eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Impetigo

Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Allan D Friedman, MD, MPH, Chairman, Division of General Pediatrics, Dept of Pediatrics, Professor of Pediatrics, Virginia Commonwealth University, VCUH Health System

Updated: Apr 27, 2009

Introduction

Background

Impetigo is a superficial pyoderma first described by Dunn and Fox in the 1860s. Impetigo is currently the most common skin infection in children and accounts for approximately one tenth of all cutaneous problems in pediatric clinics. Impetigo can be subdivided into nonbullous and bullous forms. The more common nonbullous form accounts for approximately 70% of individuals with impetigo and affects areas of traumatized skin on the face or extremities.

Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Bullous impetigo with circumscribed lesions with a thin collarette of scale.

Pathophysiology

Intact skin is usually resistant to colonization or infection by S aureus or GABHS. These bacteria can be introduced from the environment and only transiently colonize the cutaneous surface.

High temperature and humidity, underlying dermatologic disease, and young age are associated with colonization. Experimental studies have shown that inoculation of multiple strains of GABHS on to the surface of volunteer subjects did not produce cutaneous disease unless skin disruption had occurred. The teichoic acid adhesions for GABHS and S aureus require the epithelial cell receptor component, fibronectin, for colonization. These fibronectin receptors are unavailable on intact skin; however, skin disruption may reveal fibronectin receptors and allow for colonization or invasion in these disrupted surfaces. Factors that can modify the usual skin flora and facilitate transient colonization by GABHS and S aureus include high temperature or humidity, preexisting cutaneous disease, young age, or recent antibiotic treatment.

Bullous impetigo results from invasion by phage group 2 S aureus onto either intact or disrupted skin. This occurs after colonization of the upper respiratory tract, usually involving the nares. Invasion is believed to be a result of an epidermolytic toxin that disrupts epidermal cell attachments.

Frequency

United States

Impetigo accounts for approximately 10% of skin problems observed in pediatric clinics. Because it occurs more frequently in a warm humid environment, impetigo is more common in the southeastern United States than in the cooler northern states. The prevalence of impetigo varies seasonally; however, in regions that remain warm and humid throughout the year, seasonality may not occur.

International

Impetigo occurs more frequently in tropical climates and lower altitudes. Warm humid conditions combined with frequent cutaneous disruption via biting insects favor its development throughout the year in tropical climates. Geographic regions that have crowded conditions or poor hygiene also have increased prevalence of impetigo.

Mortality/Morbidity

Cellulitis, lymphangitis, suppurative lymphadenitis, and staphylococcal scalded skin syndrome occur in as many as 10% of patients with impetigo.

Acute poststreptococcal glomerulonephritis (APSGN), scarlet fever, osteomyelitis, septic arthritis, pneumonia, septicemia, guttate psoriases, and rheumatic fever have also been observed in patients with impetigo.

Age

Impetigo is found most commonly in preschool-aged children. Rapid dissemination can occur through daycare centers, nurseries, and grade schools.

Clinical

History

In nonbullous impetigo, a tiny pustule or honey-colored crusted plaque with rapid spread, occasional pruritus, and regional lymphadenopathy may follow a break in the skin. Bullous impetigo usually has a history of thin-roofed bullae that spontaneously rupture without a history of localized lymphadenopathy or cutaneous disruption.

• Nonbullous lesions
  • Lesions start as tiny pustules that evolve rapidly into honey-colored crusted plaques, which usually measure less than 2 cm in diameter.
  • A rash is usually found in exposed areas of the face and extremities where bites, abrasions, lacerations, scratches, burns, or trauma have occurred.
  • Rapid spread occurs.
  • Lesions are usually asymptomatic, with occasional pruritus.
  • Little or no surrounding erythema or edema is present.
  • Regional adenopathy is common.
• Bullous lesions
  • Thin-roofed bullae that spontaneously rupture are present.
  • Bullous lesions usually spread locally in the face, trunk, extremities, buttocks, or perineal regions.
  • These lesions may secondarily invade preexisting lesions (eg, eczema) to cause generalized lesions.
  • Minimal or no surrounding erythema occurs.
  • No regional lymphadenopathy occurs.

Physical

Generally, the patient is nontoxic and well appearing.

• Nonbullous lesions
  • A tiny vesicle or pustule that ruptures and is replaced by honey-colored crusting usually measures less than 2 cm.
  • Elevation of crust reveals a moist erythematous base.
  • Lesions are usually on the face and extremities or in areas with a break in the natural skin defense barrier.
  • Little or no surrounding erythema or edema is present.
  • Regional lymphadenopathy is present in 90% of individuals with impetigo.
• Bullous lesions
  • Thin-roofed, flaccid, and transparent bullae usually measure less than 3 cm.
  • Bullae rupture easily, within 1-2 days, leaving a rim of scale around an erythematous moist base. After desiccation, a lacquered or scalded skin appearance with a collarette of scale is noted.
  • Bullous lesions occur on intact skin, usually on the face, trunk, extremities, buttocks, and perineum.
  • No surrounding erythema or edema is present.
  • No regional adenopathy occurs.

Causes

The primary pathogen responsible for impetigo changes from decade to decade. Staphylococci were the causative agents in nonbullous impetigo until the mid 1960s. Subsequently, group A beta hemolytic streptococci (GABHS) became predominant. Since the early 1980s, the predominant pathogen is again S aureus. The etiology of bullous impetigo is almost always S aureus.

• Nonbullous impetigo
  • Most lesions are caused by S aureus and GABHS.
  • Culture results and the relative frequency of each pathogen may vary depending on geographic region, time of year, and age of the host.
  • S aureus can be cultured from impetiginous lesions in children of all ages.
  • Except for endemic areas, GABHS is uncommon in children younger than 2 years but is found commonly in preschool-aged children.
• Bullous impetigo
  • Bullous impetigo is caused almost exclusively by S aureus.
  • Phage group 2 S aureus accounts for 80% of these lesions .
  • Exfoliative toxins A and B cause a loss of cell adhesion in the superficial epidermis, split the granular cell layer, and form blisters.

Differential Diagnoses

Other Problems to Be Considered

Other bullous disorders
Stevens-Johnson syndrome
Pemphigus vulgaris
Allergic reactions (erythema multiforme, rhus dermatitis)
Tinea corporis, kerion
Nummular eczema
Linear immunoglobulin A bullous dermatosis
Bullous pemphigoid reactions
Ecchymoses
Dermatitis herpetiformis

Workup

Laboratory Studies

• Diagnosis of impetigo is usually solely based on history and clinical appearance. Occasionally, confirmation by culture and sensitivity testing of the causative organism may be warranted. Similarly, evidence of previous streptococcal skin infection may be sought in individuals in whom acute glomerulonephritis is suspected.
• Leukocytosis is present in approximately 50% of patients with impetigo.
• In patients with nonbullous lesions, after cleansing the honey-colored crusted lesion and uplifting the scab, a bacterial culture of the fresh exudate underneath the scab may be obtained.
• The following studies may be performed in patients with bullous lesions:
  • Gram stain and culture of the blister fluid reveal many polymorphonuclear WBCs and gram-positive cocci.
  • Bacterial culture yields staphylococci.
• Documentation of a recent streptococcal skin infection in the differential diagnosis of acute glomerulonephritis is accomplished best by obtaining antideoxyribonuclease B (anti-DNase B) and antihyaluronidase (AH) titers.
  • More than 92% of patients with impetigo-associated APSGN have elevated anti-DNase B titers.
  • Patients with impetigo have a poor antistreptolysin O (ASO) serologic response; only 51% of patients with impetigo-associated poststreptococcal glomerulonephritis develop an increased ASO titer.

Histologic Findings

• Typical histologic examination of bullous impetigo reveals a blister in the subcorneal or granular region.
• Polymorphonuclear cells are generally present within the vesicle.
• Acantholytic cells in the blister cavity, spongiosis, and papillary dermal edema may be present.
• Bacteria may be observed on Gram stain.
• Similar findings are present in nonbullous impetigo; however, vesicle formation is significantly smaller.

Treatment

Medical Care

Treatment of impetigo may involve local wound care along with topical or systemic antibiotic therapy.

• Local wound care: Cleansing, removal of the honey-colored crusts, and frequent application of wet dressings to areas affected by lesions are recommended.
• Topical antibiotic treatment: Topical antibiotic therapy is considered the treatment of choice for individuals with uncomplicated localized impetigo. Mupirocin has been found to clear 52-68% of patients with methicillin-resistant S aureus (MRSA) colonization. Retapamulin ointment is in a new class of topical antimicrobials and is indicated for treatment of localized impetigo in children older than 9 months. It has demonstrated excellent activity in vitro against mupirocin-resistant S aureus.²
• Systemic antibiotic treatment
• Persons with infections that are widespread, complicated, or are associated with systemic manifestations are usually treated with antibiotics that have gram-positive bacterial coverage.
• Systemic therapy is also recommended if multiple incidents of pyoderma occur within daycare, family, or athletic team settings.
• Beta-lactamase resistant antibiotics (eg, cephalosporins, amoxicillin-clavulanate, cloxacillin, dicloxacillin) are recommended. Cephalexin appears to be the drug of choice for oral antimicrobial therapy in children.
• Recently, community-acquired MRSA infections have reached epidemic proportions.³  If MRSA is suspected, alternative antibiotics include vancomycin, trimethoprim/sulfamethoxazole, and clindamycin.
• Erythromycin and clindamycin are alternatives in patients with penicillin hypersensitivity. Macrolide resistance has been increasing in the United States. Thus, avoid treatment of impetigo with erythromycin in geographic regions that are known to have a high resistance rate. Group A beta hemolytic streptococci (GABHS) and S aureus resistance to clindamycin has also been reported.

Medication

Topical antibiotics, systemic antibiotics, or a combination are effective therapies for impetigo. Empiric bacterial coverage is aimed at eradicating S aureus and group A beta hemolytic streptococci (GABHS).

Topical antibiotics

Topical antibiotic treatment with mupirocin is the treatment of choice for uncomplicated localized pyoderma, although S aureus resistance to mupirocin has been increasing.⁴

Mupirocin (Bactroban)

Naturally occurring antibiotic produced by fermentation of Pseudomonas fluorescens. Mechanism of action of mupirocin is via inhibition of bacterial protein synthesis.

Dosing

Adult

Apply to affected areas tid for 7-10 d

Pediatric

Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Prolonged use may result in growth of nonsusceptible organisms

Retapamulin (Altabax)

Topical antibiotic available as a 1% ointment. First of new antibiotic class called pleuromutilins. Inhibits protein synthesis by binding to 50S subunit on ribosome. Indicated for impetigo caused by S aureus or Streptococcus pyogenes.

Dosing

Adult

Apply topically to affected site bid for 5 d

Pediatric

<9 months: Not established
>9 months: Apply as in adults

Interactions

None known

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause irritation or pruritus at application site (1.4%); avoid application to eye area; keep out of reach of children

Systemic antibiotics

Systemic antibiotic treatment is indicated for widespread or complicated pyoderma.

Cephalexin (Biocef, Keflex, Keftab)

First-generation cephalosporin antibiotic commonly used to treat impetigo and other skin infections. As with other cephalosporins, mechanism of action is through inhibition of cell wall synthesis.

Dosing

Adult

500 mg PO q6h

Pediatric

25-50 mg/kg/d PO divided tid/qid

Interactions

Coadministration with aminoglycosides increases nephrotoxic potential

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dosage with renal insufficiency; caution in patients sensitive to penicillin

Amoxicillin and clavulanate (Augmentin)

Oral antibiotic combining broad-spectrum antibiotic amoxicillin with beta-lactamase inhibitor clavulanate. Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. Addition of clavulanate inhibits beta-lactamase producing bacteria. For children >3 mo, base dosing protocol on amoxicillin content. Because of different amoxicillin/clavulanic acid ratios in 250-mg tab (250/125) vs 250-mg chewable tab (250/62.5), do not use 250-mg tab until child weighs >40 kg.

Dosing

Adult

500 mg PO q12h or 250 mg PO q8h

Pediatric

20-45 mg/kg/d PO divided bid/tid
<3 months: 125 mg/5 mL PO susp based on amoxicillin; 30 mg/kg/d divided bid for 7 d
>3 months: If using 200 mg/5 mL or 400 mg/5 mL susp, 45 mg/kg/d PO q12h; if using 125 mg/5 mL or 250 mg/5 mL susp, 40 mg/kg/d PO q8h for 7 d
>40 kg: Administer as in adults

Interactions

Coadministration with warfarin or heparin increases risk of bleeding; avoid combination with allopurinol, which results in increased incidence of rash

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Because chewable tab contain phenylalanine, do not administer to patients with PKU

Dicloxacillin (Dycill, Dynapen)

Binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. For treatment of infections caused by penicillinase-producing staphylococci. May use to initiate therapy when staphylococcal infection is suspected.

Dosing

Adult

125-500 mg PO q6h, administer 1 h ac or 2 h pc

Pediatric

25 mg/kg/d PO divided q6h, administer 1 h ac or 2 h pc

Interactions

Decreases efficacy of oral contraceptives; may decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor PT in patients taking anticoagulant medications; toxicity may increase in patients who are renally impaired

Erythromycin (E.E.S., E-Mycin, Eryc)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double dose.

Dosing

Adult

250-500 mg (stearate/base) PO q6h

Pediatric

30-50 mg/kg/d (stearate/base) PO divided q6-8h

Interactions

Potent inhibitor of CYP450-3A4; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Clindamycin (Cleocin)

Lincosamide for treatment of serious skin and soft tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Dosing

Adult

150-450 mg PO q6h

Pediatric

10-30 mg/kg/d PO divided q6-8h

Interactions

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Contraindications

Documented hypersensitivity; regional enteritis, ulcerative colitis, hepatic impairment, antibiotic-associated colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile

Cloxacillin (Cloxapen)

For treatment of infections caused by penicillinase-producing staphylococci.

Dosing

Adult

250-500 mg PO q6h

Pediatric

50-100 mg/kg/d PO divided q6h

Interactions

Decreases efficacy of oral contraceptives; may decrease effects of anticoagulants; probenecid and disulfiram may increase penicillin levels

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with impaired renal function

Follow-up

Further Inpatient Care

• Hospital care is reserved only for impetigo with certain complications.
• If inpatient care is warranted in the child with untreated impetigo, contact isolation is recommended.

Deterrence/Prevention

• Advise the child with impetigo to avoid close contact with other children if possible. Current recommendations call for the exclusion of children with impetigo from school or daycare for 24 hours after the initiation of antibiotics.
• Inspect family members for impetiginous lesions. Failure to treat other infected persons may result in continued transmission.

Complications

• Cellulitis, lymphangitis, suppurative lymphadenitis, and staphylococcal scalded skin syndrome
  • These complications may occur in as many as 10% of patients with impetigo.
  • No correlation between the amount of impetiginous lesions and the involvement of the surrounding soft tissues, lymphatics, or regional lymph nodes has been observed.
  • Cellulitis rarely follows bullous impetigo.
• Acute poststreptococcal glomerulonephritis (APSGN)
  • APSGN appears 18-21 days after infection with nephritogenic strains of group A beta hemolytic streptococci (GABHS). Incidence of APSGN widely varies depending on the strain of GABHS.
  • No difference between the clinical appearance of impetigo due to nephritogenic and impetigo due to nonnephritogenic strains has been observed.
  • Children aged 3-7 years are most commonly affected.
  • Treatment of impetigo with systemic antibiotics does not prevent the development of APSGN in the index case. This is most likely due to the activation of the immune response resulting in APSGN prior to antibiotic treatment.
• Scarlet fever
• Osteomyelitis, septic arthritis
• Pneumonia
• Septicemia
• Guttate psoriases
• Rheumatic fever (not a complication of impetigo)

Patient Education

• For excellent patient education resources, visit eMedicine's Bacterial and Viral Infections Center and Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Impetigo, Skin Rashes in Children, and Antibiotics.

Miscellaneous

Medicolegal Pitfalls

• A practitioner is not likely to be sued because of a diagnosis or failure to make a diagnosis of impetigo. The disease may eventually heal over several weeks. Delay in treatment or incorrect treatment should not result in undue harm; however, the practitioner should be aware and anticipate known complications of impetigo.

Multimedia

Media file 1: Nonbullous impetigo with vesicles, pustules, and sharply demarcated regions of honey-colored crusts.

Media file 2: Bullous impetigo with circumscribed lesions with a thin collarette of scale.

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Keywords

impetigo, impetigo contagiosa, impetigo bullosa, streptococcal impetigo, staphylococcal impetigo, nonbullous impetigo, bullous impetigo, crusted tetter, pyoderma, group A beta hemolytic streptococci, GABHS, Staphylococcus aureus, varicella, acute poststreptococcal glomerulonephritis, APSGN, scarlet fever, osteomyelitis, septic arthritis, pneumonia, septicemia, guttate psoriases, rheumatic fever, treatment, diagnosis, lymphadenopathy

Contributor Information and Disclosures

Author

Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Lisa S Lewis, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Allan D Friedman, MD, MPH, Chairman, Division of General Pediatrics, Dept of Pediatrics, Professor of Pediatrics, Virginia Commonwealth University, VCUH Health System
Allan D Friedman, MD, MPH is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Glenn J Fennelly, MD, MPH, Director, Division of Pediatric Infectious Diseases, Jacobi Medical Center; Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine
Glenn J Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University
Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; sanofi pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None

• The Infectious Diseases Society of America have established practice guidelines for the diagnosis and management of skin and soft-tissue infections. ⁵

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