AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

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

INTRODUCTION

Section 2 of 11  

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

Background

Impetigo is a condition that is part of several different infectious skin diseases that are of a superficial nonfollicular nature.

• Impetigo contagiosa is a superficial, intraepidermal, unilocular, vesiculopustular infection. It is is the most common skin infection in children.
• Bullous impetigo is a toxin-mediated erythroderma in which the epidermal layer of the skin sloughs resulting in large areas of skin loss.
• Common impetigo is the term applied when the infection occurs in preexisting wounds. Impetigo can also present as folliculitis, which is considered to be impetigo of the hair follicles caused by Staphylococcus aureus.
• Ecthyma is a deeper, ulcerated impetigo infection, often occurring with lymphadenitis.

For a related CME/CE activity, see Strategies for Diagnosis and Treatment of Impetigo.

Pathophysiology

Impetigo is an infection caused by group A beta-hemolytic streptococci (GABHS) or coagulase-positive S aureus. The organisms are thought to enter through damaged skin and are transmitted through direct contact. After infection, new lesions may be seen on the patient with no apparent break in the skin. Frequently, however, upon close examination, these lesions will demonstrate some underlying physical damage.

The presentation of impetigo may take on more than one form. Some authors suggest that differences are due to the staphylococcal strain involved and the relative activity of the exotoxin.

In bullous impetigo, the separation of the epidermis is due to an exotoxin produced by staphylococci, which is the pathologic organism present in cases of bullous impetigo. In lesions of this type, isolation of methicillin-resistant S aureus has been as high as 20%.

On histologic examination, the lesions in all presentations reveal a subcorneal neutrophilic infiltrate.

Frequency

United States

Approximately 9-10% of all children presenting to clinics with skin complaints have impetigo.

International

About 2.6 episodes per 100 person weeks has been reported.

Multiple reports have noted a seasonal variance with peak prevalence in August and September.

Sex

Impetigo occurs equally in males and females.

Age

• Impetigo occurs more commonly in children.
• The majority (90%) of bullous impetigo cases occur in children younger than 2 years.

CLINICAL

Section 3 of 11  

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

History

In impetigo contagiosa, the lesions begin with a single 2- to 4-mm erythematous macule that rapidly evolves into a vesicle or a pustule. This vesicle is very fragile and ruptures early, leaving a crusted exudate of a honey or yellow color over the superficial erosion. The infection spreads to contiguous and distal areas through inoculation of other wounds from scratching.

Bullous impetigo presents with small or large, superficial, fragile bullae on the trunk and the extremities. Often, these quickly appear and drain so that only the remnants of ruptured bullae are seen at the time of presentation. The separation of the epidermis is due to an exotoxin produced by staphylococci, which is the pathologic organism present in cases of bullous impetigo and is directed against epidermal desmoglein 1. In lesions of this type, isolation of methicillin-resistant S aureus has been as high as 20%. Some authors assert a continuum of disease including nonbullous impetigo, bullous impetigo, and abscess formation caused by S aureus with differing exotoxin characteristics.

Typical descriptors used in impetigo are as follows:

• Tender, red rash
• Honey-colored crusts
• Pruritus
• Poorly healing wound

The following symptoms usually are absent in impetigo contagiosa but may be present in bullous impetigo:

• Fever
• Diarrhea
• Generalized weakness

Physical

• Type and location of lesions
• • Most frequently on the face (around the mouth and the nose) or at a site of trauma
  • Red macule or papule as early lesion
  • Lesions with ruptured bullae and crusted edges
  • Lesions with honey-colored crusts
  • Thin-roofed vesicle or bullae (usually nontender)
  • Pustules
  • Weeping, shallow, erythematous ulcer
  • Satellite lesions (often at multiple sites)
  • Bullae on the buttocks, trunk, and face
• Regional lymphadenopathy
• • Common in impetigo contagiosa
  • Rare in bullous impetigo

Causes

The causative agents are coagulase-positive S aureus and GABHS. S aureus is cultured consistently from the lesions, but streptococci are found only occasionally. The infection may be caused by a mixture of the 2 organisms. GABHS rarely act as the sole causative agent, as was believed 10 years ago. The incidence of community-acquired methicillin-resistant S aureus (CA-MRSA) has increased in some locales to as high as 50% of the isolates.

DIFFERENTIALS

Section 4 of 11  

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

Other Problems to be Considered

Folliculitis - Superficial hair follicle infection
Furuncle  - Deeper hair follicle infection with pus and small abscess
Erysipelas - Sharply demarcated erythematous plaque due to dermal inflammation
Insect bites
Severe eczematous dermatitis
Tinea corporis
Pemphigus vulgaris
Bullous pemphigoid

WORKUP

Section 5 of 11  

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

Lab Studies

• In special situations, such as a questionable diagnosis, the existence of epidemic conditions, or poor response to treatment, studies may be required as follows:
• • The Gram stain will reveal neutrophils with gram-positive cocci in chains or clusters.
  • Cultures of the fluid will reveal S aureus, most commonly in combination with Streptococcus pyogenes or other GABHS, but either may occur alone.
  • Antibiotic sensitivity testing may be required to isolate MRSA and identify appropriate antibiotics.
• A biopsy may be indicated.

Other Tests

• Antistreptolysin-O (ASO) titer may be weakly positive for streptococci, but it rarely is performed.
• Streptozyme is positive for streptococci, but it rarely is performed.

TREATMENT

Section 6 of 11  

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

Emergency Department Care

The emerging resistance of S aureus to beta-lactams, macrolides, and even mupirocin requires consideration of the prevalence of CA-MRSA in the locale of the patient. Treatment of bullous impetigo should now always consider this possibility. Trimethoprim-sulfamethoxazole, clindamycin, and rifampin all retain sensitivity in the vast majority of CA-MRSA strains.

• Wound cleaning with gentle abrasion is indicated. Deep abrasive scrubbing is not required.
• Topical mupirocin is adequate treatment for single lesions of nonbullous impetigo or small areas of involvement. A 7-day course is usually standard, although a few large studies have been performed to verify this as the most effective approach.
• Systemic antibiotics are indicated for extensive involvement or for bullous impetigo.
• If there are large areas of involvement resulting in denuded skin from ruptured bullae, then adequate fluid resuscitation is indicated with intravenous rehydration fluid at a volume and rate similar to standard volume replacement for burns.
• Early and appropriate treatment usually prevents scarring and localized spread.
• Good hygiene and hand washing should be encouraged. Household spread is common otherwise.

Consultations

The need for consultation is determined by the extent of involvement and the age of the patient. Neonates with bullous impetigo require a consultation with neonatology.

MEDICATION

Section 7 of 11  

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

Antibiotics are the mainstay of therapy. The drug chosen must provide coverage against coagulase-positive S aureus and GABHS. In areas with high percentage of CA-MRSA, the empiric antibiotic choice should provide coverage for this possibility.

Drug Category: Topical antibiotics

These agents pose fewer potential problems than systemic antibiotics, but their use is reserved only for cases involving lesions that are small or few in number.

Drug Category: Systemic antibiotics

Therapy must cover all likely pathogens in the context of the clinical setting.

FOLLOW-UP

Section 8 of 11  

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

Further Inpatient Care

• Inpatient care is required for patients with widespread disease or for infants at risk of sepsis and/or dehydration due to skin loss.

Further Outpatient Care

• A follow-up examination is required if lesions have not cleared in 7 days.

Transfer

• Transfer care to a neonatologist for neonates with bullous impetigo.

Deterrence/Prevention

• Avoid contact with infected persons.
• Keep wounds clean.
• Wash hands after contacting lesions or infected patients.

Complications

• Poststreptococcal glomerulonephritis (all age groups)
• Meningitis or sepsis (infants)
• Ecthyma
• Erysipelas
• Deep cellulitis
• Bacteremia
• Osteomyelitis
• Septic arthritis
• Pneumonia
• Lymphadenitis

Prognosis

• Beyond the neonatal period, patients who receive early and appropriate therapy have an excellent chance of recovery without scarring or complications.
• Neonates have a much higher incidence of developing a more generalized infection and meningitis.
• Lesions usually resolve completely in 7-10 days with treatment.
• Culture lesions to find resistant organisms if the lesions have not resolved within 7-10 days.
• Antibiotic treatment will not prevent or halt glomerulonephritis.

Patient Education

• Because of the contagious nature, children should not return to daycare or school before the lesions clear. 
• Caretakers must know how to avoid infection. A history of poor hygiene and crowded living situations are common.
• This infection is transmitted by direct contact and by fomites, including hygiene items, clothing, and toys.
• 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  

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

Medical/Legal Pitfalls

• Failure to use antibiotics with coverage against staphylococci may result in failure of treatment.
• Failure to recognize signs of dehydration and treat appropriately may result in hypovolemic and/or septic shock.

Special Concerns

• The incidence of poststreptococcal glomerulonephritis is not affected by the treatment of the infection in the index patient, but antibiotic treatment will limit the endemic nature by limiting its spread to other hosts.

ACKNOWLEDGMENTS

Section 10 of 11  

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

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Randy Park, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

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

• Allen CH, Patel B, Endom EE. Primary bacterial infections of the skin and soft tissues, changes in epidemiology and management. Clin Ped Emerg Med. 2004;5:246-255.
• Cherry JD. Contemporary infectious exanthems. Clin Infect Dis. Feb 1993;16(2):199-205. [Medline].
• Dagan R. Impetigo in childhood: changing epidemiology and new treatments. Pediatr Ann. Apr 1993;22(4):235-40. [Medline].
• Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol. Dec 1994;11(4):293-303. [Medline].
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• Epps RE. Impetigo in pediatrics. Cutis. May 2004;73(5 Suppl):25-6. [Medline].
• Leyden JJ. Review of mupirocin ointment in the treatment of impetigo. Clin Pediatr (Phila). Sep 1992;31(9):549-53. [Medline].
• Loffeld A, Davies P, Lewis A, Moss C. Seasonal occurrence of impetigo: a retrospective 8-year review (1996-2003). Clin Exp Dermatol. Sep 2005;30(5):512-4. [Medline].
• Luby S, Agboatwalla M, Schnell BM, et al. The effect of antibacterial soap on impetigo incidence, Karachi, Pakistan. Am J Trop Med Hyg. Oct 2002;67(4):430-5. [Medline].
• Nishijim S, Ohshima S, Higashida T, et al. Antimicrobial resistance of Staphylococcus aureus isolated from impetigo patients between 1994 and 2000. Int J Dermatol. Jan 2003;42(1):23-5. [Medline].
• Oranje AP, Chosidow O, Sacchidanand S, Todd G, Singh K, Scangarella N. Topical retapamulin ointment, 1%, versus sodium fusidate ointment, 2%, for impetigo: a randomized, observer-blinded, noninferiority study. Dermatology. 2007;215(4):331-40. [Medline].
• Shriner DL, Schwartz RA, Janniger CK. Impetigo. Cutis. Jul 1995;56(1):30-2. [Medline].
• Zetola N, Francis JS, Nuermberger EL, Bishai WR. Community-acquired meticillin-resistant Staphylococcus aureus: an emerging threat. Lancet Infect Dis. May 2005;5(5):275-86. [Medline].

Article Last Updated: Apr 9, 2008