GC071 It Is Red And Painful
A clinical approach to the differential diagnosis of a red, painful eye, encompassing conditions such as acute angle-closure glaucoma, anterior uveitis, keratitis, episcleritis, and scleritis that require urgent evaluation.
It Is Red and Painful — Cutaneous Infections (Bacterial, Viral, Fungal) & Blistering Diseases
This lecture, delivered by Prof. Henry H Chan, is a comprehensive tour of cutaneous infections and selected blistering diseases — conditions that present as "red, swollen, and painful" skin. It is a high-yield GC lecture because dermatology questions in HKUMed summative exams frequently test:
- Pattern recognition (spot diagnosis) of skin infections and blisters
- Clinical differentiation between conditions that look alike but carry very different prognoses (e.g., cellulitis vs. necrotising fasciitis)
- Pharmacology of antifungals and antivirals — mechanism of action, side effects, and drug selection
- Dermatological emergencies — necrotising fasciitis, SSSS, pemphigus
The lecture naturally divides into three infection categories (bacterial → viral → fungal), then pivots to blistering diseases (pemphigus vs. pemphigoid). Think of the lecture as answering: "The skin is red and painful — what's the organism, what's the depth, what's the danger, and how do I treat it?"
Cutaneous infections are classified by organism: Bacterial, Viral, Fungal [1]
This is the organising principle. Within each category, the depth of infection determines severity and management.
SECTION 1: CUTANEOUS BACTERIAL INFECTIONS
Due to Staphylococcus or Streptococcus. Vesicles or pustules that arise on erythematous base with crusting formation. In skin damaged by previous minor trauma such as scratching. [1]
Why it matters: Impetigo is a superficial bacterial infection. The lecture photographs show two useful appearances: clustered superficial erosions/vesicles with adherent crust, and the classic perinasal/perioral honey-coloured crust in a child. Bullae are flaccid and rupture easily because the split is subcorneal.
- Pathogenesis: S. aureus and/or S. pyogenes enter through micro-breaks in skin (scratching, insect bites, eczema). Exfoliative-toxin cleavage of desmoglein 1 specifically explains bullous staphylococcal impetigo; it is not the mechanism of every non-bullous lesion.
- Clinical features:
- Vesicles/pustules on erythematous base → rapid rupture → golden-yellow crusting
- Typically on face (perioral, perinasal) in children
- Non-bullous form (most common) vs. bullous form (S. aureus toxin-mediated)
- Diagnosis: Usually clinical. Culture an exudative lesion when disease is recurrent, widespread, treatment-resistant, or MRSA is suspected; routine swabbing is not required for every straightforward case.
- Treatment (current practice): Hygiene and removal/softening of crusts are foundational. A short course of topical antiseptic or, when appropriate, a topical antibiotic can be used for localised non-bullous disease; use an oral anti-staphylococcal agent for bullous, widespread, or systemically unwell cases, selected according to local resistance and allergy guidance. Do not routinely combine topical and oral antibiotics. The slide's cloxacillin-plus-ampicillin regimen is historical rather than a universal contemporary prescription [10].
Exam Tip
Bullous impetigo produces a subcorneal blister. This is the same level as the blistering classification table later in the lecture.
Erysipelas involves dermal lymphatics. Cellulitis involves deep dermis and subcutaneous tissue. Organisms: Streptococcus, Staphylococcus, Haemophilus influenzae. [1]
Why the distinction matters: Erysipelas is more superficial (dermis/lymphatics) and therefore has a sharply demarcated, raised, palpable border — you can feel the edge because the infection tracks along superficial lymphatic channels. Cellulitis is deeper (deep dermis + subcutaneous fat), so the border is poorly defined and diffuse.
| Feature | Erysipelas | Cellulitis |
|---|---|---|
| Depth | Superficial dermis + lymphatics | Deep dermis + subcutaneous tissue |
| Border | Sharply demarcated, raised, "step-off" edge | Poorly demarcated, diffuse |
| Surface | Peau d'orange (lymphatic obstruction → oedema around hair follicles) | Smooth erythema |
| Common organism | Group A Strep (most classic) | Usually beta-haemolytic streptococci; S. aureus is more relevant with purulence/penetrating trauma. H. influenzae facial cellulitis is now uncommon where Hib vaccination is established |
| Common site | Face, lower limbs | Lower limbs (most common) |
What the lecture photographs add: Facial erysipelas appears as a raised, intensely erythematous, sharply edged plaque with marked oedema; lower-limb cellulitis looks more diffuse, shiny and swollen, and may develop bullae in severe inflammation. Bullae alone do not prove necrotising infection—interpret them with pain, toxicity, rate of progression and tissue perfusion.
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Site of entry: minor skin break from scratching or tinea infection [1]
- Key clinical pearl: Always examine the toe webs. Interdigital fissuring/tinea pedis is an important, treatable portal of entry for lower-limb cellulitis and may contribute to recurrence.
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Systemic symptoms common (fever, lymphadenitis) [1]
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Antibiotics (current practice): The slide's routine IV combinations are historical. Use an oral anti-staphylococcal penicillin first when the patient can take oral therapy and is not severely unwell; reserve IV therapy for severe infection or inability to take oral treatment, review at 48 hours, and tailor for site, exposure history, MRSA risk and local susceptibility data [11]. Typical non-purulent cellulitis is primarily streptococcal; routine swabs are low yield unless skin is broken and there is an unusual exposure or penetrating injury.
High Yield
Toe-web fissuring and tinea pedis are important portals of entry for lower-limb cellulitis/erysipelas. Always check the toe webs.
Folliculitis: inflammation of hair follicle. Furuncles: follicular staphylococcal infection with pustule formation. Carbuncles: multiple furuncles grouped together to form abscess. [1]
Think of this as a spectrum of increasing severity centred on the hair follicle:
| Condition | What it is | Depth |
|---|---|---|
| Folliculitis | Superficial infection/inflammation of the hair follicle ostium | Epidermis only |
| Furuncle (boil) | Deeper infection of the entire hair follicle → abscess formation | Dermis |
| Carbuncle | Coalescence of multiple furuncles → large abscess with multiple draining sinuses | Dermis + subcutaneous |
Visual recognition: The lecture photograph shows numerous small, monomorphic papules and pustules, each centred on a follicle, scattered over the upper back. That follicular centring distinguishes folliculitis from acneiform eruptions, which also include comedones, and from a non-follicular exanthem.
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Recurrent infection: need to rule out immunocompromised (i.e., DM) [1]
- Why DM? Hyperglycaemia impairs neutrophil chemotaxis, phagocytosis, and oxidative burst → recurrent staph infections. Also consider other immunocompromised states: HIV, steroid use, haematological malignancy.
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Management:
- For a fluctuant furuncle/carbuncle, incision and drainage is the key intervention. Add systemic antibiotics for systemic illness, extensive surrounding cellulitis, immunocompromise, multiple lesions, difficult sites, failed drainage, or other high-risk features; culture purulent material when it will guide therapy.
- Uncomplicated folliculitis often responds to hygiene and removal of occlusion/friction. A blanket 3-month tetracycline course is not contemporary first-line care; confirm the diagnosis and organism in persistent or recurrent disease and choose targeted therapy.
Corynebacterium minutissimum. Involves intertriginous areas such as axilla, groins, and toe webs. Slight brown erythematous scaly patch. Pink under Wood's light. Rx: oral erythromycin, topical Whitfield's ointment. [1]
Why it's tested: Erythrasma is a great mimicker of tinea — both present in intertriginous areas with scaly patches. The discriminator is Wood's light examination:
| Feature | Erythrasma | Tinea |
|---|---|---|
| Organism | Corynebacterium minutissimum (bacterium) | Dermatophyte (fungus) |
| Wood's light | Coral-pink fluorescence (due to coproporphyrin III) | No fluorescence (except T. schoenleinii – pale green) |
| KOH microscopy | Negative for hyphae | Positive for hyphae |
| Treatment | Erythromycin (it's a bacterium!) | Antifungals |
Exam Trap
The lecture says "Pink under Wood's light" [1]. Many textbooks say "coral-red." In exams, "coral-pink" or "coral-red" fluorescence under Wood's lamp = erythrasma. Do NOT confuse with tinea versicolor (which fluoresces yellow-green due to Malassezia).
The Wood's-lamp photograph makes the clue vivid: the otherwise subtle brown intertriginous plaque becomes bright coral-red, reflecting bacterial porphyrins. Current treatment is usually a topical antibacterial (for example clindamycin or an appropriate macrolide) for limited disease, with oral therapy reserved for extensive disease; Whitfield's ointment is a historical lecture treatment.
1.5 Necrotising Subcutaneous Infection (Necrotising Fasciitis)
This is the dermatological emergency of the lecture, illustrated by a dramatic case history.
19F with preceding sore throat → painful right hip → no cutaneous abnormalities initially → next day: severe pain, K 2.4, WBC 12 → shock → fever, WBC 20, ecchymosis spreading rapidly → diagnosis: necrotising fasciitis → perineal involvement → died 30 hours after admission. [1]
Teaching points from this case:
- The initial presentation was deceptively benign — normal skin, normal joint movement. NF can begin with pain out of proportion to findings.
- The potassium of 2.4 mmol/L is clinically important but not a diagnostic clue specific to NF; it requires urgent correction and a search for its cause.
- Rapidly rising WBC and ecchymosis are late signs — by then, tissue necrosis is advanced.
- Perineal involvement = Fournier's gangrene (a specific variant of NF) [7].
Infections producing necrosis of the subcutaneous tissues that may include the fascia. Organisms: Streptococcus / mixture of aerobic and anaerobic. Common sites: limbs and perineum. Complication of cutaneous infection or preceding surgery. [1]
Fever, systemic toxicity, severe local pain. Marked tenderness, oedema. Skin becomes violaceous, bullae formation, crepitus, gangrene. Rapid progression with mortality 6 to 67%. Treatment: Surgical exploration + IV antibiotic (gentamicin, Fortum [ceftazidime]). [1]
Classification:
| Type | Organism | Context |
|---|---|---|
| Type I (polymicrobial) | Mixed aerobic + anaerobic (e.g., E. coli, Bacteroides, Clostridium) | Post-surgical, diabetic, perineal (Fournier's) |
| Type II (monomicrobial) | Group A Streptococcus (or S. aureus) | Young, otherwise healthy; can follow minor or unapparent trauma |
The young, previously well patient is compatible with Type II disease, but the preceding sore throat does not prove haematogenous seeding. NF can follow minor or unapparent trauma and can occur in otherwise healthy people [12].
Features to differentiate cellulitis from NF: [1]
- Oedema beyond the apparent limit of infection
- Development of bullae and ecchymoses
- Dermal gangrene
- Numbness in infected area (nerve destruction)
- Crepitus (gas-forming organisms)
- Severe pain disproportionate to the clinical finding
- Poor response to antibiotics
- MRI: allows early diagnosis of NF — historical slide wording; imaging must not delay surgery when suspicion is high [12]
High Yield — Discriminating NF from Cellulitis
The single most important discriminator is "pain out of proportion to clinical findings" — if the patient is screaming in pain but the skin looks only mildly erythematous, think NF. Numbness (paradoxically) can then develop as cutaneous nerves are destroyed.
| Feature | Cellulitis | Necrotising Fasciitis |
|---|---|---|
| Pain | Proportionate to erythema | Disproportionate (severe pain early, then numbness) |
| Skin changes | Erythema, warmth | Violaceous/dusky, bullae, ecchymosis, gangrene |
| Crepitus | Absent | May be present (gas-forming organisms) |
| Systemic toxicity | Mild-moderate | Severe (septic shock) |
| Response to antibiotics | Good | Poor |
| Oedema | Confined to erythema | Extends beyond visible erythema |
| Investigation | Usually clinical | Immediate surgical assessment/exploration; CT/MRI only when doubt remains and this will not delay theatre |
| Management | Oral or IV antibiotics according to severity; address portal of entry | Surgical debridement + broad IV antibiotics (surgical emergency) |
Management of NF:
- Do not wait for a score, scan, or skin necrosis. Immediate surgical consultation, aggressive exploration/debridement and sepsis resuscitation are the priorities; normal early skin or non-diagnostic imaging does not exclude NF [12].
- Start broad-spectrum IV therapy covering streptococci, staphylococci (including MRSA when relevant), Gram-negatives and anaerobes, then narrow to cultures/local guidance. The slide's gentamicin-plus-ceftazidime pair is not adequate as a stand-alone modern empiric regimen.
- Once GAS is confirmed, high-dose penicillin plus clindamycin is recommended; clindamycin suppresses toxin production [12].
- Repeat debridement often needed (look-and-re-debride at 24-48 hours)
- The slide's 6-67% mortality range is historical and heterogeneous; the CDC reports recent mortality around 15-20% for streptococcal NF, higher with age and streptococcal toxic shock [12].
Past paper relevance: The 2022 Fourth Summative MCQ tested Fournier's gangrene (Q27): "68M, diabetic, painful perineal swelling, 39°C, crepitus → Fournier's gangrene" [7]. This directly maps to this lecture section.
Less than 5 [years old]. Exfoliative toxin. Fever, tender erythematous skin, exfoliation. Positive Nikolsky sign. Diagnosis: Tzanck smear, culture. Rx: systemic antibiotics. Mortality: 4% in newborn. [1]
Pathogenesis: Certain strains of S. aureus produce exfoliative toxins (ETA and ETB) that cleave desmoglein 1 (a desmosomal cadherin concentrated in the superficial epidermis/granular layer). This causes a subcorneal/granular layer split → widespread superficial desquamation.
Visual recognition: The lecture images show tender diffuse erythema, thin wrinkled superficial bullae and broad sheet-like peeling, with crusting around facial orifices. The scale of denudation can resemble a burn, but oral/ocular/genital mucosa are characteristically spared.
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Why children < 5? Neonates and young children have:
- Immature renal clearance → cannot clear the toxin
- Lack of anti-toxin antibodies
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Nikolsky sign positive: Gentle lateral pressure on normal-appearing skin causes epidermis to shear off. This happens because the subcorneal split is extensive.
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Differentiation from TEN (Toxic Epidermal Necrolysis):
| Feature | SSSS | TEN |
|---|---|---|
| Age | < 5 years | Any age (adults more common) |
| Cause | S. aureus exfoliative toxin | Drug reaction |
| Level of split | Subcorneal/granular layer | Dermoepidermal junction (full-thickness epidermal necrosis) |
| Biopsy | Superficial cleavage, no epidermal necrosis | Full-thickness epidermal necrosis |
| Mucous membranes | Spared | Involved |
| Prognosis | Usually good in treated children; worse in adults with comorbidity/renal failure | Significant mortality; use a validated severity score such as SCORTEN |
| Treatment | Prompt systemic anti-staphylococcal antibiotics + fluids, temperature control and gentle wound care | Urgently stop culprit drug; burns/ICU-level supportive and specialist care; immunomodulation is specialist-directed |
High Yield — SSSS vs TEN
In SSSS, the split is subcorneal (superficial) and mucous membranes are spared. In TEN, the split is at the dermoepidermal junction (deep) and mucous membranes are involved. Mucosal desmoglein 3 can preserve adhesion despite toxin-mediated cleavage of desmoglein 1.
Diagnosis is primarily clinical, with biopsy if the distinction from TEN is uncertain. The slide's “Tzanck smear/culture” is not the modern core work-up: intact SSSS bullae are generally sterile because toxin is produced at a distant focus. Culture the suspected primary focus (for example conjunctiva, nasopharynx, umbilicus or another infected site) and blood when clinically indicated [13].
Classification: [1]
- Exogenous: Primary inoculation TB, Tuberculosis verrucosa cutis
- Endogenous: Lupus vulgaris, Scrofuloderma, Metastatic TB abscess, Acute miliary TB, Orificial TB
- TB due to BCG
- Tuberculids: Lichen scrofulosorum, Papulonecrotic tuberculid
- Facultative tuberculids: Erythema nodosum (EN), Erythema induratum (EI)
- Others: Lupus miliaris disseminatus faciei
This is a classification slide — know the categories rather than deep details for the exam. Key points:
- Lupus vulgaris is the most common form of cutaneous TB in previously sensitised individuals — presents as "apple-jelly nodules" on diascopy.
- Scrofuloderma = TB of skin overlying an infected lymph node (direct extension) → draining sinuses.
- EN and EI are listed as "facultative tuberculids" — they are reactive processes, not direct infection.
SECTION 2: CUTANEOUS VIRAL INFECTIONS
Viral exanthems: chickenpox, Coxsackie, infectious mononucleosis, rubella. Viral infections: warts, herpes, molluscum contagiosum. [1]
Due to HPV. Transmitted by contact. Genital wart: sexually transmitted. Wart lesions with blood vessels beneath surface. Painful in sole. Genital wart can be associated with neoplastic changes. Treated by salicylic acid, cryotherapy and cauterisation. [1]
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Pathogenesis: HPV infects keratinocytes → viral replication → epidermal hyperplasia (verrucous growth)
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Types:
- Common warts (verruca vulgaris) — hands, fingers
- Plantar warts (verruca plantaris) — painful because weight-bearing compresses them inward
- Flat warts (verruca plana) — face, dorsal hands
- Genital warts (condylomata acuminata) — HPV 6, 11 (low risk); HPV 16, 18 associated with cervical, anal, penile neoplasia
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What the photographs show: Common warts are well-circumscribed hyperkeratotic papules with a rough, papillomatous surface. Paring may reveal pinpoint thrombosed capillaries as black/red dots and interrupt normal skin lines; a corn/callus tends to preserve skin lines and has a central keratin core. Black dots are supportive, not literally pathognomonic.
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Genital HPV nuance: Visible condylomata are usually caused by low-risk HPV 6/11. Oncogenic types (especially 16/18) drive anogenital intraepithelial neoplasia and cancer, but a typical wart is not itself synonymous with cancer.
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Treatment options:
- Salicylic acid (keratolytic — dissolves keratin)
- Cryotherapy (liquid nitrogen — causes epidermal cell death)
- Cauterisation (electrosurgery)
- Imiquimod (immune response modifier — for genital warts)
Pox virus. Transmitted by contact, common in children. Can be sexually transmitted. Skin-coloured dome-shaped umbilicated papules. Sometimes itchy. Treated by salicylic acid, cryotherapy and cauterisation. [1]
- Key diagnostic feature: Umbilicated papule — the central dimple (dell/umbilication) is pathognomonic.
- Why umbilicated? The virus replicates in the central core of the papule, causing necrosis → central depression.
- In immunocompromised patients (especially HIV), molluscum can be widespread and giant.
- Molluscum is usually self-limiting. Treatment is optional and guided by symptoms, eczema, spread, cosmetic impact and immune status; destructive methods can scar. Genital lesions in adults are often sexually acquired, but site alone does not prove the route of transmission.
Highly contagious due to varicella-zoster herpes virus. Usually children. Erythema macules that quickly develop into vesicles and pustules. Associated with systemic symptoms. IP: 14 days. [1]
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Key clinical features:
- Rash appears in "crops" → lesions at different stages simultaneously ("stars in the sky" appearance)
- Centripetal distribution (trunk > extremities) — opposite to smallpox (centrifugal)
- Vesicles are described as "dewdrop on a rose petal" — superficial, clear vesicle on erythematous base
- Systemic: fever, malaise, pruritus
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Complications: Secondary bacterial infection, pneumonia (especially in adults and immunocompromised), encephalitis, cerebellar ataxia, hepatitis
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What the photograph shows: A trunk-predominant eruption with many lesions simultaneously at papular, vesicular, pustular and crusted stages—this polymorphism in successive crops is more useful than memorising a single lesion.
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Incubation period: typically 14-16 days, range 10-21 days [16]. Pregnant patients, neonates, immunocompromised people and adults/adolescents with severe disease need prompt risk assessment and specialist/local antiviral guidance.
2.4 Herpes Zoster (Shingles)
Reactivation of latent varicella-zoster virus. Dermatomal distribution. Usually elderly. Presented with painful erythematous eruption followed by vesicle and pustule formation that clustered into a herpetiform arrangement. If involved V1 can affect eye. [1]
Note: The slide says "V5" but this appears to be a slide error — cranial nerve V (trigeminal) has 3 divisions (V1/V2/V3); involvement of the ophthalmic division (V1) causes herpes zoster ophthalmicus.
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Pathogenesis: After primary varicella, VZV remains latent in dorsal root ganglia (or cranial nerve ganglia). Reactivation occurs with declining cell-mediated immunity (aging, immunosuppression) → virus travels down the sensory nerve → dermatomal eruption.
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Clinical features:
- Prodrome: Pain, burning, tingling in the dermatome 1-5 days before rash
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Clinical vignette from lecture: "Uncle Benny developed a painful rash in the left anterior chest wall, starting yesterday" — this is a classic presentation of acute herpes zoster (dermatomal pain → vesicular eruption on the chest wall) [1]
- Rash: Grouped vesicles on erythematous base in a dermatomal distribution that does NOT cross the midline
- The chest-wall photographs show a unilateral band of grouped vesicles and crusts following one sensory dermatome. “Does not cross the midline” is a useful pattern rule, not an absolute biological law; bilateral or multidermatomal disease should raise concern for immunocompromise.
- Pain: Often severe and can precede rash (can be misdiagnosed as MI, appendicitis, etc.)
- Rash: Grouped vesicles on erythematous base in a dermatomal distribution that does NOT cross the midline
Can be multidermatomal/disseminated if immunocompromised. [1] Post-herpetic neuralgia: main complication. [1] Ramsay-Hunt syndrome: ipsilateral VII and VIII nerves involvement. [1]
| Complication | Mechanism | Features |
|---|---|---|
| Post-herpetic neuralgia (PHN) | Nerve damage → chronic neuropathic pain | Pain persisting > 90 days after rash onset. Risk increases with age. |
| Herpes zoster ophthalmicus | V1 dermatome → cornea, conjunctiva, uvea | Hutchinson's sign (vesicles on tip of nose = nasociliary nerve involvement → high risk of ocular disease) |
| Ramsay-Hunt syndrome | VZV in geniculate ganglion of CN VII | Ipsilateral facial palsy + vesicles in ear canal/pinna + sensorineural hearing loss/vertigo (CN VIII involvement) |
| Disseminated zoster | Immunosuppression → viraemia | > 20 vesicles outside primary dermatome; visceral involvement (pneumonia, hepatitis, encephalitis) |
Image-derived danger signs: The forehead photograph follows the V1 distribution and extends to the eyelid/nose, consistent with herpes zoster ophthalmicus; ocular pain, photophobia, visual change, a red eye or corneal signs require urgent ophthalmic assessment. The ear photograph shows vesicles around the pinna/external canal—the cutaneous clue to Ramsay-Hunt when accompanied by ipsilateral lower-motor-neuron facial weakness, hearing symptoms or vertigo.
Clinical, viral culture, Tzanck smear, EM (electron microscopy), PCR, viral antigen detection [1]
- PCR from vesicle fluid, a lesion-base swab or crust is the most helpful confirmatory test when the diagnosis is atypical. Viral culture, electron microscopy and Tzanck smear are historical/less useful; Tzanck cannot distinguish HSV from VZV [14].
Systemic antiviral agents if less than 72 hours. Other supportive measures: 1. Pain control 2. Topical antibiotic [1]
Timing: Start as early as possible—benefit is greatest within 72 hours. Do not use 72 hours as a hard exclusion: consider treatment up to 7 days when new vesicles are still appearing or the patient is older, immunocompromised, in severe pain, or has ophthalmic/Ramsay-Hunt/non-truncal disease [14,15]. Give appropriate analgesia and clean, non-adherent local care; topical antibiotics are not routine unless there is secondary bacterial infection.
Acyclovir/valaciclovir/famciclovir: Guanosine analogue. Selectively phosphorylated by HSV and VZV thymidine kinases. Interferes with viral DNA synthesis by inhibiting viral DNA polymerase. Valaciclovir/famciclovir have better oral bioavailability. [1]
Mechanism (from first principles):
- Acyclovir enters virus-infected cells
- Viral thymidine kinase preferentially monophosphorylates acyclovir in infected cells → acyclovir monophosphate
- Host cell kinases further phosphorylate → acyclovir triphosphate
- Acyclovir triphosphate competes with dGTP for incorporation into viral DNA by viral DNA polymerase
- Once incorporated, it acts as a chain terminator (lacks the 3'-OH needed for the next nucleotide) → stops viral DNA synthesis
Why is it selective? Viral thymidine kinase activates acyclovir far more efficiently in infected cells, and the triphosphate preferentially inhibits viral DNA polymerase; this concentrates activity where virus is replicating.
| Drug | Pro-drug of | Oral bioavailability | Dosing convenience |
|---|---|---|---|
| Acyclovir | — | Low (~15-30%) | 5× daily (inconvenient) |
| Valaciclovir | L-valine ester of acyclovir | ~55% | 3× daily |
| Famciclovir | Pro-drug of penciclovir | ~77% | 3× daily |
High Yield — Antiviral Mechanism
Acyclovir is a guanosine analogue selectively activated by viral thymidine kinase → chain terminator of viral DNA polymerase. Valaciclovir and famciclovir have better oral bioavailability.
SECTION 3: CUTANEOUS FUNGAL INFECTIONS
Fungal infection classification: Superficial, Subcutaneous, Deep [1]
Superficial fungal infection: Dermatophytes and Yeast [1]
Types of superficial dermatophyte infection: [1]
- Onychomycosis (nail)
- Tinea pedis (feet)
- Tinea cruris (groin)
- Tinea corporis (trunk)
- Tinea manuum (hands)
- Tinea capitis (scalp)
Pathogenesis: Dermatophytes (Trichophyton, Microsporum, Epidermophyton) preferentially infect keratinised tissue (stratum corneum, hair and nails) by producing keratinases; mucosa is not a typical site. Deeper follicular/dermal infection can occur, particularly with topical-steroid misuse or immunosuppression.
Clinical clue: Annular lesions with central clearing and active, scaly, raised border ("ringworm" — nothing to do with actual worms).
Visual atlas from the lecture:
- Tinea cruris: an asymmetric groin/upper-inner-thigh plaque with a sharply demarcated scaly advancing edge; the scrotum is often relatively spared (unlike candidal intertrigo, which is moist and may have satellite pustules).
- Tinea corporis: annular or polycyclic plaques expand centrifugally, leaving central clearing and scale concentrated at the active rim.
- Tinea pedis: either soggy white interdigital maceration/fissuring or diffuse dry plantar/lateral scale (the “moccasin” pattern).
- Tinea manuum: the slide's side-by-side palms show unilateral diffuse dry scale against a normal opposite palm—the classic “one hand, two feet” clue. Check both feet and nails.
- Onychomycosis: yellow-brown thickening, subungual debris and onycholysis; nail dystrophy has many mimics, so confirm fungus before prolonged oral treatment.
Can be associated with immunocompromised (DM). Affects mucocutaneous areas: oral, vaginal, intertrigo. Housewife dermatitis with loss of nail cuticle can lead to candidiasis paronychia. Anti-fungal therapy useful. [1]
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Candida is a yeast (not a dermatophyte) → it CAN affect mucous membranes (unlike dermatophytes)
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Risk factors: DM, immunosuppression, antibiotics (disrupt normal flora), chronic moisture (occlusion, wet work)
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"Housewife dermatitis" — chronic wet work → loss of cuticle seal → Candida colonises the proximal nail fold → chronic paronychia (swollen, red, tender proximal nail fold)
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Genital candidiasis: The balanitis photograph shows moist erythema of the glans/prepuce with superficial scale rather than an annular advancing edge. Recurrent or severe disease should prompt assessment for diabetes, recent antibiotics, phimosis and immunosuppression; a single episode does not by itself imply immune deficiency.
3.3 Antifungal Pharmacology
This is a heavily tested pharmacology section in this lecture.
Against dermatophyte, yeast, or both. Works by inhibiting various enzymes needed for sterol synthesis in the fungal cell membrane. Should be used after skin scraping for fungal microscopy and culture. [1]
When to sample: Scrape from the active scaly edge when the morphology is atypical, treatment has failed, or systemic therapy is being considered. Confirm suspected onychomycosis before months of oral therapy. Straightforward limited tinea can often be treated clinically; sampling every patient before topical treatment is not mandatory.
Types of topical antifungal: [1]
- Keratolytic (Whitfield's ointment) — salicylic acid + benzoic acid; not truly antifungal but removes infected stratum corneum
- Undecanoate (acid zinc salt in Mycota powder)
- Thiocarbamates (tolnaftate)
- Morpholines (amorolfine) — nail lacquer for onychomycosis
- Imidazole (miconazole, clotrimazole, ketoconazole)
- Allylamines (terbinafine cream)
Fungal cell membrane contains ergosterol (equivalent to cholesterol in human cells). [1]
The ergosterol synthesis pathway is the key pharmacology concept. The slide's simplified diagram omits several intermediates; use it to locate drug targets rather than as a complete biochemical sequence:
Squalene → (squalene epoxidase) → Lanosterol → (14α-demethylase) → Fecosterol → (Δ14-reductase, Δ-fecosterol isomerase) → Episterol → Ergosterol [1]
| Enzyme Target | Drug Class | Example |
|---|---|---|
| Squalene epoxidase | Allylamines, Thiocarbamates | Terbinafine, Tolnaftate |
| 14α-demethylase (CYP51) | Azoles | Ketoconazole, Itraconazole, Fluconazole |
| Δ14-reductase and Δ-fecosterol isomerase | Morpholines | Amorolfine |
Why target ergosterol? Human cell membranes use cholesterol, not ergosterol. The enzymes in the ergosterol pathway are sufficiently different from human enzymes → selective toxicity. However, azoles' binding to CYP enzymes is not perfectly selective → they also inhibit human CYP450 → drug interactions and hepatotoxicity.
Squalene
│ squalene epoxidase ← allylamines (terbinafine)
│ thiocarbamates (tolnaftate)
↓
Squalene epoxide
↓
Lanosterol
│ 14α-demethylase ← azoles (itraconazole, fluconazole)
↓
Fecosterol
│ Δ14-reductase / Δ-fecosterol isomerase ← morpholines (amorolfine)
↓
Episterol → Ergosterol3.3.3 Systemic Antifungals
Indications for systemic antifungal: Scalp, Nail, Extensive tinea infection, Immunosuppression [1]
Why systemic for these? Topical agents cannot penetrate to the nail matrix, hair follicle root, or widespread disease adequately.
Systemic antifungals: Griseofulvin, Azoles, Allylamines [1]
- Griseofulvin: Inhibits fungal mitosis by disrupting the mitotic spindle. It remains useful for selected dermatophyte infections, especially some Microsporum tinea capitis; choice is species- and guideline-dependent.
Bind to cytochrome P-450. Fungistatic. Ketoconazole, itraconazole, fluconazole. Ketoconazole no longer used because of liver toxicity. Effective against yeast AND dermatophytes. Stay in tissue after systemic clearance: intermittent therapy useful. [1]
| Feature | Detail |
|---|---|
| Mechanism | Inhibit lanosterol 14α-demethylase (CYP51) → ↓ergosterol → destabilised fungal membrane |
| Spectrum | Yeast + dermatophytes |
| Action | Often described as fungistatic, although activity varies by drug, organism and concentration |
| Key property | Persist in keratin after systemic clearance → allows pulse/intermittent dosing (especially itraconazole for onychomycosis) |
| Major concern | CYP450 interaction → hepatotoxicity + drug interactions |
Terbinafine. Fungicidal. Effective against dermatophytes. Minimal side effects: GI upset, loss of taste, rarely rash and liver impairment. [1]
| Feature | Detail |
|---|---|
| Mechanism | Inhibit squalene epoxidase → squalene accumulation (toxic) + ↓ergosterol |
| Spectrum | Dermatophytes (less effective against yeast) |
| Action | Fungicidal (kills the fungus) |
| Side effects | GI upset, loss of taste (dysgeusia), rarely hepatotoxicity |
High Yield — Terbinafine vs Itraconazole
Terbinafine is fungicidal against dermatophytes; itraconazole covers dermatophytes and many yeasts but has substantially more CYP3A4 interactions. For dermatophyte toenail onychomycosis, continuous terbinafine outperformed intermittent itraconazole in the historical LION trial. Candida treatment depends on species, site and susceptibility—do not reduce it to “itraconazole preferred.”
LION study (Evans, BMJ 1999): Compared continuous terbinafine 250mg daily for 12-16 weeks vs. intermittent itraconazole 200mg BD for 1 week every 4 weeks for 12-16 weeks. 35 centres, 496 patients. [1]
Results — Mycological cure after 72 weeks: [1]
- Terbinafine 12 weeks: 75.7%, 16 weeks: 80.8%
- Itraconazole 12 weeks: 38.3%, 16 weeks: 49.1%
Extended LION study: 4 extra weeks of oral terbinafine may further improve cure rate. [1]
Take-home (historical evidence): In this 1999 trial, continuous terbinafine achieved higher long-term mycological cure than the tested itraconazole pulse regimens. Do not extrapolate the percentages to every nail dystrophy: confirm a fungal cause and individualise choice for organism, interactions, liver disease, heart failure risk, patient goals and local guidance.
Small study (n = 60, Jahangir, BJD 1998): Itraconazole cure rate 85.7% vs. Terbinafine cure rate 77.8% — not much difference. [1]
For tinea capitis, unlike onychomycosis, itraconazole and terbinafine show comparable efficacy. A meta-analysis for onychomycosis (Epstein, Archives of Dermatology 1998) showed terbinafine disease-free rates of 35–50% vs. itraconazole 25–40%, consistent with the LION study results [1].
Side effects of anti-fungal: GI, taste, liver, skin eruption, headache [1]
Historical slide message: hepatotoxicity can occur with systemic antifungals and may emerge after several weeks. [1]
This directly relates to the counselling scenario in the lecture:
"Elderly patient died, coroner ruled anti-fungal drug to be indirectly related." Your father with tinea pedis and onychomycosis was due to take a course of systemic anti-fungal. He is concerned. What will you do? [1]
Counselling approach:
- Acknowledge the concern
- First confirm that the nail change is fungal and that systemic treatment is worthwhile; cure is not guaranteed and cosmetic nail regrowth is slow.
- Review chronic/active liver disease, alcohol use, hepatitis status when relevant, pregnancy, heart failure (itraconazole), and interacting medicines.
- For oral terbinafine, obtain pretreatment transaminases; it is not recommended in chronic or active liver disease. The product label recommends periodic liver-function monitoring, while the exact interval follows the agent, course length, baseline risk and local protocol—not a single universal “week 4” rule [17].
- Give a symptom safety net: stop and seek care for jaundice, dark urine, pale stool, persistent nausea/anorexia, marked fatigue, right-upper-quadrant pain, progressive rash, or severe taste disturbance.
- Oral ketoconazole should not be used for routine superficial mycoses because its risk profile outweighs safer alternatives.
Exam Tip — Drug Counselling OSCE
If asked to counsel a patient about systemic antifungal therapy, mention: (1) confirm the indication/mycology, (2) check the agent-specific contraindications and baseline tests, (3) review interactions and comorbidity, (4) explain realistic cure/regrowth, and (5) give a clear liver/skin-reaction safety net. Monitoring during therapy follows the chosen drug and local protocol.
SECTION 4: BLISTERING DISEASES
Blistering disease classification by level of split: [1]
- Subcorneal: Impetigo
- Intraepidermal: Acute dermatitis, herpes, friction, erythema multiforme, pemphigus
- Subepidermal: Bullous pemphigoid, dermatitis herpetiformis, porphyria
This is a useful teaching simplification, not a complete dermatopathology taxonomy: the precise split in dermatitis, friction injury and erythema multiforme varies with mechanism and severity. For autoimmune bullous disease, confirm the level on histology and the antibody pattern on direct immunofluorescence (DIF).
Why does the level of split matter?
- Subcorneal/intraepidermal → flaccid blisters (the roof is thin → ruptures easily → erosions/crusts)
- Subepidermal → tense blisters (the entire epidermis forms the roof → more robust → blisters stay intact)
This is a fundamental principle that lets you clinically distinguish pemphigus (flaccid) from pemphigoid (tense).
4th-6th decade. Intraepidermal blister. Autoantibody against keratinocytes. Flaccid blisters in skin and mucosa. Normal skin in between lesions. Affects trunk and face, extremities spared. [1]
Nikolsky sign: positive. Skin biopsy and IMF. Serum antibody (IDIMF): against keratinocytes — level correlates with disease activity. Disease is more severe and before systemic steroid, mortality rate was 80%. [1]
Pathogenesis (from first principles):
- Autoantibodies (IgG) target desmogleins (desmoglein 3 in pemphigus vulgaris, desmoglein 1 in pemphigus foliaceus) — these are the adhesion molecules holding keratinocytes together
- Loss of cell-cell adhesion → acantholysis (individual keratinocytes separate from each other) → intraepidermal cleft → flaccid blister
- Desmoglein compensation theory:
- Oral mucosa has abundant desmoglein 3 but little desmoglein 1 → anti-Dsg3 alone causes oral erosions
- Skin has both Dsg1 and Dsg3 → need anti-Dsg1 (or both) for skin blisters
- This explains why mucosal involvement is often the FIRST manifestation of PV
Key Clinical Features:
| Feature | Detail |
|---|---|
| Age | 4th-6th decade |
| Blister type | Flaccid (intraepidermal split) |
| Distribution | Often trunk, scalp/face and flexures; limbs may also be involved |
| Mucous membranes | Commonly involved (often first site) |
| Nikolsky sign | Positive (lateral pressure on normal skin → blister) |
| Between lesions | Normal skin (no urticarial base) |
Investigations:
- Skin biopsy: The lecture micrograph shows a suprabasal cleft, rounded acantholytic keratinocytes and a basal row still attached to basement membrane—the classic “row of tombstones” appearance of pemphigus vulgaris.
- Direct IMF (DIF): "Fishnet"/intercellular IgG and C3 deposition around keratinocytes
- Serology/indirect IF: Anti-desmoglein ELISA titres often track disease activity and can support monitoring, but clinical activity remains decisive.
What the photographs show: In severe pemphigus, the fragile blister roof disappears quickly, so the dominant finding is not intact bullae but widespread irregular painful raw erosions, crust and denuded mucosa. The mouth/neck image reinforces that mucosal erosions may be prominent and can impair eating and fluid intake.
Management:
- Urgent dermatology-led wound, pain, nutrition, infection and fluid assessment.
- Rituximab plus a shorter course of systemic corticosteroid is first-line for moderate-severe pemphigus in the EADV guideline; corticosteroid with azathioprine or mycophenolate is an alternative when rituximab is unavailable or contraindicated [18].
- The slide's 80% mortality refers to the pre-corticosteroid era and must not be quoted as current treated mortality.
High Yield — Pemphigus
Pemphigus = intraepidermal acantholysis, fragile/flaccid blisters that become erosions, frequent mucosal disease, anti-desmoglein antibodies, Nikolsky often positive, and intercellular “fishnet” DIF. Historical untreated disease was often fatal; modern treatment is specialist-led and rituximab is no longer reserved only for refractory disease.
More common in elderly. Autoantibody against basement membrane. Large intact blisters arise from urticarial base. Thigh, groin, axilla. Mucosal involvement less common. Less severe than pemphigus. [1]
Skin biopsy and IMF. IDIMF: level does NOT correlate with disease activity. [1]
Pathogenesis:
- Autoantibodies (IgG) target BP antigens (BP180/BPAg2 and BP230/BPAg1) at the dermoepidermal junction (hemidesmosomes)
- Antibody binding → complement activation → neutrophil and eosinophil infiltration → protease release → destruction of the dermoepidermal junction → subepidermal split → tense blister
Key Clinical Features:
| Feature | Detail |
|---|---|
| Age | Elderly (> 60 years) |
| Blister type | Tense, large, intact (full epidermis as roof) |
| Base | Urticarial (erythematous/oedematous) |
| Distribution | Flexural — thigh, groin, axilla |
| Mucous membranes | Less commonly involved (unlike pemphigus) |
| Nikolsky sign | Usually negative (subepidermal split → harder to separate) |
| Severity | Less severe than pemphigus |
Investigations:
- Skin biopsy: Subepidermal blister with eosinophilic infiltrate
- Direct IMF: Linear IgG and C3 at the basement membrane zone
- Serology/indirect IF: Circulating anti-BP180/BP230 antibodies support diagnosis. The slide's blanket claim that antibody level “does not correlate” is too broad: BP180 NC16A ELISA can track activity and may help predict relapse, whereas indirect-IF titre is less reliable [19].
Visual recognition: The final four slides show the defining mechanical clue: very large, tense amber or haemorrhagic bullae remain intact on fingers, hands and feet because the whole epidermis forms their roof. Elsewhere, ruptured bullae leave sharply outlined erosions among intact tense blisters. Compare this with pemphigus, where widespread erosions dominate and intact blisters are hard to find.
Management:
- Superpotent topical corticosteroids are the mainstay whenever feasible, even for extensive disease; oral prednisone is an alternative when topical delivery is impractical [19].
- Choose steroid-sparing therapy according to frailty and contraindications. Doxycycline may be safer but is less rapidly effective and is mainly considered when systemic corticosteroids are undesirable; refractory disease warrants specialist immunosuppressive/biologic therapy.
| Feature | Pemphigus | Pemphigoid |
|---|---|---|
| Age | 4th-6th decade | Elderly |
| Level of split | Intraepidermal (acantholysis) | Subepidermal |
| Blister character | Flaccid | Tense |
| Base appearance | Normal skin between lesions | Urticarial base |
| Mucosal involvement | Common (often first) | Less common |
| Nikolsky sign | Positive | Negative |
| Target antigen | Desmoglein (keratinocyte) | BP180/BP230 (BMZ) |
| DIF pattern | Intercellular "fishnet" IgG + C3 | Linear IgG + C3 at BMZ |
| Antibody level vs activity | Anti-Dsg ELISA often tracks activity | BP180 ELISA may track activity; indirect-IF titre is less reliable |
| Severity | Potentially life-threatening; historical untreated mortality was very high | Often frail elderly patients; treatment toxicity and infection matter |
| Treatment | Rituximab + short-course systemic steroid for moderate-severe disease; alternatives are specialist-led | Superpotent topical steroid when feasible; systemic/steroid-sparing therapy if needed |
Exam Trap — Nikolsky Sign
Nikolsky sign is positive in pemphigus (and SSSS) but negative in pemphigoid. Don't confuse! Both pemphigus and SSSS involve intraepidermal/subcorneal splits (fragile epidermis), while pemphigoid's subepidermal split means the whole epidermis is still intact.
SECTION 5: CLINICAL APPROACH — "IT IS RED AND PAINFUL"
When a patient presents with a red, painful skin lesion:
- Onset and duration: Acute (hours-days) vs. subacute vs. chronic
- Progression: Static vs. rapidly spreading (cellulitis vs. NF)
- Pain character: Proportionate vs. disproportionate (NF red flag)
- Systemic symptoms: Fever, rigors, malaise (suggests deeper infection)
- Predisposing factors:
- Skin break, trauma, surgery
- Tinea pedis (portal of entry)
- Diabetes mellitus / immunosuppression
- Recent medications (drug eruption)
- Sexual history: If genital lesion — warts, herpes, molluscum
- Contacts: Varicella, impetigo (school contacts)
- Distribution: Dermatomal (zoster), flexural (erythrasma, candida), intertriginous (tinea cruris)
- Morphology: Macule, papule, vesicle, bulla, pustule, erosion, ulcer, crust
- Configuration: Grouped (herpes), annular (tinea), linear (contact), dermatomal (zoster)
- Distribution: Localised vs. generalised
- Blister characteristics: Flaccid (pemphigus) vs. tense (pemphigoid)
- Special signs:
- Nikolsky sign
- Hutchinson's sign (nose tip vesicles in HZ ophthalmicus)
- Crepitus (NF)
- Wood's lamp (erythrasma — coral-pink)
- Depth assessment: Superficial (subcorneal) vs. deep (subcutaneous)
- Surrounding tissue: Oedema beyond erythema, bullae, ecchymosis (NF)
| Investigation | When to use | What it shows |
|---|---|---|
| Swab/pus culture | Recurrent/widespread or non-responsive impetigo; purulent abscess; broken-skin cellulitis with unusual exposure | Organism identification and susceptibility; routine swabs are not useful in typical intact-skin cellulitis |
| KOH/fungal scraping | Suspected tinea, candida | Hyphae (dermatophytes), pseudohyphae (candida) |
| Wood's lamp | Erythrasma, tinea capitis | Coral-pink (erythrasma), green (Microsporum) |
| Viral PCR | Atypical/severe VZV or HSV | Rapid, specific viral identification; preferred over Tzanck/culture |
| Two skin biopsies | Suspected autoimmune blistering disease | Lesional edge for routine histology (level/cells); separate perilesional normal-appearing skin for DIF (antibody pattern) |
| Blood/deep-tissue cultures | Sepsis or suspected NF | Bloodstream pathogen; operative deep tissue is more informative than a superficial swab |
| Immediate surgical exploration | High clinical suspicion of NF | Diagnostic and therapeutic; imaging/laboratory scores must not delay it |
Exam Intelligence
-
Spot diagnosis (EMQ/MCQ): Photo of lesion → identify condition
- Honey-crusted lesion on face → Impetigo
- Dermatomal vesicles → Herpes zoster
- Umbilicated papules → Molluscum contagiosum
- Annular scaly plaque → Tinea corporis
- Coral-pink fluorescence → Erythrasma
- Flaccid blisters with oral erosions → Pemphigus
-
Clinical scenario (SAQ): Differentiate cellulitis from NF → list features [1]
-
Pharmacology (MCQ/SAQ): Mechanism of acyclovir, terbinafine vs. itraconazole, site of action in ergosterol pathway
-
Management (SAQ): How to treat herpes zoster (early antiviral when indicated, analgesia, eye/ear red flags, infection precautions)
-
Counselling (OSCE): Systemic antifungal risks, LFT monitoring
| Trap | Correct Answer |
|---|---|
| Confusing erythrasma with tinea | Erythrasma = bacteria (Corynebacterium), coral-pink Wood's lamp |
| Saying "V5" causes eye involvement in zoster | It's V1 (ophthalmic division) — the slide appears to contain an error |
| Calling SSSS and TEN the same thing | SSSS = subcorneal (superficial), mucosa spared, treat with antibiotics; TEN = dermoepidermal, mucosa involved, stop drug |
| Saying no pemphigoid antibody can track disease | BP180 ELISA may track activity/relapse; indirect-IF titre is less reliable |
| Treating every clinical tinea only after microscopy | Sample atypical/refractory disease and confirm nail/scalp disease before systemic therapy; limited classic tinea can be treated clinically |
High Yield Summary
-
Bacterial
- Impetigo (Staph/Strep, honey crust; bullous form has a toxin-mediated subcorneal split) → Erysipelas/Cellulitis (sharp superficial vs diffuse deeper border; inspect toe webs) → Furuncle/Carbuncle (drain fluctuant abscess; add antibiotics for risk features) → Erythrasma (Corynebacterium, coral-red Wood's lamp) → NF (pain/toxicity out of proportion, rapidly progressive; immediate surgery—do not wait for MRI) → SSSS (< 5 years, toxin, superficial peeling, Nikolsky+, mucosa spared; culture the primary focus).
-
Viral
- Warts (rough keratotic papules, thrombosed capillary dots) → Molluscum (poxvirus, umbilicated papules) → Varicella (10-21-day incubation, crops at different stages, centripetal) → Herpes zoster (unilateral dermatomal grouped vesicles; start antivirals early, but treat selected high-risk patients beyond 72 hours; recognise V1 and Ramsay-Hunt red flags).
-
Fungal
- Dermatophytes (active scaly edge; one-hand/two-feet and interdigital/moccasin patterns) → Candida (moist mucocutaneous disease, satellite lesions) → Antifungals: allylamines block squalene epoxidase; azoles block 14-alpha-demethylase. Confirm onychomycosis before oral therapy; obtain agent-specific baseline tests and monitor by risk/local protocol.
-
Blistering
- Pemphigus (suprabasal acantholysis, fragile/flaccid blisters → erosions, mucosal, Nikolsky often positive, anti-desmoglein, fishnet DIF; rituximab-based first-line therapy for moderate-severe disease) vs.
- Pemphigoid (subepidermal, large tense/haemorrhagic bullae, urticarial base, elderly, mucosa less common, linear BMZ DIF; BP180 ELISA may track activity).
Active Recall - It Is Red and Painful
[1] Lecture slides: GC 071. It is red and painful.pdf (all pages cited throughout) [2] Senior notes: Block A - It is red and painful (bacterial and viral skin infections).pdf [3] Senior notes: Block A - Dermatology PBL 2.pdf (p6 — SSSS, dermatological emergencies) [4] Lecture slides: GC 022. Visual Spot Diagnoses - Survival Guide for Primary Care.pdf [5] Senior notes: Ryan Ho Opthalmology.pdf (p16-20 — red eye differential for context) [6] Senior notes: Gen Clerk Anaes + Microbiology Summary.pdf (p20 — Gram-positive organisms) [7] Past papers: 2022 Fourth Summative MCQ.pdf (Q27 — Fournier's gangrene) [8] Past papers: 2019 Fourth Summative MCQ.pdf (p2 — dermatological EMQ) [9] Past papers: 2025 Fourth Summative MCQ.pdf (Q82 — drug allergy workup after blistering eruption) [10] NICE NG153: Impetigo — antimicrobial prescribing recommendations [11] NICE NG141: Cellulitis and erysipelas — antimicrobial prescribing recommendations [12] CDC (2025): Clinical guidance for type II necrotising fasciitis [13] Leung et al. (2018): Staphylococcal scalded skin syndrome — evaluation, diagnosis and management [14] CDC: Clinical overview of shingles (herpes zoster) [15] NHS Highland: Varicella-zoster/chickenpox and herpes-zoster/shingles antimicrobial guidance [16] CDC: Varicella diagnosis fact sheet [17] US FDA: Lamisil (terbinafine) prescribing information [18] EADV (2020): Updated S2K guideline on pemphigus vulgaris and foliaceus [19] EADV (2022): Updated S2K guideline on bullous pemphigoid
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