Impetigo

Epidemiology

Age
- Primarily affects children (especially between 2–6 years of age)
- Impetigo is highly contagious and can cause epidemics in preschools or schools.

Etiology

Pathogens: superficial bacterial skin infection
- S. aureus: majority of cases
  - Causes both bullous impetigo and nonbullous impetigo
  - The blistering in Bullous impetigo is caused by production of exfoliative toxin A, a serine protease that targets desmoglein 1 in the superficial epidermis, by certain strains of S aureus.
- S. pyogenes (GAS): causes nonbullous impetigo
- S. aureus and GAS coinfection may occur

Pathophysiology

Clinical features

Nonbullous impetigo (~70% of cases)

Lesions
- Papules that turn into small vesicles surrounded by erythema and/or pustules
  - Vesicles and pustules can rupture
  - Oozing secretion that dries to form honey-colored crusts that heal without scarring
- May be pruritic (especially pustules) but is rarely painful
- Negative Nikolsky sign
Distribution pattern
- Face (most common), especially around the nose and mouth
- Extremities
Other findings
- Regional lymphadenopathy

Bullous impetigo (~30% of cases)

Lesions
- Vesicles that grow to form large, flaccid bullae, which go on to rupture and form thin, brown crusts
- Negative Nikolsky sign
Distribution pattern
- Trunk and upper extremities
Other findings
- Systemic signs (e.g., fever, malaise, weakness) in severe cases

Tip

Impetigo should be suspected in children presenting with honey-colored crusts around the mouth and nose.

Diagnostics

Characteristic	Pemphigus Vulgaris	Bullous Pemphigoid	Bullous Impetigo
Etiology	Autoimmune disease targeting desmoglein 1 and 3	Autoimmune disease targeting BP180 and BP230	Bacterial infection (S. aureus) producing exfoliative toxins
Age Group	Middle-aged adults (40-60 years)	Elderly (>65 years)	Children, occasionally adults
Level of Skin Separation	Intraepidermal (suprabasal)	Subepidermal	Subcorneal
Autoantibodies	Anti-desmoglein 1 and 3 IgG	Anti-BP180 and BP230 IgG	None (bacterial toxin-mediated)
Clinical Presentation	• Flaccid blisters that easily rupture • Painful erosions • Mucosal involvement common • Nikolsky sign positive	• Tense bullae on normal or erythematous skin • Less mucosal involvement • Pruritus common • Nikolsky sign negative	• Superficial fragile blisters • Honey-colored crusts • Usually localized • No mucosal involvement
Common Sites	Oral mucosa, scalp, face, trunk	Flexural areas, trunk, extremities	Face, extremities, trunk
Diagnosis	• Direct immunofluorescence: intercellular IgG • Histology: acantholysis	• Direct immunofluorescence: linear IgG at basement membrane • Histology: subepidermal blister	• Gram stain: gram-positive cocci • Culture: S. aureus
Treatment	• Systemic corticosteroids • Steroid-sparing agents (rituximab, azathioprine) • Topical therapy	• Systemic corticosteroids • Steroid-sparing agents • Topical steroids	• Topical antibiotics • Systemic antibiotics if extensive
Prognosis	Chronic, potentially life-threatening if untreated	Better than PV, but chronic	Excellent with treatment
Complications	• Secondary infections • Fluid/electrolyte imbalance • Malnutrition	• Secondary infections • Side effects of treatment	• Usually self-limited • Rarely systemic infection

Treatment