eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Impetigo

Author: Lisa S Lewis, MD, Consulting Staff, Division of Emergency Medicine, Children's Hospital Medical Center of Cincinnati
Coauthor(s): Allan D Friedman, MD, MPH, Chairman, Division of General Pediatrics, Dept of Pediatrics, Professor of Pediatrics, Virginia Commonwealth University, VCUH Health System
Contributor Information and Disclosures

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 ...

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

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Nonbullous impetigo with vesicles, pustules, and ...

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


Bullous impetigo with circumscribed lesions with ...

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

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Bullous impetigo with circumscribed lesions with ...

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



Staphylococcus aureus, group A beta hemolytic streptococci (GABHS), or mixed flora may invade disrupted skin following bites, cuts, abrasions, varicella, or other trauma.1 Certain serotypes of GABHS (eg, types 49, 55, 57, 59) are associated with impetigo and acute glomerulonephritis. Bullous impetigo may affect intact skin and is usually caused by S aureus infection .

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.

More on Impetigo

Overview: Impetigo
Differential Diagnoses & Workup: Impetigo
Treatment & Medication: Impetigo
Follow-up: Impetigo
Multimedia: Impetigo
References
Further Reading
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Further Reading

  • 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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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

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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

 
 
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