OVERVIEW: What every practitioner needs to know

Are you sure your patient has impetigo? What are the typical findings for this disease?

Impetigo is a common, superificial, bacterial infection of the skin, which may occur in a bullous or non-bullous form.

Nonbullous impetigo (also known as Impetigo contagiosa) presents with the following:

Plaques with honey-colored crust (may start as papule or pustule)

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Often asymptomatic, although pain and itching are possible

Healing without scarring, but often with postinflammatory pigmentation abnormalities

Typically affects exposed areas, especially face and extremities

Bullous impetigo presents with the following:

Fragile, superficial bullae or pustules

Round, erythematous erosions

Surrounding collarette of scale

Lesions may cluster

Evidence of autoinoculation

Often asymptomatic, although pain and itching are possible

Healing without scarring, but often with postinflammatory pigmentation abnormalities

Involvement of diaper area is common in infants, as is involvement of the abdomen; exposed areas (face and extremities) are involved at other ages

What other disease/condition shares some of these symptoms?

A wide variety of dermatologic conditions may be mistaken for impetigo. They include the following:

Herpes simplex viral infections

Arthropod bite reactions, especially bullous reactions


Chronic bullous disease of childhood

Staphylococcal scalded skin syndrome

Child abuse



Nummular eczema

Pemphigus foliaceus (also targets desmoglein-1)

Ecthyma gangrenosum

Subcorneal pustular dermatosis

Molluscum contagiosum

Prurigo, neurotic excoriations

Contact dermatitis, especially from neomycin




Eosinophilic folliculitis

Hidradenitis suppurativa

Cold abscesses of hyper-IgE syndrome

Acute generalized exanthematous pustulosis

What caused this disease to develop at this time?

Exposure to a carrier of Staphylococcus aureus (usually nasal colonization) or someone infected with S. aureus, or exposure to someone colonized or infected with Streptococcus pyogenes (usually skin colonization); direct contact.

Patients who have skin conditions with traumatized or compromised skin barriers (e.g., eczema, insect bites, abrasions, varicella, eczema herpeticum, tinea capitis, neurotic excoriations) are particularly susceptible to development of impetigo, often as superinfections.

Additional predisposing factors may include the following:

Hot, humid weather

Sports, especially contact sports

Crowded living situations and sharing household items (e.g., personal hygiene products)

Poor hygiene


Intravenous drug use

School or day care attendance

What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?

Typically, impetigo is a clinical diagnosis; laboratory studies are generally not necessary. The diagnosis may be confirmed by culturing Staphylococcus aureus or Streptococcus pyogenes from foci of infection, but this is usually reserved for unusual, persistent, or severe cases.

Would imaging studies be helpful? If so, which ones?

Chest radiography is useful if there is a concern for pneumonia as a complication. Magnetic resonance imaging (MRI) can be used if there is a concern for complicating osteomyelitis.

If you are able to confirm that the patient has impetigo, what treatment should be initiated?

Perform gentle cleansing.

Apply moist compresses.

Remove crusts.

Drain pustules and bullae in sterile fashion.

Topical antibiotics for localized, mild, and/or uncomplicated cases (e.g., mupirocin ointment applied three times daily for 7-10 days). Other topical options include retapamulin, polymyxin, erythromycin, bacitracin, and gentamicin.

Administer oral antibiotics for more severe, widespread, and/or complicated disease, with gram-positive coverage. The antibiotic choice should be based on local resistance patterns. It is important to provide treatment that would be effective for both
Staphylococcus aureus and
Streptococcus pyogenes. Common choices include beta-lactamase resistant antibiotics such as cephalexin, erythromycin, or amoxicillin-clavulanate.

Consider oral antibiotics for emerging or potential outbreaks (e.g., multiple cases in a nursery school, day care, home, or on a sports team).

Consider providing an antibiotic that will be effective for methicillin-resistant
Staphylococcus aureus (MRSA), although MRSA is more closely linked to abscesses and furuncles than impetigo. Options include trimethoprim-sulfamethoxazole (but this antibiotic has poor
Streptococcus pyogenes coverage), clindamycin, or vancomycin.

Neonates with bullous impetigo should be treated with intravenous antibiotics.

Consider whether the patient or a close contact is a carrier (e.g., in a nursery outbreak or in the case of recurrent disease).

Consider intermittent intranasal and perianal mupirocin ointment for decolonization (e.g., twice daily for 1 week/month).

Contact precautions/isolation are necessary if the patient is hospitalized.

Exclude from school or sports for at least 24 hours after initiating antibiotics.

Consider dilute bleach baths (1/4-1/2 cup of regular 6% bleach for a 40-gallon bathtub, approximately 10 minutes a few times a week) or a chlorhexidine gluconate wash for recurrent disease.

What are the adverse effects associated with each treatment option?

Drug rashes may occur with antibiotics, including toxic epidermal necrolysis with trimethoprim-sulfamethoxazole and red man syndrome with vancomycin.

Gastrointestinal upset may occur with oral antibiotics.

Contact dermatitis may occur with topical antibiotics, especially neomycin.

Antibiotic resistance may develop.

If the decision is made to avoid antibiotics, there may be an increased risk for spread to other individuals.

What are the possible outcomes of impetigo?

Complications are uncommon. Impetigo usually resolves on its own in several weeks without treatment (i.e., antibiotics). However, treatment may prevent uncommon complications as well as prevent spread to other individuals. Many individuals struggle with recurrent disease. Most treatments have only a low risk of side effects.

What causes this disease and how frequent is it?

Impetigo is the most common pediatric bacterial skin infection.

Up to 2% of visits to pediatricians result from impetigo.

More than 70% of cases of impetigo are nonbullous impetigo.

A compromised skin barrier facilitates infection.

Athough bullous impetigo is caused only by Staphylococcus aureus, nonbullous impetigo may be caused by either S. aureus or Streptococcus pyogenes. Overall, Staphylococcus aureus is a more common cause of impetigo than
Streptococcus pyogenes (the latter tending to occur in preschool-aged children).

In some cases of impetigo, both Staphylococcus aureus and Streptococcus pyogenes may be cultured.

Bullous impetigo is infection with particular
Staphylococcus aureus strains that produce epidermolytic toxin (exfoliative toxin).

How do these pathogens/genes/exposures cause the disease?

Bullous impetigo is mediated by several epidermolytic toxins produced by particular strains of
S. aureus.Epidermolytic toxin-A (ET-A) is most often implicated in bullous impetigo. ET-A targets and cleaves desmoglein-1, an important epidermal adhesion protein. This allows invasion of the S. aureus and local blistering.

S. aureus and Streptococcus pyogenes can cause nonbullous impetigo when they are inoculated through an impaired skin barrier (which leads to exposed fibronectin).

S. pyogenes produces streptolysins.

Panton-Valentine leukocidin is often expressed by MRSA. This toxin targets neutrophils and monocytes and is associated with more aggressive disease.

Other clinical manifestations that might help with diagnosis and management

Impetigo is a highly contagious condition.

Exudative, draining lesions sometimes develop, and infrequently patients with impetigo experience fever of regional lymphadenopathy (typically with nonbullous impetigo).

Occasionally lesions take on the appearance of warty plaques or ulcers.

What complications might you expect from the disease or treatment of the disease?

Complications are unusual, but the following may occur:

Ecthyma (deeper, more serious infection into the dermis)


Septic arthritis




Staphylococcal scalded skin syndrome

Poststreptoccocal glomerulonephritis

Guttate psoriasis or scarlet fever (but not rheumatic fever)

Are additional laboratory studies available; even some that are not widely available?

A skin biopsy is rarely needed. A skin biopsy would typically reveal a subcorneal blister (better defined in bullous impetigo) with polymorphonuclear leukocytes, acantholytic cells, and bacteria visible on Gram stain.

A Tzanck smear may help evaluate for herpes simplex virus infection or varicella.

A potassium hydroxide scraping may help rule out tinea.

A scabies preparation may help rule out scabies.

Anti-DNAse B (or, less commonly, anti-streptolysin O) may be elevated in
S. pyogenes infection.

Antihyaluronidase titers may indicate streptococcal infection.

Leukocytosis is sometimes seen.

Blood culture results are rarely positive.

How can impetigo be prevented?

Prompt evaluation and treatment of staphylococcal infections, as well as treatment of asymptomatic carriers will help prevent spread of infection to others.

Infection control measures should be used to avoid outbreaks (e.g., barrier protocols, hand washing, treatment of infected workers or family, mupirocin ointment for nasal carriers, frequent washing of towels). Infected skin should be covered to minimize spread to others. Dilute bleach baths may help prevent recurrent disease.

It is essential to keep any underlying or associated skin condition (e.g., atopic dermatitis) under good control, or avoid the condition if possible (e.g., arthropod bite reactions).

What is the evidence?

Geria, AN, Schwartz, RA. “Impetigo update: new challenges in the era of methicillin resistance”. Cutis. vol. 85. 2010. pp. 65-70. (This article provides a review of impetigo and addresses appropriate management for methicillin-resistant infection.)

Schachner, L. “Treatment of uncomplicated skin and skin infections in the pediatric and adolescent patient populations”. J Drugs Dermatol. vol. 4. 2005. pp. s30-3. (This article describes the growing predominance of Staphylococcus aureus, compared with Streptococcus pyogenes, as the cause of impetigo.)

Berk, DR, Bayliss, SJ. “MRSA, scalded skin syndrome, and other cutaneous bacterial emergencies”. Pediatr Ann. vol. 39. 2010. pp. 627-33. (This article reviews cutaneous bacterial infections, their treatment, and methods to prevent their spread.)

Ongoing controversies regarding etiology, diagnosis, treatment

There is controvery regarding the need for oral versus topical antibiotics. There is controvery regarding the need for treatment at all, given that impetigo is generally self-limited. It is still uncertain if treating impetigo caused by Streptococcus pyogenes indeed alters the risk for poststreptococcal glomerulonephritis.

There has been a recent push to reconsider the role of gentian violet as a viable treatment option. A multivalent vaccine against S. pyogenes is also under development. Topical fusidic acid is a treatment option outside of the United States, but
Staphylococcus aureus resistance is emerging.