Dermatology · Bacterial Skin Infections
The facts most likely to be tested
Non-bullous impetigo is the most common form, characterized by honey-colored crusts typically found on the face.
Staphylococcus aureus is the most common causative pathogen, followed by Streptococcus pyogenes (Group A Strep).
Bullous impetigo is caused by exfoliative toxin A produced by S. aureus, resulting in flaccid bullae that rupture to leave a thin, varnish-like crust.
Topical mupirocin or retapamulin is the first-line treatment for localized, non-bullous impetigo.
Oral antibiotics such as cephalexin or dicloxacillin are indicated for widespread lesions or cases involving multiple family members.
Post-streptococcal glomerulonephritis is a potential, though rare, complication of impetigo caused by nephritogenic strains of S. pyogenes.
Impetigo is highly contagious and spreads through direct contact, requiring strict hygiene and exclusion from school until 24 hours after starting antibiotic therapy.
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A 5-year-old boy is brought to the clinic by his mother due to a skin rash on his face. Physical examination reveals several small, erythematous papules around the nose and mouth that have progressed to vesicles with honey-colored crusts. The child has no fever, and there is no evidence of systemic toxicity. The surrounding skin is not warm or tender, and there is no lymphadenopathy.
What is the most appropriate initial management for this patient?
Topical mupirocin
The clinical presentation of honey-colored crusts is pathognomonic for non-bullous impetigo, which is effectively treated with topical antibiotics like mupirocin.
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Etiology / Epidemiology
Highly contagious superficial skin infection common in children 2-5 years old; caused by Staphylococcus aureus or Streptococcus pyogenes.
Clinical Manifestations
Presents as honey-colored crusts on the face; non-bullous is the most common form.
Diagnosis
Clinical diagnosis; bacterial culture is the gold standard if the diagnosis is uncertain.
Treatment
Mupirocin is the first-line topical treatment; avoid systemic antibiotics unless widespread.
Prognosis
Excellent; post-streptococcal glomerulonephritis is a rare but serious complication.
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Epidemiology & Etiology
Most common in children 2-5 years old living in warm, humid climates. Transmission occurs via direct contact or fomites. Staphylococcus aureus is the most common pathogen, followed by Group A Streptococcus.
Pertinent Anatomy
Infection is limited to the epidermis, specifically the stratum corneum. This superficial location explains the lack of systemic symptoms in localized cases.
Pathophysiology
Bacterial colonization occurs at sites of minor skin trauma or insect bites. S. aureus produces exfoliative toxins that cause the separation of the epidermis, leading to the formation of vesicles and bullae.
Clinical Manifestations
Non-bullous impetigo presents as papules that progress to vesicles and pustules, eventually rupturing to form honey-colored crusts. Bullous impetigo features large, flaccid bullae, often seen in infants. Red flags include fever or systemic toxicity, which suggest progression to cellulitis or erysipelas.
Diagnosis
Diagnosis is primarily clinical. If the presentation is atypical or resistant to therapy, a bacterial culture of the exudate is the gold standard to guide antibiotic selection.
Treatment
For limited disease, apply mupirocin ointment three times daily. For extensive lesions or outbreaks, use oral cephalexin or dicloxacillin. Do not use topical steroids as they exacerbate the infection.
Prognosis
Prognosis is excellent with appropriate therapy. Monitor for post-streptococcal glomerulonephritis, which may occur 1-3 weeks after infection, characterized by hematuria and hypertension.
Differential Diagnosis
Contact dermatitis: pruritic, lacks honey-colored crusts
Herpes simplex: grouped vesicles on an erythematous base
Tinea corporis: annular lesions with central clearing
Ecthyma: deeper ulcerations extending into the dermis
Cellulitis: diffuse, non-crusted erythema with warmth