Key Points
- Honey-colored crusted erosions are classic for nonbullous impetigo.
- Both group A streptococci and Staphylococcus aureus can cause nonbullous disease.
- Use topical therapy for a limited number of lesions and oral therapy for numerous, bullous, or outbreak-associated lesions.
- Oral regimens should cover both streptococci and S aureus.
- Culture is useful for treatment failure, recurrent disease, outbreaks, or suspected resistant organisms.
- Systemic toxicity or deep tenderness suggests a diagnosis beyond simple impetigo.
Algorithm
- Identify superficial crusted or bullous lesions without evidence of deep infection.
- Assess lesion number, distribution, systemic symptoms, outbreak context, and MRSA risk.
- Use topical antibiotic therapy for limited localized disease.
- Use oral therapy for numerous lesions, bullous disease, or impractical topical treatment.
- Culture unusual, recurrent, outbreak-associated, or treatment-resistant disease.
- Address underlying eczema, scabies, or skin trauma.
- Provide hygiene and lesion-covering instructions to limit spread.
Clinical Synopsis & Reasoning
Nonbullous impetigo typically begins as papules or vesicles that rupture and form characteristic honey-colored crusts, often around the nose, mouth, or exposed extremities. It is caused by Staphylococcus aureus, group A Streptococcus, or both. Bullous impetigo is caused by toxin-producing S aureus and produces fragile superficial bullae that rupture into moist erosions. Patients are usually well; fever, marked tenderness, rapidly spreading erythema, or systemic toxicity should prompt evaluation for cellulitis, deeper infection, or another diagnosis.
The diagnosis is usually clinical. Bacterial culture is useful when MRSA is suspected, disease is recurrent, an outbreak is being investigated, or lesions fail standard therapy. HSV can mimic impetigo around the mouth, and eczema herpeticum should be considered when painful monomorphic erosions occur in a patient with atopic dermatitis. Tinea, contact dermatitis, insect bites, and scabies with secondary crusting are other common mimics.
Post-streptococcal glomerulonephritis can follow streptococcal impetigo, but antibiotic treatment has not been proven to reliably prevent this immune complication. Rheumatic fever is not a typical sequela of impetigo. The practical goals are cure, limiting transmission, and recognizing deeper infection.
Treatment Strategy & Disposition
For a small number of localized lesions, use topical mupirocin or another recommended topical antimicrobial according to local susceptibility and formulary. Gently soaking or cleansing crusts can improve contact with topical medication. Oral therapy is preferred for numerous lesions, bullous impetigo, outbreaks, or situations in which topical treatment is impractical. CDC guidance recommends therapy active against both group A Streptococcus and S aureus.
Common oral options for methicillin-susceptible disease include cephalexin or dicloxacillin. When community MRSA is a realistic concern, select therapy based on local susceptibility and the need to maintain streptococcal coverage. Avoid routine incision and drainage unless a true abscess is present. Treat underlying eczema, scabies, or other barrier disruption that is driving recurrent infection.
Cover draining lesions when feasible, reinforce hand hygiene, avoid sharing towels or razors, and keep children out of close-contact activities according to local school or public-health rules until effective therapy has begun. Recurrent clustered household cases may warrant evaluation for shared exposures or colonization strategies under clinician guidance.
Epidemiology / Risk Factors
- Impetigo is especially common in young children.
- Warm humid environments, close contact, minor trauma, eczema, insect bites, and scabies increase risk.
- Transmission occurs through direct contact and contaminated items.
- Outbreaks can occur in households, schools, athletic settings, and crowded environments.
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| Clinical examination | Usually establishes diagnosis | Superficial crusts, erosions, or bullae | No routine labs in uncomplicated disease |
| Bacterial culture | Guides resistant or recurrent cases | S aureus, GAS, or both | Useful after treatment failure |
| Urinalysis | Evaluates suspected post-streptococcal nephritis | Hematuria or proteinuria | Only when compatible symptoms develop |
Therapy Overview
| Scenario | Treatment |
|---|---|
| Few localized nonbullous lesions | Topical antibiotic therapy |
| Numerous lesions or outbreak setting | Oral antibiotic active against S aureus and group A streptococci |
| Bullous impetigo | Oral therapy is commonly used because disease is toxin-producing S aureus |
| Treatment failure or recurrent infection | Culture and reassess diagnosis and resistance |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Mupirocin | Inhibits bacterial isoleucyl-tRNA synthetase | Days | Localized impetigo | Resistance with overuse |
| Cephalexin | First-generation cephalosporin cell-wall inhibition | Days | Oral therapy for MSSA and streptococcal disease | Allergy and local resistance considerations |
| Dicloxacillin | Antistaphylococcal beta-lactam | Days | MSSA and streptococcal disease | Frequent dosing and GI effects |
| MRSA-active oral agent | Agent-dependent antimicrobial action | Days | Selected patients with MRSA concern | Ensure streptococcal coverage when needed |
Prognosis / Complications
- Most uncomplicated impetigo resolves with appropriate treatment.
- Untreated disease can spread locally and to close contacts.
- Cellulitis and deeper infection are uncommon but important complications.
- Post-streptococcal glomerulonephritis is an uncommon immune complication after streptococcal skin infection.
Patient Education / Counseling
- Wash hands after touching lesions and avoid sharing towels, clothing, or razors.
- Keep draining areas covered when practical.
- Complete the prescribed course and do not save topical antibiotic for unrelated future rashes.
- Seek care if fever, rapidly expanding redness, severe pain, or new swelling develops.
Notes
Impetigo is usually a visual diagnosis, so the most important skill is recognizing when the appearance no longer fits a superficial infection. Deep pain, rapidly progressive swelling, hypotension, or systemic toxicity should move the clinician toward cellulitis, abscess, necrotizing infection, or another serious process.
Antibiotic choice should reflect local resistance. The enduring principle from CDC guidance is that oral therapy for nonbullous impetigo must address both major pathogens rather than assuming every case is purely streptococcal.
Bullous and nonbullous impetigo also differ in the way lesions should be interpreted. Bullae that are widespread, accompanied by systemic illness, or associated with diffuse tenderness in a young child should prompt consideration of staphylococcal scalded skin syndrome rather than routine outpatient impetigo. Around the eye, rapidly increasing edema or pain with eye movement changes the problem to possible preseptal or orbital cellulitis. In recurrent disease, clinicians should look for an untreated driver such as eczema, nasal colonization, scabies, or close-contact transmission. Decolonization is not a universal first step and should be reserved for appropriate recurrent-infection strategies rather than prescribed after a single uncomplicated episode.
References
- CDC Clinical Guidance for Group A Streptococcal Impetigo — Link
- CDC Group A Streptococcal Clinical Guidance — Link
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