Community Associated MRSA, CA-MRSA

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    Dr.T.V.Rao.MD

    COMMUNITY ASSOCIATED- MRSA(CA-MRSA)

    DR.T.V.RAO MD 1

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    Staphylococci: Gram positive cocci( from Greek staphyle, means bunch of

    grapes ) that occur singly and in pairs,

    short chains and irregular grape-likeclusters.

    DR.T.V.RAO MD 2

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    MRSA Discovered in 1981 Found on skin and in the nose of 1 in 3

    healthy people - symptomless carriers

    Widespread in hospitals andcommunity

    Resistant to most antibiotics

    When fatal - often due to septicaemia

    DR.T.V.RAO MD 3

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    METHICILLIN RESISTANT

    STAPHYLOCOCCUS Methicillin-resistant Staphylococcus aureus

    (MRSA) are identified as nosocomial pathogens

    throughout the world . Established risk factors

    for MRSA infection include recent hospitalizationor surgery, residence in a long-termcare facility,

    dialysis, and indwelling percutaneous medical

    devices and catheters. Recently, however, casesof MRSA have been documented in healthy

    community-dwelling persons without established

    risk factors for MRSA acquisition.DR.T.V.RAO MD 4

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    Healthcare system is evolving to an increased use of outpatientprocedures and long-term care

    Many long-term-care facilities now experience infection rates comparable to thosein acute hospital settings

    Outbreaks are common

    High rates of colonization with resistant strains

    THE LANDSCAPE OF

    HEALTHCARE-ASSOCIATED (HCA) INFECTIONS

    Nicolle LE. Clin Infect Dis. 2000;31:752-756.

    Hospital or

    Acute care setting

    Home careOutpatient facility

    Long-term-care facility

    DR.T.V.RAO MD 5

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    S. aureus

    Penicillin

    [1950s]

    Penicillin-resistant

    S. aureus

    EVOLUTION OF DRUG RESISTANCE IN S. AUREUS

    Methicillin

    [1970s]

    Methicillin-resistant

    S. aureus(MRSA)

    Vancomycin-resistant

    enterococci (VRE)

    Vancomycin

    [1990s]

    [1997]

    Vancomycin

    intermediate-resistantS. aureus(VISA)

    [ 2002 ]

    Vancomycin

    -resistant S.aureus

    DR.T.V.RAO MD 6

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    0

    10

    20

    30

    40

    50

    60

    1989

    1991

    1993

    1995

    1997

    1999

    2001

    2003

    2005

    PercentRe

    sistance

    Methicillin-ResistantStaphylococcus aureus (MRSA)

    U.S. Non-Intensive Care

    U.S. Intensive CareThe Nebraska Medical Center

    Source: National Nosocomial InfectionsSurveillance (NNIS) System

    DR.T.V.RAO MD 7

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    INFECTION CLASSIFICATION

    Infections historically identified as community acquiredor hospital acquired, based on location and time of symptom

    onset

    Community-acquired (CA): hospitalization 48 hours

    Hospital-acquired (HA): hospitalization > 48 hours

    Associated with inherent assumptions:Hospital-acquired infectionsCommunity-acquired infections

    Patients with compromised defenses

    Environment with resistant microorganisms

    Often associated with invasive devices or

    medical procedures

    Otherwise healthy patients

    Environment with little selective pressure,

    fewer resistant microorganisms

    Develop spontaneously

    Siegman-Igra Y, et al. Clin Infect Dis. 2002;34:1431-1439.

    DR.T.V.RAO MD 8

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    They are apparently acquired in the

    community, these infections are

    referred to as community-acquired

    (CA)-MRSA (. CA-MRSA infections

    have been reported in North

    America, Europe, Australia, and New

    Zealand . The recent genomic

    sequence of a CA-MRSA isolate

    indicated the presence not only of a

    novel smaller variant of the

    methicillin-resistance locus(SCCmecIVa, according to Baba et

    al. designation , but also that of the

    locus for the Panton-Valentine

    leukocidin (PVL).

    COMMUNITY ACQUIRED MRSA

    DR.T.V.RAO MD 9

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    TERMINOLOGY OF CA-MRSA

    DR.T.V.RAO MD 10

    Terminology has been inconsistent Community-Onset

    (CO) MRSA: infection

    diagnosed or index culture collected in community

    Established risk factors (RFs): recent hospitalization,surgery, dialysis, long-tern care; indwelling catheter or

    percutaneous medical device; history of MRSA

    Community-Acquired MRSA: Used for CO infections or CO

    infections in patients without established RFs, but difficultto establish with certainty where acquisition occurred

    Community-Associated MRSA: CO infections in persons

    without established RFs

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    CA-MRSA: A COMPLEX ISSUE Epidemiologic and clinical risk factors cannot reliably

    distinguish between MRSA and

    MSSA in patients with community-acquired

    S aureus infections

    CA-MRSA strains are emerging with resistance to some

    non--lactam classes of antibiotics

    Strains resistant to fluoroquinolones and

    aminoglycosides have been isolated

    The distinction between CA- and HA-MRSA strains is

    blurring

    1. Miller LG, et al. Clin Infect Dis. 2007;44:471-482. 2. Del Giudice P, et al. Br J Dermatol. 2006;154:118-124. 3. Gonzalez BE, et al. Infect Control Hosp Epidemiol.

    2006;27:1051-1056. 4. Klevens RM, et al. Emerg Infect Dis. 2006;12:1991-1993. 5. Maree CL, et al. Emerg Infect Dis. 2007;13:236-242.

    DR.T.V.RAO MD 11

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    COMMUNITY-ASSOCIATED MRSA Methicillin-resistant S aureus strains are endemic in

    many communities

    Strains from the community may be referred to as either

    community-associatedorcommunity-acquired(CA) MRSA

    CA-MRSA is genetically different from the strains normally

    associated with hospital-acquired infections

    CA-MRSA first emerged in the 1990s

    Outbreaks of CA-MRSA have been reported2

    CA-MRSA infections most often involve skin

    and soft tissue1-3

    1. Zetola N, et al. Lancet Infect Dis. 2005;5:275-286. 2. McDonald LC. Clin Infect Dis. 2006;42:S65-S71. 3. Naimi TS, et al. JAMA. 2003;290:2976-2984.

    DR.T.V.RAO MD 12

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    GROWING INCIDENCES OF CA-MRSA Patients with HCA infections have an increased risk

    of infection with MRSA compared to patients with CAinfections

    Identifying and treating patients in a timelymanneris critical

    The prevalence of MRSA is increasing in the community and hospital

    settings

    Infection with MRSA is associated withnegative outcomes

    MRSA is frequently associated with

    inappropriate treatmentDR.T.V.RAO MD 13

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    WHATS DIFFERENT ABOUTCA-MRSA?

    SCCmec IV (V) is mobile and in variety ofbackground strains

    Replicate more rapidly than HA-MRSA (23 minvs 46 min) More fit than HA-MRSA

    MW2 sequence vs 5 HA-MRSA reveal 19putative virulence genes: 4 Enterotoxins, 11exotoxins (PVL), collagen adhesin, etc. Morevirulent?

    LD is 5x less than HA-MRSA (no single geneappears responsible)

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    Necrotizing cytotoxin

    Associated withabscesses and severe

    pneumonia Also found in some

    methicillinsusceptible

    S. aureus (MSSA)isolates

    PANTON-VALENTINE LEUKOCIDIN

    (PVL) TOXIN

    DR.T.V.RAO MD 15

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    COMMON CLINICAL PRESENTATIONS OF CA-MRSA

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    RECURRENT FURUNCULOSIS

    Very little data indicating long-term benefit of decolonizationregimens. Toxicity/cost/resistance

    Combination of topical, mucosal, and systemic antibiotics: Oral TMP-SMX, nasal mupirocin, chlorhexidine showers x 5d

    Bleach baths (1 teaspoon of bleach per gallon of water) x 10minutes 2 times/wk

    Environmental cleaning (bedclothes, towels, surfaces)

    Close contacts? Pets? Environment?

    DR.T.V.RAO MD 17

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    WHAT IS PVL (PANTON-VALENTINE

    LEUKOCIDIN)?

    1st described in 1932

    Bicomponent synergistic membrane-tropic toxin

    Encoded by lukS-PV and lukF-PV genes

    Assembled as hetero-oligimers thatsynergistically act to form pores in cell

    membranes (lysis) of pmns andmonocytes/macrophages

    Associated with necrotizing skin and soft tissueinfections and pneumonia

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    The PVL locus iscarried on a

    bacteriophage and is

    present in only a small

    percentage ofS. aureus

    isolates from France,

    where this locus is

    associated with skininfections, and

    occasionally, severe

    necrotizing pneumonia

    LOCATION OF PANTON-VALENTINE LEUKOCIDIN (PVL).

    DR.T.V.RAO MD 19

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    Nosocomial infection

    Community-acquired infection

    Methicillin-resistant S aureus

    0

    25

    50

    75

    100

    1970 1980 2000

    Year

    Resistantisolates(%)

    1990

    Nosocomial infection

    Community-acquired infection

    Methicillin-resistant S aureus

    0

    25

    50

    75

    100

    1970 1980 2000

    Year

    Resistantisolates(%)

    1990

    Nosocomial infection

    Community-acquired infection

    Methicillin-resistant S aureus

    0

    25

    50

    75

    100

    1970 1980 2000

    Year

    Resistantisolates(%)

    1990

    Prevalence of MRSA

    increasing in hospitals

    and in the community1

    INFECTIONS DUE TO COMMUNITY- AND

    HEALTHCARE-ASSOCIATED MRSA

    1. McDonald LC. Clin Infect Dis. 2006;42:S65-S71. 2. Naimi TS, et al. JAMA. 2003;290:2976-2984.

    Infections associatedwith CA-MRSA (n = 131)2

    Infections associatedwith HA-MRSA (n = 937)2

    Skin/Soft tissue 75%

    Otitis media/externa7%

    Respiratory tract 6%

    Bloodstream 4%

    Urinary tract 1%

    Other 8%

    Skin/Soft tissue 75%

    Otitis media/externa7%

    Respiratory tract 6%

    Bloodstream 4%

    Urinary tract 1%

    Other 8%

    Skin/Soft tissue 37%

    Otitis media/externa 1%

    Respiratory tract 22%

    Bloodstream 9%

    Urinary tract 20%

    Other 12%

    Skin/Soft tissue 37%

    Otitis media/externa 1%

    Respiratory tract 22%

    Bloodstream 9%

    Urinary tract 20%

    Other 12%

    Infections associatedwith CA-MRSA (n = 131)2

    Infections associatedwith HA-MRSA (n = 937)2

    Skin/Soft tissue 75%

    Otitis media/externa7%

    Respiratory tract 6%

    Bloodstream 4%

    Urinary tract 1%

    Other 8%

    Skin/Soft tissue 75%

    Otitis media/externa7%

    Respiratory tract 6%

    Bloodstream 4%

    Urinary tract 1%

    Other 8%

    Skin/Soft tissue 37%

    Otitis media/externa 1%

    Respiratory tract 22%

    Bloodstream 9%

    Urinary tract 20%

    Other 12%

    Skin/Soft tissue 37%

    Otitis media/externa 1%

    Respiratory tract 22%

    Bloodstream 9%

    Urinary tract 20%

    Other 12%

    DR.T.V.RAO MD 20

    DECIPHERING MRSA STRAINS

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    DECIPHERING MRSA STRAINS:HA-MRSA VS. CA-MRSA

    HA-MRSA CA-MRSA

    Genetic characteristics SCC mectype I, II, or III SCC mectypeIV

    Commonresistance

    -lactamsMacrolides

    AminoglycosidesQuinolones

    Lincosamides

    -lactams

    Macrolides

    Panton-Valentine

    leukocidin (PVL)exotoxinNot common Common

    1. Carleton HA, et al. J InfectDis. 2004;190:1730-1738. 2. Drew RH. Pharmacotherapy. 2007;27:2027-249. 3. Zetola N, et al. Lancet Infect Dis. 2005;5:275-286. 4. Klevens RM, et al.

    Emerg Infect Dis. 2006;12:1991-1993.

    HA-MRSA = strains first isolated in the hospital (nosocomial pathogen);

    CA-MRSA = strains first isolated in the community setting.

    DR.T.V.RAO MD 21

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    PANTON-VALENTINE LEUKOCIDIN

    Panton-Valentine leukocidin (PVL) is a cytotoxinone of the

    -pore-forming toxins. The presence of PVL is associated with

    increased virulence of certain strains (isolates) of

    Staphylococcus aureus. It is present in the majority of

    community-associated Methicillin-resistant Staphylococcusaureus (CA-MRSA) isolates studied] and is the cause of

    necrotic lesions involving the skin or mucosa, including necrotic

    hemorrhagic pneumonia. PVL creates pores in the membranes

    of infected cells. PVL is produced from the genetic material of abacteriophage that infects Staphylococcus aureus, making it

    more virulent.

    DR.T.V.RAO MD 22

    http://en.wikipedia.org/wiki/Panton-Valentine_leukocidinhttp://en.wikipedia.org/wiki/Panton-Valentine_leukocidin
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    PANTON-VALENTINE LEUKOCIDIN (PVL)

    Panton-Valentine leukocidin (PVL) is one of many

    toxins associated with S. aureus infection. Because it

    can be found in virtually all CA-MRSA strains that

    cause soft-tissue infections, it was long described as akey virulence factor, allowing the bacteria to target and

    kill specific white blood cells known as neutrophils. This

    view was challenged, however, when it was shown that

    removal of PVL from the two major epidemic CA-MRSAstrains resulted in no loss of infectivity or destruction of

    neutrophils in a mouse model.[

    DR.T.V.RAO MD 23

    http://en.wikipedia.org/wiki/Panton-Valentine_leukocidinhttp://en.wikipedia.org/wiki/Panton-Valentine_leukocidin
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    CA-MRSA: Whats Going On?

    SCCmec I-V, mecIV is most commonly found in CA-MRSA; 25 KB,

    mobileDR.T.V.RAO MD 24

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    Patients with MRSA infection

    (n = 100 isolates)

    Infection

    with typical

    CA-MRSA

    strain

    Healthcare-related risk factors?

    Yes

    (n = 73)

    No

    (n = 27)

    Infection

    with typical

    HA-MRSA

    strain

    Infection

    with typical

    CA-MRSA

    strain

    Infection

    with typical

    HA-MRSA

    strain

    22%

    (16/73)

    70%

    (19/27)

    77%

    (56/73)

    26%

    (7/27)

    Patients with MRSA infection

    (n = 100 isolates)

    Infection

    with typical

    CA-MRSA

    strain

    Healthcare-related risk factors?

    Yes

    (n = 73)

    No

    (n = 27)

    Infection

    with typical

    HA-MRSA

    strain

    Infection

    with typical

    CA-MRSA

    strain

    Infection

    with typical

    HA-MRSA

    strain

    22%

    (16/73)

    70%

    (19/27)

    77%

    (56/73)

    26%

    (7/27)

    DISTINCTION BETWEEN CA-MRSA

    AND HA-MRSA IS BLURRING

    Klevens RM, et al. Emerg Infect Dis. 2006;12:1991-1993.

    CA-MRSA strains are emerging in the healthcare setting, while

    HA-MRSA strains are moving out into the community

    DR.T.V.RAO MD 25

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    THE DISTINCTION BETWEEN CA AND HA

    IS BLURRING!

    Characterized 132 cases of MRSA BSI in Atlanta

    34% of MRSA were USA 300

    28% of pts with HA BSI factors

    20% of pts with nosocomial BSI

    0%

    20%

    40%

    60%

    80%

    100%

    Total (n=116) HA (n=107) Noso (n=49)

    USA800

    USA500

    USA100USA300

    Seybold U, et al. ClinInfect Dis, 2006

    DR.T.V.RAO MD 26

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    1. In all pus forminglesions

    Gram stain andculture of pus

    2. In all systemicinfections

    Blood culture

    3. In infections of other

    tissues Culture of relevant

    tissue or exudate

    DIAGNOSIS

    DR.T.V.RAO MD 27

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    On isolating any MRSA strains

    with clinical and epidemiological

    suspicion of CA-MRSA, further

    laboratory characterization

    needs to be undertaken to

    support the diagnosis. SCCmectyping is performed by

    determining the combination of

    two attributes: the class of the

    mecgene complex, and with the

    type of the ccr(chromosomalcassette recombinase) gene

    complex

    CA-MRSA DIAGNOSIS

    DR.T.V.RAO MD 28

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    The mecgene complex,

    comprises classes A to C,

    and the latter comprises

    types 1 to 3. The technique

    employed is polymerasechain reaction (PCR), either

    using individual reactions or

    in a multiplex format.9-11 In

    addition, the presence ofthe PVL gene is also

    detected by PCR.

    CA-MRSA DIAGNOSIS

    DR.T.V.RAO MD 29

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    SENSITIVITY AND RESISTANCE PATTERNS

    OF STAPHYLOCOCCUS AUREUS

    MRSA

    DR.T.V.RAO MD 30

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    Community-associated

    methicillin-resistant

    Staphylococcus aureus strain

    (note golden colour) showing

    resistance to -lactams and

    susceptibility to multipleantimicrobials. Key: Resistant

    to penicillin (P) and cefoxitin

    (FOX); Susceptible to

    erythromycin (E), clindamycin

    (DA), gentamicin (CN),tetracycline (TE),

    chloramphenicol

    (C),ciprofloxacin (CIP),

    rifampicin (RD) and

    cotrimoxazole (SXT).

    CA-MRSA DIAGNOSIS

    DR.T.V.RAO MD 31

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    PLATE 1B: A MECA GENE NEGATIVE STAPHYLOCOCCUS AUREUSWITH HIGH B-LACTAMASE ACTIVITY SHOWING BORDERLINE RESISTANCE TO OXACILLIN

    (BORSA) WHILST THERE IS AN INHIBITORY ZONE OF 7.5 MM AROUND THE CEFOXITIN

    (FOX 10) DISC.DR.T.V.RAO MD 32

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    NON-MULTIPLE RESISTANT MRSA SUSCEPTIBLE

    TO COTRIMOXAZOLE

    DR.T.V.RAO MD 33

    : A MECA GENE POSITIVE STAPHYLOCOCCUS AUREUS(MRSA) BUT LACKING

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    : A MECA GENE POSITIVE STAPHYLOCOCCUS AUREUS(MRSA) BUT LACKING B-LACTAMASE ACTIVITY. NOTE THE LARGE ZONES AROUND PENICILLIN (P 0.5) AND

    OXACILLIN (OX 1) DISCS BUT THE REDUCED INHIBITORY ZONE AROUND CEFOXITIN

    (FOX 10).

    DR.T.V.RAO MD 34

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    : MRSA WITH INDUCIBLE CLINDAMYCIN RESISTANCE (ICR): NO INHIBITORY

    ZONE AROUND ERYTHROMYCIN (E 5) AND A FLATTENED INHIBITORY ZONE

    AROUND CLINDAMYCIN (DA 2) NEAR THE ERYTHROMYCIN DISC.

    DR.T.V.RAO MD 35

    : STAPHYLOCOCCUS AUREUS NCTC 6571 NOTE THE APPROXIMATE

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    : STAPHYLOCOCCUS AUREUSNCTC 6571. NOTE THE APPROXIMATE

    INHIBITORY ZONE SIZES AROUND PENICILLIN (P 0.5), CEFOXITIN (FOX

    10) AND VANCOMYCIN (VA 5) DISCS ARE 12 MM, 10 MM AND 3 MM

    RESPECTIVELY

    DR.T.V.RAO MD 36

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    PLATE 4: MRSA WITH REDUCED SUSCEPTIBILITY TO VANCOMYCIN (VISA/GISA).

    NOTE THE REDUCED ZONE AROUND VANCOMYCIN (VA 5) AND TEICOPLANIN (TEC

    15) DISCS.DR.T.V.RAO MD 37

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    Further typing ofCA-MRSAstrains is possible using various

    methods, including pulsed-field

    gel electrophoresis (PFGE),

    multilocus sequence typing

    (MLST) and S. aureus protein A

    (spa) typing.5,12 These methods

    are employed when it is

    necessary to delineate

    epidemiological relationships

    among CA-MRSA strains isolatedfrom different sources, such as in

    outbreak settings

    EPIDEMIOLOGICAL TYPING

    DR.T.V.RAO MD 38

    OPTIMIZING INITIAL

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    OPTIMIZING INITIAL

    ANTIMICROBIAL THERAPY

    Initial therapy is often empiric and should cover all pathogensthat may be present

    Knowledge of underlying risk factors for antimicrobial

    resistance and local Antibiogram contribute to correct

    treatment choice

    Appropriate antimicrobial therapy includes an agent or regimen

    that is effective against the causative pathogen(s)

    Broad-spectrum therapy is often recommended

    Adequate empiric therapy should not be delayed

    1. Kollef MH. Drugs 2003;63(20):2157-2168. 2. The American Thoracic Society and the Infectious Diseases Society of America.Am J Respir Crit Care Med. 2005;171:388-416.

    DR.T.V.RAO MD 39

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    TREATING MRSA INFECTIONS

    Agents with anti-MRSA activity include:

    Limitations of some agents include:

    Emerging resistance, changing susceptibilities

    Bacteriostatic rather than bactericidal activity

    Decreased penetration or inactivity in some tissues

    (eg, lung)

    Side effects/toxicity

    Drew RH. Pharmacotherapy. 2007;27:227-249.

    TMP-SMX = trimethoprim-sulfamethoxazole.

    Vancomycin Linezolid Daptomycin

    Tigecycline TMP-SMX Clindamycin

    Vancomycin Linezolid Daptomycin

    Tigecycline TMP-SMX Clindamycin

    DR.T.V.RAO MD 40

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    TREATMENT OF CA-MRSA

    Most disease is skin & soft tissue (75% - 80%)

    Data suggests that many cases can be treated

    with I&D without Abx

    73% of pts in one study received antibiotics to

    which the organisms was resistant. No difference

    in number of follow-up visits, subsequent need forI&D, or change in antibiotic therapy (Fridkin, NEJM,

    2005)

    DR.T.V.RAO MD 41

    TREATMENT ALGORITHM: DISTINGUISHING

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    TREATMENT ALGORITHM: DISTINGUISHINGBETWEEN HCA AND CA INFECTIONS IS A CRITICAL

    STEP

    1. American Thoracic Society.Am J Respir Crit Care Med. 2005;171:388-416. 2. Mandell LA, et al. Clin Infect Dis. 2007;44:S27-S72.

    Treat with: Extended spectrum antipseudomonal

    cephalosporin, carbapenem,or -lactam/-lactamase inhibitor

    +

    Antipseudomonal fluoroquinoloneor aminoglycoside

    +/- Anti-MRSA agent

    Patient presents to hospital with suspected pneumonia

    Underlying risk factors for healthcare-associated infection?

    Recent hospitalization Residence in nursing home

    Home infusion therapy Chronic dialysis

    Home wound care Family member with resistant pathogen

    Community-acquired

    pneumonia suspected

    Treat with (non-ICU treatment): Respiratory fluoroquinolone

    or -lactam + macrolide

    Healthcare-associated

    pneumonia suspected

    NoYes

    Note: Local prevalence and susceptibilitypatterns should be used when choosing an

    empiric antibiotic regimen

    Treat with: Extended spectrum antipseudomonal

    cephalosporin, carbapenem,or -lactam/-lactamase inhibitor

    +

    Antipseudomonal fluoroquinoloneor aminoglycoside

    +/- Anti-MRSA agent

    Patient presents to hospital with suspected pneumonia

    Underlying risk factors for healthcare-associated infection?

    Recent hospitalization Residence in nursing home

    Home infusion therapy Chronic dialysis

    Home wound care Family member with resistant pathogen

    Community-acquired

    pneumonia suspected

    Treat with (non-ICU treatment): Respiratory fluoroquinolone

    or -lactam + macrolide

    Healthcare-associated

    pneumonia suspected

    NoYes

    Note: Local prevalence and susceptibilitypatterns should be used when choosing an

    empiric antibiotic regimen

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    0 4 8 12 24 36 4810

    2

    103

    104

    105

    106

    107

    108

    109

    1010

    Bacteria[CFU/mL]

    Time (hours)

    LinezolidRifampin

    SXT

    SXT+Rifampin

    Clindamycin

    Minocycline

    Control

    Time-kill curves for all isolates of MethicillinResistant Staphylococcus Aureus (12)

    Kaka, et al

    IDSA, 2005

    DR.T.V.RAO MD 43

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    DR.T.V.RAO MD 44

    NEW DRUGS ON TRAILS FOR USE

    IN STAPHYLOCOCCAL INFECTIONS

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    INVESTIGATIONAL

    ANTI-STAPHYLOCOCCAL ANTIBIOTICS

    Glycopeptides

    Ortivancin (Intermune)

    Dalbovancin (Vicuron)

    Telavancin (Theravance)

    DHFR inhibitor

    Iclaprim (Arpida)

    Novel B-lactams Ceftobiprole

    BMS-247243, RWJ 54428, CB-181963, BAL 5788, S-3578

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    OTHER POTENTIALANTI-STAPHYLOCOCCAL AGENTS

    Capsule 5/8 Vaccine (NABI): - FDA fast tracked announced 10/12/04;Halt in development 11/05

    Staph capsule IG (NABI & Biosynexus) (Halt 11/05)

    Lysostaphin (Biosynexus)

    Aurexis (Inhibitex) anti-ClfA

    Veronate (Inhibitex) Adhesin Ab (neonates)

    Aurograb (NeuTec) Ab vs ABC transporter

    Peptide deformylase inhibitors

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    Cover all wounds

    Train athletes in first aid for

    wounds and signs of infection

    Encourage good hygiene

    Discourage sharing of items

    Establish routine cleaning

    schedules for shared

    equipment

    Encourage players to reportskin lesions

    PREVENTION AND CONTROL

    DR.T.V.RAO MD 47

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    Multi-component strategies

    used (difficult to assess

    individual contribution of

    each)

    Strategies focusing on

    increased awareness, early

    detection and appropriate

    management, enhanced

    hygiene, and maintenance ofa clean environment appear

    to have been successful at

    interrupting transmission

    CA-MRSA OUTBREAK CONTROL

    MEASURES

    DR.T.V.RAO MD 48

    UNIVERSAL INFECTION

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    UNIVERSAL INFECTION

    CONTROL PRECAUTIONS

    Devised in US in the 1980s in response togrowing threat from HIV and hepatitis B

    Not confined to HIV and hepatitis B Treat ALL patients as a potential bio-hazard

    Adopt universal routine safe infectioncontrol practices to protect patients, selfand colleagues from infection

    DR.T.V.RAO MD 49

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    UNIVERSAL PRECAUTIONS Hand washing

    Personal protective equipment [PPE]

    Preventing/managing sharps injuries

    Aseptic technique

    Isolation Staff health

    Linen handling and disposal

    Waste disposal

    Spillages of body fluids

    Environmental cleaning

    Risk management/assessment

    DR.T.V.RAO MD 50

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    HAND WASHING

    Single most effective action to prevent HAI -resident/transient bacteria

    Correct method - ensuring all surfaces are cleaned -more important than agent used or length of timetaken

    No recommended frequency - should be determinedby intended/completed actions

    Research indicates:

    poor techniques - not all surfaces cleaned frequency diminishes with workload/distance

    poor compliance with guidelines/training

    DR.T.V.RAO MD 51

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    YOUR HABITS KEEP THE PEOPLE AT RISK

    NASAL CAVITY A SOURCE OF INFECTION

    DR.T.V.RAO MD 52

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    MAKE HAND WASHING A HABIT

    SOME BODY WATCHING YOU

    DR.T.V.RAO MD 53

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    Programme created by Dr.T.V.Rao MD

    for Medical Professionals in theDeveloping World Email

    [email protected]