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Impetigo
Author
Larry M Baddour, MD, FIDSA
Section Editors
Daniel J Sexton, MD
Sheldon L Kaplan, MD
Deputy Editor
Elinor L Baron, MD, DTMH
Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2012. |This topic last updated: nov 28, 2012.
INTRODUCTION Impetigo is a contagious superficial bacterial infection observed most frequently in children. It may be
classified as primary impetigo (direct bacterial invasion of previously normal skin) or secondary impetigo (infection at sites
of minor skin trauma such as abrasions, minor trauma, and insect bites, or underlying conditions such as eczema).
Pyoderma and impetigo contagiosa are sometimes used as synonyms for impetigo.
Impetigo is most frequently observed in children ages two to five years, although older children and adults may also be
affected. The infection usually occurs in warm, humid conditions and is easily spread among individuals in close contact;
risk factors include poverty, crowding, poor hygiene, and underlying scabies [1]. Carriage of group A streptococcus (GAS)
and Staphylococcus aureus predisposes to subsequent impetigo [2].
CLINICAL MANIFESTATIONS Variants of impetigo include non-bullous impetigo, bullous impetigo, and ecthyma.
Poststreptococcal glomerulonephritis and rheumatic fever following impetigo have also been described.
Non-bullous impetigo Non-bullous impetigo is the most common form of impetigo. Lesions begin as papules that
progress to vesicles surrounded by erythema. Subsequently they become pustules that enlarge and break down to form
thick, adherent crusts with a characteristic golden appearance; this evolution usually occurs over about one week (picture
1 and picture 2). Lesions usually involve the face and extremities. Multiple lesions may develop but tend to remain welllocalized. Regional lymphadenitis may occur, although systemic symptoms are usually absent.
Bullous impetigo Bullous impetigo is a form of impetigo seen in young children in which the vesicles enlarge to form
flaccid bullae with clear yellow fluid, which later becomes darker and more turbid; ruptured bullae leave a thin brown crust
[3,4]. Usually there are fewer lesions than in non-bullous impetigo, and the trunk is more frequently affected.
Bullous impetigo is due to strains of S. aureus that produce exfoliative toxin A, a toxin that causes loss of cell adhesion in
the superficial epidermis by targeting the protein desmoglein 1 [5]. This mechanism is related to the pathophysiology of
pemphigus, in which autoantibodies are directed against the same protein [6]. (See "Pemphigus".)
Ecthyma Ecthyma is an ulcerative form of impetigo in which the lesions extend through the epidermis and deep into
the dermis. They consist of "punched-out" ulcers covered with yellow crust surrounded by raised violaceous margins [7].
POST INFECTIOUS SEQUELAE
Poststreptococcal glomerulonephritis Most cases of poststreptococcal glomerulonephritis are believed to result
from streptococcal impetigo rather than streptococcal throat infection [8].
It is unclear whether antimicrobial therapy for impetigo reduces the risk of poststreptococcal glomerulonephritis [9]. (See
"Poststreptococcal glomerulonephritis in children".)

Rheumatic fever In Australian aboriginal communities, where acute rheumatic fever is hyperendemic, low rates of
streptococcal pharyngitis and high rates of impetigo have been observed [10]. Observers have hypothesized that
streptococcal skin infections such as impetigo may be protective against pharyngitis but may be followed by invasive
sequelae such as acute rheumatic fever.
MICROBIOLOGY The principal pathogen is S. aureus. Beta-hemolytic streptococci (primarily group A, but occasionally
other serogroups such as C and G) accounts for a minority of cases, either alone or in combination with S. aureus [11-13].
The relative frequency of S. aureus infections has changed with time. It was predominant in the 1940s and 1950s, after
which group A streptococci became more prevalent. Since the 1990s, S. aureus has become more common again [14],
though impetigo due to community-acquired methicillin-resistant S. aureus (CA-MRSA) has occurred in a small minority of
cases [15]. This may be due, in part, to the observation that CA-MRSA strains that harbor exfoliative genes have rarely
been reported; strains associated with impetigo usually have the exfoliative genes [16]. Bullous impetigo is caused by
strains of S. aureus that produce a toxin causing cleavage in the superficial skin layer (see 'Bullous impetigo' above).
Streptococcal colonization of intact skin precedes inoculation via breaches in the skin; bacteria may be subsequently
transferred from the skin to the upper respiratory tract. The group A streptococcus virulence factor, emm protein, can be
encoded by one of five chromosome patterns of emm genes (denoted A through E) [17]. Pharyngeal strains usually have
patterns A-C, while nearly all impetigo strains have patterns D or E [18]. The impetigo strains patterns are rarely observed
among invasive clinical isolates [19].
DIAGNOSIS The diagnosis of impetigo is made on the basis of clinical manifestations. Impetigo may be distinguished
from contact dermatitis in that impetigo lesions are painful whereas contact dermatitis lesions are pruritic. Diagnostic
confusion can also occur with other skin diseases including bullous pemphigoid and Stevens Johnsons syndrome. (See
"Stevens-Johnson syndrome and toxic epidermal necrolysis: Clinical manifestations; pathogenesis; and diagnosis" and
"Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid", section on 'Bullous
pemphigoid'.)
Cultures of pus or bullae fluid may be useful in patients who fail to respond to empiric therapy, although swabs of intact
skin are not helpful and should not be performed.
Serologic testing for streptococcal antibodies is not useful for the diagnosis of impetigo; the anti-streptolysin O (ASO)
response is weak, likely because skin lipids suppress streptolysin O response [20-22]. Anti-deoxyribonulease B (antiDnase B) and antihyaluronidase (AHT) response are more reliable than the ASO response following GAS skin infections.
However, serologic testing can be helpful in the setting of impetigo with subsequent presumed poststreptococcal
glomerulonephritis.
TREATMENT Treatment of impetigo is important for reducing spread of infection and for hastening the resolution of
discomfort and cosmetic appearance [23]. The treatment of impetigo should include antimicrobial therapy with activity
against beta-hemolytic streptococci and S. aureus. Options include both topical and oral systemic therapy; local
resistance patterns should be considered in antibiotic selection [24].
Topical therapy Topical therapy should be administered if there are a limited number of lesions without bullae. Topical
therapy has fewer side effects and lower risk for contributing to bacterial resistance compared to oral therapy [23].
Mupirocin, fusidic acid, and retapamulin are probably equally effective topical therapies [23,25-33]; fusidic acid is not
available in the United States.
An alternative to topical antibiotics is hydrogen peroxide cream; it was as effective as fusidic acid in a randomized trial of
256 patients with impetigo (efficacy 70 to 80 percent) [26].

Although the components of over-the-counter triple antibiotic ointments (consisting of bacitracin-neomycin-polymyxin B)

do have some activity against the organisms causing impetigo, they may not be as effective for treatment [27]. Bacitracin
and neomycin can also cause contact dermatitis.
Oral antibiotics Oral antibiotic therapy should be used for impetigo when the lesions are bullous, and when it is
impractical to use topical therapy either due to the extent or location of lesions. Appropriate agents include dicloxacillin,
cephalexin, or clindamycin (table 1) [28,29]. In the setting of beta-lactam allergy or suspected MRSA (table 2), appropriate
choices are outlined in the Table (table 3). (See "Treatment of skin and soft tissue infections due to methicillin-resistant
Staphylococcus aureus in adults" and "Evaluation and management of suspected methicillin-resistant Staphylococcus
aureus skin and soft tissue infections in children", section on 'Antimicrobial therapy'.)
Macrolides are not adequate therapy given increasing resistance among S. pyogenes and S. aureus [30,31]. Penicillin
was previously useful for treatment of impetigo but is no longer adequate given the significant role of S. aureus (most
strains of which produce beta-lactamase that can inactivate penicillin and ampicillin) [32]. Fluoroquinolones should NOT
be used to treat impetigo, as MRSA resistance to this class is widespread and resistance can develop on therapy.
Trimethoprim-sulfamethoxazole has activity against MRSA but does not have activity against streptococci. (See
"Treatment of skin and soft tissue infections due to methicillin-resistant Staphylococcus aureus in adults" and "Evaluation
and management of suspected methicillin-resistant Staphylococcus aureus skin and soft tissue infections in children",
section on 'Antimicrobial therapy'.)
Follow-up The duration of antimicrobial therapy should be tailored to clinical improvement; seven days of treatment is
usually sufficient [33]. Crusted lesions can be washed gently. Handwashing is important for reducing spread among
children, and other preventive measures employed in reducing the spread of staphylococci may also be helpful [34,35].
(See "Prevention and control of methicillin-resistant Staphylococcus aureus in adults".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, The Basics and Beyond
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the Basics. The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and
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pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level
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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to
your patients. (You can also locate patient education articles on a variety of subjects by searching on patient info and the
keyword(s) of interest.)

Basics topics (see "Patient information: Impetigo (The Basics)")

Beyond the Basics topics (see "Patient information: Impetigo (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Impetigo is a contagious superficial bacterial infection manifesting on the face and extremities with lesions that
progress from papules to vesicles, pustules, and crusts. Less common manifestations include bullous impetigo
and ecthyma. Impetigo may be followed by poststreptococcal glomerulonephritis or rheumatic fever. (See 'Clinical
manifestations' above.)

The principal pathogen is S. aureus; beta-hemolytic streptococci (primarily group A, but occasionally other
serogroups such as C and G) cause a minority of cases, either alone or in combination with S. aureus. (See
'Microbiology' above.)

For management of impetigo with a small number of non-bullous lesions, we recommend treatment with topical
therapy rather than oral therapy (Grade 1A). (See 'Treatment' above.)

For all other forms of impetigo, we recommend treatment with oral antibiotic therapy (Grade 1B). Appropriate
agents include dicloxacillin, cephalexin, or clindamycin (table 1). In the setting of beta-lactam allergy or suspected
MRSA, appropriate choices include clindamycin or linezolid (table 4). (See 'Treatment' above.)

The duration of antimicrobial therapy should be tailored to clinical improvement; seven days is usually sufficient.
(See 'Treatment' above.)

Handwashing is important for reducing spread among children, and other preventive measures employed in
reducing the spread of staphylococci may also be helpful. (See "Prevention and control of methicillin-resistant
Staphylococcus aureus in adults".)
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REFERENCES

1. Lejbkowicz F, Samet L, Belavsky L, Bitterman-Deutsch O. Impetigo in soldiers after hand-to-hand combat training. Mil
Med 2005; 170:972.
2. Dajani AS, Ferrieri P, Wannamaker LW. Natural history of impetigo. II. Etiologic agents and bacterial interactions. J Clin
Invest 1972; 51:2863.
3. Edlich RF, Winters KL, Britt LD, Long WB 3rd. Bacterial diseases of the skin. J Long Term Eff Med Implants 2005; 15:499.
4. Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis 2002; 22:42.
5. Amagai M, Matsuyoshi N, Wang ZH, et al. Toxin in bullous impetigo and staphylococcal scalded-skin syndrome targets
desmoglein 1. Nat Med 2000; 6:1275.
6. Stanley JR, Amagai M. Pemphigus, bullous impetigo, and the staphylococcal scalded-skin syndrome. N Engl J Med 2006;
355:1800.
7. Hewitt WD, Farrar WE. Bacteremia and ecthyma caused by Streptococcus pyogenes in a patient with acquired
immunodeficiency syndrome. Am J Med Sci 1988; 295:52.
8. Baltimore RS. Treatment of impetigo: a review. Pediatr Infect Dis 1985; 4:597.
9. Weinstein L, Le Frock J. Does antimicrobial therapy of streptococcal pharyngitis or pyoderma alter the risk of
glomerulonephritis? J Infect Dis 1971; 124:229.
10. McDonald MI, Towers RJ, Andrews RM, et al. Low rates of streptococcal pharyngitis and high rates of pyoderma in
Australian aboriginal communities where acute rheumatic fever is hyperendemic. Clin Infect Dis 2006; 43:683.
11. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol 1994; 11:293.
12. Demidovich CW, Wittler RR, Ruff ME, et al. Impetigo. Current etiology and comparison of penicillin, erythromycin, and
cephalexin therapies. Am J Dis Child 1990; 144:1313.
13. Baddour LM. Primary skin infections in primary care: An update. Infect Med 1993; 10:42.
14. Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Pediatr Ann 1993; 22:235.
15. Liu Y, Kong F, Zhang X, et al. Antimicrobial susceptibility of Staphylococcus aureus isolated from children with impetigo in
China from 2003 to 2007 shows community-associated methicillin-resistant Staphylococcus aureus to be uncommon and
heterogeneous. Br J Dermatol 2009; 161:1347.
16. Del Giudice P, Hubiche P. Community-associated methicillin-resistant Staphylococcus aureus and impetigo. Br J
Dermatol 2010; 162:905; author reply 905.
17. Wasserzug O, Valinsky L, Klement E, et al. A cluster of ecthyma outbreaks caused by a single clone of invasive and
highly infective Streptococcus pyogenes. Clin Infect Dis 2009; 48:1213.
18. Bessen DE, Sotir CM, Readdy TL, Hollingshead SK. Genetic correlates of throat and skin isolates of group A streptococci.
J Infect Dis 1996; 173:896.
19. Fiorentino TR, Beall B, Mshar P, Bessen DE. A genetic-based evaluation of the principal tissue reservoir for group A
streptococci isolated from normally sterile sites. J Infect Dis 1997; 176:177.
20. Kaplan EL, Anthony BF, Chapman SS, et al. The influence of the site of infection on the immune response to group A
streptococci. J Clin Invest 1970; 49:1405.
21. Bisno AL, Nelson KE, Waytz P, Brunt J. Factors influencing serum antibody responses in streptococcal pyoderma. J Lab
Clin Med 1973; 81:410.
22. Kaplan EL, Wannamaker LW. Suppression of the antistreptolysin O response by cholesterol and by lipid extracts of rabbit
skin. J Exp Med 1976; 144:754.
23. Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo. Cochrane Database Syst Rev 2012;
1:CD003261.
24. Yun HJ, Lee SW, Yoon GM, et al. Prevalence and mechanisms of low- and high-level mupirocin resistance in
staphylococci isolated from a Korean hospital. J Antimicrob Chemother 2003; 51:619.

25. Koning S, Verhagen AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. Cochrane Database Syst Rev 2004;
:CD003261.
26. Christensen OB, Anehus S. Hydrogen peroxide cream: an alternative to topical antibiotics in the treatment of impetigo
contagiosa. Acta Derm Venereol 1994; 74:460.
27. Bass JW, Chan DS, Creamer KM, et al. Comparison of oral cephalexin, topical mupirocin and topical bacitracin for
treatment of impetigo. Pediatr Infect Dis J 1997; 16:708.
28. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue
infections. Clin Infect Dis 2005; 41:1373.
29. Kumar A, Murray DL, Hanna CB, et al. Comparative study of cephalexin hydrochloride and cephalexin monohydrate in the
treatment of skin and soft tissue infections. Antimicrob Agents Chemother 1988; 32:882.
30. Daniel R. Azithromycin, erythromycin and cloxacillin in the treatment of infections of skin and associated soft tissues.
European Azithromycin Study Group. J Int Med Res 1991; 19:433.
31. Parish LC. Clarithromycin in the treatment of skin and skin structure infections: two multicenter clinical studies.
Clarithromycin Study Group. Int J Dermatol 1993; 32:528.
32. Ferrieri P, Dajani AS, Wannamaker LW. A controlled study of penicillin prophylaxis against streptococcal impetigo. J Infect
Dis 1974; 129:429.
33. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract 2003; 53:480.
34. Luby SP, Agboatwalla M, Feikin DR, et al. Effect of handwashing on child health: a randomised controlled trial. Lancet
2005; 366:225.
35. Kowalski TJ, Berbari EF, Osmon DR. Epidemiology, treatment, and prevention of community-acquired methicillin-resistant
Staphylococcus aureus infections. Mayo Clin Proc 2005; 80:1201.
Topic 7655 Version 9.0

GRAPHICS Impetigo vesiculopustules

Impetigo vesiculopustules with crusting. Courtesy of Larry M Baddour, MD.

Impetigo

Reproduced with permission from: Stedman's Medical Dictionary. Copyright 2008 Lippincott Williams & Wilkins.

Empiric antimicrobial therapy for impetigo (excluding MRSA)

Adults

Children*

Oral therapy
Dicloxacillin

500 mg orally every six hours

25 mg/kg/day in 4 divided doses

Cephalexin

500 mg orally every six hours

25 mg/kg/day in 4 divided doses

Clindamycin

300 mg orally every six hours

15-25 mg/kg/day in 3 divided doses

Erythromycin

250 mg orally every six hours

40 mg/kg/day in 4 divided doses

Maximum single dose should not exceed dose for adults.

 Note local prevalence of inducible clindamycin resistance; see text.

 Macrolides may not be adequate therapy given increasing resistance among S. pyogenes and S. aureus; note local
resistance patterns.

Risk factors for MRSA

Recent hospitalization
Residence in a long term care facility
Recent antibiotic therapy
HIV infection
Men who have sex with men
Injection drug use
Hemodialysis
Incarceration
Military service
Sharing needles, razors or other sharp objects
Sharing sports equipment
Diabetes
Prolonged hospital stay

Options for oral treatment of methicillin-resistant Staphylococcus aureus (MRSA)

Treatment

Adult dose

Pediatric dose (children >28 days)*

Clindamycin

300 to 450 mg orally three times daily

40 mg/kg per day orally divided in three or four doses

Trimethoprimsulfamethoxazole

1 DS tab orally twice daily

8 to 12 mg trimethoprim component/kg per day orally

divided in two doses

100 mg orally twice daily

45 kg: 4 mg/kg per day orally divided in two doses

>45 kg: 100 mg orally twice daily

200 mg orally once, then 100 mg

orally twice daily

4 mg/kg orally once, then 4 mg/kg per day divided in two

doses

600 mg orally twice daily

<12 years: 30 mg/kg per day orally divided in three doses

12 years: 600 mg orally twice daily

Doxycycline

Minocycline

Linezolid

DS: double strength.

* Dosing for neonates is provided separately. (See table "Treatment of cellulitis in neonates.")

 Not recommended for children <8 years of age.

Data adapted from: Liu C, Bayer A, Cosgrove SE, et al. Clinical Practice Guidelines by the Infectious Diseases Society of
America for the Treatment of Methicillin-Resistant Staphylococcus Aureus Infections in Adults and Children. Clin Infect Dis
2011; 52:e18.

Parenteral antimicrobial therapy for infections due to methicillin-resistant

Staphylococcus aureus (MRSA) in adults
Drug
Vancomycin

Adult dose
30 mg/kg IV every 24 hours in 2 equally divided doses; not to exceed 2 g/24 hours unless
concentrations in serum are inappropriately low

Daptomycin
Skin and soft tissue
infection

4 mg/kg IV once daily

Bacteremia

6 mg/kg IV once daily*

Linezolid

600 mg IV (or orally) twice daily

Ceftaroline

600 mg IV every 12 hours

Tigecycline

100 mg IV once, thereafter 50 mg IV every 12 hours

IV: intravenously.

* Because daptomycin exhibits concentration-dependent killing, some experts recommend doses of up to 8 to 10 mg/kg IV
once daily, which appear safe, though additional studies are needed[1,2].

References:

1.

Figueroa DA, Mangini E, Amodio-Groton M, et al. Safety of high-dose intravenous daptomycin treatment: three-year
cumulative experience in a clinical program. Clin Infect Dis 2009; 49:177-80.

2.

Benvenuto M, Benziger DP, Yankelev S, Vigliani G. Pharmacokinetics and tolerability of daptomycin at doses up to 12
milligrams per kilogram of body weight once daily in healthy volunteers. Antimicrob Ther Chemother 2006; 50:3245-9.

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