Superficial bacterial skin infection (S. aureus or S. pyogenes) producing honey-colored crusted erosions; highly contagious in children.
Also known as: impetigo, non-bullous impetigo, bullous impetigo, ecthyma
Overview
Highly contagious superficial bacterial skin infection caused predominantly by Staphylococcus aureus and Streptococcus pyogenes. Classified as non-bullous (most common), bullous, or ecthyma (ulcerative deeper variant).
Epidemiology
Most common bacterial skin infection in children ages 2-5; peak incidence in summer/fall. Affects ~140 million people globally. Bullous impetigo predominantly in neonates and young children. Higher rates in crowded conditions, hot/humid climates, and individuals with atopic dermatitis.
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Question 1DermatologyEasy
A 4-year-old boy who attends daycare is brought in with several lesions around the mouth and nares that began as small vesicles and have evolved into golden, honey-colored crusts. He is afebrile and otherwise well, and the lesions are mildly itchy but not painful. Which of the following is the most likely diagnosis?
AHerpes simplex virus infection
BAtopic dermatitis
CVaricella
DContact dermatitis
EImpetigo
Reveal answer & full explanation
Correct answer: E — Impetigo
AHerpes simplex virus infection
BAtopic dermatitis
CVaricella
DContact dermatitis
EImpetigo✓
Why Impetigo is correct
Non-bullous impetigo is the most common bacterial skin infection in young children and spreads readily in daycare settings
The hallmark is golden, honey-colored crusting that develops from initial vesicles, classically around the mouth and nares
Staphylococcus aureus is the leading cause, followed by group A Streptococcus
The well, afebrile child with superficial perioral crusts fits a localized superficial pyoderma rather than a systemic or chronic process
Why the others are wrong
Contact dermatitis — produces erythema, edema, and vesicles in the distribution of an external allergen and does not form honey-colored crust (anchoring on the initial vesicles)
Herpes simplex virus infection — causes grouped vesicles on an erythematous base that ulcerate and are painful, without the characteristic honey crust (buzzword-matching the word "vesicles")
Atopic dermatitis — a chronic, intensely pruritic eczematous condition favoring flexural skin, not an acute perioral crusted eruption (premature closure on a common pediatric rash)
Varicella — a daycare child with vesicles that crust over invites chickenpox, but varicella is a widespread, intensely itchy eruption concentrated on the trunk with lesions in different stages and often fever, not a few perioral lesions with honey-colored crust (anchoring on the vesicle-to-crust evolution)
Question 2DermatologyEasy
A 6-year-old boy presents with a honey-crusted, golden-yellow lesion on his nose and around his mouth. His 3-year-old sibling developed similar lesions. He has no fever. What is the most likely diagnosis?
AContact dermatitis
BVaricella
CImpetigo
DHerpes labialis
EPerioral dermatitis
Reveal answer & full explanation
Correct answer: C — Impetigo
AContact dermatitis
BVaricella
CImpetigo✓
DHerpes labialis
EPerioral dermatitis
Why impetigo is correct
Impetigo is the most common bacterial skin infection in children
Caused by S. aureus (most common) or S. pyogenes
Non-bullous (crusted) form presents with honey-colored crusts on the face around the mouth and nose
Highly contagious, explaining sibling spread
Why the others are wrong
Herpes labialis — shows grouped vesicles on an erythematous base, not honey-colored crusts
Perioral dermatitis — papulopustules that spare the vermilion border, typically after topical steroid use, not honey-colored crusts
Contact dermatitis — pruritic, sharply demarcated erythema and vesicles limited to the site of allergen or irritant contact, with no crusting
Varicella — sibling spread of a crusting rash makes chickenpox tempting, but varicella produces a generalized, intensely pruritic eruption of vesicles that appear in successive crops, so lesions are seen in different stages of evolution, rather than golden honey-colored crusts confined to the nose and mouth
Additional high-yield points
Treatment for localized disease: mupirocin 2% ointment three times daily (TID) x 5 days
Oral antibiotics (cephalexin or dicloxacillin) used for widespread, bullous, or recurrent disease
MRSA coverage with trimethoprim-sulfamethoxazole (TMP-SMX) or doxycycline if MRSA is suspected
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Non-bullous impetigo: bacteria invade skin through breaks in barrier, producing intraepidermal pustules that rupture and crust. Bullous impetigo: S. aureus phage group II produces exfoliative toxin (ET-A) that cleaves desmoglein-1 in the granular layer → flaccid bullae. Ecthyma: deeper dermal invasion → ulcerative crusted lesion that heals with scar.
Non-bullous: thin-walled vesicle/pustule on erythematous base → rapidly ruptures → erosion with honey-colored (yellow-brown) crust; face (perioral, perinasal), extremities; well-demarcated; minimal surrounding inflammation
Bullous: flaccid clear/cloudy bullae 1-5 cm on intact skin (no erythematous base required) that rupture leaving collarette of scale and varnish-like brown crust; trunk, extremities, intertriginous areas; neonates and young children
Ecthyma: punched-out ulcer with adherent yellow-gray crust and surrounding violaceous halo; lower extremities; heals with scarring
Regional lymphadenopathy in 90% of non-bullous cases
Classic findings
Honey-colored crust on superficial erosions in a child; flaccid bullae with brown varnish-like crusts (bullous form).
Differential diagnosis
Herpes simplex (HSV) — Grouped vesicles on erythematous base, prodromal tingling, recurrent in same site; Tzanck/PCR positive
Varicella — Generalized eruption in different stages, fever, vesicles on erythematous base ('dew drop on rose petal')
Contact dermatitis with secondary infection — Pattern matches exposure; pruritus predominant before crusting
Tinea corporis with secondary infection — Annular plaque with peripheral scale; KOH positive
Staphylococcal scalded skin syndrome (SSSS) — Diffuse erythema and superficial desquamation; positive Nikolsky; fever; young child
Ecthyma gangrenosum (vs ecthyma) — Necrotic ulcer with black eschar in neutropenic patient; Pseudomonas bacteremia
Diagnostic workup
Diagnostic criteria
Clinical: characteristic honey-colored crusted lesions or flaccid bullae in a typical patient; culture confirms organism and susceptibility.
Labs
Clinical diagnosis usually sufficient
Gram stain and culture of exudate (especially in suspected MRSA, treatment failure, severe disease, outbreaks)
Anti-DNase B and anti-streptolysin O titers (rising in post-streptococcal glomerulonephritis surveillance — not routine); after impetigo the ASO response is often weak, so anti-DNase B is the preferred marker
Urinalysis in the weeks after streptococcal impetigo if PSGN suspected (hematuria, edema, HTN)
Imaging
Not indicated
Diagnostic algorithm
Variant
Hallmark
Therapy
Non-bullous
Honey-colored crusts on face/extremities
Topical mupirocin × 5 d (limited); oral cephalexin/dicloxacillin × 7 d (extensive)
Bullous
Flaccid bullae → varnish-like brown crust (toxin-mediated)
Oral cephalexin/dicloxacillin; admit neonates
Ecthyma
Punched-out ulcer with adherent crust, scars on healing
Oral antibiotics × 7-10 d; local wound care
MRSA-suspected
Treatment failure, purulent, abscess
Clindamycin, TMP-SMX, or doxycycline based on susceptibilities
Impetigo variants and antimicrobial selection.
Treatment
First-line
Limited (≤5 lesions, small body area, non-bullous): topical mupirocin 2% ointment TID × 5 days OR topical retapamulin 1% ointment BID × 5 days OR topical ozenoxacin 1% cream BID × 5 days
Extensive, bullous, ecthyma, or treatment failure (systemic antibiotics × 7 days): cephalexin 25-50 mg/kg/day divided QID (pediatric) or 250-500 mg QID (adult); dicloxacillin 12.5 mg/kg/day pediatric or 250-500 mg QID adult — covers MSSA and S. pyogenes
Penicillin-allergic (non-anaphylactic): cephalexin acceptable; (anaphylactic): clindamycin 10-30 mg/kg/day pediatric or 300-450 mg QID adult, or doxycycline (≥8 years)
MRSA suspected: clindamycin (check D-test for inducible resistance), trimethoprim-sulfamethoxazole, doxycycline, linezolid; mupirocin remains effective for many MRSA strains
Hygiene: hand washing, nail trimming, separate towels and bedding, cover lesions; may return to school or daycare at least 12 hours after starting antibiotics, with lesions covered (CDC, AAP Red Book) — crusted lesions are still infectious
Decolonization for recurrent: intranasal mupirocin BID × 5 days + chlorhexidine washes + household decontamination
Bullous impetigo (neonates)
Low threshold for hospital admission, IV antibiotics (nafcillin, oxacillin, vancomycin if MRSA risk)
Differentiate from staphylococcal scalded skin syndrome which requires broader management
Ecthyma
Systemic antibiotics (as above) × 7-10 days
Local wound care with gentle debridement
Counsel: heals with scarring (unlike standard impetigo)
Second-line / adjunct
Mupirocin resistance documented in some regions — fusidic acid or retapamulin are alternatives
Bleach baths for recurrent disease in atopic dermatitis patients
Treat underlying skin disease (scabies, eczema)
Complications
Cellulitis, lymphangitis, bacteremia
Post-streptococcal glomerulonephritis (PSGN) — 1-5% incidence after streptococcal skin infection, latent period longer after skin infection (about 3 weeks, up to 6) than after pharyngitis (about 10 days); antibiotic treatment does NOT prevent PSGN once infection established
Acute rheumatic fever classically follows streptococcal pharyngitis; CDC now recognizes that ARF can also follow group A strep skin infection such as impetigo, but that link is less established — PSGN is the expected nonsuppurative sequela of impetigo
Staphylococcal scalded skin syndrome (SSSS) from toxin spread
Scarlet fever
Permanent scarring from ecthyma
Recurrence with persistent nasal/skin S. aureus colonization
PANCE pearls
Honey-colored crust on a child's face = impetigo. Topical mupirocin × 5 days is sufficient for limited disease.
Bullous impetigo is caused by S. aureus exfoliative toxin (same family that produces SSSS); the bullae are typically on intact-appearing skin without erythematous halo.
Antibiotic treatment of streptococcal impetigo does NOT prevent post-streptococcal glomerulonephritis once infection is established — but does prevent transmission and other complications.
Recurrent impetigo warrants S. aureus decolonization (intranasal mupirocin + chlorhexidine).
Ecthyma heals with scarring; standard impetigo does not.
References
IDSA 2014 — Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America (Stevens et al., Clin Infect Dis 2014)
AAP Red Book 2024 — American Academy of Pediatrics. Red Book: 2024-2027 Report of the Committee on Infectious Diseases, 33rd ed. — Group A Streptococcal Infections and Staphylococcus aureus chapters
AAFP 2014 — Impetigo: Diagnosis and Treatment (Hartman-Adams, Banvard, Juckett, Am Fam Physician 2014)
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