Impetigo and bacterial skin infection — branching viva

Opening question

Examiner: Take me through this child. What is the diagnosis, and what is your frame for managing it? [1]

Candidate: The most likely diagnosis is non-bullous impetigo — the honey-coloured, weeping crust spreading from the nose across the cheek and onto the sibling, in an otherwise well, afebrile child, is the classic presentation of the commonest bacterial skin infection of childhood. My frame is three-layered: treat the individual lesion with the least antibiotic that will work, control the household and school spread, and watch for the post-streptococcal complications. Because the child is well with localised lesions, this is a community-managed case with a short topical course and clear advice on exclusion and hygiene. [1] [2]

Examiner: How do you classify impetigo, and which form is dangerous? [1]

Candidate: Two forms. Non-bullous impetigo is about seventy percent — the honey-coloured crust, caused by Staphylococcus aureus or group A streptococcus. Bullous impetigo is about thirty percent — flaccid bullae caused exclusively by exfoliative-toxin-producing S. aureus. The dangerous end of the same spectrum is staphylococcal scalded skin syndrome, where the toxin circulates systemically in a neonate or young infant and causes widespread tender erythema and sheet-like desquamation. This child has the benign form; I would still examine for any sign of deeper extension or toxin-mediated appearance. [1] [8]

Branch 1 — pathophysiology

Examiner: Explain the mechanism that unites bullous impetigo and staphylococcal scalded skin syndrome. [8]

Candidate: Certain phage-group II strains of Staphylococcus aureus produce exfoliative toxins A and B, which are serine proteases that cleave the extracellular domain of desmoglein-1 in the granular layer of the epidermis. Desmoglein-1 is the adhesion molecule holding the superficial keratinocytes together. When it is cleaved the superficial epidermis splits, fluid accumulates, and a bulla forms. In bullous impetigo the toxin acts locally at the staphylococcal focus; in staphylococcal scalded skin syndrome the toxin circulates in the bloodstream and cleaves desmoglein-1 across the whole skin surface. [8]

Examiner: Why are the mucous membranes spared? [8]

Candidate: Because mucosal epithelium co-expresses desmoglein-3, which holds the cells together even when desmoglein-1 is cleaved. The intact desmoglein-3 compensates, so the mouth, eyes and genitals are spared in staphylococcal scalded skin syndrome. This is the bedside clue that separates it from Stevens-Johnson syndrome and toxic epidermal necrolysis, which involve the mucosae. [8]

Branch 2 — diagnosis and investigations

Examiner: How will you confirm impetigo here? [1]

Candidate: The diagnosis is clinical — the honey-coloured crust on an erythematous base in a well child is enough to start empiric therapy. I would not swab uncomplicated disease. I reserve a swab of the active lesion for the atypical, recurrent, non-healing, severe or treatment-non-responsive case, to identify the organism and its sensitivities, including methicillin resistance. In recurrent or household-clustered disease I would swab the nares and skin folds to identify staphylococcal carriage for a decolonisation strategy. [1]

Examiner: And if this child's sibling later presents with a fluctuant abscess? [6]

Candidate: That changes the management entirely. An abscess is treated by incision and drainage first, not antibiotics. The placebo-controlled trials of trimethoprim-sulfamethoxazole for uncomplicated skin abscess showed only a modest benefit of antibiotics over placebo added to drainage, so I would drain and add an MRSA-active antibiotic only for the severity flags — large size, multiple lesions, extensive surrounding cellulitis, fever, very young age, or immunocompromise. [6]

Branch 3 — treatment and the extent-matched pathway

Examiner: What treatment will you give this child? [1]

Candidate: For localised non-bullous impetigo, a short topical course is first-line. UK NICE recommends topical hydrogen peroxide 1% cream applied two to three times daily for up to five days, with topical fusidic acid 2% three times daily for five days as the alternative; where mupirocin is used it is applied three times daily for five days. I would advise gentle cleansing, hand hygiene, and exclusion from school until the lesions are dry or healed or until 24 hours into effective treatment. [1]

Examiner: When would you use an oral antibiotic instead? [1]

Candidate: For widespread, bullous, severe or non-responsive impetigo, an oral anti-staphylococcal antibiotic is first-line — five days of oral flucloxacillin (child 1 to 5 years 125 mg four times daily), or cephalexin in Australasian practice, with clarithromycin or erythromycin for the penicillin-allergic child. If community-acquired MRSA is suspected, I would use trimethoprim-sulfamethoxazole or clindamycin instead of a beta-lactam, because a beta-lactam does not cover MRSA. [5] [1]

Branch 4 — remote and recurrent disease

Examiner: How does management change in a remote endemic community? [3]

Candidate: In a remote endemic community where group A streptococcal impetigo predominates and scabies co-exists, the National Healthy Skin Guideline approach supports a short three-day oral course of co-trimoxazole (trimethoprim 8 mg/kg/day in two divided doses) or a single weight-based intramuscular dose of benzathine benzylpenicillin. The non-inferiority trial showed oral co-trimoxazole was non-inferior to injection, so the oral course is a practical alternative. Crucially, I would treat the scabies concurrently, because scabies is the portal of entry driving recurrence, and address the household and environmental determinants. [3] [2]

Examiner: And if the child keeps coming back with recurrent sores? [7]

Candidate: Then I move from treating the lesion to treating the carrier and the household. A decolonisation strategy combines dilute bleach baths or chlorhexidine washes with intranasal mupirocin for five to seven days applied to the child and all colonised household members, alongside treatment of scabies and underlying atopic dermatitis. The bleach-bath trial evidence supports this combination for recurrent disease, and the principle is that the child who keeps coming back is trading staphylococci with the people around them. [7]

Branch 5 — complications

Examiner: What complication must you screen for over the coming weeks? [2]

Candidate: Post-streptococcal glomerulonephritis, which follows skin infection with nephritogenic group A streptococcal strains one to three weeks later. It presents with haematuria — often tea- or cola-coloured urine — oedema, hypertension and oliguria. I would warn the family about these features and check blood pressure, urinalysis, renal function, complement C3 and streptococcal serology if they occur. [2]

Examiner: Does this child need rheumatic-fever prophylaxis? [2]

Candidate: No. Skin-derived group A streptococcal infection is nephritogenic but not rheumatogenic. Impetigo can cause glomerulonephritis but not acute rheumatic fever, which follows throat infection alone. So a child with impetigo does not need rheumatic-fever prophylaxis, and reaching for it would be to misapply throat logic to the skin. [2]

Wrap

Examiner: Summarise the bacterial skin-infection stance in one sentence. [1]

Candidate: Recognise the form and the danger, make a clinical diagnosis, treat localised disease with a short topical course and widespread disease with a short oral anti-staphylococcal course, drain the pus, use an MRSA-active agent where MRSA is prevalent, decolonise the carrier and the household when disease recurs, admit the toxin-mediated neonate for intravenous therapy and burns-style care, and watch for post-streptococcal glomerulonephritis — because impetigo is common and benign until the toxin, the invasion or the immune complex makes it not. [1] [8]