Inappropriate Antibiotic Use and MRSA for Augusta State Nov 2007

7/31/2019 Inappropriate Antibiotic Use and MRSA for Augusta State Nov 2007

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A Worldwide Crisis:

Inappropriate AntibioticUse & Resistant Bacterial

InfectionsJames A. Wilde MD

Associate Professor of Emergency Medicine and PediatricsDirector Pediatric Emergency Medicine

Medical College of Georgia

Medical Director, Georgia United Against Antibiotic Resistant Disease (GUARD)


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Viruses

Parasites-need other cells to provide food and means ofreproducing (sucks the life out of a cell)

Attack humans by invading cells of certain tissues

Hepatitis virus: attacks the liver cells Encephalitis virus: attacks the brain cells

Cold virus: attacks the throat and breathing passages

Diarrhea virus: attacks the small intestine

Can live dormant in the environment for years

Difficult to treat Multiply rapidly and easily transmitted by blood and body

secretions

Antibiotics DO NOT WORK against viruses!


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Bacteria

Can live and grow wherever they find food Environment: mountain streams, ocean water, rotting

animal or plant, sewer, topsoil, food

Humans & Animals: blood, skin, throat, lungs, urinary

bladder, intestine

Good versus Bad Bacteria

Some copy and grow every 20 minutes

Makes them difficult to treat: we are outnumbered
http://aapredbook.aappublications.org/cgi/content/full/2003/1/3.119/123_01


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http://aapredbook.aappublications.org/cgi/content/full/2003/1/3.119/123_01


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Diseases Caused by

Viruses and Bacteria

Virus

Common cold

Diarrhea (99%)

Acute Bronchitis

Influenza (flu)

Measles

Chicken Pox

AIDS

Rabies

Hepatitis

Bacteria

Urine infections

Strep Throat

Boils/abscesses

Gangrene

Some pneumonia

Ear infections (half)

Sinus infections (< half)

Bubonic Plague

Tuberculosis


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How Do We Treat Infections?

Bacterial infections

Immune system (white blood cells, etc)

Antibiotics (Penicillin, etc.) help to kill bacteria

Viruses

Immune system

Anti-viral medications: not very helpfulAntibiotics have NO EFFECT against viruses!


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How do Antibiotics Kill Bacteria?

Interfere with bacterial metabolism orreproduction Crowbar in a clock tower

Viruses have completely differentmetabolism and reproductive mechanisms

Crowbar has no effect on a waterfall

Bacteria are killed by antibiotics, but noantibiotic is effective against all bacteria Must match the antibiotic to the disease


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Fact:Bacteriaare the cause of themajority of deaths due to sepsis,

meningitis, and pneumonia in the U.S.

But: Most infections are due to viruses.

Therefore: Most infections are not

serious or life threatening.


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Fact: Virus

Most viral infections get better all bythemselves in 1-3 weeks

No medications are required for resolutionof colds, flu, stomach virus

Treat symptoms with Over the Countermedications & TLC (moms chicken soup)


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Treatment of Acute

Bronchitis

0

20

40

60

80

100

0 2 4 6 8 10 12 14 16 18

Days with cough

%

Patients

No Antibiotic

(+) Antibiotic

Stott, BMJ 1976


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A Doctors Approach to Infections

Fever does not cause brain damage

Underlying source of the fever can cause brain

damage

A viral infection is a nuisance

A bacterial infection can be deadly

SO

The doctors task is to decide who has infection

due to a virus and who has infection due to a

bacteria.


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Antibiotic Prescription Rate: Private

Physicians

Colds: 51%

Upper respiratory infections: 52%

Bronchitis: 66%

These antibiotics are unnecessary!!!

Gonzales et al., JAMA, 1997


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Problems With Inappropriate Use of

Antibiotics

They dont help the patient at all when used for thewrong disease/illness

Side effects: diarrhea, rash, allergy Unnecessary expense: 75% of outpatient antibiotics

are used for respiratory infections (viruses)

Development ofresistance: the antibioticwont work when you really DO need it for a bacterialinfection Penicillin no longer works for impetigo or urine infections


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Chronology of Development of Antibiotic

Resistance

Antibiotic Year introduced Resistance identified

Penicillin 1942 1940Streptomycin 1947 1947

Tetracycline 1952 1956

Erythromycin 1955 1956

Gentamicin 1967 1970Vancomycin 1956 1987


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New Resistant Bacteria

How Bacteria Become Resistant

Susceptible Bacteria

Resistant Bacteria

Resistance Gene Transfer


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Resistant Genes

More than 400 resistance genes have beenidentified

These genes allow the bacteria to shield

themselves from the antibiotic Resistance genes can be transferred from

one bacterial species to another: spread of

resistance is RAPID Remember: Some bacteria can copy themselves

(double) every 20 minutes!


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Mechanisms of Resistance

Enzymatic

degradation

Decreased entry

Efflux pump

Altered target site

Bypass pathway


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S. aureus

Penicillin

[1950s]

Penicillin-resistant

S. aureus

Evolution of Drug Resistance in

S. aureusMethicillin

[1970s]

Methicillin-resistant

S. aureus(MRSA)

Vancomycin-resistant

enterococci (VRE)

Vancomycin

[1990s]

[1997]

Vancomycin

intermediate-resistantS. aureus

(VISA)

[ 2002 ]Vancomycin-

resistantS. aureus


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0

10

20

30

40

50

60

70

1989 1991 1993 1995 1997 1999 2001 2003

Year

PercentResistance

Proportion ofS. aureus NosocomialInfections Resistant to Oxacillin (MRSA)

Among Intensive Care Unit Patients,

1989-2003*

*Source: NNIS System, data for 2003 are incomplete


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Emergence of Vancomycin

Resistant Enterococci

Source: NNIS Data

0

5

10

15

20

25

30

1989

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

P

ercentResis

tance

Non-Intensive Care Unit Patients

Intensive Care Unit Patients


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USNew Antibacterial AgentsYear No. Approved Agents

1991 20 Multiple agents

1992 3 Temafloxacin, lomefloxacin, cefpodoxime

1993 1 Piperacillin/Tazobactam

1994 0 Lowest number of new agents (22) since 1988

1995 2 Dirithromycin, ceftibutin1996 4 Meropenem, levofloxacin, sparfloxacin, Cefepime

1997 2 Grepafloxacin, Trovafloxacin

1998 0 Rivaled 1994

1999 3 Dalfopristin/quinupristin, gatifloxacin, moxifloxacin2000 1 Linezolid

2001 2 Ertapenem, ceftidoren

2002 0 89 drugs approved, no antibacterial agents

2003 2 Daptomycin, gemifloxacin


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The development of new antibiotics

without having mechanisms to insuretheir appropriate use is much like

supplying your alcoholic patientswith a finer brandy.

- Dennis Maki, 1998

- From Managing the Minefield Satellite Symposium

Annual Meeting of the Infectious Diseases Society of America


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It gets worse

Farmers routinely use

antibiotics in animal feed!

Wh U A tibi ti i A i l


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Why Use Antibiotics in Animal

Feed?

Promotes growth

Decreases amount of

feed needed

Prevents infectiousdiseases (examples?)

Facilitates confinement

housing Lowers cost to consumer


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How does this affect me?

Animals harbor the same bacteria on their

skin and in their guts as humans

The antibiotics used in animal feed are

similar to those used in humans

Resistant bacteria develop in animals the

same as in humans

Resistant bacteria are spread from animals

to humans


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EID 1999; Vol 5

Decrease in VRE After Removing

Avoparcin From Animal Feed


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National Effort to Stop Unwarranted

Antibiotics

Surveillance

Prevention and Control

Research

Product Development

Education 28 Coalitions in U.S.

Agency forHealth Care Research and

Quality Department ofDefense

EnvironmentalProtection

Agency

Health CareFinancing

Administration

Health Resources andServices

Administration

Department ofAgriculture

Department ofVeterans Affairs


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Local Efforts: GUARD Coalition

GeorgiaUnitedAgainstAntibioticResistantDisease

2002-2006: Funded by the Centers for Disease Control

and Prevention (CDC), part of Get Smart program

2002-Spring 2005: Oversight by Georgia Department ofPublic Health

Spring 2005: Officially became part of and managed by

the Medical College of Georgia

Medical Director: Jim Wilde, MD, FAAP (MCG faculty)


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GUARD Coalition Members

Medical Association of Georgia

GA chapter American Academyof Pediatrics

GA chapter American Academyof Family Physicians

Blue Cross Blue Shield Georgia Hospital Association

GA Assn Infection ControlNurses

GA Department of PublicHealth

PHARMA

US Centers for Disease Controland Prevention

Medical College of Georgia

Emory University

GA PTA

many individual physicians,nurses and other healthprofessionals


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GUARD Goals

Community education about appropriateuse of antibiotics

Physician education How to recognize bacterial infections

Rising rates of resistant bacteria

New antibiotics and their proper use

Create and distribute educational materials


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So, what can I do?

Educate yourself: most infections dont

require antibiotics

Talk to your doctor to see if antibiotics are

appropriate for you and/or your child

Dont use leftover antibiotics

Dont use someone elses antibiotics

Follow instructions-take them properly

Spread the wordnot the bacteria!


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His life is in

OUR hands


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The ravaging epidemic of AIDS has

shocked the worldWe will face similar

catastrophes againWe have too manyillusions that we cangovern the

remaining vital kingdoms, the microbes,that remain our competitors of last

resort for dominion of the planet

1988, Dr. Joshua Lederberg,Nobel Laureate


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CA-MRSA

First noted as emerging problem in late 1990s

Increasing rate of MRSA infections in patientswith none of the usual risk factors

Initially noted in prisons Sports teams

Getting national attention 2002/2003

Unusual sensitivity pattern: did not exhibit multi-drug antibiotic resistance typical of earlier strainsof hospital acquired MRSA (HA-MRSA)


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(CA-MRSA, cont)

New Staph strain now referred to as Community

Associated MRSA, or CA-MRSA

Primarily USA 300 clone on PFGE, also USA 400

First isolated in 2000 Many people are colonized but exhibit no symptoms

(carrier)

Panton-Valentine leukocidin (PVL) toxin: lethal to

neutrophils, induces abscess formation

90% of CA-MRSA, < 5% of HA-MRSA


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MRSA Summary

Health care associated: HA-MRSA Risk factors (hospitalization,

nursing home, surgery, etc)

Multidrug Resistant >90% erythromycin, clindamycin,

quinolone (FQ) resistant

Different PFGE

PVL negative

SCC mec I, II, III

Community-associated: CA-MRSA Poorly defined risk factors

(children/day care, prisons, sportsteams, MSM, Native Americans)

-lactam resistant; often resistant to

erythromycin; more susceptible to

other agents (clindamycin,

TMP/Sulfa, FQ)

PFGE USA300, USA 400

PVLpresent SEC mec IV


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CA-MRSA: Epidemiology

Has quickly become the predominant Staph

aureusspecies in most communities

King, Blumberg, et alAnn Int MedNov 2003

Surveillance Aug to Nov 2003, Atlanta (Grady Hosp)

MRSA caused 72% of all skin and soft tissue infections

63% of all MRSA was CA-MRSA

Medical College of Georgia data similar by 2005


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MRSA i M di l C ll f G i


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MRSA in Medical College of Georgia

(Adult Hospital)

1993-2005

0.00

1.00

2.00

3.00

4.00

5.00

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

2003

2004

2005

cases/1000

patientday

Nosocomial Entered with

MRSA i th CMC M di l C ll f G i


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MRSA in the CMC, Medical College of Georgia

1999-2005

0.00

1.00

2.00

3.00

4.00

5.00

6.00

7.00

8.00

1999 2000 2001 2002 2003 2004 2005

c

ases/1000p

atientdays

Nosocomial Entered with


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Risk factors for CA-MRSA

Children

Breaks in Skin/abrasions

Sharing towels/razors

Incarceration

Men having sex with men Contact sports participants


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Clinical Manifestations, CA-MRSA

Vast majority are skin and soft tissue

infections (SSTI)

Many SSTI come in the form of abscesses

Multiple abscesses may be present

Recurrence common

****Often mistaken for a spider bite

Increasing number of invasive infections

over the past 2-3 years


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? Spider Bite?Slide provided by Melissa Tobin DAngelo, Georgia DHR

Carbuncle


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Carbuncle

Slide provided by Melissa Tobin DAngelo, Georgia DHR


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Abscess


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Abscess

Slide provided by Melissa Tobin DAngelo, Georgia DHR


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Cellulitis with AbscessSlide provided by Jim Wilde MD


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CA-MRSA: Changing Patterns

Seybold, Blumberg et al., Clinical Inf Dis,

March 2006: CA-MRSA as a cause of blood

stream infections (BSI)

116 cases MRSA BSI over 7 months, 2004

MRSA USA 300 accounted for 34%

20% of nosocomial MRSA BSI were USA 300

Crude in-hospital mortality 22%


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(changing patterns, continued)

MMWR, April 13 2007

Report of severe community acquired

pneumonia due to CA-MRSA, LA and GA 10 patients, median age 17 y (eight < 30y)

All had influenza-like illness, 6 confirmed flu

6/10 died, median 3.5 days after symptom onset

Five isolates studied by CDC, all USA-300


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National Prevalence study of MRSA in US

Healthcare Facilities: APIC Report June

2007

Survey done in 1,237 hospitals in the US

Oct/Nov 2006

Symptomatic patients (infections) and

targeted high risk patients

Overall rate 4.6%

Majority were HA-MRSA


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Invasive MRSA infections in the US. Klevens et

al.,Journal of the American Medical

Association(JAMA) October 19, 2007

Surveillance data collected from 9 UScommunities

Extrapolation to US population

Estimated 18,650 deaths per year

Over 90% of deaths due to HA-MRSA


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VI. Management of CA-MRSA SSTI Abscesses should be drained

Drainage alone in many cases is definitive therapy

Strong recommendation to obtain culture Helps to define local epidemiology/resistance pattern

Antibiotics in selected cases Abscess greater than 5 cm diameter

Significant area of cellulitis

Systemic symptoms

For impetigo or simple cellulitis, considerantibiotic therapy directed at CA-MRSA

Most CA-MRSA infections are easily treated ifmanaged appropriately


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Suggested Antibiotics for CA-MRSA Outpatient

Trimethoprim/Sulfamethoxisole Cellulitis: Add beta-lactam to cover for strep

Clindaymcin Doxycycline

Avoid quinolones if possible (Cipro, Levofloxacin)

DO NOT use Rifampin as monotherapy

CDC recommendation: If local CA-MRSA prevalenceexceeds 15%, beta-lactams (penicillins andcephalosporins) should not be used as monotherapy forskin and soft tissue infections


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Inpatient managementFor severe or life-threatening infections suspected

to be due to CA-MRSA, initial empiric therapyshould include Vancomycin PLUS a beta-lactamase resistant beta-lactam antimicrobialagent Oxacillin

Nafcillin

Ampicillin/Sulbactam

Ref: 2003 Red Book, American Academy of Pediatrics: page 567


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Parenteral (IV) antibiotics for MRSA: options

Vancomycin

Not as active as beta-lactam antibiotics against susceptibleStaph aureus

Linezolid

Quinupristin/Dalfopristin (Synercid)

Daptomycin

Deactivated by Surfactant: Not for pneumonia

Tigacycline


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Decolonization efforts

Intranasal Mupirocin

Chlorhexidine body washes

Efficacy data are lacking Reacquisition common

Generally not recommended

May be reasonable in certain situations

Multiple documented recurrences

Ongoing transmission in well-defined, closely associated cohort

such as a household, sports team, etc.


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Tips for the public

See your doctor for boils or pustules or

tender/red/swollen areas on the skin

Do not attempt to drain abscesses at home

If fever present, or if sore is enlarging rapidly,

seek medical care immediately

Dont attempt self treatment with old antibiotics

Recurrence is common; follow up with your MD


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For More Information on GUARD

ContactDr. Jim Wilde MD, FAAP

Director, GUARD Coalition

(706) 533-2925

[email protected]

www.guard-ga.org
http://www.guard-ga.org/http://www.guard-ga.org/http://www.guard-ga.org/http://www.guard-ga.org/

Inappropriate Antibiotic Use and MRSA for Augusta State Nov 2007

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