eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Impetigo

John Ratz, MD, MBA, Staff Dermatologist, Mohs Surgeon, Center for Dermatology and Skin Surgery, Inc
Daniel B Ward Jr, MD, Clinical Assistant Professor, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina

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.

Differential Diagnoses

Erythema Multiforme (Stevens-Johnson Syndrome)
Herpes Simplex
Herpes Zoster
Pediculosis
Staphylococcal Infections
Varicella-Zoster Virus

Other Problems to Be Considered

Nonbullous impetigo
Varicella
Tinea corporis
Rhus dermatitis 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

Laboratory Studies

• Impetigo can usually be diagnosed based on 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 is rarely 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, may also contain occasional gram-positive cocci and numerous neutrophils.

Treatment

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 two 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

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

Antibiotics

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

Penicillin V (Penicillin VK, Veetids)

Interferes with cell wall mucopeptide synthesis during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Not recommended for staphylococcal impetigo.

Dosing

Adult

500 mg PO q6h

Pediatric

<50 lb: 500 mg/d PO divided qid for 10 d
>50 lb: Administer as in adults

Interactions

Probenecid can increase effects; coadministration of tetracyclines can decrease effects

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 impaired renal function

Cephalexin (Keflex)

Recommended for impetigo caused by S aureus resistant to erythromycin. First-generation cephalosporin arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primary activity against skin flora. Used for skin infections or prophylaxis in minor procedures.

Dosing

Adult

500 mg PO q6h for 10 d

Pediatric

25-50 mg/kg/d PO q6h for 10 d; not to exceed 3 g qd

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 dose in renal impairment

Amoxicillin clavulanate (Augmentin)

Indicated for skin and skin structure infections caused by beta-lactamase–producing strains of S aureus that are resistant to erythromycin.
Administration with food may decrease GI adverse effects.

Dosing

Adult

500 mg of amoxicillin with 125 mg of clavulanate PO tid for 7-10 d

Pediatric

Children > 3 months: Base dosing protocol on amoxicillin content; due to different amoxicillin-to-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
<40 kg: 6.7-13.3 mg/kg of amoxicillin and 1.7-3.3 mg/kg of clavulanate PO tid for 7-10 d
>40 kg: Administer as in adults

Interactions

Administer at least 1 h apart from aminoglycosides to prevent mutual inactivation; coadministration with warfarin or heparin increases risk of bleeding

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Prescribe for a minimum of 10 d to eliminate organism and prevent sequelae (eg, endocarditis, rheumatic fever); following treatment, perform culture to confirm streptococci eradication

Clindamycin (Cleocin)

Alternative therapy for S aureus resistant to erythromycin. 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

300 PO q8h for 10 d

Pediatric

Administer as in adults

Interactions

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

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

Possible cross-sensitivity between clindamycin and doxorubicin; adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

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 S 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 at application site (1.4%); avoid application to eye area; keep out of reach of children

Follow-up

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 parasitic 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

Special Concerns

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

Multimedia

Media file 1: Bullous impetigo on the buttocks. Courtesy of Medical University of South Carolina, Department of Dermatology.

Media file 2: Following dermabrasion, this patient developed nonbullous impetigo in the same area as several herpes simplex lesions.

Media file 3: A nummular eczema lesion on the knee, impetiginized with Staphylococcus aureus.

References

1. 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].

2. Cunha BA. Antibiotic Essentials. Royal Oak, Mich: Physicians Press:2005.

3. Dajani AS, Ferrieri P, Wannamaker L. Endemic superficial pyoderma in children. Arch Dermatol. Oct 1973;108(4):517-22. [Medline].

4. 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].

5. Dillon HC Jr. Topical and systemic therapy for pyodermas. Int J Dermatol. Oct 1980;DA - 19810424(8):443-51. [Medline].

6. Drug Information for the Health Care Professional. USP DI-Volume I. 17^th ed. Chicago, Ill: Rand McNally; 1997.

7. 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].

8. Elias PM, Levy SW. Bullous impetigo. Occurrence of localized scalded skin syndrome in an adult. Arch Dermatol. Jun 1976;112(6):856-8. [Medline].

9. 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].

10. Ginsburg CM. Staphylococcal toxin syndromes. Pediatr Infect Dis J. Apr 1991;10(4):319-21. [Medline].

11. 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.

12. 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.

13. Hirschmann JV. Topical antibiotics in dermatology. Arch Dermatol. Nov 1988;124(11):1691-700. [Medline].

14. Kahn RM, Goldstein EJ. Common bacterial skin infections. Diagnostic clues and therapeutic options. Postgrad Med. May 1 1993;93(6):175-82. [Medline].

15. 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.

16. 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].

17. 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].

18. Scales JW, Fleischer AB Jr, Krowchuk DP. Bullous impetigo. Arch Pediatr Adolesc Med. Nov 1997;151(11):1168-9. [Medline].

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

Contributor Information and Disclosures

Author

John Ratz, MD, MBA, Staff Dermatologist, Mohs Surgeon, Center for Dermatology and Skin Surgery, Inc
John Ratz, MD, MBA is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Micrographic Surgery and Cutaneous Oncology, American College of Physicians, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery, International Society for Dermatologic Surgery, and Southern Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Daniel B Ward Jr, MD, Clinical Assistant Professor, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina
Daniel B Ward Jr, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Gregory William Rutecki, MD, Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University
Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

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