Skin & Subcutaneous Tissue

Impetigo and ecthyma: outpatient management

Clinical Overview and When to Suspect Impetigo/Ecthyma

— Staphylococcus aureus (including community-acquired MRSA) — now the dominant pathogen in the US, especially for bullous and nonbullous impetigo.

— Streptococcus pyogenes (group A strep, GAS) — classic cause; more often implicated in ecthyma and in nonbullous impetigo in hot/humid climates.

— Mixed S. aureus + GAS infection is common.

— Nonbullous impetigo (~70%): honey-crusted erosions, typically perinasal/perioral or on extremities; mostly children 2–5 yr.

— Bullous impetigo: flaccid bullae from local S. aureus exfoliative toxin A; infants and young children; trunk/intertriginous areas.

— Ecthyma: "punched-out" ulcers with adherent crust and surrounding erythema; heals with scarring; lower extremities; associated with poor hygiene, malnutrition, immunosuppression, insect bites, diabetes.

— Honey-colored crusts on the face of a school-aged child, especially with siblings or daycare contacts affected.

— Recurrent superficial pustules in an athlete (wrestlers, football), or military recruits — think MRSA.

— Crusted ulcers on the shins of an unhoused or diabetic adult after minor trauma.

— Secondary infection ("impetiginization") overlying eczema, scabies, varicella, or insect bites.

Board pearl: A child with crusted lesions plus 2 weeks later cola-colored urine = post-streptococcal glomerulonephritis following GAS impetigo — but treating impetigo does not prevent PSGN (unlike rheumatic fever after pharyngitis).

Impetigo is a superficial bacterial skin infection of the epidermis; ecthyma is its ulcerative form extending into the dermis. Both are common outpatient diagnoses in primary care, pediatrics, and urgent care.

Microbiology:

Three clinical forms:

When to suspect (outpatient red flags that should trigger the diagnosis):

Epidemiology pearls: Peak incidence late summer/early fall, warm humid climates, crowded living, contact sports, daycare. Spreads via direct contact and fomites.

Presentation Patterns and Key History

— Begins as a small red macule or papule → rapidly evolves to a vesicle/pustule → ruptures within hours leaving a honey-colored ("golden") crust on an erythematous base.

— Often starts at sites of minor skin breakdown: nostrils, around mouth, scratches, insect bites, eczema patches.

— Itching common, pain mild, systemic symptoms absent. No fever in uncomplicated disease.

— Flaccid, fragile bullae with clear-to-yellow fluid → rupture leaves a thin "collarette" of scale and a varnish-like base.

— Trunk, axillae, diaper area, neck folds; predominantly neonates and infants.

— Caused by localized S. aureus exfoliative toxin; no mucosal involvement (key contrast with SSSS, which is generalized).

— Begins similar to impetigo but evolves over days into a deep, punched-out ulcer 0.5–3 cm with thick gray-yellow crust and a violaceous, indurated border.

— Heals slowly (weeks) with scarring — a defining historical feature.

— Predisposing factors to elicit: poverty/crowding, diabetes, IV drug use, prior skin trauma, neutropenia, lymphedema, recent travel to tropics.

— Duration, evolution (vesicle → crust vs. ulcer with scar potential).

— Sick contacts: siblings, daycare, sports teammates, household members.

— Recurrence pattern — recurrent furuncles/impetigo in family suggests S. aureus colonization (nares, axilla, groin).

— Underlying skin disease (atopic dermatitis is the #1 predisposer).

— Prior MRSA infection or hospitalization.

— Immunization status (especially varicella), and recent varicella/scabies.

— Allergies, antibiotic exposure, and any prior topical/oral antibiotic use for this episode.

Key distinction: Honey crust = impetigo (epidermal, heals without scar). Punched-out ulcer with violaceous rim healing with scar = ecthyma (dermal). Same organisms, different depth — and ecthyma always needs systemic antibiotics.

Nonbullous impetigo history:

Bullous impetigo history:

Ecthyma history:

Key history questions every visit:

Physical Exam Findings and Severity Assessment

— Inspect entire body, not just the lesion presented — children often have multiple sites and undiscovered atopic dermatitis or scabies.

— Examine nares, perineum, and umbilicus in infants for S. aureus reservoir.

— Palpate regional lymph nodes — mild reactive lymphadenopathy is common; tender fluctuant nodes suggest abscess/lymphadenitis.

— Multiple discrete 1–2 cm erosions with adherent honey-colored crusts, satellite lesions from autoinoculation.

— Surrounding erythema minimal; no induration; lesions do not blanch with surrounding cellulitis pattern.

— Thin-walled bullae 1–5 cm, often already ruptured leaving a moist erythematous base with a collarette of scale.

— Nikolsky sign negative (positive would suggest SSSS or pemphigus).

— Punched-out shallow ulcer with raised, indurated, often violaceous rim and a firmly adherent crust.

— Removing crust reveals a purulent ulcer base. Surrounding cellulitis may be present.

— Most often on lower extremities, buttocks, dorsum of feet.

— Vital signs: fever, tachycardia, hypotension → suggests cellulitis, bacteremia, or progression beyond simple impetigo.

— Look for streaking lymphangitis, crepitus, dusky discoloration, pain out of proportion → emergent referral for necrotizing infection.

— In infants with bullous lesions: assess for generalized desquamation, perioral crusting, irritability → SSSS, requires admission.

Step 3 management: Document number of lesions, anatomic distribution, and presence/absence of cellulitis on every visit — this single line drives the choice between topical mupirocin (limited disease) and oral antibiotics (extensive, bullous, ecthyma, or systemic features).

Systematic skin exam approach:

Nonbullous impetigo exam:

Bullous impetigo exam:

Ecthyma exam:

Hemodynamic/systemic assessment (often overlooked but Step 3-relevant for triage):

Diagnostic Workup — Initial Evaluation

— Failure of empiric therapy after 48–72 hours.

— Recurrent disease or recurrent furunculosis in patient/household.

— Outbreak setting (daycare, athletic team, correctional facility, military).

— Suspected MRSA based on local prevalence (>10–15% community MRSA) or risk factors (prior MRSA, athletes, IDU, household exposure).

— All ecthyma lesions — deeper, more likely to require tailored therapy, and may harbor gram-negatives (especially Pseudomonas in immunocompromised → ecthyma gangrenosum).

— Bullous impetigo in a neonate (toxin-mediated, may herald SSSS).

— Unroof an intact pustule or bulla; swab the moist base after removing crust, not the dry crust itself.

— Send for aerobic culture and susceptibilities. Gram stain often shows gram-positive cocci in clusters (staph) or chains (strep).

— CBC, CRP, blood cultures only if systemic toxicity, fever, or suspected bacteremia/cellulitis.

— Basic metabolic panel and urinalysis if PSGN suspected (edema, hematuria, hypertension, cola urine 1–2 weeks after impetigo).

— ASO titers are poorly elevated after skin GAS infection — anti-DNase B is the better serologic marker for post-streptococcal disease following pyoderma.

Board pearl: A child with hematuria 2 weeks after honey-crusted skin lesions — order C3 (low), anti-DNase B (elevated), UA, and BP. ASO is unreliable after cutaneous GAS. PSGN risk is not reduced by antibiotic treatment of impetigo, unlike acute rheumatic fever after pharyngitis (which is prevented).

Impetigo is fundamentally a clinical diagnosis. Routine laboratory or imaging studies are not required for uncomplicated cases and add cost without benefit.

When to obtain a wound culture with gram stain and susceptibilities:

How to culture properly:

Labs rarely needed but consider:

Imaging: Not indicated routinely. Reserve ultrasound for suspected abscess, MRI for suspected deeper infection (osteomyelitis, necrotizing fasciitis).

Diagnostic Workup — Advanced and Confirmatory Studies

— Nasal swab for S. aureus carriage in patients with ≥2 episodes in 6 months or family clustering.

— Consider swabbing axilla, groin, and perineum — extranasal carriage is increasingly recognized.

— Pulsed-field gel electrophoresis or whole-genome sequencing only in outbreak investigation by public health.

— Atypical morphology, chronic non-healing lesions, or failure of two appropriate antibiotic courses.

— Suspected mimics: bullous pemphigoid, pemphigus, herpes, varicella, contact dermatitis, cutaneous leishmaniasis, ecthyma gangrenosum.

— Send biopsy for histology + tissue culture (bacterial, fungal, mycobacterial) and direct immunofluorescence if autoimmune blistering suspected.

— Nonbullous impetigo: subcorneal pustule with neutrophils and gram-positive cocci.

— Bullous impetigo: intraepidermal cleavage at the granular layer from exfoliative toxin acting on desmoglein-1 (same target as pemphigus foliaceus and SSSS).

— Ecthyma: full-thickness epidermal necrosis with dermal inflammation and ulceration.

— Ecthyma gangrenosum in a febrile neutropenic patient: lesions begin as painless red macules → hemorrhagic bullae → necrotic ulcers with black eschar. Obtain blood cultures + tissue culture/Gram stain — Pseudomonas aeruginosa bacteremia until proven otherwise. This is a hematology/oncology emergency, not outpatient impetigo.

— Recurrent staph skin infections in children: consider HIV testing, hyper-IgE syndrome (Job), chronic granulomatous disease if very recurrent + deep abscesses.

— Photograph lesions if patient consents — facilitates telehealth follow-up and outbreak tracking.

Key distinction: "Ecthyma" (strep/staph, outpatient, treatable) vs. "ecthyma gangrenosum" (Pseudomonas bacteremia in neutropenia, ICU-level, IV antipseudomonal therapy emergently) — share a name, share nothing else.

Decolonization screening (recurrent disease):

When to biopsy:

Histology features (rarely tested but useful):

Special situations:

Documentation for follow-up:

Risk Stratification and First-Line Management Logic

— Limited nonbullous impetigo (few lesions, localized to one body region, no bullae, no systemic symptoms, immunocompetent host) → topical therapy alone.

— Extensive impetigo (numerous lesions, multiple body areas, or unable to apply topical reliably) → oral antibiotics.

— Bullous impetigo → oral antibiotics (toxin-mediated; topicals insufficient).

— Ecthyma (any extent) → oral antibiotics, always — dermal involvement.

— Systemic symptoms, surrounding cellulitis, immunocompromise, neonate → oral antibiotics ± referral.

— Low risk → cover MSSA + GAS: cephalexin or dicloxacillin.

— High risk (prior MRSA, household MRSA, athletes, IDU, incarceration, high local prevalence) → doxycycline, TMP-SMX, or clindamycin.

— Wash affected areas gently with soap and water; remove crusts with warm compresses.

— Cover lesions with gauze.

— Hand hygiene; separate towels/linens; clip fingernails short in children.

— Exclusion from school/daycare/sports until 24 hours of effective antibiotic therapy and lesions can be covered.

— Treat household contacts only if symptomatic; consider decolonization for recurrent disease.

Step 3 management: The exam loves the dyad "limited lesions → mupirocin or ozenoxacin topically" vs. "extensive/bullous/ecthyma → cephalexin (or doxycycline/TMP-SMX if MRSA risk)". Memorize this branchpoint cold — it appears verbatim in stems.

Step 1 — Confirm it's impetigo/ecthyma and not a mimic (varicella, HSV, scabies with secondary infection, contact dermatitis, tinea, candidiasis).

Step 2 — Stratify by extent and depth — this single decision drives therapy:

Step 3 — Assess MRSA risk to choose oral agent:

Step 4 — General hygiene measures (counsel every patient):

Step 5 — Schedule follow-up: Re-assess at 48–72 hours if not improving; full re-evaluation if worsening sooner.

Pharmacotherapy — First-Line Regimens

— Mupirocin 2% ointment — apply to lesions TID × 5 days. First-line; covers MSSA, MRSA, GAS.

— Retapamulin 1% ointment — BID × 5 days; alternative; not approved <9 mo.

— Ozenoxacin 1% cream — BID × 5 days; quinolone topical, effective against MRSA.

— Apply after gently soaking off crusts with warm water.

— Cephalexin 250–500 mg PO QID × 7 days (peds: 25–50 mg/kg/day divided QID).

— Dicloxacillin 250–500 mg PO QID × 7 days (less palatable for children).

— Amoxicillin-clavulanate acceptable alternative.

— Doxycycline 100 mg PO BID × 7 days (avoid <8 yr and pregnancy).

— TMP-SMX 1–2 DS tabs PO BID × 7 days (avoid late pregnancy, G6PD caution; weak GAS coverage — pair with cephalexin if GAS also suspected).

— Clindamycin 300–450 mg PO QID (peds 10–20 mg/kg/day TID) — covers MRSA + GAS; check local D-test for inducible resistance.

— Linezolid — reserved for resistant or refractory cases.

— Topical: 5 days.

— Oral impetigo: 7 days.

— Ecthyma: 7 days, extend to 10 if slow response.

— Topical neomycin, bacitracin, polymyxin — inadequate for impetigo per IDSA; common board trap.

— Oral macrolides — high GAS and S. aureus resistance; avoid.

— Topical fusidic acid available outside US but not standard.

Board pearl: "Mupirocin TID × 5 days" for limited lesions; "cephalexin 7 days" for extensive disease or ecthyma without MRSA risk; "doxycycline or TMP-SMX" when MRSA is on the table. OTC bacitracin/Neosporin is the wrong answer.

Topical therapy (limited nonbullous impetigo):

Oral therapy — MSSA/GAS (no MRSA risk):

Oral therapy — MRSA coverage:

Penicillin allergy: Clindamycin or doxycycline acceptable; cephalexin safe in non-anaphylactic penicillin allergy.

Treatment duration:

What NOT to use:

Decolonization and Recurrent-Disease Pharmacology

— ≥2 documented S. aureus skin infections in 6 months in same patient.

— Multiple household members affected.

— Outbreaks among athletes or in families with recurrent disease despite appropriate acute therapy.

— Intranasal mupirocin 2% ointment BID × 5 days to both nares.

— Chlorhexidine 4% body wash daily × 5–14 days (or dilute bleach baths: ¼ cup household bleach in full bathtub, 2× weekly × several weeks — especially in pediatric atopic dermatitis with recurrent infection).

— Wash all bedding, towels, and clothing in hot water.

— Avoid sharing razors, towels, athletic gear.

— Consider treating all symptomatic and high-risk household contacts simultaneously to prevent ping-pong reinfection.

— Optimize underlying atopic dermatitis (topical steroids, emollients) — uncontrolled eczema is the single largest driver of recurrent impetigo in children.

— Trim fingernails; address nasal picking, thumb sucking.

— Screen and treat scabies if pruritic and crusted lesions coexist.

— Reassess diagnosis (consider HSV, eczema herpeticum, tinea, contact dermatitis, scabies).

— Obtain culture and susceptibilities if not already done.

— Escalate from topical to oral; or change oral agent to cover MRSA.

— Evaluate adherence and barrier — children may need parental supervision of applications.

— Always systemic antibiotics; debride crust at visit and instruct on warm soaks.

— If diabetic or immunocompromised with leg ulcer, broaden coverage and consider wound culture for gram-negatives.

— In tropical travelers, consider cutaneous diphtheria, leishmaniasis, or buruli ulcer as mimics.

CCS pearl: On a CCS recurrent-impetigo case, order "mupirocin nasal BID × 5 days" + "chlorhexidine wash daily" + "counsel hygiene" + "screen household contacts" — these four orders move the clock and resolve the case.

When to consider decolonization (outpatient, Step 3-favorite):

Standard 5–10 day decolonization bundle:

Adjunctive measures:

Failure of first-line therapy at 48–72 hours — algorithm:

Ecthyma-specific pharmacologic notes:

Special Populations — Elderly and Renal/Hepatic Impairment

— Ecthyma more common than impetigo in this group; lower-extremity ulcers frequently misdiagnosed as venous stasis or pressure injury.

— Always examine the entire leg — concurrent stasis dermatitis, venous ulcer, cellulitis, or DVT may coexist.

— Lower threshold for oral antibiotics and dermatology/wound-care referral.

— Assess functional status, social support, and ability to perform wound care; impaired dexterity or vision is a major adherence barrier.

— Cephalexin — reduce dose or extend interval if CrCl <30 mL/min (e.g., 250–500 mg q12h).

— TMP-SMX — reduce by 50% if CrCl 15–30; avoid if CrCl <15 or risk of hyperkalemia (especially with ACEi/ARB or spironolactone in CKD).

— Doxycycline — no renal dose adjustment needed; preferred when renal function is poor.

— Clindamycin — no renal adjustment; caution in hepatic impairment (hepatically metabolized).

— Mupirocin topical — systemic absorption negligible; safe in CKD/ESRD.

— Doxycycline — use with caution in severe hepatic disease.

— Clindamycin — reduce dose in severe disease.

— Cephalexin — generally safe.

— TMP-SMX + warfarin → INR spike, bleeding. Check INR within 3–5 days or choose alternative.

— TMP-SMX + ACEi/ARB/spironolactone → hyperkalemia, especially in CKD.

— Doxycycline + warfarin → mild INR increase.

— Clindamycin + neuromuscular blockers → enhanced blockade.

— Avoid concurrent PPI/antacids/iron/calcium within 2 hours of doxycycline (chelation).

Step 3 management: In an older diabetic with leg ecthyma on warfarin and lisinopril, avoid TMP-SMX — choose doxycycline (or cephalexin if MRSA risk low). Anticipate and document this interaction in your note — pure board fodder.

Elderly patients with impetigo or ecthyma:

Renal impairment dosing adjustments:

Hepatic impairment:

Drug-interaction pitfalls in the elderly:

Special Populations — Pregnancy, Pediatrics, Neonates

— Topical mupirocin is safe (category B, minimal absorption) — first-line for localized disease.

— Oral cephalexin and dicloxacillin — safe throughout pregnancy.

— Clindamycin — safe; useful for MRSA coverage in pregnancy.

— Avoid: doxycycline (tooth/bone effects after 2nd trimester), TMP-SMX (1st trimester: neural tube defects; 3rd trimester: kernicterus risk).

— Lactation: cephalexin, dicloxacillin, clindamycin, mupirocin all compatible; doxycycline short courses likely acceptable; avoid prolonged TMP-SMX in jaundiced or G6PD-deficient infants.

— Most common infection in children 2–5 years; honey crusts perinasally/perioral.

— Topical mupirocin approved ≥2 months; retapamulin ≥9 months; ozenoxacin ≥2 months.

— Cephalexin 25–50 mg/kg/day divided QID — first-line oral; palatable suspension.

— Clindamycin suspension — covers MRSA but bitter taste limits adherence.

— Doxycycline now considered safe for short courses (≤21 days) even <8 years per AAP/CDC (Rocky Mountain spotted fever data extended to other indications).

— Daycare/school exclusion until ≥24 hours on effective antibiotics and lesions can be covered.

— Lower threshold for admission, especially if <2 months, ill-appearing, poor feeding, or fever.

— Differentiate from SSSS (generalized, Nikolsky positive, mucosal sparing) and congenital HSV (vesicles, sepsis).

— Empiric IV nafcillin or cefazolin ± vancomycin if MRSA risk; obtain blood cultures.

— Wrestlers, football players — recurrent CA-MRSA; team-wide decolonization may be needed.

— Counsel about not sharing equipment, towels; shower after practice.

Board pearl: Pregnant patient with extensive impetigo → cephalexin PO × 7 days. If MRSA coverage required → clindamycin. Never doxycycline or TMP-SMX in 1st or 3rd trimester.

Pregnancy:

Pediatric considerations:

Neonates with bullous impetigo:

Adolescents/athletes:

Complications and Adverse Outcomes

— Cellulitis/erysipelas — spread beyond superficial epidermis; tender erythema, warmth, fever. Requires systemic antibiotics.

— Abscess formation — fluctuant nodule; requires incision and drainage with antibiotics in selected cases.

— Lymphangitis and lymphadenitis — red streaking; treat with oral antibiotics, monitor closely.

— Scarring and post-inflammatory dyspigmentation — common after ecthyma; counsel patients (especially darker skin types) and use sun protection.

— Bacteremia, osteomyelitis, septic arthritis, endocarditis — more likely in S. aureus, especially MRSA, and in immunocompromised hosts.

— Pneumonia in MRSA bacteremia (e.g., PVL-positive strains).

— Staphylococcal scalded skin syndrome (SSSS) — diffuse exfoliation from hematogenous toxin spread; admit and IV antibiotics.

— Streptococcal toxic shock syndrome — rare from skin source; fever, hypotension, multiorgan failure.

— Post-streptococcal glomerulonephritis (PSGN) — 1–2 weeks (occasionally up to 6 weeks) after GAS impetigo. Hematuria, edema, hypertension, low C3. Self-limited in most children; supportive care, BP control, salt restriction.

— Acute rheumatic fever does NOT follow skin infection — only follows GAS pharyngitis. High-yield board distinction.

— Guttate psoriasis can be triggered by recent strep infection (usually pharyngeal but also pyoderma).

— Common with S. aureus colonization; addressed via decolonization (see chunk 8).

— C. difficile with clindamycin.

— TMP-SMX: Stevens-Johnson syndrome, hyperkalemia, hyponatremia, marrow suppression.

— Doxycycline: photosensitivity, esophagitis (take upright with water).

Key distinction: PSGN can follow either GAS pharyngitis or pyoderma; rheumatic fever follows only pharyngitis. Treating impetigo does not prevent PSGN, but does prevent local spread and transmission.

Local complications:

Systemic/invasive complications (uncommon but feared):

Post-streptococcal sequelae:

Recurrence:

Pharmacologic adverse outcomes:

When to Escalate Care — ICU, Consult, or Inpatient Triage

— Systemic toxicity: fever, tachycardia, hypotension, altered mental status, or appearing ill.

— Rapidly spreading or extensive cellulitis, lymphangitis, or suspected necrotizing infection.

— Neonates and young infants (<2 months) with bullous impetigo or any systemic features → admit, IV antibiotics, blood cultures, consider SSSS workup.

— Immunocompromised hosts: neutropenia, transplant, HIV with low CD4, biologic immunosuppression — consider ID consult and broader coverage.

— Failure of two appropriate outpatient antibiotic courses.

— Suspected ecthyma gangrenosum (febrile, neutropenic patient with necrotic skin lesion) → emergent hospitalization, blood cultures, IV antipseudomonal therapy (cefepime, piperacillin-tazobactam, or meropenem ± aminoglycoside).

— Suspected SSSS (Nikolsky positive, generalized exfoliation, mucosal sparing) → admit, IV antistaph antibiotics, fluid/electrolyte management, pediatric or burn unit if extensive.

— Suspected streptococcal TSS or necrotizing fasciitis → ED, surgical consult, broad-spectrum IV antibiotics + clindamycin (toxin suppression).

— Dermatology: atypical lesions, treatment failure, suspected autoimmune blistering disease, recurrent disease, chronic non-healing ecthyma.

— Infectious Disease: recurrent MRSA, immunocompromised host, unusual organisms (mycobacteria, leishmaniasis), outbreak investigation.

— Pediatrics/neonatology: neonate with bullous impetigo.

— Public health: outbreaks in schools, daycares, athletic teams, correctional facilities.

CCS pearl: On a CCS case of a febrile infant with bullae and Nikolsky sign → change location to pediatric ward, order IV nafcillin (or vancomycin), blood culture, CBC, BMP, dermatology consult, "isolate" the infant, and IV fluids. Don't try to manage SSSS in the office.

Refer or admit when any of the following are present:

Specialist referral pathways:

Inpatient workup for severe disease: Blood cultures × 2, CBC, BMP, lactate, CRP, wound culture, consider echocardiogram if S. aureus bacteremia confirmed.

Key Differentials — Other Skin Infections

Key distinction: Honey crusts = impetigo. Fluctuant nodule = furuncle (I&D first). Diffuse non-purulent redness = cellulitis. Grouped painful vesicles = HSV (give acyclovir, not cephalexin). Confusing one for another is a classic exam trap.

Within the bacterial/superficial-infection category, distinguish:

Folliculitis — pustules centered on hair follicles; superficial. Treated with topical antibiotics, hygiene. No honey crust.

Furuncle/carbuncle (boils) — deeper follicular infection; tender fluctuant nodule. Management = incision and drainage, ± antibiotics if >2 cm, systemic symptoms, multiple sites, immunocompromise, or facial location.

Cellulitis — diffuse, non-fluctuant erythema/warmth/tenderness without crusts or ulcers. GAS predominates; treated with cephalexin (or clindamycin/doxycycline if purulent/MRSA risk).

Erysipelas — sharply demarcated, raised, fiery red plaque, usually face or shins; GAS classic; treat with penicillin or amoxicillin.

Staphylococcal scalded skin syndrome (SSSS) — generalized exfoliation from hematogenous spread of exfoliative toxin; Nikolsky positive; mucosa spared; admission required.

Necrotizing fasciitis — pain out of proportion, dusky skin, crepitus, systemic toxicity; emergent surgical debridement + broad IV antibiotics.

HSV/eczema herpeticum — grouped vesicles on erythematous base, painful, often punched-out erosions in atopic dermatitis patient; Tzanck smear, PCR; treat with acyclovir.

Varicella/zoster — vesicles in various stages (varicella) or dermatomal (zoster); secondary impetiginization common.

Tinea corporis — annular plaques with peripheral scale; KOH positive; topical antifungal.

Candidal intertrigo — beefy red plaques in skin folds with satellite pustules; topical antifungal.

Scabies — burrows, intense pruritus, web spaces, genitals; family members affected; permethrin 5% or oral ivermectin.

Key Differentials — Non-Infectious Mimics

Key distinction: Bullous impetigo (young child, no mucosa, toxin-mediated, antibiotics resolve) vs. pemphigus/pemphigoid (older patient, mucosa often involved, autoimmune, antibiotics do nothing — needs steroids/immunosuppression). When a "bullous impetigo" doesn't respond to cephalexin in a 65-year-old, think biopsy with DIF.

Bullous pemphigoid — tense bullae on erythematous or normal skin in elderly; pruritic; oral mucosa often spared; DIF: linear IgG and C3 at basement membrane. Confirmation requires biopsy; treat with topical/systemic corticosteroids, immunosuppressants.

Pemphigus vulgaris — flaccid bullae, mucosal involvement (oral erosions), Nikolsky positive; DIF: intercellular IgG. Distinguished from bullous impetigo by mucosal involvement, age, chronicity.

Contact dermatitis (allergic or irritant) — vesicles, oozing, crusting; pruritic; geometric/linear pattern (poison ivy) or in distribution of contactant (nickel, fragrance). No bacterial pathogens; treat with topical steroids and avoidance.

Atopic dermatitis flare — chronic relapsing eczematous patches; flexural in older children; often secondarily impetiginized — may need both topical steroid and antibiotic.

Sweet syndrome — tender erythematous plaques with neutrophilic infiltrate; fever; often associated with malignancy or IBD; responds to systemic steroids.

Pyoderma gangrenosum — rapidly enlarging painful ulcer with violaceous undermined border; associated with IBD, RA; biopsy + clinical; treat with immunosuppression, not antibiotics. Avoid debridement (pathergy).

Cutaneous leishmaniasis — chronic ulcer in returning traveler (Middle East, Latin America); biopsy/PCR.

Cutaneous anthrax — painless ulcer with black eschar in exposed worker (wool, hides).

Insect bite reactions — central punctum, grouped, pruritic; may be impetiginized.

Burns/excoriations — historical context distinguishes.

Discoid lupus, vasculitis ulcers — chronic, atypical morphology; biopsy.

Secondary Prevention and Long-Term Plan

— Daily bathing with mild soap; thorough hand hygiene.

— Cover any cuts, abrasions, or insect bites with clean dressings.

— Trim fingernails short; discourage nose picking and scratching of lesions.

— Avoid sharing towels, razors, athletic gear, bedding.

— Launder linens and clothing in hot water after each acute episode.

— Optimize atopic dermatitis — daily emollients, topical corticosteroids/calcineurin inhibitors for flares; this is the highest-yield intervention to prevent recurrent impetigo in children.

— Treat coexistent scabies in household (permethrin for all contacts).

— Manage diabetes, venous insufficiency, lymphedema in adults with recurrent ecthyma.

— Nasal mupirocin BID × 5 days + chlorhexidine body wash daily × 5–14 days; consider repeating monthly × several months in highly recurrent cases.

— Dilute bleach baths (¼ cup household bleach per full tub) 2× weekly for atopic dermatitis with recurrent S. aureus.

— Treat all symptomatic household members; consider screening asymptomatic household contacts in persistent cases.

— Identify and treat all cases; emphasize equipment cleaning, no sharing.

— Exclude affected individuals until 24 hours on antibiotics and lesions covered.

— Report to public health when applicable; coordinate with school/coach/employer.

Step 3 management: Don't end the visit at the antibiotic prescription. Address eczema control, hygiene, family screening, school exclusion, and follow-up — Step 3 tests the plan, not just the diagnosis.

After acute treatment, build a prevention package for every patient:

Hygiene and barrier measures:

Treat the underlying skin disease:

Decolonization for recurrent disease (see chunk 8):

Outbreak control (athletic teams, daycares, military):

Patient education materials: Provide written instructions in patient's language and reading level; verify comprehension via teach-back.

Vaccination opportunity: Verify and update routine immunizations — varicella vaccine reduces a major risk factor for secondary impetigo.

Follow-Up, Monitoring, and Counseling

— 48–72 hour check-in (in-person, phone, or telehealth) to confirm clinical response — fewer new lesions, less erythema, drying of crusts.

— End of treatment (~7 days): confirm resolution; for ecthyma, expect slower healing and possible residual hyperpigmentation/scarring; book a 2- to 4-week visit.

— Recurrent disease pathway: any second episode within 6 months → initiate decolonization workup at that visit.

— Topical mupirocin: no labs needed.

— Oral cephalexin/dicloxacillin: no routine labs.

— TMP-SMX: consider BMP within 1 week if on ACEi/ARB, spironolactone, or in CKD (K+, Cr); INR if on warfarin.

— Doxycycline: counsel photoprotection; check Hb in prolonged courses.

— Clindamycin: monitor for diarrhea/C. difficile.

— For confirmed GAS pyoderma or unclear etiology, monitor BP and urinalysis at the 2- to 4-week follow-up to screen for PSGN in children, especially during outbreaks. Hematuria, edema, hypertension → urgent evaluation.

— Expected course and red flags (fever, spreading redness, severe pain, dark urine, decreased urine output).

— Adherence: full course of antibiotics; don't stop when lesions look better.

— Return-to-school/sport criteria: 24 hours of effective antibiotics + ability to cover lesions.

— Family education: hand hygiene, towel separation, no sharing of personal items.

— Smoking cessation, glycemic control, weight management — chronic risk factor mitigation for recurrent infection in adults.

Board pearl: "Cola-colored urine and periorbital edema 2 weeks after honey-crusted skin lesions" → check BP, UA, C3, anti-DNase B for PSGN. Reassure: usually self-limited in children with supportive care, but document the diagnosis and follow-up.

Follow-up cadence:

Monitoring parameters by therapy:

Post-streptococcal monitoring:

Counseling points to document:

Telehealth utility: Photo-based follow-up is appropriate for stable, improving impetigo — efficient, value-based, and increasingly tested.

Ethical, Legal, and Patient Safety Considerations

— Most US jurisdictions require exclusion until ≥24 hours of effective antibiotic therapy and lesions are able to be covered.

— Document this in the chart and provide a written return-to-school note. Failure to do so can perpetuate outbreaks and creates liability.

— Individual impetigo cases are generally not reportable, but outbreaks in schools, daycare, athletic teams, or correctional facilities are reportable to local public health departments in most states. Know your jurisdiction.

— MRSA outbreaks may trigger formal public health investigation.

— Discuss the choice between topical vs. oral therapy, potential adverse effects (TMP-SMX rash, doxycycline photosensitivity, clindamycin C. difficile), and rationale for MRSA coverage.

— For pediatric patients, obtain informed consent from a parent/guardian; address minor's assent for older children.

— In adolescents, particularly athletes, discuss confidentiality vs. team safety obligations carefully.

— When prescribing TMP-SMX or doxycycline, check the active medication list for warfarin, methotrexate, ACEi/ARB, spironolactone, sulfonylureas, and isotretinoin — interaction risks are easily missed in a brief acute-care visit. Document the medication reconciliation.

— Communicate the diagnosis and plan to the primary care physician if the encounter occurred in urgent care or ED. A missed handoff for a child with new bullae or a diabetic with ecthyma is a sentinel-event-grade error.

— Mupirocin and cephalexin are affordable generics; default to these unless contraindicated. Avoid prescribing high-cost retapamulin or ozenoxacin when generics suffice.

— Address structural risk factors (crowding, homelessness, inadequate sanitation) and connect to social services when relevant.

Step 3 management: A pharmacy alert for a TMP-SMX + warfarin interaction is never to be ignored — choose an alternative (cephalexin or doxycycline) or arrange close INR monitoring. Documenting this decision is both safe practice and Step 3 gold.

School and daycare exclusion:

Communicable disease reporting:

Informed consent and shared decision-making:

Patient safety — transition of care:

Equity and access:

Documentation essentials: Diagnosis, extent, MRSA risk assessment, antibiotic chosen and rationale, allergies, return precautions, follow-up plan, school note.

High-Yield Associations and Rapid-Fire Facts

Board pearl: Every "honey-colored crust" question stem expects "mupirocin if limited; cephalexin if extensive" — and a follow-up on PSGN screening if hematuria or edema appears 2 weeks later.

Honey-colored crust → nonbullous impetigo → S. aureus > GAS.

Flaccid bullae in infant, Nikolsky negative, mucosa spared → bullous impetigo (local exfoliative toxin A, S. aureus).

Nikolsky positive + generalized exfoliation + mucosa spared → SSSS (hematogenous toxin spread).

Nikolsky positive + mucosal involvement → think pemphigus vulgaris or SJS/TEN, not impetigo.

Punched-out ulcer with violaceous rim healing with scar → ecthyma.

Necrotic black eschar in febrile neutropenic patient → ecthyma gangrenosum (Pseudomonas bacteremia).

Bullous impetigo toxin target = desmoglein-1 (same as pemphigus foliaceus and SSSS).

Cola-colored urine 1–2 weeks after impetigo → PSGN; low C3, elevated anti-DNase B (ASO unreliable after skin GAS).

Acute rheumatic fever follows GAS pharyngitis only, not pyoderma.

Eczema herpeticum mimics impetigo but lesions are punched-out, painful, monomorphic vesicles → treat with acyclovir.

First-line topical = mupirocin 2% TID × 5 days.

First-line oral (low MRSA risk) = cephalexin × 7 days.

First-line oral (MRSA risk) = doxycycline, TMP-SMX, or clindamycin × 7 days.

Decolonization = nasal mupirocin BID × 5 days + chlorhexidine body wash daily; consider dilute bleach baths in atopic dermatitis.

Avoid OTC bacitracin/neomycin — inadequate for impetigo.

Macrolides — high resistance; avoid as first-line.

Pregnancy: cephalexin yes; clindamycin yes; doxycycline no after 1st trimester; TMP-SMX avoid 1st and 3rd trimesters.

Return to school after 24 hours on effective antibiotics with lesions covered.

Wrestler/football team outbreaks → think CA-MRSA, team-wide decolonization.

Daycare child with impetigo → check siblings, treat symptomatic contacts, communicate with daycare.

Diabetic with leg ulcer → think ecthyma; oral antibiotics + wound care.

Board Question Stem Patterns

Key distinction: Always parse the stem for: lesion morphology (crust vs. ulcer vs. bulla vs. vesicle), extent (few vs. many), MRSA risk factors, host (infant, pregnant, diabetic, immunocompromised), and timing (post-infectious findings). These five features dictate the right answer.

Stem 1 — Classic peds impetigo: 4-year-old with honey-colored crusts perinasally, afebrile, attends daycare. Best initial therapy? → Topical mupirocin TID × 5 days. Distractor: oral amoxicillin (overkill); bacitracin OTC (inadequate).

Stem 2 — Extensive disease: 8-year-old with crusted lesions on face, arms, and legs. Next step? → Oral cephalexin × 7 days + hygiene counseling + school exclusion until 24 hours on antibiotics.

Stem 3 — Bullous impetigo in infant: Afebrile 6-month-old with flaccid bullae in axilla, Nikolsky negative, mucosa clear. Diagnosis/treatment? → Bullous impetigo, treat with oral cephalexin or dicloxacillin. Distractor: SSSS — that would have generalized exfoliation and positive Nikolsky.

Stem 4 — MRSA-suspected: High school wrestler with recurrent pustular lesions, teammates affected. Best oral agent? → Doxycycline, TMP-SMX, or clindamycin + decolonization protocol for team.

Stem 5 — Ecthyma in diabetic: 65-year-old with punched-out leg ulcers with crust after working in garden. Management? → Wound culture, oral cephalexin × 7–10 days (or MRSA-active if risk), wound care, glycemic optimization.

Stem 6 — PSGN follow-up: 7-year-old with periorbital edema, hypertension, and cola-colored urine 2 weeks after honey-crusted lesions. Best test? → C3 (low) and anti-DNase B (elevated); UA shows RBC casts. Manage supportively.

Stem 7 — Pregnancy: 28-week pregnant patient with extensive impetigo. Best oral therapy? → Cephalexin (avoid doxycycline and TMP-SMX in late pregnancy).

Stem 8 — Treatment failure: Child treated with mupirocin × 5 days without improvement. Next step? → Reassess diagnosis, culture, switch to oral antibiotic with MRSA coverage if risk factors.

Stem 9 — Recurrent disease: Child with 3rd episode in 4 months. Best preventive intervention? → Nasal mupirocin BID × 5 days + chlorhexidine body wash; screen family.

Stem 10 — Differential trap: Adolescent with painful clustered vesicles on lip with crusting after a cold. Diagnosis? → HSV, not impetigo; treat with acyclovir.

One-Line Recap

Impetigo and ecthyma are clinical diagnoses driven by S. aureus and GAS, treated outpatient with topical mupirocin for limited disease and oral cephalexin (or doxycycline/TMP-SMX/clindamycin when MRSA risk is present) for extensive impetigo, bullous impetigo, and all ecthyma — with attention to hygiene, school exclusion, decolonization for recurrence, and post-infectious PSGN surveillance.

Board pearl: Honey crust → mupirocin or cephalexin → cover lesions → exclude 24 hours → screen for PSGN if hematuria appears. Master this sequence and impetigo/ecthyma questions on Step 3 become near-automatic.

Treatment branchpoint: Limited nonbullous → topical mupirocin TID × 5 days. Extensive, bullous, ecthyma, or systemic features → oral antibiotics × 7 days (cephalexin if no MRSA risk; doxycycline/TMP-SMX/clindamycin if MRSA risk).

Sequelae to remember: PSGN can follow GAS pyoderma (low C3, anti-DNase B positive) but rheumatic fever does NOT — that requires pharyngitis. Antibiotics do not prevent PSGN but do reduce spread.

Don't miss the mimics: SSSS (generalized exfoliation, Nikolsky positive, mucosa spared, admit), ecthyma gangrenosum (Pseudomonas bacteremia in neutropenia), eczema herpeticum (acyclovir), bullous pemphigoid in the elderly (biopsy/DIF, steroids — not antibiotics).

Beyond the prescription: School exclusion until 24 hours on antibiotics with covered lesions; decolonization (nasal mupirocin + chlorhexidine) for recurrent disease; treat underlying atopic dermatitis; check warfarin/ACEi/ARB interactions before prescribing TMP-SMX; and arrange 48–72 hour follow-up plus a 2-week visit for PSGN screening when GAS is suspected.