AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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 2 separate forms—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 2 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

• Impetigo affects males and females.
• In adults, incidence in males is greater.

Age

• Nonbullous impetigo can affect all ages, but it affects children aged 2-5 years most commonly.
• Bullous impetigo affects all ages, but historically it occurs more often in newborns and older infants. Some authors disagree, stating that adult cases often are underreported.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

• Patients 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.
• Lesions usually have been present for days or weeks rather than months. The lesions usually are painless, although patients may report burning and pruritus.
• Constitutional symptoms usually are 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 occasionally are reported.
  • One report described an outbreak among rugby players, which demonstrates an opportunity for impetigo to be spread during contact sports.

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 from 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.

• 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 usually are 1-2 cm. 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 rarely is encountered.

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 increasingly is 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.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Nonbullous impetigo
Varicella
Tinea corporis
Rhus species or other contact dermatitis
Nummular eczema
Linear immunoglobulin A bullous dermatosis
Thermal or chemical burns
Pemphigus vulgaris
Bullous pemphigoid
Dermatitis herpetiformis
Bullous-fixed drug reaction
Staphylococcal scalded skin syndrome
Bullous insect bites
Bullous impetigo
Seborrheic dermatitis
Atopic dermatitis
Allergic contact dermatitis
Epidermal dermatophyte infection
Tinea capitis
Scabies
Pediculosis capitis

WORKUP

Section 5 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
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Lab Studies

• Impetigo usually can be diagnosed from the clinical picture.
• Culture of the involved skin confirms the diagnosis and identifies the causative organism, thereby helping the physician choose appropriate antibiotic therapy.
• • The presence of gram-positive cocci in chains indicates S pyogenes.
  • Gram-positive cocci in clusters indicate S aureus.
  • A culture obtained from intact bullae of bullous impetigo reveals S aureus, phage group II.

• If acute glomerulonephritis presents in a patient with a recent history of impetigo, use a titer of antibodies to streptococcal components (eg, antideoxyribonuclease [DNAse] B, antihyaluronidase, and antistreptolysin O [ASO] titers) to identify a possible etiology for the renal findings.

Histologic Findings

The epidermal cleavage plane is subcorneal in both bullous and nonbullous impetigo. Obtaining biopsies, which rarely is necessary to establish the diagnosis, reveals neutrophils migrating within the epidermis, an inflammatory infiltrate of neutrophils and lymphocytes in the upper dermis, and subcorneal blisters containing occasional acantholytic cells. The blisters of nonbullous impetigo, which are slight and transient, also may contain occasional gram-positive cocci and numerous neutrophils.

TREATMENT

Section 6 of 11  

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• Clinical
• Differentials
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• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

Medical management may involve topical therapy alone or a combination of systemic and topical therapies.

• Topical therapy
• • First, remove the infected crusts and debris with soap and water. If the infection is mild and localized, topical mupirocin alone may be the only necessary therapy. Studies indicate this topical antibiotic, although expensive, is as effective as oral erythromycin for treating impetigo. Furthermore, the cost difference between these 2 treatments may be offset by the increased incidence of adverse effects associated with erythromycin.
  
  
  • Disadvantages of topical treatment are that it cannot eradicate organisms from the respiratory tract and applying topical medications to extensive lesions is difficult.
  
  
  • No studies indicate that other topical antibiotics are as effective as systemic therapy.


• Systemic therapy
• • When infection is moderate to severe or accompanied by lymphadenopathy, systemic therapy is indicated.
  
  
  • The drug preferred for impetigo caused by S pyogenes is penicillin. Substitute clindamycin in patients who are allergic to penicillin.
  
  
  • In cases caused by S aureus, clindamycin or cephalexin may be used.
  
  
  • Treat erythromycin-resistant S aureus impetigo with a cephalosporin (eg, cephalexin, clindamycin).

MEDICATION

Section 7 of 11  

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The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

FOLLOW-UP

Section 8 of 11  

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• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Follow-up is important to ensure complete clearing of lesions. Request that patients schedule follow-up visits if lesions worsen or do not improve after beginning therapy.

Complications

• Acute poststreptococcal glomerulonephritis
• • Acute poststreptococcal glomerulonephritis (AGN) is a rare but potential complication of nonbullous impetigo.
  • It occurs in less than 1% of cases, depending on the nephritogenic potential of the S pyogenes strain involved. Many strains have no nephritogenic potential, but types M-60 and M-49 cause AGN in 70% and 25% (respectively) of patients with impetigo caused by these strains.
  • Interestingly, in certain tropical and subtropical climates, skin infection is the most common infection preceding nephritis. Rheumatic fever, however, is not a risk following streptococcal impetigo because it develops after streptococcal pharyngitis. Use anti-DNAse B, antihyaluronidase, and ASO titers to provide evidence of a recent streptococcal infection.

• Other complications (rare)
• • Cellulitis
  • Erysipelas
  • Scarlet fever
  • Erythema multiforme

  • Urticaria

• Untreated lesions may progress to ecthyma.

Prognosis

• With appropriate treatment, lesions usually heal in 2-3 weeks or less; however, patients with eczema or an underlying parasite infection may have a prolonged course.
• Patients typically do not have scars, but postinflammatory pigment alterations may occur.

Patient Education

• Discourage touching the lesions.
• Inform patients about early and proper care of predisposing factors (eg, insect bites, minor trauma). Recommend that patients apply a topical antibiotic to minor skin traumas.
• 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

Section 9 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Special Concerns

• Impetigo may become endemic or epidemic in certain populations during the summer months. Consider antibiotic prophylaxis in these populations.

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.
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Media file 2:  Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.
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Media file 3:  A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.
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Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Cunha BA. Antibiotic Essentials. Royal Oak, Mich: Physicians Press:2005.
• Dajani AS, Ferrieri P, Wannamaker L. Endemic superficial pyoderma in children. Arch Dermatol. Oct 1973;108(4):517-22. [Medline].
• 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].
• Dillon HC Jr. Topical and systemic therapy for pyodermas. Int J Dermatol. Oct 1980;DA - 19810424(8):443-51. [Medline].
• Drug Information for the Health Care Professional. USP DI-Volume I. 17^th ed. Chicago, Ill: Rand McNally; 1997.
• el Tayeb SH, Nasr EM, Sattallah AS. Streptococcal impetigo and acute glomerulonephritis in children in Cairo. Br J Dermatol. Jan 1978;98(1):53-62. [Medline].
• Elias PM, Levy SW. Bullous impetigo. Occurrence of localized scalded skin syndrome in an adult. Arch Dermatol. Jun 1976;112(6):856-8. [Medline].
• 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].
• Ginsburg CM. Staphylococcal toxin syndromes. Pediatr Infect Dis J. Apr 1991;10(4):319-21. [Medline].
• Hay RJ, Adriaans BM. Bacterial Infections. In: Champion RH, Breathnach SM, Burns AD, et al, eds. Textbook of Dermatology. 6^th ed. Oxford, England: Blackwell Science; 1998:1097-1179.
• Hirschmann JV. Bacterial infections of the skin. In: Sams WM Jr, Lynch PJ, eds. Principles and Practice of Dermatology. 2^nd 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.
• Ludlam H, Cookson B. Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team. Lancet. Aug 9 1986;2(8502):331-3. [Medline].
• 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].

Article Last Updated: May 4, 2007