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August/September
2007: VOLUME
1, NUMBER 3
Community-acquired
Methicillin-resistant S. Aureus (CA-MRSA) Skin and Soft Tissue
Infections
In
this Issue...
Community-acquired
methicillin-resistant S. aureus (CA-MRSA) has emerged as a
frequent cause of skin and soft tissue infections in adults and children.
Over the past year, new data have become available to assist clinicians
in how to better diagnose, manage, and prevent these infections. In
this issue, we review the epidemiology of skin and soft tissue infections,
the association between antibiotic use and CA-MRSA, the role of antibiotic
therapy in the management of these infections, issues involved in selecting
appropriate therapy, and approaches to the prevention of CA-MRSA skin
infections. |
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Course
Directors
John
G. Bartlett, MD
Professor of Medicine
Department of Medicine
The Johns Hopkins
University
School of Medicine
Baltimore, MD
Paul
G. Auwaerter, MD
Associate Professor
of Medicine
Clinical Director
Division of Infectious
Diseases
The Johns Hopkins
University
School of Medicine
Baltimore, MD
Sara
E. Cosgrove, MD, MS
Assistant Professor
of Medicine
Division of Infectious
Diseases
Director
Antibiotic Management
Program
Associate Hospital
Epidemiologist
The Johns Hopkins
University
School of Medicine
Baltimore, MD |
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GUEST
AUTHOR OF THE MONTH |
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Commentary
& Reviews: |
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Sara
E. Cosgrove, MD, MS
Assistant
Professor of Medicine, Division of Infectious Diseases
The Johns
Hopkins University School of Medicine |
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Guest
Faculty Disclosures
Sara
E. Cosgrove, MD, MS, has disclosed that she is a research
investigator for Merck. She is on the Advisory Boards of Ortho McNeil
and Cadence Pharmaceuticals.
Unlabeled/Unapproved Uses
The author has indicated
that there will be no reference to unlabeled or unapproved uses of
drugs or products in this presentation.
Program
Directors' Disclosures |
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the conclusion of this activity, participants should be able to: |
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Describe
the evolving epidemiology of CA-MRSA |
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Discuss
key issues regarding antibiotic therapy of skin and soft tissue
infections caused by CA-MRSA |
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Explain
the role of decolonization in management of CA-MRSA infections |
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COMPLETE
THE
POST-TEST
Step
1.
Click on the appropriate link
below. This will take you to the post-test.
Step
2.
If you have participated in a
Johns Hopkins on-line course, login. Otherwise, please register.
Step
3.
Complete the post-test and course
evaluation.
Step
4.
Print out your certificate.
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Infections
due to methicillin-resistant Staphylococcus aureus (MRSA)
were first observed decades
ago, mostly in hospitalized
patients with significant
comorbidities. MRSA remained
largely a hospital-associated
pathogen until the early
2000s, when otherwise healthy
people with no clear exposure
to the healthcare system
began to present with MRSA skin and soft tissue infections. Rates of
infections with so called community-acquired MRSA (CA-MRSA) have risen
over the past 5 years to the point where most clinicians have had at
least some experience treating patients with CA-MRSA infections.1 Nevertheless,
the results of a study by
Moran and colleagues examining
the etiology of purulent
skin and soft tissue infections
presenting to 11 university-affiliated
emergency departments across
the US are striking: 59%
of all infections were caused by MRSA, with the majority of these infections
caused by USA300, the predominant CA-MRSA strain in the US. Risk factors
for CA-MRSA in this study included history of prior MRSA infection,
reported spider bite, contact with another person with a similar infection,
and use of any antibiotic in the past month.
Prior use of antibiotics as a
risk factor for CA-MRSA was also demonstrated in a large study using
a database of ~3.2 million patients in general practices in the United
Kingdom by Schneider-Linder and colleagues. Exposure to any antimicrobial
drug within the year was an independent predictor of MRSA, and this
association was most marked for patients who received fluoroquinolones
or macrolides. Interestingly, the use of fluoroquinolones has previously
been implicated as increasing the incidence of MRSA colonization, perhaps
by increasing fibronectin-binding protein and allowing for increased
adherence of MRSA in the nasal mucosa.2 The association between
antibiotic use and subsequent CA-MRSA colonization and infection provides
an additional reason to limit antibiotic use in the outpatient setting
as much as possible.
Traditionally, antibiotics have
not been recommended as adjunctive
therapy to incision and drainage
in skin abscesses; however, most studies were in the pre-CA-MRSA era.3 Three
of the studies reviewed here
provide conflicting data on the
role of antibiotics in skin and
soft tissue infections caused
by CA-MRSA. Both the Moran and Miller studies noted that receipt of
an antibiotic that was inactive against CA-MRSA did not affect patient
outcomes, while Ruhe and colleagues found that receipt of inactive antibiotics
was associated with treatment failure. Failure to undergo incision and
drainage was the major predictor of treatment failure in the Miller
study; this variable could not be independently assessed in the Ruhe
study because of the study design. Fridkin and colleagues also observed
that receipt of inactive antibiotics did not appear to affect outcomes
of patients with skin and soft tissue infection in a large study evaluating
MRSA disease in 3 communities.4
While incision and drainage is
clearly the mainstay of management of CA-MRSA skin infections, the Centers
for Disease Control and Prevention have recommended that adjunctive
antibiotic therapy be considered in patients with:
- severe
or rapidly progressive
infections
- the
presence of extensive
associated cellulitis
- signs
and symptoms of systemic
illness
- diabetes
or other immune suppression
- advanced
age
- location
of the abscess in an area where complete drainage is difficult, and
- lack
of response to incision
and drainage alone5
In addition, therapy should be
given before incision and drainage in patients with prosthetic heart
valves or other conditions placing them at high risk for endocarditis.6
If antibiotics are used, then
an agent that is known to have
activity against CA-MRSA should be chosen rather than a β-lactam.
Clindamycin, tetracyclines, and trimethoprim-sulfamethoxazole are the
agents most commonly used for CA-MRSA infection. Unfortunately, the
study by Han and colleagues demonstrates decreased rates of susceptibility
to clindamycin and tetracycline
in an outpatient clinic in Boston. This finding underscores the importance
of examining local susceptibility data when making decisions about antibiotic
choice and also emphasizes the importance of judicious antibiotic use
when managing these infections to prevent increasing rates of resistance.
Recurrent infection and infection
among multiple household members
are frequently seen in patients
with CA-MRSA skin and soft tissue infections. The study by Wiese-Posselt
and colleagues provides the first published evidence that an aggressive
decolonization strategy, consisting of a combination of personal decolonization
and cleaning of the environment and personal items, could control an
outbreak of S. aureus skin
infections in the community setting.
All patients who present with
CA-MRSA skin infections should be questioned about other household members
with similar symptoms, and should be advised to undertake the household
cleaning protocols described in the Wiese-Posselt study. If patients
experience recurrence, or if other household members develop symptoms
despite these measures, then decolonization with mupirocin to the nares
(if nasal swabs grow MRSA) and antiseptic skin and throat washes can
be considered for the patient and all household members. Systemic antibiotics
should not be used for decolonization alone.
CA-MRSA has emerged as a significant
pathogen, and new research continues to advance our understanding of
its epidemiology and approaches to prevention and treatment.
References
| 1. |
Crum
NF, Lee RU, Thornton SA, et al. Fifteen-year
study of the changing epidemiology of methicillin-resistant Staphylococcus
aureus. Am J Med. 2006;119:943-951. |
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| 2. |
Weber
SG, Gold HS, Hooper DC, Karchmer AW, Carmeli Y. Fluoroquinolones
and the risk for methicillin-resistant Staphylococcus aureus in
hospitalized patients. Emerg Infect Dis. 2003;9:1415-1422. |
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| 3. |
Llera
JL, Levy RC. Treatment
of cutaneous abscess: a double-blind clinical study. Ann
Emerg Med. 1985;14:15-19. |
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| 4. |
Fridkin
SK, Hageman JC, Morrison M et al. Methicillin-resistant
Staphylococcus aureus disease in three communities. N Engl
J Med. 2005
Apr 7;352(14):1436. |
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| 5. |
Gorwitz
RJ, Jernigan DB, Powers JH, Jernigan JA, and Participants in the
CDC Convened Experts’ Meeting on Management of MRSA in the
Community. Strategies for clinical management of MRSA in the community:
Summary of an experts’ meeting convened by the Centers for
Disease Control and Prevention. 2006.
Available at: www.cdc.gov/ncidod/dhqp/ar_mrsa_ca_04meeting.html |
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| 6. |
Wilson
W, Taubert KA, Gewitz M, et al. Prevention
of Infective Endocarditis. Guidelines From the American Heart
Association. American Heart Association Rheumatic Fever, Endocarditis
and Kawasaki Disease Committee, Council on Cardiovascular Disease
in the Young; Council on Clinical Cardiology; Council on Cardiovascular
Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary
Working Group. Circulation. 2007 Apr 19; [ePub ahead of
print]. |
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EMERGENCE
OF MRSA IN THE EMERGENCY DEPARTMENT |
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| Moran
GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S.
aureus infections among patients in the emergency department. N
Engl J Med. 2006;355:666-674. |
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Moran
et al studied patients aged 18 or older with acute, purulent skin
and soft-tissue infections in 11 university-affiliated emergency
departments in August 2004. Patients were eligible for enrollment
if they had symptoms for less than 1 week. Demographics, risk factors,
and information about clinical presentation were recorded, and multivariate
analysis was performed to assess risk factors for MRSA infection. S.
aureus isolates were sent to the Centers for Disease Control
and Prevention (CDC) for evaluation of toxin production and Staphylococcal
cassette chromosome mec (SCCmec) typing.
Four hundred twenty-two
patients were enrolled with a mean age of 39 years. Infections consisted
of abscesses (81%), infected wounds (11%), and cellulitis with a
purulent exudate (8%). Three hundred twenty of 422 (76%) had wound
cultures that grew S. aureus, and 249 (78%) of these isolates
were methicillin resistant. Thus, 59% of all infections were caused
by MRSA. Two hundred sixteen of the 218 MRSA isolates that were tested
at the CDC were CA-MRSA strains (212 were USA300, 2 were USA400,
and 2 were USA1000). The vast majority were SCCmec type
IV (98%) and produced the Panton-Valentine leukocidin toxin (98%).
All MRSA isolates were susceptible to trimethoprim-sulfamethoxazole,
95% were susceptible to clindamycin, and 92% were susceptible to
tetracyclines.
Independent risk
factors for MRSA infection were black race, use of any antibiotic
in the past month, reported spider bite, history of MRSA infection,
and close contact with a person with a similar infection. The majority
of patients were treated with incision and drainage and antibiotic
therapy (66%); 19% received incision and drainage alone, 10% received
antibiotics alone, and 5% received neither. In 100 of 175 (57%) MRSA
infections, the antibiotic prescribed was not effective based on
susceptibility testing; however, this did not seem to have an effect
on cure.
This study indicates
that CA-MRSA is now the most common cause of skin infections in patients
who present to urban emergency departments. This diagnosis should
be considered in patients who present with cellulitis associated
with an abscess, isolated abscesses, or lesions that look like spider
bites. In this study, as in some others, use of an antibiotic without
activity against MRSA did not appear to affect outcomes, suggesting
that incision and drainage is the most important part of therapy. |
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THE
ASSOCIATION BETWEEN ANTIBIOTICS AND
CA-MRSA IN OUTPATIENTS |
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| Schneider-Lindner
V, Delaney JA, Dial S, Dascal A, Suissa S. Antimicrobial
drugs and community-acquired methicillin-resistant Staphylococcus
aureus, United Kingdom. Emerg Infect Dis. 2007;13:994-1000. |
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Schneider-Lindner
et al performed a case-control study to determine the impact of receipt
of antibiotics and subsequent development of CA-MRSA among a group of
adult patients with no previous diagnosis of MRSA who had not been hospitalized
in the past 2 years. All data came from the records of ~3.2 million
patients from >400 general practices in the United Kingdom. Case
patients had a clinical diagnosis of MRSA between 2000 and 2004 based
on diagnosis codes; however, the most common code did not differentiate
between MRSA colonization and infection. Ten control patients per case
patient were matched on practice and age. With adjustment for variables
such as age, BMI, and underlying medical conditions, the association
between antibiotics and MRSA diagnosis was determined using multivariate
analysis.
One thousand nine hundred eighty-one
patients with an MRSA diagnosis were eligible for the study and were
matched to 19,779 control patients. After adjustment for demographics
and comorbid conditions, exposure to any antimicrobial drug in the preceding
30 to 365 days remained an independent predictor of MRSA, conferring
a 3-fold increased risk of this diagnosis. The association was stronger
for patients who received more prescriptions (adjusted odds ratio [OR]
= 6.24 for ≥4 prescriptions) and for patients who received macrolides
(adjusted OR = 2.5) and fluoroquinolones (adjusted OR = 3.37). Nearly
40% of case patients had received no antibiotics in the year before
diagnosis of MRSA.
This study suggests that there
is an association between prior
antibiotic exposure and the development of colonization or infection
with CA-MRSA, although one third of patients who developed CA-MRSA had
no prior antibiotic exposure. The strongest correlation was with 2 antibiotic
classes commonly prescribed in the outpatient setting, macrolides and
fluoroquinolones. This lends further evidence to the notion that limiting
antibiotic prescriptions to essential use in the outpatient setting
benefits individual and public health. The data source used in the study,
records from a national primary care database in the United Kingdom,
did not contain information as to whether patients were infected or
just colonized with MRSA; however, most outpatients are not routinely
screened for MRSA colonization, suggesting that most were likely infected.
In addition, specific data regarding the place of residence of study
subjects, such as long-term care facilities or group homes where hospital-acquired
strains may be present, was not reported. Finally, due to the retrospective
nature of the study, no strain typing was performed to confirm that
the isolates were actually community-acquired strains of MRSA. |
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THE
ROLE OF ANTIBIOTIC THERAPY |
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| Ruhe
JJ, Smith N, Bradsher RW, Menon A. Community-onset methicillin-resistant
Staphylococcus aureus skin and soft-tissue infections: impact of
antimicrobial therapy on outcome. Clin Infect Dis. 2007;44:777-784. |
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| Miller
LG, Quan C, Shay A, et al. A prospective investigation of
outcomes after hospital discharge for endemic, community-acquired
methicin-resistant and –susceptible Staphylococcus aureus skin infection. Clin
Infect Dis. 2007:44:483-492. |
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Ruhe
and colleagues performed a retrospective
cohort study of 492 adult patients with 531 episodes of community-onset
MRSA skin and skin structure infections (abscesses, furuncles or carbuncles,
and cellulitis) at 2 tertiary care center clinics to determine the impact
of appropriate antibiotic therapy on patient outcomes. The day of the
first incision and drainage procedure (if performed), or the day of
the first positive wound culture result, was defined as zero time. Treatment
failure, the primary outcome, was defined as a documented worsening
of signs of infection at least 2 days after zero time, accompanied by
one of more of the following: performance of an additional incision
and drainage, hospital admission, occurrence of a new MRSA skin or soft
tissue infection while on therapy, or persistence of cultures growing
MRSA after completion of antibiotic therapy. Demographics, comorbidities,
and information about clinical presentation were recorded, and multivariate
analysis was performed to assess risk factors for treatment failure.
Miller and colleagues performed
a prospective study of 117 patients who were hospitalized for CA-MRSA
or CA-MSSA (community-acquired methicillin-susceptible S. aureus)
skin infections between February and October of 2004. At the time of
enrollment, patients underwent a survey regarding exposures, and data
on risk factors and comorbidites were collected. After hospital discharge,
patients were contacted by telephone at 30 days, and again at 120 days,
after enrollment and asked about clinical outcomes, new infections in
themselves or family members, and antibiotic use. The primary outcome
was non-response at 30 days, defined as: 1) infection relapse at the
original site, 2) new S. aureus skin infection, or 3) need
for a new course of antibiotic treatment. Secondary outcomes included
the need for additional surgery, rehospitalization, and new skin infection
in a family member.
In the Ruhe study, 361 infections
were abscesses, 116 were cellulitis, and 54 were furuncles and carbuncles.
All cases of cellulitis were associated with another skin lesion such
as folliculitis, a skin ulcer, or an abscess. Appropriate antimicrobial
therapy was given in 312 (59%) cases. Forty-five (8.5%) patients had
treatment failure, defined as the need for additional incision and drainage
in 38 patients, subsequent hospitalization in 20, new lesion in 2, and
microbiological failure in 1. Twenty-nine of these 45 patients received
inappropriate therapy, the majority of which was with a β-lactam
agent. Failure to start appropriate therapy within 48 hours of zero
time was the only independent predictor of treatment failure (adjusted
OR = 2.8, 95% CI 1.26-6.22). This finding was also seen in the subgroup
of 427 episodes in which incision and drainage was performed at zero
time. Size of the lesion was not associated with treatment failure.
In the Miller study, 84% of patients
were adults and 16% were children. Seventy patients had CA-MRSA infections
and 47 had CA-MSSA infections. Patients with CA-MRSA were younger (median
age 37 vs 46 years), less likely to have diabetes (20% vs 49%), and
more likely to have a history of snorting drugs (30% vs 10%). Thirty-six
(31%) patients experienced non-response at 30 days; there was no difference
in rates of response among patients with CA-MRSA infection (33%) and
CA-MSSA infection (28%). Failure to undergo incision and drainage was
more common in non-responders – 20% did not undergo incision and
drainage compared to only 1% of responders. Receipt of inappropriate
antibiotic therapy was not associated with a higher failure rate.
These studies provide conflicting
data on the impact of appropriate antibiotic therapy on the outcomes
of patients with skin infections caused by CA-MRSA. In the Ruhe study,
receipt of inappropriate antibiotics for CA-MRSA skin and soft tissue
was associated with treatment failure. The relative effect of incision
and drainage on outcome, which would be expected to be significant,
could not be assessed in this study because zero time was defined as
the time of incision and drainage, if performed. However, in the subgroup
of patients who underwent incision and drainage, appropriate choice
of antibiotics also improved outcomes. The participants in this study
attended clinics at a tertiary care medical center and a VA hospital,
and may have had more comorbidities than average (eg, 17% had diabetes),
but none of the comorbidities measured in the study were associated
with treatment failure. Although the authors had a standardized definition
for failure, the retrospective nature of the study may have led to bias
in assessing outcomes.
In the Miller study, receipt
of inappropriate antibiotics was not associated with treatment failure.
In contrast to Ruhe, this study assessed both CA-MSSA and CA-MRSA skin
infections in patients who were ill enough to be hospitalized. Because
patients were followed prospectively, outcomes may be more reliable;
however, the numbers of patients who failed and received inappropriate
antibiotic therapy were quite small. Incision and drainage was the only
predictor of treatment failure, emphasizing the importance of this procedure
in the management of skin infections caused by S. aureus. |
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INCREASING
RESISTANCE TO FIRST-LINE ORAL AGENTS |
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| Han
LL, McDougal LK, Gorwitz RJ, et al. High frequencies of
clindamycin and tetracycline resistance in methicillin-resistant
Staphylococcus aureus pulsed-field type USA300 isolated collected
at a Boston ambulatory health center. J Clin Microbiol. 2007;45:1350-1352. |
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Han
et al studied 123 CA-MRSA isolates from patients presenting to a community
health center in Boston between May 2004 and November 2005 to assess
resistance to the antibiotics commonly used for management of CA-MRSA
(clindamycin, tetracycline, levofloxacin, and mupirocin). One hundred
fifteen isolates had a known source – 90% were from skin and soft
tissue sites and 10% were from the nares or nasopharynx. Eighty-three
percent of total isolates were MRSA strain type USA300, the predominant
CA-MRSA strain in the US; 59% were USA300-0114, and 24% were USA300-0247.
Both strains had significant rates of resistance to several commonly
used antibiotics, as detailed in the table below:
In addition, 12 isolates with
resistance to erythromycin, levofloxacin, clindamycin, and tetracycline
were sent to the CDC; these isolates were susceptible to minocycline
and doxycycline. All 12 were found to be resistant to mupirocin.
This study demonstrates that
there are areas in the US where there is increasing resistance to agents
that are commonly used to treat CA-MRSA skin and soft tissue infections,
in particular clindamycin and tetracycline. This finding emphasizes
the importance of examining local resistance data when determining empiric
antibiotic choices for these infections. The high prevalence of fluoroquinolone
resistance is not surprising, as resistance to fluoroquinolones arises
quickly and commonly in S. aureus strains; consequently, fluoroquinolone
use is discouraged in the management of skin and soft tissue infections
caused by S. aureus. Of great concern is this study’s finding
of concomitant mupirocin resistance in the highly resistant strains,
given that mupirocin is the only commercially available agent for S.
aureus decolonization of the nares. One encouraging finding, though,
is that all isolates retained susceptibility to trimethoprim-sulfamethoxazole,
an effective agent in the management of MRSA skin and soft tissue infections.
It is important to remember that trimethoprim-sulfamethoxazole has poor
activity against Group A streptococci; thus, its use as monotherapy
for routine cellulitis in which Group A streptococci are suspected as
a pathogen is discouraged. |
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THE
ROLE OF DECOLONIZATION |
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| Wiese-Posselt
M, Heuck D, Draeger A, et al. Successful termination of
a furunculosis outbreak due to lukS-lukF-positive, methicillin-susceptible
Staphylococcus aureus in a German village by stringent decolonization,
2002-2005. Clin Infect Dis. 2007;44(11):e88-95.
Epub 2007 Apr 25. |
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Wiese-Posselt
and colleagues report on the investigation and termination of an outbreak
of S. aureus that began in 1998 in a German village of 144
residents in 58 households. The MSSA strain causing the outbreak contained
the lukS-lukF gene which encodes for Panton-Valentine leukocidin,
the toxin that has been implicated in causing aggressive skin infections
in CA-MRSA strains. A retrospective cohort study was performed to assess
risk factors for infection. All village residents who consented to participate
completed a standardized questionnaire about demographics, risk factors,
comorbidities, and occurrence of furuncles since 1998. A “case” was
defined as a person with a skin abscess >0.5 cm or an abscess in
another organ occurring from 1998-2004; a “case contact” was a household
member, a friend, or relative with whom time was spent or personal objects
were shared, or a person with whom skin contact occurred.
The intervention to control transmission
of MSSA was an aggressive decolonization protocol for the affected patient
and all household members initiated in July 2004. The protocol consisted
of 5 days of the following:
- mupirocin
ointment to the nares
3 times daily
- daily
treatment of skin and
hair with an octenidin-based wash
- gargling
with 0.1% chlorhexidine
solution 3 times daily
- daily
disinfection of personal
items such as combs, razors, glasses, and jewelry
- daily
disinfection of the bathtub
or shower floor
- daily
changing and hot water
washing of towels, sheets, and clothing
- enhanced
hand hygiene with alcohol-based hand gel, and
- minimized
contact with other villagers
during the 5-day period
Nasal swab specimens were obtained
at 3 days, 7 weeks, and 20 weeks after the decolonization protocol,
and physicians were asked to report any new cases of furunculosis.
From 1998 to 2005, 42 primary
cases and 59 relapses of furuncles or abscesses occurred in 27 people.
Fifteen (36%) patients required hospitalization. One hundred forty-one
of 144 (98%) villagers participated in the study. Independent risk factors
for development of furuncles and abcesses were nasal colonization with lukS-lukF-positive S.
aureus (adjusted OR 9.2, 95% CI 1.2-73.1), contact with case patients
(adjusted OR 4.7, 95% CI 1.3-17.3), being a member of the local fire
brigade (adjusted OR 5.5, 95% CI 1.6-19.0), sharing objects with neighbors
(adjusted OR 3.6, 95% CI 1.1-12.2), and having a chronic skin disease
(adjusted OR 12.3, 95% CI 1.5-100.2).
Fifty-three patients underwent
the decolonization protocol. All nasal cultures were negative at 3 days.
At 7 weeks, 4 (8%) patients were found to be colonized with lukS-lukF-positive S.
aureus and received 10 days of trimethoprim-sulfamethoxazole and
rifampicin. At 20 weeks no patients were colonized with lukS-lukF-positive S.
aureus. Clinical follow-up of patients revealed 1 new case of furunculosis
and 3 relapses; these patients and their household contacts underwent
the decolonization protocol again. In the year following decolonization,
no new or recurrent cases were identified.
This study demonstrates that
an aggressive decolonization strategy can lead to control of S.
aureus infections in the community. Although the patients in the
study had infections caused by MSSA, the predominant strain contained
the same virulence factor—Panton-Valentine leukocidin—as do many CA-MRSA
strains. It is important to note that the decolonization protocol involves
the use of nasal decolonization with mupirocin and skin decolonization
in combination with cleaning of the environment (eg, bathtubs and showers)
and items that contact skin (eg, sheets, towels, clothing); when used
alone, these individual approaches are less likely to be as effective
as when combined. Patients with infections in this study had similar
risk factors for infection that have been identified for CA-MRSA infections,
including contact with another infected patient, sharing objects, and
having underlying skin disease. |
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At
the conclusion of this activity, participants should be able to:
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Describe
the evolving epidemiology of CA-MRSA |
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Discuss
key issues regarding antibiotic therapy of skin and soft tissue
infections caused by CA-MRSA |
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Explain
the role of decolonization in management of CA-MRSA infections |
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| Internet
CME Policy — back
to top |
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The
Office of Continuing Medical Education (CME) at The Johns Hopkins
University School of Medicine is committed to protect the privacy
of its members and customers. The Johns Hopkins University SOM CME
maintains its Internet site as an information resource and service
for physicians, other health professionals and the public.
Continuing Medical
Education at The Johns Hopkins University School of Medicine will
keep your personal and credit information confidential when you participate
in a CME Internet based program. Your information will never be given
to anyone outside of The Johns Hopkins University School of Medicine's
CME program. CME collects only the information necessary to provide
you with the services that you request. |
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| Faculty
Disclosure — back
to top |
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As
a provider accredited by The ACCME, it is the policy of The Johns
Hopkins University School of Medicine to require the disclosure
of the existence of any significant financial interest or any other
relationship a faculty member or a provider has with the manufacturer(s)
of any commercial product(s) discussed in an educational presentation.
The Program Directors reported the following:
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John
G. Bartlett, MD has disclosed that he has served on
the HIV Advisory Board for GlaxoSmithKline, Abbott, Bristol-Myers
Squibb, Pfizer and Tibotec. He is also on the Policy Board for
Johnson & Johnson. |
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Paul
G. Auwaerter, MD has disclosed that he has served as
a consultant for Novartis, Pfizer, Ortho-McNeil, Schering-Plough,
and Genzyme. He is on the Speakers' Bureau for Schering-Plough
and has also disclosed that he is a Stock Shareholder for Johnson
& Johnson. |
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Sara
E. Cosgrove, MD, MS has disclosed that as a co-investigator,
she has received grants or research support from Merck and served
on the Advisory Boards for Ortho-McNeil and Cadence Pharmaceuticals. |
Guest
Authors Disclosures |
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| Disclaimer
Statement — back
to top |
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| The
opinions and recommendations expressed by faculty and other experts
whose input is included in this program are their own. Use of The
Johns Hopkins University School of Medicine name implies review
of educational format design and approach. Please review the complete
prescribing information of specific drugs or combination of drugs,
including indications, contraindications, warnings and adverse effects
before administering pharmacologic therapy to patients. |
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© 2007
JHUSOM and eInfections Review
Created by DKBmed. |
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COMPLETE
THE
POST-TEST
Step
1.
Click on the appropriate link below. This
will take you to the post-test.
Step
2.
If you have participated in a Johns Hopkins
on-line course, login. Otherwise, please register.
Step
3.
Complete the post-test and course evaluation.
Step
4.
Print out your certificate.
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