Document 6464978

CONCISE REVIEW FOR CLINICIANS
Epidemiology, Treatment, and Prevention of Community-Acquired
Methicillin-Resistant Staphylococcus aureus Infections
ToDD J. KowALSKi, MD;
ELIE F . BERBARI,
since first described In 1 9 6 1 , methiclllln-resistant Staphylococcus
aureus (MRSA) has become a common nosocomial pathogen. Substantial Increases In MRSA Infections among nonhospitallzed patients are being reported. Methiciilin-reslstant S aureus is the most
common isolate from skin and soft tissue infections in seiected
centers In the United States. Community-acquired iVIRSA strains
differ from nosocomial strains In clinicaily relevant ways, such as in
their propensity to cause skin and soft tissue infection and severe
necrotizing pneumonia. Ciinicians in numerous speciaities, particuiarly primary care physicians, wiil likely evaluate patients presenting with community-acquired iVIRSA and should become famiiiar
with the epidemioiogy and clinicai characteristics of and evoiving
therapeutic and preventive strategies for this infection.
tVlayo Clin Proc. 2005;80(9):1201-1208
CA = community-acquired; CAP = CA pneumonia; MRSA = methicllllnresistant Staphylococcus aureus; MSSA = methlcillln-sensltlve 5
aureus; PVL = Panton-Valentlne leukocldln; SCC = staphylococcal cassette cartridge; TMP-SMX = trimethoprltn-sulfamethoxazole
A
ccumulating evidence reveals the emergence of methicillin-resistant Staphylococcus aureus (MRSA) in
the community.' Many of these community isolates are
distinctly different from nosocomial strains. The emergence of these distinct MRSA isolates in the community,
coined community-acquired MRSA (CA-MRSA), has become a topic of intense interest. The incidence of CA-MRSA
infection seems to be increasing in the United States and
worldwide. Primary care clinicians will need to be knowledgeable about the epidemiology, clinical syndromes,
treatments, and preventive strategies associated with CAMRSA.
THE CHANGING FACE OF S AUREUS
Shortly after the introduction of penicillin in the 1940s,
penicillin-resistant S aureus isolates were described first in
hospitals and subsequently in the community.' Today, the
vast majority of staphylococcal isolates carry plasmids
encoding a penicillinase-rendering penicillin resistance.
From the Departnnent of Internal Medicine and Division of infectious Diseases, (Vlayo Ciinic Coiiege of Medicine, Rochester, Minn.
A question-and-answer section appears at the end of this articie.
individuai reprints of this articie are not avaiiabie. Address correspondence to
Douglas R. Osmon, MD, MPiH, Division of Infectious Diseases, Mayo Clinic
Coiiege of Medicine, 200 First St SW, Rochester, MN 55905.
© 2005 Mayo Foundation for Medical Education and Research
Mayo Clin Proc.
MD;
AND DOUGLAS R . OSMON,
MD, MPH
Methicillin, a penicillinase-resistant semisynthetic penicillin, was introduced in 1961. Less than 1 year later, MRSA
was reported.' Today, MRSA is a
common nosocomial isolate and acFor editorial
counts for more than 50% of S aureus
comment,
isolates from intensive care units in
see page 1122
the United States.^ In 1982, MRSA
was first reported outside of the hospital among intravenous drug users in Detroit, Mich.' Subsequently, MRSA
was described in Polynesian populations in western Australia and in pediatric populations in the southern and
midwestem United States."*'* In 1999, a report of the deaths
of 4 children due to severe MRSA infections in Minnesota
and North Dakota garnered much attention.' A burgeoning
body of literature continues to detail the emergence of CAMRSA. These community isolates are composed of a heterogeneous mix of strains, some apparently well suited to
survival and propagation in the community.
WHAT CONSTITUTES CA-iVIRSA?
There is no universally accepted definition of what constitutes CA-MRSA. Epidemiologically oriented studies base
the definition on the timing of MRSA isolation in culture
relative to hospital admission (ie, <24-72 hours), with or
without excluding patients with established MRSA risk
factors (recent hospitalization, hemodialysis, indwelling
catheters, etc).* Numerous epidemiological studies have
suggested that hospitals were the primary MRSA reservoir
and that hospital contact accounted for most MRSA infections in the community.* In contrast, outbreaks and small
case series of MRSA infections in the community were
notable for the lack of any health care exposure among
cases.^'^ These reports elucidated characteristics differentiating CA-MRSA from local nosocomial strains.
Molecular analysis (eg, pulse-field gel electrophoresis
analysis) revealed distinct strains compared with local
nosocomial isolates.' These distinct community strains
often expressed resistance to p-lactams alone, in contrast
to the multidrug-resistance pattern that typified nosocomial strains. Clinicians also noted a predilection for skin
and soft tissue infection in these outbreaks.' The discovery of a novel resistance element in CA-MRSA, in conjunction with molecular epidemiological insights, has
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COMMUNITY-ACQUIRED METHICILLIN-RESISTANT STAPHYLOCOCCUS
TABLE 1 . Representative Antimicrobial Susceptibiiities (%) of
Community-Associated and Heaith Care-Associated iVIRSA*t
Antimicrobial
Cotnmutiityassociated
Health careassociated
Oxacillin
Ciprofloxacin
Clindamycin
Erythromycin
Gentamicin
Rifampin
Tetracycline
Ttitnethoprim-sulfamethoxazole
Vancotnycin
0
79
83
44
94
96
92
95
100
0
16
21
9
80
94
92
90
100
*Resistance data vary by geographic region. MRSA = methicillin-resistant Staphylococcus aureus.
tSee Table 2 and text for treatment recommendations; susceptibility does
not necessarily indicate appropriate monotherapy.
Adapted from JAMA,'^ with permission. Copyrighted 2003, American
Medical Associatioti. All rights reserved.
added substantially to our understanding of these apparent
differences.
Methicillin resistance is mediated via a chromosomally
incorporated resistance gene, mecA, which confers altered
binding of P-lactams to penicillin binding protein 2a. The
mecA gene is packaged in a cassette called the staphylococcal cassette cartridge (SCC), which aids in successful chromosomal incorporation.'" Until 2002, only 3 SCC types (IIII) were known, but a novel fourth type has been isolated
from CA-MRSA." It is becoming clear that the smaller
type IV cassette, which usually does not include multiple
other resistance elements, predominates among CA-MRSA
strains.'^ Rapid molecular diagnostics are available to test
for the mecA gene in vitro and eventually will likely be
available to directly test clinical specimens. These tests
may prove useful to more rapidly diagnose MRSA infections.'^ A recent San Francisco-based study used both epidemiological and molecular techniques to characterize CAMRSA.''' The strong association between type IV cassettes
and CA-MRSA was confirmed. Furthermore, the study
suggested that most MRSA infections in the community
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were related to a growing community reservoir, not a hospital reservoir, of MRSA.
Methicillin-resistant S aureus infections in the community are composed of escaped nosocomial isolates (particularly among people with traditional MRSA risk factors)
and novel community isolates of MRSA,the latter of which
we deem to be true CA-MRSA. Regardless of origin, the
growing community reservoir of MRSA poses daunting
new challenges to the control and treatment of MRSA
infections.
Currently, CA-MRSA sensu stricto can be distinguished
by the following characteristics: (1) the lack of multidrugresistant phenotype, (2) the presence of exotoxin virulence factors, (3) type IV SCC, and (4) molecular distinction from nosocomial strains. Only an isolate's lack of
multidrug-resistant phenotype is readily available to practicing clinicians outside of research settings. Table 1'^
shows representative resistance patterns among CAMRSA compared with nosocomial strains. These susceptibility patterns are dynamic and may vary markedly by
region. Already, CA-MRSA strains have encroached on
health care settings to cause nosocomial outbreaks, and
increasing antimicrobial resistance patterns have been observed among type IV isolates.''''.'^ Table l"*-'-"'''-" highlights differences between CA-MRSA and nosocomial
MRSA.
Community-acquired MRSA strains tend to have associated exotoxins. The most common is the Panton-Valentine leukocidin (PVL) toxin, which is lethal to neutrophils
and is associated with skin and soft tissue infections (specifically cellulitis, cutaneous abscesses, and furuncles) as
well as severe necrotizing pneumonia.^" Historically an
uncommon virulence factor (present in <5% of isolates),
PVL is emerging with CA-MRSA and probably in part
explains the predilection for skin and soft tissue infections." Recent in vitro work revealed that PVL-positive
strains of Staphylococcus bind preferentially to damaged
respiratory epithelium.^' This correlates clinically with data
TABLE 2. Characteristics of CA-iVIRSA vs Health Care-Associated M R S A * * * ' " " "
At-risk groups or conditions
SCC type
Antimicrobial resistance
PVL toxin
Associated clinical syndromes
CA-MRSA
Health care-associated MRSA
Children, competitive athletes, prisoners, soldiers,
selected ethnic populations (Native Americans/
Alaska Natives, Pacific Islanders), intravenous
drug users, men who have sex with men
Type IV
p-Lactam resistance alone, common (Table 1)
Frequent
Skin and soft tissue infections (furuncles, skin
abscesses), postinfluenza necrotizing pneumonia
(see text)
Residents in long-term care facility, patients with diabetes
mellitus, patients undergoing hemodialysis/peritoneal
dialysis, prolonged hospitalization, intensive care unit
admission, indwelling intravascular catheters
Types I, II, and III
Multidrug resistance, common (Table 1)
Rare
Nosocomial pneumonia, nosocomial- or catheter-related urinary
tract infections, intravascular catheter or bloodstream
infections, surgical-site infections
*CA = community-acquired; MRSA = methicillin-resistant Staphylococcus aureus, PVL = Panton-Valentine leukoeidin; SCC = staphylocoecal cassette
cartridge.
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COMMUNITY-ACQUIRED METHICILLIN-RESISTANT STAPHYLOCOCCUS
showing that PVL-associated pneumonias are associated
with prior influenzalike illnesses." It is postulated that
PVL contributes to enhanced community fitness, perhaps
through enhanced transmission from draining wounds.
Other exotoxins, including that responsible for staphylococcal scalded skin syndrome, have been described in community strains.^' A recent prospective study^"* suggests that
CA-MRSA possesses enhanced infectivity and virulence.
This report showed at least a 12-fold greater attack rate
among MRSA nasally colonized soldiers compared with
methicillin-sensitive S aureus (MSSA) colonized soldiers
over an 8- to 10-week period. Furthermore, PVL-positive
strains were found in all patients whose illness was severe
enough to require hospitalization.
POPULATIONS AT RISK
The incidence of CA-MRSA varies regionally, but comprehensive epidemiological studies have not been published
recently. Local prevalence data and antibiograms should be
updated and monitored. Attendant to this, clinicians need to
culture appropriate sources (furuncles, soft tissue abscesses, etc). The incidence of CA-MRSA varies also by
age and is reported consistently in younger patients than is
nosocomial MRSA.'' Outbreaks have occurred in several
discrete patient populations. Identified at-risk populations
include children (particularly those in day care centers),
soldiers, prisoners, homeless persons, intravenous drug users, and men who have sex with men.^*-^""^' Certain ethnic
groups also have been associated with outbreaks including
Pacific Islanders, Native Americans/Alaska Natives, and
Pacific and Canadian aboriginals." Competitive athletes,
specifically those who participate in fencing, rugby, football, and wrestling, have been involved in outbreaks among
high school, college, and professional teams." Recently, an
outbreak occurred in a group of divers .^^ A lack of personal
hygiene and a lack of basic infection-control principles
probably contribute considerably to these outbreaks.^' Patients with recent or frequent antimicrobial use or persons
who were recently hospitalized, have contact with others
who have skin and soft tissue infections, or live in crowded
quarters are also at ris
CLINICAL SYNDROMES
Skin and soft tissue infections and lower respiratory infections account for much of the current clinical literature
about CA-MRSA. Community-acquired MRSA has been
reported less frequently in endocarditis, brain abscesses,
bacteremia, sinusitis, and musculoskeletal infections.'""^''
Recent reports about CA-MRSA causing necrotizing
fasciitis, myositis, osteomyelitis, prosthetic joint infection.
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•
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and complicated parapneumonic effusions highlight the
various clinical settings and syndromes with which this
pathogen has been associated.'^"^^ Such diverse manifestations may become recognized more frequently over time as
the prevalence and physician awareness of this pathogen
increase.
Community-acquired MRSA should be considered in
the differential diagnosis of skin and soft tissue infections,
particularly among patients at risk or slow to respond to plactam therapy. Furunculosis and cutaneous skin abscesses
are the most common manifestations, but simple cellulitis
also can occur. Recurrent furunculosis and transmission to
close contacts (family members, teammates, etc) occur
frequently.^' The dermonecrotic lesions encountered may
be misdiagnosed as spider bites, and such lesions should
suggest CA-MRSA."" Infections may be severe, possibly
because of enhanced virulence and/or ineffective initial
antimicrobial therapy. A strain causing staphylococcal
scalded skin syndrome has emerged in Asia."" Although
skin and soft tissue infections account for most of the
morbidity associated with CA-MRSA, mortality is exceedingly uncommon.
Reports of lethal community-acquired pneumonias
(CAPs) due to CA-MRSA are mounting. S aureus is an uncommon cause of CAP, one exception being postinfluenza
infection. Two reports have detailed CA-MRSA CAP from
the 2003-2004 influenza season."^^^ Combined, 19 cases
were reported in the United States. All had documented or
suspected influenza preceding infection. Despite primarily
young, healthy hosts, mortality exceeded 25%, and survivors often had prolonged stays in intensive care units with
attendant morbidity. Of 15 isolates tested, 14 expressed the
PVL toxin. Clinical features of PVL-positive necrotizing
pneumonias may include leukopenia, hemoptysis, influenza prodrome, concomitant furunculosis, and a fulminant
and often fatal course."
TREATiVIENT
SKIN AND SOFT TISSUE INFECTIONS
When choosing an empirical antimicrobial for skin and soft
tissue infections, one should consider the likelihood that
MRSA is the etiologic agent, the severity of the infection,
and pertinent host factors including immunologic status
(eg, diabetes mellitus and human immunodeficiency virus),
allergies, and factors that may impede follow-up. P-Lactam
agents currently remain the antimicrobial of choice for
most skin and soft tissue infections in many if not most
parts of the country. If CA-MRSA is strongly suspected on
the basis of local prevalence data or epidemiological and/or
clinical clues, empirical-directed therapy is indicated. Recently, interim guidelines for the evaluation and manage-
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COMMUNITY-ACQUIRED METHICILLIN-RESISTANT STAPHYLOCOCCUS
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TABLE 3. Potential Outpatient Oral Therapies for iVIiid or Moderate Skin and Soft Tissue Infections
When CA-MRSA Is Suspected In Adults*'"
Antimicrobial
Usual dosage
Notes
TMP-SMX DSt
(160 mg/800 mg)
Minocycline
Doxycycline
Clindamycin
1 DS tablet every 12 h
If P-hemolytic streptococci infection also is suspected, consider
p-lactam therapy as well
If p-hemolytic streptococci infection also is suspected, consider
P-lactam therapy as well
Request double disk diffusion test for inducible resistance if
isolate is erythromycin-resistant and clindamycin-susceptible
100 mg every 12 h
100 mg every 12 h
300-450 mg every 6 h
*A11 furuncles and abscesses should be drained, cultured, and tested for susceptibilities; mild furuncles alone (<5 cm)
do not require systemic antimicrobials. CA-MRSA = community-acquired methicillin-resistant Staphylococcus
aureus; DS = double-strength; TMP-SMX = trimethoprim-sulfamethoxazole.
tAdjust dose for renal insufficiency.
ment of CA-MRSA skin and soft tissue infections have
been posted on the Internet by the Infectious Disease Society of Washington and by Washington state and county
health departments."" When possible, incision and drainage
should be performed, and an aerobic bacterial culture
should be obtained. Culture and in vitro susceptibility results should dictate which pathogen-specific antimicrobial
to use. For small (<5 cm) cutaneous abscesses with no
significant surrounding cellulitis or systemic symptoms,
drainage alone is sufficient, provided close follow-up is
available."^
Empirical antimicrobial therapy is indicated for patients
with larger abscesses, cellulitis, systemic symptoms, or
serious comorbidities. Moderate cases treated early and
appropriately may permit successful outpatient therapy.
Adult patients without serious comorbidities for whom
outpatient treatment is believed appropriate can be given
trimethoprim-sulfamethoxazole (TMP-SMX), minocycline, doxycycline, or clindamycin (Table 3). No randomized prospective data are available to support one oral agent
over another in this setting. However, the following points
should be considered when choosing an outpatient oral
regimen.
Clindamycin is a bacteriostatic antimicrobial that binds
to the bacterial ribosomal 50S subunit, thereby inhibiting
protein synthesis. Inhibition of protein production is probably beneficial in some toxin-mediated bacterial syndromes, such as streptococcal toxic shock syndrome and
necrotizing fasciitis. To date, no published data suggest
similar benefits when treating PVL-positive staphylococcal strains. Numerous treatment failures have been attributed to inducible clindamycin resistance .''* A clue to the
potential presence of such lies in the in vitro susceptibility
results: any erythromycin-resistant but clindamycin-susceptible strain may harbor inducible resistance. Either an
efflux pump or ribosomal methylation that impedes drug
binding mediates erythromycin resistance. The latter also
may confer clindamycin resistance. To evaluate for the
presence of inducible clindamycin resistance, the microbi1204
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ology laboratory should perform double disk diffusion testing (D testing) on any erythromycin-resistant, clindamycin-susceptible isolate for which clindamycin therapy is
being considered. Some microbiology laboratories may do
this routinely, others only on clinician request. Alternatives
to clindamycin should be considered for inducibly resistant
strains.
P-Hemolytic streptococci (groups A, B, C, and G) are
another extremely common cause of skin and soft tissue
infections, particularly erysipelas and cellulitis. Clindamycin is usually active against these microbes, but TMP-SMX
and tetracyclines are not recommended. Accordingly, if
clinical suspicion for (3-hemolytic streptococci and MRSA
is high (eg, high-risk patient with cellulitis), combination
therapy with a penicillinase-resistant (3-lactam (eg, dicloxacillin, cephalexin) and either a tetracycline or TMP-SMX
provides adequate outpatient antimicrobial coverage. Although clindamycin is usually active against P-hemolytic
streptococci, bacterial isolates are cultured rarely from cellulitis; hence, MRSA strains would not likely be tested for
inducible resistance. Close monitoring of the therapeutic
response is indicated.
Among patients with severe skin and soft tissue infections, marked systemic symptoms, or mitigating comorbid
conditions, hospitalization, parenteral antimicrobials, and
appropriate surgical drainage are preferred. Vancomycin
remains the initial agent of choice for serious skin infections in which MRSA is suspected until culture and sensitivity data are available to tailor therapy. After substantial
clinical improvement, some patients may be able to complete their antimicrobial course with an oral agent.
Several other antimicrobials are available for treatment
of CA-MRSA. Linezolid has been approved for treatment
of MRSA skin and soft tissue infection, is highly bioavailable, and is active against MRSA."" Expense, drug
interactions, and the potential for promoting linezolid resistance make this drug undesirable for widespread outpatient
use. Newer fluoroquinolones (eg, gatifloxacin, moxifloxacin, and levofioxacin) have enhanced activity against Staph-
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COMMUNITY-ACQUIRED METHICILLIN-RESISTANT STAPHYLOCOCCUS
ylococcus, and combined with rifampin, appear effective in
diverse clinical scenarios."" Increasing fluoroquinolone resistance among CA-MRSA isolates and limited experience
for this indication suggest that fluoroquinolones should not
be first-line agents for empirical treatment.''' Daptomycin
and quinupristin-dalfopristin are relatively new parenteral
agents, each with activity against MRSA and with Food
and Drug Administration approval for skin and soft tissue
infection. Each appears to be similar in efficacy to vancomycin for skin and soft tissue infection."'•''' Daptomycin is
taken once daily, making it an attractive option for outpatient therapy. Cost and concern about promoting resistance
weigh against its routine use over vancomycin.
Therapy duration is usually 7 to 14 days, depending on
severity of the infection, therapeutic response, and host
factors. One recent study suggested that 5 days' duration is
equivalent to 10 days' duration for uncomplicated cellulitis, but MRSA was not suspected in this patient population." In most instances, 7 to 10 days' duration is adequate.
In severe cases or in patients who are slow to respond or are
vulnerable hosts, treatment for 14 days or longer may be
needed.
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TABLE 4. Suggested Measures to Limit the Spread of CA-MRSA*
Personal and caregiver hygiene measures
Shower daily using soap and hot water
Wash hands frequently and/or use sanitation gels
Cover wounds with dry, clean dressings
Avoid contact with wound drainage (use gloves)
Avoid sharing towels, razors, clothing, personal items
Clean cuts and abrasions with soap and water
Environmental and organizational control measures
Routinely clean shared equipment (eg, wrestling mats, benches,
athletic equipment, whirlpools)
Clean and disinfect contaminated surfaces
Launder contaminated clothes and/or linens in hot water with
detergent or bleach
Limit participation in contact sports unless adequate wound coverage
can be obtained
Use a barrier (eg, clothes, towels) to bare skin when in contact with
shared equipment or surfaces (eg, sauna benches, exercise
machines, massage tables)
Health care-initiated measures
Use antimicrobials judiciously
Recognize and treat CA-MRSA lesions early
Educate and counsel patients and caregivers about appropriate wound
care
Consider decolonization strategies for recurrent disease or in localized
outbreaks in consultation with infectious disease physicians
*See text for references. CA-MRSA = community-acquired methicillinresistant Staphylococcus aureus.
PNEUMONIA
The potential confiuence of widespread PVL-positive
MRSA colonization in the community with an influenza
pandemic bodes dire consequences. Therefore, although
CA-MRSA pneumonia is much less common than skin and
soft tissue infections, the associated morbidity, mortality,
and therapeutic challenges merit discussion. It is now prudent to consider CA-MRSA as an etiology of severe CAP
in the correct clinical context. Severe necrotizing pneumonia with or without hemoptysis after an influenzalike illness in high-risk patients warrants therapy directed against
MRSA."*^ Unfortunately, effective therapeutic options are
limited. Vancomycin traditionally has been used, but at
routine dosages, it concentrates poorly in alveoli and is
known to be inferior to P-lactam therapy for severe MSSA
pneumonia.'^ Linezolid was associated with greater clinical
cure rates than vancomycin in 1 retrospective subgroup
analysis of a prospective nosocomial pneumonia study."
However, whether this is replicable and applicable to CAMRSA CAP remains to be seen. Daptomycin is inactivated
by surfactant and has been shown to be inferior to
ceftriaxone for CAP. Thus, it is an inappropriate treatment
for pneumonia.^" The fulminant nature of these infections is
presumably related to PVL toxin. Therefore, it is unclear
whether more active antimicrobials alone will translate into
better clinical outcomes. New and novel therapeutic approaches are needed for this severe infection. Combination
therapies (eg, vancomycin plus rifampin, TMP-SMX, or
clindamycin), although unproven, merit further investiga-
Mayo Clin Proc.
tion. Intravenous immunoglobulin neutralizes PVL toxin in
vitro, but the clinical relevance of this remains undefined.
Patients with known or suspected CA-MRSA necrotizing
pneumonia should be treated in consultation with infectious disease and critical care specialists.
PREVENTION
There is great interest in measures to abort and prevent CAMRSA outbreaks. Education of health care providers, patients, caregivers, high-risk populations, and appropriate
organizations about CA-MRSA and adherence to basic
infection-control principles are key to preventive strategies. Informed physicians are in a better position to recognize, treat, and appropriately counsel patients with CAMRSA. Data are limited about which specific control interventions may be most effective. Measures that may help
prevent outbreaks are listed in Table 4. Simple personal
hygiene interventions appear effective in aborting outbreaks .-^'•^'•^^ Daily hot showers, use of antibacterial soaps
and hand sanitizer, and appropriate care and coverage of any
draining lesions with clean dry bandages should be stressed
to patients. Personal items that may facilitate transmission,
such as towels, razors, and clothing, should not be shared.
Community-acquired MRSA wound drainage is considered
highly infectious, and adequate coverage of draining lesions
is important. When appropriate coverage cannot be attained,
athletes should be withheld from competition."
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From an organizational perspective, in addition to ensuring access to the previously mentioned interventions, targeted environmental sanitation may be helpful. For instance,
appropriate laundering of towels with hot water and detergent and routine cleaning of shared equipment (eg, wrestling
mats, football pads, whirlpools, etc) should be used.
Some outbreaks have been associated with frequent or
recent antimicrobial use.^' Limiting inappropriate antimicrobial use may be beneficial in preventing outbreaks and
is recommended.
Methicillin-resistant S aureus decolonization has been
attempted both to abort outbreaks and to prevent disease
recurrence. Various decolonization strategies have been
tried, but convincing evidence of their effectiveness among
outpatients with CA-MRSA is lacking. Decolonization
strategies have included various combinations of systemic
antimicrobials (either TMP-SMX, tetracyclines, or
clindamycin each with or without rifampin), mupirocin
nasal ointment, and chlorhexidine body washes, usually for
5 to 7 days.'"-'* Prolonged low-dose clindamycin may prevent recurrent MSSA furunculosis but has not been investigated among CA-MRSA cases; inducible resistance may
limit its effectiveness in this setting." Rifampin temporarily eradicates staphylococcal nasal carriage but should
not be given as monotherapy because resistance may
emerge rapidly. Mupirocin resistance is described in nosocomial MRSA, but the extent in community strains is unknown.'* In the absence of compelling outcome data, routine attempts at decolonization of all patients presenting
with CA-MRSA is not recommended.'" However, in cases
of recurrent disease among individuals or families or in
outbreak settings among discrete patient populations, it is
probably a worthwhile intervention. Currently, no one regimen can be recommended over another. In vitro antimicrobial susceptibilities should be used to aid in picking an
appropriate regimen. Rifampin has numerous drug interactions that need to be considered before including it in a
decolonization program.
CONCLUSIONS
Community-acquired MRSA is an emerging infectious
cause of morbidity and mortality among previously healthy
persons in the United States and worldwide. Accumulating
evidence suggests that these heterogeneous strains are particularly suited to community survival and spread. It remains to be seen whether CA-MRSA will become the
predominant staphylococcal phenotype in the community,
as penicillin-resistant S aureus did. If so, CA-MRSA promises to affect nearly every medical specialty. Primary care
clinicians will likely see most cases manifest as skin and
soft tissue infections and will need to recognize, diagnose.
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and appropriately treat this pathogen. Use of preventive
strategies and sage counsel to patients and caregivers may
prove invaluable in limiting its spread.
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1207
COMMUNITY-ACQUIRED METHICILLIN-RESISTANT STAPHYLOCOCCUS
Questions About CA-MRSA
1. Which one, of the following patient populations is not
associated with CA-MRSA outbreaks?
a.
b.
c.
d.
e.
Prisoners
Teachers
Soldiers
Athletes
Alaska Natives
2. Which one of the following clinical manifestations is
not associated with the PVL toxin?
a.
b.
c.
d.
e.
Endocarditis
Cellulitis
Furunculosis
Necrotizing pneumonia
Cutaneous abscesses
3. Which one. of the following statements about
CA-MRSA therapy is true!
a. TMP-SMX monotherapy is adequate when
P-hemolytic streptococci infection also is
suspected
b. Clindamycin is proved superior to minocycline for
CA-MRSA skin and soft tissue infections
c. TMP-SMX dosing does not need to be adjusted in
renal insufficiency
'
d. Daptomycin is the preferred therapy against
CA-MRSA CAP
e. Clindamycin-inducible resistance has been
associated with treatment failures and should be
evaluated with a double disk diffusion test
1208
Mayo Clin Proc.
•
AUREUS
4. Which one, of the following antimicrobials should
never be used as monotherapy against CA-MRSA
because resistance may emerge rapidly?
a.
b.
c.
d.
e.
TMP-SMX
Minocycline
Rifampin
Clindamycin
Vancomycin
5. Which one of the following helps distinguish
CA-MRSA from health care-associated MRSA?
a. Penicillinase
b. Type I SCC
c. Type IV SCC
d. Vancomycin resistance
e. Linezolid resistance
Correct answers:
l.b,2.a,
September 2005;80(9):120J-1208
3.e, 4 . c , 5 . c
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