscess, septic
arthritis, osteomyelitis, septic tenosynovitis or
4. Systemic symptoms
Deciding what the bacteria on
our skin are doingIf transient bacteria become resident bacteria
May colonizei.e., present but
not invadingMay cause an infection
Mom’s criteria105 organism/ gm
of tissue> 1 ml of pus
redness, warmth, purulent secretions,
pain, tenderness
If you order a swabWhy are you ordering it
To see if Colonizedi.e., present but
not invading
To identify the cause of an infection
MRSA surveillanceswab
Report will say Yes MRSA present or
No MRSA found
Order Wound swab
Report will tell what Antibiotics you can use
Remember chronic ulcers will chronically grow bacteria GO BACK 1 SLIDE if do not know if colonization or infection
Lab report says MRSA positive
What does that mean?
Why was the swab taken?Clinically what does the pt look like
No obvious infectionPatient colonized
Mom says infectedUse results to help guide
therapy for an infected wound
Patient needs to be placed under contact precautions
You do not need To order any further
MRSA screening swabsIPC will order
Use informationto treat infection
(infectious diseases)
What does Treatment look like for MRSA 10?
Septra Population has 8% rash rate Causes problems with breast feeding
moms Premies do not do well Issues with G-6PD deficiency
Clindamycin: Not good if local C. difficile happens to
be F strain (very high association with Clindamycin
Tastes terrible as liquid
What does Treatment look like for MRSA 10? Tetracyclines
Are not given to young children Vancomycin
IV medication Linezolid
PO or IV Currently must fail Vancomycin to get Issues re hemogloblin
In the Adult HPTP World
Ancef Some people fail on Day 3 ??? Had mixed MSSA and
MRSA infection. Ancef kills MSSA but leaves MRSA untouched
Ancef + Septra (Tetracycline, clindamycin) Ancef + clindamycin works well with the “aggressive
MSSA + Group A strep” cellulitis + Group A Ancef + Vancomycin
Cellulitis in face ICU patient with Staph in blood
Vancomycin Pt known to have MRSA
Colonization has been associated with subsequently developing
infection Reported rates have varied
Low 15% High > 30% Nosocomial bacteremia rate RR 30 (NEJM 2001, von Eiff) SSI 2-9 fold increase risk of infection (but decolonization
pre-op mupirocin did not decrease risk) Renal patients (meta-analysis)
Decrease by 78% risk of BSI in hemodialysis patients
Decrease by 66% risk of BSI in peritonneal dialysis patients
Tacconelli 2003 Clin Infect Dis
Should we decolonize patients because colonized patients have a high risk of
developing an active infection
What is Decolonization?
Use of topical and/or systemic agents to eradicate/reduce MRSA carriage on skin and mucus membranes
Purpose is to reduce risk of transmission in healthcare settings
Efficacy dependent on multiple factors related to the patient e.g. health status, wounds, foreign bodies, feeding tubes, compliance
To Decolonize or Not
Who should we try to decolonize
All patients? Choose subsets of patients
All patients with access lines? All patients with more than 3 infections in six
months? All patients who will be compliant
No patient Cazaban 2007 ICHE looked at outcomes. If had
non-pneumonia MRSA infection in hospital no worse outcome than MSSA. Just be smarter when we treat
How Has Decolonization Been Done
Most reviews do not support intranasal mupirocin alone UNLESS short term use for patients about to undergo major surgery
(e.g. cardiac, ortho) OR conventional methods have failed to control an outbreak
(e.g. NICU) Multiple agent intervention more successful and
generally used for very selected patient populations or HCWs (e.g. surgeons). Generally use combinations of mupirocin, CHG, and if susceptible combos of clindamycin or SXT or rifampin
How Has Decolonization Been Done
Most groups have used nasal mupirocin + 2% CHG body washes
Some groups have used PO Vancomycin to resolve GI carriage Some have treated positive urine
2nd commonest first clinical isolate in CHR is urine (Dan Gregson)
Some have treated positive vaginal culture Some have treated positive throat cultures
Andy Simor’s StudyClin Infect Dis 2007
2% CHG wash 2% intranasal mupirocin Rifampin x 7 days Doxycycline x 7 days
(can TB land tolerate this medical use of their VERY IMPORTANT drug)
Andy’s results
Significant eradication at 3 months 75% with program, 32% without
At 8 months 54% still negative (so 21% returned to
be positive)
My roadside conversations with Tom Louie
Yes you can decolonize MRSA 2 Interesting because are the folks with
the “holes” (stasis ulcer, PEGs etc) Very hard to decolonize MRSA 10
2% CHG in nares works better than mupirocin
The “core” patients are not in easy to do locations
Can you do this in the high risk areas of jails, drop in centers, ER, Urgent Care
Can you do this in high risk clinical areas (HPTP, SAC, STI)
We couldn’t do it the acute care settings and Tom responded by making an outpatient clinic
Summary RecommendationsFor Decolonization
No group or organization has supported decolonization for all patients
Some support for selected Decolonization (if mupirocins) Dialysis patients Recurrent infections Infection control measure
Do Not use routine decolonization in pre-op or non-surgical patients
Good Hand
Hygiene as
prevention
remains good
plan but can we
do it
Transient floraResident flora
Good Hand Hygiene for everyone
Start of activity, End of activity
StaffPatients
VolunteersVisitors
Are we now where we were in the early 1980s with HIV?In the 1980’s we learnt that we could
not tell if someone is HIV positive or not
VIEW ALL BLOOD AND BODY SUBSTANCES as potentially carrying BLOODBORNE PATHOGENS
Should we assume that everyone and everything is
MRSA positive?
MRSA prevalence rates are growing in the community
Risk factor are breaking down No magic way to detect MRSA
Here are four actions you can take to protect your children
from MRSA1. If your child has a booboo, put a
bandage on it. MRSA is usually spread by skin-to-skin contact. Bandages protect broken skin from MRSA and also reduce the risk of spreading MRSA to family members and friends if a wound already is infected.
Here are four actions you can take to protect your children
from MRSA2. Wash your hands with soap and water, and don't be timid about nagging kids to wash their hands, too. Boring, but it works.
If you are cleaning a woundClean potentially contaminated surfaces with ¼ cup bleach(5.25%) to 4 gallons of water)
Wear gloves when cleaning a wound but REMEMBER you MUST ALSO WASH your hands.
Here are four actions you can take to protect your children
from MRSA3. Discourage sharing of towels,
razors, and other hygiene items, which are often implicated in MRSA outbreaks. That's one reason MRSA outbreaks have been more common in school athletic teams. This could be the best way ever to scare boys off towel-snapping! Also, tell kids not to share clothes or other personal items.
Here are four actions you can take to protect your children
from MRSA4. Call the doctor ASAP if a family
member has a skin infection and also a fever. Most staph infections look like a bump or infected area that is red, swollen, painful, and warm to the touch. Rapid treatment with the right antibiotics makes it easier to get rid of the bug.
Will MRSA always be anAntibiotic Resistant Organism?
12 Classes of anti-S. aureus drugs Class Oral (n=9 ) IV (n=12)
Penicillin Cloxacillin Cloxacillin
Cephalosporin Keflex Ancef
Carbapenum Meropenum
Sulfa “septra” “septra”
Macrolides All Azithromycin
Lincomycins Clindamycin Clindamycin
Tetracyclines All
Glycopeptide Vancomycin
Quinolones Not cipro* Levo, Moxi
Others LinezolidFusidic AcidRifampin
Linezolid, Tigecycline, Daptomycin, Synercid
*CIPRO has an MIC that just works but that also means it often fails against S. aureus. Spain has a > 30% resistance rate
**Rifamycins work but not alone
New Anti Staph AgentsAntimicrobial
AgentClass Route of
Administration
Ceftobiprole Cephalosporin IV
Ceftaroline Cephalosporin IV
Cethromycin Ketolide Oral
Dalbavancin Lipoglycopeptide IV
Doripenem Carbapenem
IV
Iclaprim Diaminopyrimidine IV
Oritavancin Glycopeptide IV
Prulifloxacin Quinolone Oral
Telavancin Lipoglycopeptide IV
The Future Infectious diseases is hoping that the new
IV cephalosporins and carbapenem are as good as we think
The new cephalosporins target the PBP2’ i.e., the PBP that Mec A makes
Side effects-Ceftobiprole (rash, nausea, bad taste) -Ceftaroline (mild headache)
We hope that at some of the other drugs in development pan out, a new oral agent would be wonderful
These are very broad spectrum antibiotics
Question for 2010-2012
At some point in the not distant future we will have more MRSA than MSSA. MRSA will become our new “Norm” of S. aureus
We will have at least 3 new antibiotics from 2 classes that will be bactercidal for MRSA
Could we “de ARO” MRSA as we did in the 1960’s re penicillin resistant S. aureus?
Could we “de-ARO” MRSAPro Scientifically, likely yes The system does not have enough beds
or staff to deal with private rooms needsCon Would likely die in the media Government has a lot at stake We should not be transmitting organisms
MRSA Outbreak reporting
Any person who knows or has reason to suspect the existence of MRSA: In epidemic form; Occurring at an unusually high rate; or That is caused by a nuisance or other
threat to public health, Shall immediately notify the regional
MOH by the fastest means possible
Alberta Government Guidelines
Summary
Failure to quickly and appropriately treat serious infections will result in poor
patient outcomes.
In mid 2007, 35% of ER isolates of S. aureus were MRSA
18% kids MRSA swab positive 2007
CA-MRSA 10 will likely permanently alter S. aureus’
disease profileThere will be more abscesses and soft tissue infection More person to person transmission
(gene(s) from CoNS) 10% of the infections will be very serious (?
new pathogen markers) Repeat infection since MRSA 10 seems to
result in a poor antibody response Very high rate of colonization becoming
infection
Very different from MRSA 2, 6, 8Very different from MRSA 2, 6, 8
I do not believe we have seen all that MRSA 10 will
do CHR had a really nasty episiotomy MRSA
infection. I think we may see MRSA looking like Group B Streptococcus and Listeria in newborns because I think the Europeans are correct, MRSA 10 is carried in the vagina
There is an increasing sense that MRSA 10 are sexually transmitted infections
I do not believe we have seen all that MRSA 10 will
do S. aureus causes secondary bacterial
pneumonias after influenza infections. We have not yet had a bad influenza year to go sour with secondary MRSA pneumonia
We have not really seen MRSA prosthetic joint infections yet. The paper on osteomyelitis suggests this may be very true.
http://www.cps.ca/English/surveillance/cpsp/studies/Questionnaire/MRSA.pdf
CANADIAN PAEDIATRIC SURVEILLANCE PROGRAM
Please complete the following sections for the case identified above. Reporting to the CPSP does not preclude
a responsibility to report cases of MRSA directly to the province according to each province’s legislation
on notifiable disease reporting. Patient and reporter information will be kept confidential.
2305 St. Laurent Blvd.Ottawa, ON K1G 4J8
Tel: 613-526-9397, ext. 239 Fax: 613-526-3332 [email protected] or www.cps.ca/cpsp
Questions?
ReferencesGuidelines for the prevention and management of
CA-MRSA: a perspective for Canadian health care practitioners
Can J Infect Dis Med Microbiol 2006 (supplC): 4c-24c
Control and treatment of MRSA in Canadian paediatric health care institutions.
Paediar Child Health 2006;11:163-165
Ca-MRSA: Implications for the Care of Children Paediatrics and Child Heatlh 2007;12(4) 323-324
Consensus Statement for the management of MRSA infections in Neonatal ICUs Susan Gerber
ICHE Feb 2006 27(2): 139-145
CDC Sept 8, 2008launched program to teach parents about MRSA