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.
●(See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
●(See "Impetigo".)
●(See "Infectious folliculitis".)
●(See "Skin and soft tissue infections in neonates: Evaluation and management".)
●(See "Methicillin-resistant Staphylococcus aureus (MRSA) in children: Prevention and control".)
●(See "Staphylococcus aureus in children: Overview of treatment of invasive infections".)
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 "Human bites: Evaluation and management", section on 'Spectrum of antibiotic coverage' and "Animal bites (dogs, cats, and other mammals): Evaluation and management", section on 'Spectrum of antibiotic coverage'.)
•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 "Primary 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 a retrospective review of data from 38 hospitals between 2012 and 2018, blood cultures were positive in only 0.6 percent of emergency department encounters and 1 percent of hospitalization encounters for children with SSTIs who had a blood culture obtained [19]. 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 "Methicillin-resistant Staphylococcus aureus (MRSA): Microbiology and laboratory detection".)
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 [2,9,12,20]. 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 [21]; 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 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 [22]. In addition, nasal and wound isolates may be discordant with respect to antimicrobial susceptibility and pulsed-field gel electrophoresis [23].
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 "Primary 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 "Invasive group A streptococcal infections 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 3A-B); 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 [24]. (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) [25]. 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 3A-B). (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 "Prevention of endocarditis: Antibiotic prophylaxis and other measures".)
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 [3,10,26]. 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 [27-29]. 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 [30]. 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 [28,31-34]. Nonetheless, adjunctive antibiotics are beneficial in preventing recurrence, subsequent drainage procedures, and secondary spread [30].
Adjunctive antibiotics — Although drainage is the mainstay of therapy for purulent SSTI, adjunctive antibiotics are also typically administered (algorithm 1 and table 3A). Adjunctive antibiotics are associated with clinical improvement and may prevent recurrence, subsequent drainage, and secondary spread [30,35,36].
●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 3A). The choice of initial empiric therapy should be determined by local susceptibility patterns.
Second-line parenteral agents include ceftaroline, linezolid, daptomycin, dalbavancin, tedizolid (for children ≥12 years of age), oritavancin (for children ≥18 years of age), and telavancin (for children ≥18 years of age). Among these, we prefer ceftaroline or linezolid. Although experience with dalbavancin in children is limited, it may be reasonable for children who would not be able to complete therapy with an oral agent. 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) [37]. 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 and the oral suspension is not well tolerated by children (table 2 and table 3A-B). 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 [3,10,29]:
●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 [38-40]. However, given temporal and geographic variability [41,42] 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 [43-46]. 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 [47,48].
In a meta-analysis of four randomized trials (including 2406 participants) of patients who underwent drainage for a skin or soft tissue abscess [26,27,29,49], 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) [30]. 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 [37,50,51] and observational studies [13,28,52-54] 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 [35].
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".)
●Risk factors for MRSA – 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 3A-B) [3].
Options for parenteral therapy include clindamycin and vancomycin. Linezolid, ceftaroline, daptomycin, or dalbavancin is also available for children with complicated SSTI. Tedizolid is available for children ≥12 years [55], but its use is limited by cost. (See 'Considerations for antibiotic selection' below.)
●No risk factors for MRSA – 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; the oral suspension of dicloxacillin is poorly tolerated by children. We also tend to avoid dicloxacillin because it must be given four times per day (table 2 and table 3A-B) [56]. 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) [57]. 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 [58]. 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 3A). 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
●Hospitalization for parenteral therapy – 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 "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
●Initial parenteral therapy in emergency department or "short stay" unit – 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
●Outpatient oral therapy – 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 3A-B) [10,11,21,59]. Information regarding local susceptibility patterns can be obtained from local public health officials or hospital laboratories. In several geographic areas of the United States (Northeast, West), resistance to trimethoprim-sulfamethoxazole increased among methicillin-resistant S. aureus (MRSA) isolates between 2012 and 2018 [60]. 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) [57,58,61-66], clindamycin [30,35,37,43,50,67,68], trimethoprim-sulfamethoxazole (TMP-SMX) [4,30,37,47,54,68,69], tetracycline/doxycycline [31,70,71], vancomycin [72-74], linezolid [73-78], ceftaroline [79-81], daptomycin, and dalbavancin [82,83] for the treatment of SSTI in children [84]. 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 [85]. When the etiologic agent and susceptibility are known, antimicrobial therapy can be further narrowed as indicated.
Avoiding vancomycin, clindamycin, linezolid, tedizolid, ceftaroline, daptomycin, and dalbavancin 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 [20]. (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 [56]. Flavoring can be can be added to clindamycin solution to overcome the unpleasant taste [86,87]; 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 [88-91]. Thus, doxycycline may be used for ≤21 days in children of all ages [91]. Tedizolid is available only for children ≥12 years of age [55].
●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 [10,92]. The use of tedizolid and dalbavancin 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, tedizolid, and dalbavancin 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. Dalbavancin may be an attractive option for management of children for whom completing therapy with an oral antibiotic is challenging for some reason, such as children with short bowel syndrome or those requiring parenteral nutrition.
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 3A-B). 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 antimicrobial agent, clinical syndrome, and clinical response.
●Antibiotics other than dalbavancin – For antibiotics other than dalbavancin, 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 treated with antibiotics other than dalbavancin 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 [93]. 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.
●Dalbavancin – For children <18 years of age, dalbavancin is given in a single intravenous dose. Its effective half-life is approximately nine days [82,94].
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 [95].
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 [25].
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 [23,96-99]. 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 [100]. Strategies to eliminate colonization are sometimes used, but the effectiveness of this approach in reducing recurrences is not clear [101]. (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 [102]. Conditions that predispose to recurrent cellulitis include obesity, immunosuppression, edema due to impaired lymphatic drainage, venous insufficiency, and tinea pedis [103-111].
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)")
SUMMARY AND RECOMMENDATIONS
●Etiology – Purulent/fluctuant skin and soft tissue infections (SSTI) usually are caused by Staphylococcus aureus (either methicillin-susceptible S. aureus [MSSA] or methicillin-resistant S. aureus [MRSA]). Cellulitis is usually caused by group A Streptococcus and other beta-hemolytic streptococci, 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 'Etiology' above.)
●Evaluation – The history and examination of a child with suspected S. aureus or streptococcal SSTI focuses on risk factors for MRSA (table 1), factors predisposing to infection with other pathogens, the type and extent of SSTI (eg, abscess (picture 5), furuncle, carbuncle (picture 3), cellulitis, erysipelas (picture 4), impetigo (picture 1B)), and associated systemic signs (eg, fever >38°C [100.4°F], hypotension, tachycardia). (See 'History' above and 'Examination' above.)
Laboratory evaluation is necessary to determine the microbiologic etiology of SSTI.
•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.
•We obtain blood cultures from patients with signs of serious systemic infection (eg, prolonged fever, tachycardia, hypotension), neutropenia or immunodeficiency, animal bites, or immersion injuries.
•We do not obtain routine nasal cultures from children presenting with possible MRSA SSTI. (See 'Laboratory evaluation' above.)
●Management – Our approach to the management of suspected S. aureus or streptococcal SSTI in children varies with the clinical status of the child and the type of SSTI (algorithm 1 and algorithm 2 and algorithm 3):
•For children with SSTI and hemodynamic instability, we suggest initial parenteral antimicrobial coverage for MRSA, MSSA, and beta-hemolytic Streptococcus (table 2) (Grade 2C); additional coverage for gram-negative pathogens may be necessary. (See 'SSTI and hemodynamic instability' above.)
•For most hemodynamically stable children with purulent/fluctuant SSTI, we suggest adjunctive antibiotic therapy in addition to drainage rather than drainage alone (algorithm 1 and table 3A) (Grade 2B). (See 'Purulent/fluctuant SSTI' above.)
-For hemodynamically stable children with cellulitis and no risk factors for MRSA, we provide empiric antimicrobial coverage for beta-hemolytic Streptococcus and MSSA (algorithm 2 and table 3A). For children with risk factors for MRSA, we provide empiric antimicrobial coverage for beta-hemolytic Streptococcus and MRSA (algorithm 2 and table 3A). (See 'Cellulitis' above.)
-For hemodynamically stable children with erysipelas, we provide empiric antimicrobial coverage for beta-hemolytic Streptococcus (algorithm 3 and table 3A). (See 'Erysipelas' above.)
•For children with localized impetigo or folliculitis and no systemic signs (fever, hypotension, tachycardia), we provide topical antibiotic therapy. For children with multiple sites of impetigo or folliculitis, we provide systemic antimicrobial therapy. (See "Impetigo", section on 'Treatment' and "Infectious folliculitis", section on 'Staphylococcal folliculitis'.)
●Response to therapy – Response to therapy is indicated by clinical improvement after 48 hours. Additional drainage procedures and/or change in or initiation of 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 or observation if adjunctive antibiotics were not administered initially (table 2 and table 3A-B). (See 'Response to therapy' above.)
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