Suspected Staphylococcus aureus and

streptococcal skin and soft tissue infections

in children >28 days: Evaluation and
management
Author: Sheldon L Kaplan, MD
Section Editor: Morven S Edwards, MD
Deputy Editor: Mary M Torchia, MD
Contributor Disclosures
Literature review current through: Jun 2021. | This topic last updated: Jun 10, 2021.

INTRODUCTION

The evaluation and management of suspected Staphylococcus aureus and

streptococcal skin and soft tissue infections (SSTIs) in children older than 28 days
will be reviewed here. Clinical features of SSTI; the evaluation and management
of suspected S. aureus or streptococcal SSTI in neonates; the epidemiology,
prevention, and control of methicillin-resistant Staphylococcus aureus (MRSA)
infections in children; and the treatment of invasive MRSA infections in children
are discussed separately.

ETIOLOGY

Methicillin-resistant S. aureus (MRSA) is the most common

identifiable cause of skin and soft tissue infection (SSTI) in many
communities and should be suspected in most children with SSTI
(along with methicillin-susceptible S. aureus [MSSA] and group
A Streptococcus [GAS]). The relative frequency of S.
aureus compared with GAS depends upon the type of SSTI:
●Purulent/fluctuant SSTI – Purulent/fluctuant SSTIs (eg,
abscess, furuncle, carbuncle) usually are caused by S.
aureus (either MSSA or MRSA). MSSA and MRSA cannot be
differentiated clinically or epidemiologically [1,2]. (See "Cellulitis
and skin abscess: Epidemiology, microbiology, clinical
manifestations, and diagnosis", section on 'Skin abscess'.)
●Cellulitis and erysipelas – Cellulitis is usually caused by GAS
and other beta-hemolytic streptococci (groups B, C, G, and F) but
also may be caused by S. aureus, particularly in children with risk
factors for MRSA (table 1). Erysipelas is usually caused by beta-
hemolytic Streptococcus. (See "Cellulitis and skin abscess:
Epidemiology, microbiology, clinical manifestations, and
diagnosis", section on 'Cellulitis and erysipelas' and "Methicillin-
resistant Staphylococcus aureus infections in children:
Epidemiology and clinical spectrum", section on 'Epidemiology
and risk factors'.)
●Impetigo and folliculitis – Impetigo and folliculitis usually are
caused by S. aureus (either MSSA or MRSA). (See "Impetigo",
section on 'Microbiology' and "Infectious folliculitis", section on
'Staphylococcal folliculitis'.)

EVALUATION

History — Important aspects of the history in a child with skin and

soft tissue infection (SSTI) include [3]:
●Risk factors for community-associated or community-onset
health care-associated methicillin-resistant S. aureus (MRSA)
infection (table 1) – MRSA isolates in children with health care risk
factors are more likely to be resistant to clindamycin and other
commonly used drugs than isolates from children without risk
factors [4-6]. Perhaps the most important risk factor is living in a
community with a high proportion (≥15 percent) of MRSA among
community S. aureus isolates. (See "Methicillin-resistant
Staphylococcus aureus infections in children: Epidemiology and
clinical spectrum", section on 'Epidemiology and risk factors'.)
Although past history of MRSA is a risk factor for MRSA, past
history of MRSA SSTI does not necessarily mean that the current
infection is caused by MRSA [7], particularly if the episodes are
separated by >12 months or the child has a predisposing
condition, such as eczema [8].
●Factors that may suggest pathogens other than S. aureus and
group A Streptococcus include:
•Animal exposure or human or animal bites – May result in
polymicrobial infection. (See "Animal bites (dogs, cats, and
other animals): Evaluation and management", section on
'Microbiology' and "Human bites: Evaluation and
management", section on 'Microbiology'.)
•Travel history – Travel to an endemic area may suggest
pathogens such as Corynebacterium diphtheriae. (See "Skin
lesions in the returning traveler" and "Epidemiology and
pathophysiology of diphtheria" and "Clinical manifestations,
diagnosis, and treatment of diphtheria".)
•Hobbies – Hobbies that involve water exposure may increase
the risk of pathogens such as Aeromonas or Mycobacterium
 marinum. (See "Soft tissue infections following water
exposure".)
•Traumatic lesions, especially those associated with dirt,
increase the likelihood of polymicrobial infections including
bacteria as well as fungi.
•An underlying condition expands the spectrum of pathogens
that need to be considered (eg, Pseudomonas aeruginosa in
neutropenic patient).
●Allergy to antibiotics – May affect choice of therapy.
(See 'Systemic antimicrobial therapy' below.)
Examination — Examination determines the type of SSTI. Important
aspects of the examination include general appearance (eg, well- or
ill-appearing), systemic signs (eg, fever >38°C [100.4°F],
hypotension, tachycardia), and the extent of involvement (eg, type,
localization, and size of the SSTI).
●Impetigo is a superficial bacterial infection that manifests with
lesions that progress from papules to vesicles, pustules, and
crusts (picture 1A-B). (See "Impetigo".)
●Folliculitis is a superficial bacterial infection of the hair follicles
with purulent material in the epidermis (picture 2A-B).
(See "Infectious folliculitis".)
●A skin abscess is a collection of pus within the dermis and
deeper skin tissues. (See "Cellulitis and skin abscess:
Epidemiology, microbiology, clinical manifestations, and
diagnosis", section on 'Skin abscess'.)
●A furuncle (or "boil") is an infection of the hair follicle in which
purulent material extends through the dermis into the
subcutaneous tissue, where a small abscess forms.
(See "Cellulitis and skin abscess: Epidemiology, microbiology,
clinical manifestations, and diagnosis", section on 'Skin abscess'.)
●A carbuncle is a coalescence of several inflamed follicles into a
single inflammatory mass with purulent drainage from multiple
follicles in the epidermis (picture 3). (See "Cellulitis and skin
abscess: Epidemiology, microbiology, clinical manifestations, and
diagnosis", section on 'Skin abscess'.)
●Erysipelas is an infection of the upper dermis and superficial
lymphatics. It is characterized by clear demarcation between
involved and uninvolved tissue; the erysipelas lesion is raised
above the level of the surrounding skin (picture 4). Patients with
erysipelas tend to have acute onset of symptoms with systemic
manifestations, including fever and chills. (See "Cellulitis and skin
abscess: Epidemiology, microbiology, clinical manifestations, and
diagnosis", section on 'Cellulitis and erysipelas'.)
●Cellulitis is an infection of the deep dermis and subcutaneous fat
without an underlying suppurative focus (eg, cutaneous abscess,
septic arthritis, etc); it manifests with erythema, edema, and
warmth. (See "Cellulitis and skin abscess: Epidemiology,
microbiology, clinical manifestations, and diagnosis", section on
'Cellulitis and erysipelas'.)
●Necrotizing soft tissue infections are characterized by fulminant
tissue destruction and systemic signs of toxicity.
(See "Necrotizing soft tissue infections".)
●Pyomyositis is a purulent infection of skeletal muscle that arises
from hematogenous spread, usually with abscess formation [3].
(See "Pyomyositis".)
●Toxic shock syndrome (staphylococcal or streptococcal) is a
clinical illness characterized by rapid onset of fever, rash,
 hypotension, and multiorgan system involvement; diffuse macular
erythroderma is a sign of toxic shock syndrome.
(See "Staphylococcal toxic shock syndrome" and "Invasive group
A streptococcal infection and toxic shock syndrome:
Epidemiology, clinical manifestations, and diagnosis".)
Laboratory evaluation — Laboratory evaluation is necessary to
determine the microbiologic etiology of SSTI, which may influence
treatment decisions. Various bacterial and viral pathogens can cause
skin lesions that are clinically indistinguishable from staphylococcal or
streptococcal infections; MRSA and methicillin-susceptible S.
aureus (MSSA) cannot be differentiated clinically or epidemiologically
[1,2]. (See "Impetigo" and "Infectious folliculitis" and "Cellulitis and
skin abscess: Epidemiology, microbiology, clinical manifestations,
and diagnosis".)
●Gram stain, culture, and susceptibility testing of purulent
material – We obtain specimens for Gram stain, culture, and
susceptibility testing from patients with purulent skin lesions
(abscess, furuncle, carbuncle, draining cellulitis or wound) if
purulent material can be obtained [9-11]. Results of these studies
guide the choice of empiric and pathogen-directed antimicrobial
therapy [2,7,12,13]. It is particularly important to obtain wound
cultures from immunocompromised patients and those with
severe local infections, systemic signs of infection, recurrent or
multiple abscesses, an epidemiologic link to individuals with
MRSA infection, and those who have failed initial treatment [9,14].
The Gram stain may help to guide empiric therapy. Gram stain
identification of gram-positive cocci in clusters provides early
indication of staphylococcal infection. Gram stain identification of
gram-positive cocci in chains provides early identification of
streptococcal infection.
●Blood culture – We obtain blood cultures from patients who
have signs of serious systemic infection (eg, prolonged fever,
tachycardia, hypotension), neutropenia or severe cell-mediated
immunodeficiency, animal bites, or immersion injuries [3,14,15].
In a retrospective review, blood cultures were positive in 12.5
percent of immunocompetent children hospitalized with
complicated SSTI (defined as surgical or traumatic wound
infection, SSTI requiring surgical intervention [other than routine
incision and drainage], or infected ulcer or burn), and none of
those with uncomplicated SSTI [16]. In observational studies,
blood cultures are rarely positive in children with uncomplicated
SSTI [17,18]. In addition, blood cultures may be positive for
contaminants, which may necessitate follow-up cultures or
prolong intravenous antibiotic therapy.
●Susceptibility testing – If S. aureus is isolated in bacterial
culture, susceptibility testing is necessary to distinguish MRSA
from MSSA [1]. In some laboratories, methicillin resistance may
be detected rapidly using commercially available molecular tests
for the mecA gene that leads to methicillin resistance.
(See "Rapid detection of methicillin-resistant Staphylococcus
aureus".)
Susceptibility testing is important in monitoring the local
proportion of S. aureus infections caused by MRSA and the
prevalence of resistance to various classes of antimicrobials
[2,9,12,19]. S. aureus isolates associated with SSTI should be
tested for susceptibility to beta-lactam antibiotics, trimethoprim-
sulfamethoxazole,
tetracyclines, erythromycin, clindamycin, vancomycin, linezolid,
and possibly daptomycin [20]; isolates associated with SSTI
requiring parenteral therapy also should be tested for
susceptibility to ceftaroline in selected circumstances (eg, high
rates of clindamycin resistance, children with renal dysfunction,
inflammatory bowel
disease, Clostridioides (formerly Clostridium) difficile-associated
disease, or intolerance to vancomycin). A D test or automated test
for inducible resistance to clindamycin should be performed on
isolates that are resistant to erythromycin but susceptible to
clindamycin if clindamycin therapy is being considered.
(See 'Treatment setting' below and "Methicillin-resistant
Staphylococcus aureus infections in children: Epidemiology and
clinical spectrum", section on 'Microbiologic
characteristics' and "Overview of antibacterial susceptibility
testing", section on 'Inducible clindamycin resistance testing'.)
Beta-hemolytic Streptococcus usually is susceptible to penicillin
and other beta-lactam antibiotics; susceptibility testing is not
necessary. (See "Treatment and prevention of streptococcal
pharyngitis in adults and children", section on 'Treatment of initial
episodes'.)
●Nasal cultures – We do not obtain routine nasal cultures from
patients presenting with possible MRSA infection [9]. The
predictive value of screening for colonization is not known [21]. In
addition, nasal and wound isolates may be discordant with
respect to antimicrobial susceptibility and pulsed-field gel
electrophoresis [22].
 MANAGEMENT APPROACH

The discussion below focuses on the management of

purulent/fluctuant skin and soft tissue (SSTI), cellulitis, erysipelas,
and superficial SSTI in children. The management of muscle
infections and necrotizing soft tissue infections is discussed
separately. (See "Pyomyositis", section on
'Treatment' and "Necrotizing soft tissue infections", section on
'Treatment'.)
The management of invasive SSTI (ie, SSTI that extend beyond the
skin and soft tissues) is also discussed separately.
(See "Staphylococcus aureus bacteremia in children: Management
and outcome" and "Group A streptococcal (Streptococcus pyogenes)
bacteremia in children" and "Staphylococcus aureus in children:
Overview of treatment of invasive infections", section on 'Empiric
antimicrobial therapy'.)
Our approach to management is largely consistent with guidelines
provided by the American Academy of Pediatrics Committee on
Infectious Diseases and the Infectious Diseases Society of America
(algorithm 1 and algorithm 2 and algorithm 3) [3,10,11].
SSTI and hemodynamic instability — Children with localized skin
infections and associated hemodynamic instability generally have
either a systemic infection or toxic shock syndrome. Treatment of
toxic shock syndrome is discussed separately. (See "Staphylococcal
toxic shock syndrome", section on 'Management' and "Invasive group
A streptococcal infection and toxic shock syndrome: Treatment and
prevention", section on 'Streptococcal toxic shock syndrome'.)
For activity against S. aureus and group A Streptococcus (GAS) in
hemodynamically unstable children with SSTI, we suggest an empiric
parenteral regimen
of vancomycin plus either nafcillin or oxacillin (table 2 and table 3);
additional activity against gram-negative pathogens may be
necessary. The combination of vancomycin and nafcillin or oxacillin
is necessary to maximize coverage for both methicillin-resistant S.
aureus (MRSA) and methicillin-susceptible S. aureus (MSSA), as
well as beta-hemolytic Streptococcus. We do not add gentamicin for
synergy; the potential risk of nephrotoxicity with even low-doses of
gentamicin outweighs the theoretic benefit [23]. (See 'Considerations
for antibiotic selection' below.)
For children who are unable to receive penicillin antibiotics,
monotherapy with parenteral linezolid or daptomycin is an
alternative; ceftaroline is an alternative for children without a history
of anaphylaxis to penicillin or cephalosporin antibiotics. Consultation
with an expert in infectious diseases is suggested. The role of
ceftaroline in critically ill children with SSTI remains to be determined.
It provides an important option in communities with high rates
of clindamycin resistance; health care-associated SSTIs with onset in
the community or the hospital; and children with renal dysfunction,
inflammatory bowel disease, C. difficile-associated disease, or
intolerance to vancomycin.
Purulent/fluctuant SSTI — Skin abscesses, furuncles, and
carbuncles are purulent/fluctuant SSTI. Cellulitis also may be
associated with purulent drainage or exudate in the absence of a
drainable abscess (sometimes called purulent cellulitis, although the
terminology for this clinical constellation is inconsistent) [3,10].
Purulent/fluctuant SSTI usually are caused by S. aureus.
(See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical
manifestations, and diagnosis", section on 'Microbiology'.)
Drainage — We recommend incision and drainage of purulent and
fluctuant lesions (algorithm 1). Point-of-care ultrasonography may be
helpful in identifying lesions appropriate for incision and drainage (eg,
abscess) [24]. Application of moist heat may help to promote drainage
of small furuncles that are not amenable to incision and drainage
[3,12]. Although drainage is the mainstay of therapy, we also typically
administer adjunctive antibiotics (table 2 and table 3). (See 'Systemic
antimicrobial therapy' below.)
Children with cardiac conditions predisposing to adverse outcomes
from infectious endocarditis (eg, unrepaired cyanotic congenital heart
disease, repaired congenital heart defects with prosthetic defects,
etc) should receive prophylactic antibiotics before incision and
drainage. (See "Techniques for skin abscess
drainage" and "Antimicrobial prophylaxis for the prevention of
bacterial endocarditis", section on 'Clinical approach'.)
Purulent fluid should be sent for Gram stain, culture, and susceptibility
testing [11]. (See 'Laboratory evaluation' above.)
Drainage is the mainstay of therapy for purulent SSTI [3,10,25]. For
purulent/fluctuant SSTI that are <5 cm (2 inches) in diameter
(including surrounding erythema/cellulitis) in children ≥9 years and <4
cm (1.6 inches) in children 12 months through 8 years, drainage
appears to be more important than antimicrobial therapy [26-28]. The
effectiveness of drainage for purulent SSTI is supported by a meta-
analysis of four randomized trials in which most patients (>83 percent)
achieved successful outcomes whether they were assigned to
antibiotic therapy or placebo after incision and drainage [29]. In
additional randomized and observational studies, most patients with
uncomplicated MRSA skin abscesses who underwent incision and
drainage or spontaneous drainage improved despite adjunctive
antibiotics ineffective against MRSA [27,30-33]. Nonetheless,
adjunctive antibiotics are beneficial in preventing recurrence,
subsequent drainage procedures, and secondary spread [29].
Adjunctive antibiotics — Although drainage is the mainstay of
therapy for purulent SSTI, adjunctive antibiotics are also typically
administered (algorithm 1 and table 3). Adjunctive antibiotics are
associated with clinical improvement and may prevent recurrence,
subsequent drainage, and secondary spread [29,34,35].
●For hemodynamically stable children with purulent/fluctuant
SSTI of the face, hand, or perineum and hemodynamically stable
children from communities in which ≥10 to 15 percent of S.
aureus isolates are MRSA, we provide initial coverage for
MRSA. Clindamycin, doxycycline, and trimethoprim-
sulfamethoxazole (TMP-SMX) are options for oral therapy;
clindamycin and vancomycin are options for initial parenteral
therapy (table 3). The choice of initial empiric therapy should be
determined by local susceptibility patterns.
Second-line parenteral agents
include ceftaroline, linezolid, daptomycin, and tedizolid (for
children ≥12 years of age). Among these, we prefer ceftaroline or
linezolid. However, second-line parenteral agents are rarely used
because of cost. (See 'Systemic antimicrobial therapy' below.)
In a multicenter randomized trial, TMP-SMX
and clindamycin were similarly efficacious in the treatment of
uncomplicated SSTI in children and adults (with cure rates of 80
to 90 percent in both treatment arms) [36]. Trials comparing
clindamycin or TMP-SMX with doxycycline are lacking.
 ●For hemodynamically stable children with purulent/fluctuant
SSTI that do not involve the face, hand, or perineum and who are
from communities in which <10 to 15 percent of S. aureus isolates
are MRSA, we provide coverage for
MSSA. Cefuroxime, cephalexin, dicloxacillin, and cloxacillin (not
available in the United States) are options for oral therapy. Among
these, we prefer cephalexin because of its narrow spectrum and
three times a day dosing. We tend to avoid dicloxacillin because
it must be given four times per day (table 2 and table
3). Clindamycin, TMP-SMX, and doxycycline are alternatives for
children who are unable to receive penicillin and cephalosporin
antibiotics.
Cefazolin, clindamycin, nafcillin, and oxacillin are options for
parenteral therapy. (See 'Considerations for antibiotic
selection' below.)
Adjunctive antibiotics are particularly important for children with
[3,10,28]:
●Systemic signs
●Underlying medical problems that increase the risk of poor
response or complications (eg, primary immune deficiency,
diabetes mellitus)
●Multiple sites of infection
●Age <12 months
●Lesions ≥5 cm (2 inches) in diameter (including surrounding
erythema/cellulitis) in children age ≥9 years and ≥4 cm (1.6
inches) in diameter in children age 12 months through 8 years
●Lesions of the face, hand, or perineum (which are difficult to
drain)
●Lesions near an implanted device
Most strains of MRSA that cause SSTI in the community are relatively
susceptible to clindamycin, TMP-SMX, and doxycycline [37-39].
However, given temporal and geographic variability [40,41] and the
challenges of distinguishing true community-onset infections from
community-onset health care-associated infections, empiric therapy
should be determined by local resistance patterns. Some strains are
resistant to one or more of these antibiotics, and some have
susceptibility patterns similar to nosocomial isolates [42-45]. We do
not use fluoroquinolones (eg, ciprofloxacin) or macrolides
(eg, erythromycin, azithromycin) for the treatment of MRSA SSTI
because community isolates of MRSA are relatively resistant to them
[46,47].
In a meta-analysis of four randomized trials (including 2406
participants) of patients who underwent drainage for a skin or soft
tissue abscess [25,26,28,48], fewer patients receiving adjunctive
antibiotics than placebo had treatment failure (7.7 versus 16.1
percent, calculated risk difference 7.4 percent, 95% CI 2.8-12.1
percent) or developed new lesions within 10 to 30 days (6.2 versus
15.3 percent, calculated risk difference 10 percent, 95% CI 7.2-12.8
percent) [29]. Although the rate of adverse events was increased
among antibiotic recipients (calculated risk difference 4.4 percent,
95% CI 1.0-7.8 percent), most of the adverse events were mild (eg,
gastrointestinal symptoms, mild rashes).
Other randomized trials [36,49,50] and observational studies
[13,27,51-53] suggest that, in addition to incision and drainage as
indicated, appropriate antimicrobial therapy is associated with clinical
improvement, particularly for children with lesions ≥4 to 5 cm (1.6 to
2 inches) in diameter, depending on age, but even for smaller lesions.
The effect of adjunctive antimicrobial therapy on secondary spread
has not been well studied, but there is some evidence to suggest that
adjunctive antibiotics are beneficial in preventing secondary spread
[34].
Cellulitis — Antimicrobial therapy is the cornerstone of therapy for
typical (nonpurulent) cellulitis (algorithm 2). Typical cellulitis usually is
caused by beta-hemolytic streptococci, particularly GAS, but also
may be caused by S. aureus. (See "Cellulitis and skin abscess:
Epidemiology, microbiology, clinical manifestations, and diagnosis".)
●For hemodynamically stable children with typical cellulitis
and risk factors for MRSA (table 1), we provide initial coverage
for both beta-hemolytic Streptococcus and MRSA.
Options for oral therapy include monotherapy with clindamycin or
combination therapy with a beta-lactam antibiotic
(eg, amoxicillin or cephalexin) plus either TMP-SMX
or doxycycline. Among these, we prefer monotherapy with
clindamycin unless the local prevalence of clindamycin-
resistant S. aureus is ≥15 percent (table 2 and table 3) [3].
Options for parenteral therapy
include clindamycin and vancomycin. Linezolid, ceftaroline,
or daptomycin is also available for children with complicated
SSTI. Tedizolid is available for children ≥12 years [54], but its use
is limited by cost. (See 'Considerations for antibiotic
selection' below.)
●For hemodynamically stable children with typical cellulitis and no
risk factors for MRSA (table 1), we provide initial coverage for
both beta-hemolytic Streptococcus and MSSA. We broaden
coverage to include MRSA if initial therapy is unsuccessful.
(See 'Failure to respond' below.)
 First-generation cephalosporins (eg, cephalexin, cefadroxil),
second-generation cephalosporins
(eg, cefuroxime), cloxacillin (not available in the United States),
and dicloxacillin are options for oral therapy. Among these, we
prefer cephalexin because of its narrow spectrum and three times
a day dosing. We tend to avoid dicloxacillin because it must be
given four times per day (table 2 and table 3) [55]. Clindamycin is
an alternative for children who are unable to receive penicillin or
cephalosporin antibiotics.
Cefazolin, clindamycin, nafcillin, and oxacillin are options for
parenteral therapy. (See 'Considerations for antibiotic
selection' below.)
For patients with cellulitis and no risk factors for MRSA, it is not
necessary to provide empiric coverage for MRSA. In a multicenter
randomized trial in 153 patients (predominantly adults) with
nonpurulent cellulitis, the cure rates were comparable among
those treated with cephalexin (82 percent) and combination
cephalexin/TMP-SMX (85 percent) [56]. In another multicenter
trial, 500 patients >12 years of age with nonpurulent cellulitis were
randomly assigned to empiric treatment with cephalexin plus
either TMP-SMX or placebo [57]. Cure rates at 14 to 21 days did
not differ between groups, although the results were imprecise
(76.2 versus 69 percent, difference 7.3 percent, 95% CI -1.0 to
15.5).
Erysipelas — Antimicrobial therapy is the cornerstone of therapy for
erysipelas (picture 4). For children with erysipelas, we provide
antimicrobial coverage for beta-hemolytic Streptococcus (algorithm
3 and table 3). Options for oral therapy include amoxicillin and
penicillin; cephalexin and clindamycin are alternatives. Options for
parenteral therapy include cefazolin, nafcillin, oxacillin,
and ceftriaxone; clindamycin is an alternative for children who cannot
receive penicillin or cephalosporin antibiotics. (See "Cellulitis and skin
abscess: Epidemiology, microbiology, clinical manifestations, and
diagnosis", section on 'Cellulitis and erysipelas'.)
Impetigo or folliculitis — Impetigo and folliculitis are superficial
SSTI. For localized, superficial SSTI in children without systemic
symptoms, we provide outpatient management with topical antibiotics
(eg, mupirocin) [3,10,11]. (See "Impetigo", section on 'Limited
impetigo' and "Infectious folliculitis", section on 'Staphylococcal
folliculitis'.)
For superficial SSTI that involves multiple sites, we provide oral
antimicrobial therapy that includes coverage for both S. aureus and
beta-hemolytic Streptococcus. (See "Impetigo", section on 'Extensive
impetigo and ecthyma' and "Infectious folliculitis", section on
'Staphylococcal folliculitis'.)

SYSTEMIC ANTIMICROBIAL THERAPY

Treatment setting — We generally hospitalize the following

children with skin and soft tissue infection (SSTI) for parenteral
antimicrobial therapy:
●Systemic signs, including fever (>38°C [100.4°F]), tachycardia,
hypotension, or systemic inflammatory response syndrome
(see "Systemic inflammatory response syndrome (SIRS) and
sepsis in children: Definitions, epidemiology, clinical
manifestations, and diagnosis", section on 'Systemic
inflammatory response syndrome')
 ●Rapid progression of erythema
●Limb-threatening infection (eg, necrotizing soft tissue infection,
pyomyositis) (see "Necrotizing soft tissue infections", section on
'Treatment')
●Children with underlying medical problems that may be
associated with poor response or complications (eg, malignancy,
primary immune deficiency, diabetes mellitus)
●Children who are unable to tolerate oral medications
●Children with SSTI close to an implanted device
We usually provide the first one or two doses of antimicrobial
therapy parenterally (eg, in an emergency department observation
or "short stay" unit if one is available) for SSTI in:
●Children (of any age) with multiple sites of nonsuperficial
infection (ie, infections other than impetigo or folliculitis)
●Children <5 years with abscesses on the face or perineum
●Children age 29 days through 11 months with SSTI ≥3 cm (1.2
inches) in diameter (including surrounding erythema/cellulitis) or
age 12 months through 4 years with SSTI ≥4 cm (1.6 inches) in
diameter
We typically initiate antimicrobial therapy orally for children with
indications for antimicrobial therapy who do not meet the above
criteria for hospitalization or initial parenteral therapy.
Considerations for antibiotic selection — The choice of the initial
antimicrobial regimen is guided by clinical features, desired spectrum
of coverage, and local S. aureus susceptibility data (table 2 and table
3) [10,11,20,58]. Information regarding local susceptibility patterns
can be obtained from local public health officials or hospital
laboratories. When the etiologic agent and susceptibility are known,
antimicrobial therapy can be narrowed as indicated.
In vitro susceptibility studies, observational studies, and randomized
trials support the effectiveness of beta-lactam antibiotics (eg,
penicillins, cephalosporins) [56,57,59-
64], clindamycin [29,34,36,42,49,65,66], trimethoprim-
sulfamethoxazole (TMP-SMX)
[4,29,36,46,53,66,67], tetracycline/doxycycline [30,68,69], vancomyc
in [70-72], linezolid [71-76], ceftaroline [77-79], and daptomycin for
the treatment of SSTI in children [80]. Few studies have directly
compared one of these agents with another.
Factors that may help in choosing among antimicrobial regimens that
provide adequate coverage for S. aureus and/or beta-
hemolytic Streptococcus include:
●Antimicrobial stewardship – When multiple therapeutic
options are available for empiric therapy, the option with the
narrowest therapeutic range should be prioritized [81]. When the
etiologic agent and susceptibility are known, antimicrobial therapy
can be further narrowed as indicated.
Avoiding vancomycin, clindamycin, linezolid, tedizolid, ceftarolin
e, and daptomycin when the isolate is methicillin-susceptible and
the patient is not allergic to beta-lactam antibiotics may help to
minimize promotion of resistance to these drugs, which are crucial
to the treatment of invasive infections [19]. (See "Staphylococcus
aureus in children: Overview of treatment of invasive infections",
section on 'MRSA infections'.)
●Local prevalence of clindamycin-resistant S. aureus –
Avoidance of clindamycin may be warranted if the prevalence of
clindamycin-resistant S. aureus is ≥15 percent.
●Ability of the child to swallow pills and palatability of liquid
antibiotics – Therapeutic options may be limited if the child
cannot swallow pills. Adherence to oral therapy may be
challenging if oral solutions are unpalatable [55]. Flavoring can be
can be added to clindamycin solution to overcome the unpleasant
taste [82,83]; alternately, the contents of clindamycin capsules
can be emptied into a small amount of chocolate syrup,
applesauce, or yogurt.
●Age of the child – Tetracycline antibiotics may cause
permanent tooth discoloration if used repeatedly for children <8
years. However, doxycycline binds less readily to calcium than
other tetracycline antibiotics and, in some studies, was not
associated with visible teeth staining in children <8 years [84-87].
Thus, doxycycline may be used for ≤21 days in children of all ages
[87]. Tedizolid is available only for children ≥12 years of age [54].
●Cost, adverse effects, and clinical experience – The use
of linezolid for SSTI is limited by cost and toxicity (bone marrow
suppression, peripheral and optic neuropathy) if used for a
prolonged time [10,88]. The use of tedizolid is also limited by cost.
These agents should be reserved for those who do not respond
to or cannot tolerate other agents or whose isolates are resistant
to clindamycin and TMP-SMX.
Clinical experience with ceftaroline, daptomycin, and tedizolid in
children with SSTI is limited and their role remains to be
determined. Nonetheless, they provide an important option in
communities with high rates of clindamycin resistance; health
care-associated SSTIs with onset in the community or the
hospital; and children with renal dysfunction, inflammatory bowel
disease, C. difficile-associated disease, or intolerance
to vancomycin.
Switching from parenteral to oral therapy — Results of antibiotic
susceptibility testing should be used to make decisions about which
oral antibiotic to use for continuation of systemic therapy (table
2 and table 3). For children with negative cultures or in whom cultures
were not obtained, we usually continue/initiate clindamycin for
children with nonpurulent SSTI and continue clindamycin or switch to
TMP-SMX for children purulent/fluctuant SSTI.

For children with systemic signs and underlying medical problems

that increase the risk of poor response or complications (eg,
malignancies, primary immune deficiency, diabetes mellitus), we
continue parenteral therapy at least until all of the following criteria
are met:

●Resolution of systemic symptoms and fever

●Improvement in other clinical findings (see 'Monitoring
response' below)
●Antibiotic susceptibility results are available
●Child is able to tolerate an oral agent

For children with multiple sites of infection, children <5 years with
abscesses of the face or perineum, and children age 29 days through
11 months in children with SSTI ≥3 cm (1.2 inches) in diameter
(including surrounding erythema/cellulitis) or age 12 months through
4 years with SSTI ≥4 cm (1.6 inches), we switch to oral therapy after
one or two doses of parenteral therapy provided that the child is well-
appearing, able to tolerate oral medications, and able to adhere to
oral regimen and follow-up plans.

Total duration — The total duration of systemic therapy for

staphylococcal or streptococcal SSTI is not well studied. It depends
upon the clinical syndrome and clinical response. A duration of five
days is generally adequate for purulent/fluctuant SSTI, cellulitis,
erysipelas, impetigo, and folliculitis, provided the patient improves
clinically and the course is uncomplicated. The duration may be
extended if the clinical response is inadequate or complications
develop.
Our suggested five-day course of therapy for uncomplicated SSTI in
children is supported by stratified analysis of randomized trial that
compared 3 with 10 days of antibiotic therapy (TMP-SMX) following
surgical drainage of uncomplicated skin abscess [89]. Children with
MRSA infection who were assigned to three days of therapy had
increased rates of treatment failure, defined as persistent or
increased size of the original abscess requiring additional antibiotic
therapy or surgical incision and drainage and one-month recurrence.

RESPONSE TO THERAPY

Monitoring response — Response to therapy is indicated by clinical

improvement after 48 hours. In children who are admitted to the
hospital for antimicrobial therapy, we monitor the skin and soft tissue
infection (SSTI) for improvement or progression, the patient's vital
signs, and culture and susceptibility results (if obtained).
Children who are treated for SSTI in the outpatient setting should be
instructed to seek medical care promptly if they develop systemic
symptoms or if local symptoms worsen [12]. They should be seen for
follow-up within 48 hours (whether or not antimicrobial therapy is
prescribed). Follow-up is essential to ensure clinical improvement and
determine the need for additional drainage or change in antimicrobial
therapy [90].
Failure to respond — Additional drainage procedures and/or
initiation of or change in antimicrobial therapy (guided by culture and
susceptibility results, if available) may be warranted for patients who
have not improved after 48 hours of observation or antimicrobial
therapy (table 2). Patients with purulent/fluctuant lesions who did not
respond to incision and drainage alone should be treated with
antibiotics; repeat incision and drainage also may be warranted.
Possible explanations for failure to respond in patients receiving an
agent to which their isolate is susceptible include inadequate drainage
(if drainage was performed), reformation of the abscess, development
of a new abscess, or poor compliance with oral therapy.
Ultrasonography may identify residual, recurrent, or new abscesses
that require drainage [24].
If cultures remain negative and new or reformed abscesses are not
identified, a change to second-line empiric therapy may be indicated
(table 2).
Recurrence
●Purulent infection – Reported recurrence rates for methicillin-
resistant S. aureus (MRSA) SSTI range from 19 to 63 percent,
even after successful treatment [22,91-94]. It is important to look
for local predisposing conditions (eg, pilonidal cyst, hidradenitis
suppurativa, foreign material) in children who have recurrent SSTI
at the same site. (See "Pilonidal disease", section on 'Clinical
manifestations' and "Hidradenitis suppurativa: Pathogenesis,
clinical features, and diagnosis", section on 'Clinical
manifestations'.)
Recurrence is usually treated in the same way as the initial
episode. In a retrospective analysis of 264 MRSA isolates from
105 otherwise healthy children (birth to 18 years) with recurrent
MRSA SSTI, 90 percent of recurrent infections were caused by a
strain identical to that in the previous episode [95]. Strategies to
eliminate colonization are sometimes used, but the effectiveness
of this approach in reducing recurrences is not clear [96].
(See "Methicillin-resistant Staphylococcus aureus (MRSA) in
children: Prevention and control", section on 'Children with
recurrent MRSA infection'.)
For patients with recurrent infection due to S. aureus, attempting
decolonization is reasonable. (See "Methicillin-resistant
Staphylococcus aureus (MRSA) in children: Prevention and
control", section on 'Children with recurrent MRSA infection'.)
●Nonpurulent infection – Recurrences occur in approximately
14 percent of cellulitis cases within one year and 45 percent of
cases within three years, usually in the same location [97].
Conditions that predispose to recurrent cellulitis include obesity,
immunosuppression, edema due to impaired lymphatic drainage,
venous insufficiency, and tinea pedis [98-106].
Management of recurrent cellulitis includes evaluation for
alternative diagnoses. Predisposing conditions should be
identified and alleviated if possible. The approach to antimicrobial
therapy for recurrent cellulitis is the same as that for the initial
episode. (See "Cellulitis and skin abscess: Epidemiology,
microbiology, clinical manifestations, and diagnosis", section on
'Differential diagnosis'.)
 PREVENTION Patient education regarding methods to

prevent spread of infection to others is an essential component of

management of methicillin-resistant S. aureus skin and soft tissue
infection [9]. (See "Methicillin-resistant Staphylococcus aureus
(MRSA) in children: Prevention and control", section on 'Prevention in
the community'.)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected

countries and regions around the world are provided separately.
(See "Society guideline links: Skin and soft tissue
infections" and "Society guideline links: Management of
Staphylococcus aureus infection".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The

Basics" and "Beyond the Basics." The Basics patient education
pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might
have about a given condition. These articles are best for patients who
want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer,
more sophisticated, and more detailed. These articles are written at
the 10th to 12th grade reading level and are best for patients who want
in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic.
We encourage you to print or email these topics to your patients. (You
can also locate patient education articles on a variety of subjects by
searching on "patient education" and the keyword[s] of interest.)

●Basics topic (see "Patient education: Methicillin-resistant

Staphylococcus aureus (MRSA) (The Basics)")
●Beyond the Basics topic (see "Patient education: Methicillin-
resistant Staphylococcus aureus (MRSA) (Beyond the Basics)")