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MI5.{1,3-4} | Anaerobic & Skin/Soft-Tissue Infections — SDL Guide (Part 2)

Skin and Soft-Tissue Infections — Bacterial

A layered skin cross-section and clinical comparison diagram classifying bacterial skin and soft-tissue infections by depth from impetigo to necrotising fasciitis and myonecrosis. — **Panel A:** Skin depth overview showing epidermis, dermis, hair follicle, superficial lymphatics, subcutaneous tissue, fascia, and skeletal muscle with infection zones for impetigo, folliculitis, furuncle, carbuncle, erysipelas, cellulitis, necrotising fasciitis, and myonecrosis.. **Panel B:** Superficial SSTIs showing impetigo with honey-coloured crusts, folliculitis centered on hair follicles, furuncle as a deep follicular abscess, carbuncle as coalescent follicles with subcutaneous extension, and a CA-MRSA callout for furuncles and skin abscesses.. **Panel C:** Erysipelas versus cellulitis comparison showing sharply demarcated raised plaque caused by Group A Streptococcus in upper dermis and superficial lymphatics versus diffuse poorly marginated oedema caused by Staphylococcus aureus or Streptococcus pyogenes in deep dermis and subcutaneous tissue.. **Panel D:** Deep infection danger panel showing necrotising fasciitis type I as polymicrobial fascial necrosis with gas and dishwater fluid, necrotising fasciitis type II as rapidly spreading Group A Streptococcus often without gas, and Clostridium perfringens myonecrosis with gas in muscle..

Bacterial SSTIs classified by depth of tissue involved:

Superficial (epidermis/dermis):
- Impetigo: S. aureus (bullous — exfoliatin toxin) or S. pyogenes (crusted); honey-coloured crusts on face in children; non-scarring; treat with topical mupirocin or oral penicillin
- Folliculitis: S. aureus in hair follicles; superficial pustules; sycosis barbae in beard area
- Furuncle / Carbuncle: deeper S. aureus infection; carbuncle = multiple follicles + subcutaneous extension; risk of bacteraemia in diabetics
- Erysipelas: S. pyogenes (Group A Strep); sharply demarcated, raised, bright-red plaque; involves upper dermis + superficial lymphatics; face/leg; treat with penicillin
- Cellulitis: S. aureus or S. pyogenes; involves deeper dermis and subcutaneous tissue; diffuse, poorly marginated redness + oedema; no gas; treat with IV nafcillin or cloxacillin

Deep / Fascia / Muscle:
- Necrotising fasciitis type I: Polymicrobial (anaerobes + facultatives); diabetes, peripheral vascular disease predispose; rapidly spreading necrosis; gas on CT; "dishwater" fluid from wound; requires emergency surgical debridement
- Necrotising fasciitis type II: Mono-microbial — Group A Strep (S. pyogenes); "flesh-eating bacteria"; toxic shock syndrome toxin; extremely rapid; often no gas
- Myonecrosis (gas gangrene): C. perfringens — as above

MRSA (Methicillin-Resistant S. aureus):
- Community-acquired CA-MRSA causes furuncles, skin abscesses; treat with trimethoprim-sulfamethoxazole, doxycycline, or vancomycin
- Hospital-acquired HA-MRSA: surgical wound infections, IV line infections

SELF-CHECK

A young boy has multiple honey-coloured crusted lesions around the nose and mouth after a minor abrasion. No fever, no deep tissue involvement. Gram stain of the crust shows Gram-positive cocci in chains. What is the most likely diagnosis and its causative organism?

A. Bullous impetigo caused by Staphylococcus aureus (exfoliatin toxin)

B. Non-bullous impetigo caused by Streptococcus pyogenes

C. Erysipelas caused by Streptococcus pyogenes

D. Folliculitis caused by Staphylococcus aureus

Reveal Answer

Answer: B. Non-bullous impetigo caused by Streptococcus pyogenes

Honey-coloured crusted lesions on the face in a child after minor trauma is the classic presentation of non-bullous impetigo caused by Streptococcus pyogenes (Group A Strep) or sometimes S. aureus. Gram-positive cocci in chains point to Streptococcus. Bullous impetigo (option A) is caused by S. aureus exfoliatin toxin and presents with intact flaccid bullae, not crusts. Erysipelas (option C) involves the dermis with a sharply raised border, not surface crusts.

Fungal, Viral, and Parasitic Skin Infections

A multi-panel medical diagram classifying fungal and viral skin infections with clinical lesions, diagnostic microscopy, and key distinguishing features. — **Panel A:** Classification map showing superficial fungal infections, subcutaneous fungal infections, and viral skin infections with representative disease examples.. **Panel B:** Dermatophytosis with annular tinea lesion, KOH branching septate hyphae, Wood's lamp green fluorescence with Microsporum, and labels for tinea corporis, pedis, unguium, and capitis.. **Panel C:** Subcutaneous fungal infections showing sporotrichosis with rose thorn prick and nodular lymphangitis, chromoblastomycosis with verrucous lesion and Medlar bodies, and mycetoma with Madura foot, draining sinuses, and grains.. **Panel D:** Viral vesicular infections showing varicella lesion stages, dermatomal herpes zoster with preceding pain, herpes simplex vesicles, and Tzanck smear multinucleated giant cells with Cowdry type A inclusions.. **Panel E:** Molluscum contagiosum showing dome-shaped pearly papules with central umbilication and magnified papule structure..

Dermatophytoses (Superficial fungal infections):
- Trichophyton, Microsporum, Epidermophyton spp.; affect keratinised layers (stratum corneum, hair, nails)
- Tinea corporis (ringworm body), tinea pedis (athlete's foot), tinea unguium (onychomycosis), tinea capitis (scalp ringworm)
- Diagnosis: KOH preparation — branching, septate hyphae; Wood's lamp (green fluorescence with Microsporum); culture on Sabouraud Dextrose Agar (SDA)

Subcutaneous fungal infections:
- Sporotrichosis (Sporothrix schenckii) — rose thorn prick → nodular lymphangitis (ascending nodules along lymphatics on arm); KOH — 'cigar-shaped' yeast; treat with itraconazole
- Chromoblastomycosis (Fonsecaea spp.) — verrucous skin lesions; tissue shows Medlar bodies (muriform cells) — brown, thick-walled, sclerotic cells
- Mycetoma — Madura foot; can be actinomycetoma (Nocardia, Actinomyces) or eumycetoma (Madurella); grains (granules) in discharge

Viral skin infections:
- Varicella (Chickenpox): VZV; centripetal distribution; successive crops; papule → vesicle → pustule → crust; Tzanck smear: multinucleated giant cells (Cowdry type A inclusions)
- Herpes Zoster: VZV reactivation; dermatomal; severe pain precedes rash
- Herpes simplex (HSV 1/2): oral/genital vesicles; Tzanck smear positive; PCR for definitive diagnosis
- Molluscum contagiosum: Poxvirus; dome-shaped papules with central umbilication; Henderson-Patterson (molluscum) bodies on HE stain
- Measles (Rubeola): Koplik spots (pathognomonic buccal mucosa) → maculopapular rash; systemic

Parasitic skin infections:
- Scabies: Sarcoptes scabiei mite; burrows in finger webs, wrists; intense night itch; skin scraping + microscopy = mite/eggs/scybala
- Cutaneous larva migrans: Ancylostoma braziliense hookworm larvae — serpiginous tracks in skin; barefoot walking on contaminated sand/soil

Infective vs. Non-Infective Skin Lesions (MI5.4)

A five-panel educational diagram compares infective and non-infective skin lesions using clinical cues, morphology examples, mimics, and systemic infections with characteristic rashes. — **Panel A:** Main comparison showing infective unilateral warm tender erythematous lesion with pustules, crusting, oedema, fever, lymphadenopathy, antimicrobial response, and exposure history versus non-infective bilateral symmetrical plaques with autoimmune, allergic, atopic, psoriatic, and corticosteroid-response clues.. **Panel B:** Diagnostic decision strip showing clinical features suggesting infection versus inflammatory, allergic, or autoimmune non-infective aetiology.. **Panel C:** Common infective morphology examples: impetigo with honey-colored crust and superficial erosion, erysipelas with raised sharply demarcated erythema, and cellulitis with diffuse poorly demarcated erythema and oedema.. **Panel D:** Non-infective mimics showing psoriasis, atopic dermatitis, and autoimmune-associated rash patterns with symmetry and systemic associations.. **Panel E:** Systemic infections with prominent skin involvement: S. aureus bacteremia, S. pyogenes scarlet fever, Neisseria meningitidis purpura, rickettsial eschar and rash, viral exanthems, secondary syphilis palmar/plantar rash, dengue haemorrhages, and leptospirosis with jaundice and conjunctival suffusion..

Differentiating infective from non-infective skin disease is a key clinical skill:

Features suggesting infection:
- Acute onset
- Localised heat, tenderness, erythema, oedema
- Pustules, vesicles, crusts
- Fever, lymphadenopathy
- Response to antimicrobials
- Identified contact/exposure history (epidemiological link)

Features suggesting non-infective aetiology (inflammatory/allergic/autoimmune):
- Bilateral, symmetrical distribution
- Associated with systemic features of autoimmune disease (arthritis, lupus, IBD)
- Response to corticosteroids
- Personal/family history of atopy, psoriasis

Systemic infections with prominent skin involvement (microbes causing systemic disease + skin):
- S. aureus — bacteraemia → embolic skin lesions, Janeway lesions (infective endocarditis)
- S. pyogenes — scarlet fever (erythrogenic toxin → diffuse sandpaper rash)
- Neisseria meningitidis — purpuric/petechial rash (meningococcaemia)
- Rickettsia spp. — eschar + maculopapular rash (scrub typhus, Rocky Mountain spotted fever)
- VZV, measles, rubella — exanthems
- Secondary syphilis (T. pallidum) — copper-coloured palmar/plantar rash
- Dengue — skin haemorrhages, positive tourniquet test
- Leptospirosis — jaundice + conjunctival suffusion

Five-panel dermatology collage comparing impetigo honey crust, erysipelas raised border, cellulitis diffuse erythema, varicella lesions at different stages, and tinea corporis ring lesion. — **Panel A:** Impetigo: honey-colored crust, superficial erosion, perioral distribution, surrounding mild erythema. **Panel B:** Erysipelas: raised sharply demarcated border, bright red erythema, edema, lower limb skin. **Panel C:** Cellulitis: diffuse erythema, poorly defined margin, warmth/swelling zone, spreading soft-tissue inflammation. **Panel D:** Varicella: macule, papule, clear vesicle, pustule, crust, lesions at different stages. **Panel E:** Tinea corporis: annular ring lesion, central clearing, scaly active edge, erythematous raised border.

SELF-CHECK

A patient develops ascending nodular skin lesions on the dorsum of his right hand and forearm following a thorn prick while gardening. The lesions are non-tender and painless. KOH preparation of material from a nodule shows cigar-shaped yeast forms. What is the diagnosis?

A. Chromoblastomycosis caused by Fonsecaea pedrosoi

B. Sporotrichosis caused by Sporothrix schenckii

C. Mycetoma caused by Madurella mycetomatis

D. Cutaneous larva migrans caused by Ancylostoma braziliense

Reveal Answer

Answer: B. Sporotrichosis caused by Sporothrix schenckii

The classic triad for sporotrichosis: (1) trauma with a thorn or plant material, (2) ascending nodular lymphangitis along the arm, (3) cigar-shaped or fusiform yeast on KOH/culture. Sporothrix schenckii is a dimorphic fungus — mould in soil/environment, cigar-shaped yeast at 37°C in tissue. Treatment: itraconazole for 3–6 months. Chromoblastomycosis shows Medlar bodies (muriform cells) in tissue. Mycetoma forms triad of swelling + sinuses + grains.

CLINICAL PEARL

Necrotising fasciitis — the 'dishwater' clue: The intraoperative finding of non-purulent, thin, grey-brown 'dishwater' fluid emerging from fascial planes, with absence of frank pus and easy blunt dissection through necrotic fascia, confirms necrotising fasciitis. This is a surgical emergency — every hour of delay worsens mortality. The clinical triad: pain out of proportion to skin findings + skin necrosis + systemic toxicity = NF until proven otherwise.

Interactive practice: Quick Recall

Interactive practice: Multiple Choice

Interactive practice: True / False

Interactive practice: Multiple Choice