eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections
Impetigo
Updated: Nov 5, 2009
Introduction
Background
Impetigo is an acute, contagious, superficial pyogenic skin infection that occurs most commonly in children, especially those who live in hot humid climates. Clinically, physicians recognize two separate forms of impetigo—bullous and nonbullous. Bullous impetigo is caused almost exclusively by Staphylococcus aureus, whereas nonbullous impetigo is caused by S aureus, group A Streptococcus (Streptococcus pyogenes), or a combination of both.
Pathophysiology
Impetigo most often develops at a site of minor trauma or insult in which the integrity of the skin is disrupted. Causative organisms enter the epidermis. Alternatively, scratching may directly inoculate bacteria beneath the skin surface, causing impetiginization.
The sequence of spread of the two causative organisms differs. S pyogenes is spread from a person who is infected or colonized with the bacteria onto the skin of another individual, where it may cause impetigo. The organism then colonizes the nose and throat. S aureus, in contrast, spreads first to the nose. It then spreads to the skin, where it may cause impetigo.
Race
Impetigo can affect people of all races.
Sex
- In adults, impetigo is more common in men.
Age
- Nonbullous impetigo can affect all ages, but it most commonly affects children aged 2-5 years.
- Bullous impetigo affects all ages, but, historically, it occurs more often in newborns and older infants. Some authors disagree, stating that adult cases often go underreported.
Clinical
History
- Patients with impetigo may report a history of minor trauma, insect bites, scabies, herpes simplex, varicella, or eczema at the site of infection, and any history of preexisting skin disease should raise the clinician's index of suspicion.
A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.
- Lesions have usually been present for days or weeks rather than months. The lesions are usually painless, although patients may report burning and pruritus.
- Constitutional symptoms are usually absent.
- Obtain a history of contacts and living conditions; crowding and poor hygiene can be contributing factors to the spread of impetigo.
- Clusters in families and outbreaks in institutions are occasionally reported.
- One report described an outbreak among rugby players, which demonstrates an opportunity for impetigo to be spread during contact sports.1
Physical
- Nonbullous impetigo
- Lesions first begin as thin-walled vesicles or pustules on an erythematous base. The lesions promptly rupture, releasing their serum, which dries and forms a light brown, honey-colored crust.
- Multiple lesions generally occur at the same site, often coalescing. The affected area of skin may enlarge as the infection spreads peripherally.
- Skin on any part of the body can be involved, but the face and extremities are affected most commonly.
- Pruritus of infected areas may result in excoriations due to scratching.
- As the lesions resolve, either spontaneously or after antibiotic treatment, the crusts slough from the affected areas and heal without scarring.
- If the course of disease is prolonged and patients do not seek treatment, as many as 90% will develop regional lymphadenopathy.
Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.
- Bullous impetigo
- Lesions may form on grossly normal or previously traumatized skin.
- The vesicles do not rupture as easily or quickly as in nonbullous lesions, but they do enlarge into bullae that are usually 1-2 cm in diameter. The bullae initially contain a clear yellow fluid that subsequently turns cloudy and dark yellow.
- After 1-3 days, the lesions rupture and leave a thin, light brown, varnishlike crust.
- Central healing results in circinate lesions.
- In contrast to nonbullous impetigo, bullous impetigo may involve the buccal mucous membranes, but regional lymphadenopathy is rare.
Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.
Causes
- Nonbullous impetigo
- S aureus, group A streptococcus (S pyogenes), or both may be the causative agent(s) in nonbullous impetigo, but researchers disagree about which organism more often plays the primary role in infection.
- Early studies pointed to streptococci, but recent investigations suggest that S aureus is increasingly the primary infectious organism, especially in industrialized nations.
- Evidence indicates that the primary organism varies with geography and climate; streptococcal impetigo is more common in developing nations and warm climates.
- Streptococci are the most common primary cause when both organisms are present.
- Bullous impetigo
- S aureus phage group II type 71 is the predominant causative organism. This strain of bacteria produces an exfoliatin toxin that causes subcorneal epidermal cleavage.
- In immunodeficient or immunocompromised patients, the toxin may disseminate hematogenously and lead to generalized staphylococcal scalded skin syndrome.
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References
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Cunha BA. Antibiotic Essentials. Royal Oak, Mich: Physicians Press:2005.
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Dajani AS, Ferrieri P, Wannamaker LW. Natural history of impetigo. II. Etiologic agents and bacterial interactions. J Clin Invest. Nov 1972;51(11):2863-71. [Medline].
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Ferrieri P, Dajani AS, Wannamaker LW, et al. Natural history of impetigo. I. Site sequence of acquisition and familial patterns of spread of cutaneous streptococci. J Clin Invest. Nov 1972;51(11):2851-62. [Medline].
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Hirschmann JV. Bacterial infections of the skin. In: Sams WM Jr, Lynch PJ, eds. Principles and Practice of Dermatology. 2nd ed. New York, NY: Churchill Livingstone; 1993:79-88.
Hirschmann JV. Topical antibiotics in dermatology. Arch Dermatol. Nov 1988;124(11):1691-700. [Medline].
Kahn RM, Goldstein EJ. Common bacterial skin infections. Diagnostic clues and therapeutic options. Postgrad Med. May 1 1993;93(6):175-82. [Medline].
Lee PK, Weinberg AN, Swartz MN, et al. Pyodermas: Staphylococcus aureus, Streptococcus, and Other Gram-Positive Bacteria. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al, eds. Dermatology in General Medicine. 4th ed. New York, NY: McGraw-Hill; 1999:2182-2207.
Mertz PM, Marshall DA, Eaglstein WH, et al. Topical mupirocin treatment of impetigo is equal to oral erythromycin therapy. Arch Dermatol. Aug 1989;125(8):1069-73. [Medline].
Rice TD, Duggan AK, DeAngelis C. Cost-effectiveness of erythromycin versus mupirocin for the treatment of impetigo in children. Pediatrics. Feb 1992;89(2):210-4. [Medline].
Scales JW, Fleischer AB Jr, Krowchuk DP. Bullous impetigo. Arch Pediatr Adolesc Med. Nov 1997;151(11):1168-9. [Medline].
Further Reading
Keywords
impetigo, skin infection, cutaneous infection, bullous impetigo, nonbullous impetigo, Staphylococcus aureus, S aureus, Streptococcus pyogenes, S pyogenes, group A Streptococcus, GAS, group A streptococci, streptococci, staphylococci
