5-Mark Detailed Answers

1. Staphylococcal Scalded Skin Syndrome (SSSS)
2. Taenia capitis (Tinea capitis) and its management
3. MDR in Leprosy
4. Scabies - Management

SHORT NOTE 1: Staphylococcal Scalded Skin Syndrome (SSSS)

Definition

Etiology & Pathogenesis

• Caused by exfoliative toxins A and B (ETA and ETB) produced by Group 2 Staphylococcus aureus, phage types 71 or 55
• The bacteria reside at a distant focus (pharynx, nose, ear, conjunctiva) - the skin lesions themselves are sterile
• Toxins specifically cleave desmoglein-1 (the same target as pemphigus foliaceus autoantibodies), causing a split below the granular layer of the epidermis
• Since mucous membranes have predominantly desmoglein-3 (not desmoglein-1), they are characteristically spared

Clinical Features

• Abrupt onset with skin redness and tenderness in periorificial areas (around eyes, nose, mouth) and intertriginous areas (neck, groin, axillae)
• Fever (variable), intense skin tenderness simulating a sunburn
• Nikolsky sign is positive - skin slips off with gentle lateral pressure
• Large sheets of epidermis separate (exfoliation in sheets)
• Sparing of palms, soles, and mucous membranes - key distinguishing feature from TEN
• Blisters form easily where pressure is applied (e.g., ECG lead placement)

Diagnosis

• Clinical - primarily
• Frozen section biopsy of blister roof: cleavage is below the granular layer (superficial) - NOT full-thickness necrosis as seen in TEN
• Cultures from primary site of infection (nares, perianal, periocular areas) - NOT from skin lesions (they are sterile)
• Differentiated from Stevens-Johnson Syndrome/TEN: SSSS has no mucosal involvement, more superficial split, affects younger patients

Treatment

• First-line: Penicillinase-resistant penicillin (e.g., dicloxacillin or cloxacillin) + IV fluids + supportive care
• Clindamycin may be added (inhibits toxin production via ribosomal mechanism), but only if culture shows susceptibility (resistance is increasing)
• Wound care and fluid replacement (similar to burn management)

SHORT NOTE 2: Tinea Capitis (Taenia Capitis) and its Management

Definition

Epidemiology

• Most common in children aged 3-14 years
• Reduced after puberty due to fungistatic fatty acids in sebum
• More common in children of African descent
• Spread via fomites (combs, caps, pillowcases); hairs can harbor organisms for >1 year
• Causative organisms: T. tonsurans (most common in USA/UK), M. canis (most common in Europe)

Clinical Types

Diagnosis

• KOH mount of hair stubs: ectothrix vs endothrix pattern
• Wood's lamp: green fluorescence (Microsporum species)
• Fungal culture (gold standard) on Sabouraud's dextrose agar
• Dermoscopy: comma hairs, corkscrew hairs

Management

• Griseofulvin (oral) - drug of choice, especially in children: 20-25 mg/kg/day for 6-8 weeks (ultramicronized form)
• Terbinafine (oral) - preferred for Trichophyton species, 4 weeks
• Itraconazole or Fluconazole as alternatives
• Adjunct: Selenium sulfide or ketoconazole shampoo (2-3x/week) to reduce shedding and transmission
• Treat household contacts and screen carriers

SHORT NOTE 3: MDR in Leprosy

Background

Standard MDT Regimen (WHO 1982)

Definition of MDR Leprosy

Mechanisms of Resistance

• Dapsone resistance: Mutations in folP1 gene (dihydropteroate synthase)
• Rifampicin resistance: Mutations in rpoB gene (RNA polymerase beta subunit)
• Fluoroquinolone resistance: Mutations in gyrA/gyrB genes

Management of MDR Leprosy

1. Ofloxacin (or other fluoroquinolones)
2. Minocycline
3. Clarithromycin

Leprosy Reactions (Management)

• Type 1 (Reversal reaction): Prednisone 1-2 mg/kg/day in tapering doses over ~3 months
• Type 2 (ENL): Thalidomide 100-400 mg/day (first-line); prednisolone for women of childbearing age
• Methylprednisolone pulse IV for severe nerve damage

SHORT NOTE 4: Scabies - Management

Causative Agent

Clinical Features (briefly)

• Intense nocturnal pruritus (due to sensitization to mite antigens)
• Pathognomonic burrows in web spaces of fingers, wrists, genitalia, periareolar area
• Nodular scabies: persistent pruritic nodules on scrotum/penis
• Crusted (Norwegian) scabies: in immunocompromised (HIV, steroids, neurologic disease) - hyperkeratotic, teeming with mites, minimally pruritic, highly contagious

Treatment

• Ivermectin 200 mcg/kg orally as a single dose, repeated after 1-2 weeks
• Drug of choice for crusted scabies (use oral + topical combination)
• Also useful in immunocompromised patients and institutional outbreaks

Additional Measures

• Treat all household contacts simultaneously (even if asymptomatic) - essential to prevent reinfestation
• Decontaminate clothing and bedding (wash in hot water >50°C or seal in plastic bag for 72 hours)
• Nodular scabies: intralesional steroids, tar preparations, or excision
• Crusted scabies: combination oral ivermectin + topical permethrin or benzyl benzoate; keratolytics (5% salicylic acid) to reduce crust

Post-treatment

• Pruritus may persist for 2-4 weeks after successful treatment (due to dead mites/antigens) - this does not indicate treatment failure
• Scabicide should not be repeated too early unless reinfestation is confirmed

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