Vesiculobullous Diseases Flashcards
Bullous pemphigoid clinical presentation
- chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an erythematous or normal skin base
- can present as urticarial plaques without bullae
- common sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth in 33%
Bullous pemphigoid pathophysiology
• IgG produced against dermal-epidermal basement membrane proteins (hemidesmosomes) leads to subepidermal bullae
Bullous pemphigoid epi
• mean age of onset: 60-80 yr old, F=M
Bullous pemphigoid invesigations
- immunofluorescence shows linear deposition of IgG and C3 along the basement membrane
- anti-basement membrane antibody (IgG) (pemphigoid antibody detectable in serum)
Bullous pemphigoid prognosis
heals without scarring, usually chronic
rarely fatal
Bullous pemphigoid management
- prednisone 0.5-1 mg/kg/day until clear, then taper ± steroid-sparing agents (e.g. immunosuppressants such as azathioprine, cyclosporine, mycophenolate mofetil)
- topical potent steroids (clobetasol) may be as effective as systemic steroids in limited disease
- tetracycline ± nicotinamide is effective for some cases
- IVIg and plasmapheresis for refractory cases
Pemphigus vulgaris clinical presentation
- autoimmune blistering disease characterized by flaccid non-pruritic intraepidermal bullae/vesicles on an erythematous or normal skin base
- may present with erosions and secondary bacterial infection
- sites: mouth (90%), scalp, face, chest, axillae, groin, umbilicus
- Nikolsky’s sign: epidermal detachment with shear stress
- Asboe-Hansen sign: pressure applied to bulla causes it to extend laterally
Pathophysiology pemphigus vulgaris
IgG against epidermal desmoglein-1 and -3 lead to loss of intercellular adhesion in the epidermis
Pemphigus vulgaris epidemiology
- 40-60 yr old, M=F, higher prevalence in Jewish, Mediterranean, Asian populations
- paraneoplastic pemphigus may be associated with thymoma, myasthenia gravis, malignancy, and use of D-penicillamine
Pemphigus vulgaris investigations
- immunofluorescence: shows IgG and C3 deposition intraepidermally
- circulatng serum anti-desmoglein IgG antibodies
Pemphigus vulgaris prognosis
- lesions heal with hyperpigmentation but do not scar
* may be fatal unless treated with immunosuppressive agents
Pemphigus vulgaris management
• prednisone 1-2 mg/kg until no new blisters, then 1-1.5 mg/kg until clear, then taper ± steroid-sparing agents (e.g. azathioprine, cyclophosphamide, cyclosporine, IVIg, mycophenolate mofetil, rituximab)
Pemphigus vulgaris vs Bullous pemphigoid
VulgariS = Superficial, intraepidermal, flaccid lesions
PemphigoiD = Deeper, tense lesions at the dermal-epidermal junction
Pemphigus Foliaceus description, pathophysiology and treatment
An autoimmune intraepidermal blistering disease that is more superficial than pemphigus vulgaris due to antibodies against desmoglein-1, a transmembrane adhesion molecule.
Appears as crusted patches, erosions and/or flaccid bullae that usually start on the trunk.
Localized disease can be managed with topical steroids. Active widespread disease is treated like pemphigus vulgaris
Dermatitis herpetiformis clinical presenntation
- grouped papules/vesicles/urticarial wheals on an erythematous base, associated with intense pruritus, burning, stinging, excoriations
- lesions grouped, bilaterally symmetrical
- common sites: extensor surfaces of elbows/knees, sacrum buttocks, scalp
Dermatitis herpetiformis pathophysiology
- transglutaminase IgA deposits in the skin alone or in immune complexes leading to eosinophil and neutrophil infiltration
- 90% have HLA B8, DR3, DQWZ
- 90-100% associated with an often subclinical gluten-sensitive enteropathy (i.e. celiac disease)
- 30% have thyroid disease; increased risk of intestinal lymphoma in untreated comorbid celiac disease; iron/folate deficiency is common
Dermatitis herpetiformis epidemiology
20-60 year old
M:F = 2:1
Dermatitis herpetiformis investigations
biopsy
immunofluorescencce shows IgA depots in perilesional skin
Dermatitis herpetiformis management
- dapsone (sulfapyridine if contraindicated or poorly tolerated)
- gluten free diet for life – this can reduce risk of lymphoma
Porphyria Cutanea Tarda clinical presentation
- skin fragility followed by formation of tense vesicles/bullae and erosions on photoexposed skin
- gradual healing to scars, milia
- periorbital violaceous discolouration, diffuse hypermelanosis, facial hypertrichosis
- common sites: light-exposed areas subjected to trauma, dorsum of hands and feet, nose, and upper trunk
Porphyria Cutanea Tarda Pathophysiology
- uroporphyrinogen decarboxylase deficiency leads to excess heme precursors
- can be associated with hemochromatosis, alcohol abuse, DM, drugs (estrogen therapy, NSAIDs), HIV, hepatitis C, increased iron indices
Porphyria cutanea tarda epidemiology
• 30-40 yr old, M>F
Porphyria Cutanea Tarda investigations
- urine + 5% HCl shows orange-red fluorescence under Woods lamp (UV rays)
- 24 h urine for uroporphyrins (elevated)
- stool contains elevated coproporphyrins
- immunofluorescence shows IgE at dermal-epidermal junctions
Porphyria Cutanea Tarda management
discontinue aggravating substances (alcohol, estrogen therapy)
- phlebotomy to decrease body iron load
- low dose hydroxychloroquine
Exanthematous drug reaction clinical presentation
- morphology: erythematous macules and papules ± scale
- spread: symmetrical, trunk to extremities
- time course: 7-14 d after drug initiation, fades 7-14 d after withdrawal
Exanthematous drug reaction epidemiology
most common cutaneous drug reaction; increased in presence of infections
common causative agents: penicillin, sulfonamides, phenytoin
Exanthematous drug reaction management
weight risks and benefits of drug discontinuation
antihistamins, emollients, topical steroids
Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) clinical presentation
- morphology: morbilliform rash involving face, trunk arms; can have facial edema
- systemic features: fever, malaise, cervical lymphadenopathy, internal organ involvement (e.g. hepatitis, arthralgia, nephritis, pneumonitis, lymphadenopathy, hematologic abnormalities, thyroid abnormalities)
- spread: starts with face or periorbitally and spreads caudally; no mucosal involvement
- time course: onset 1-6 weeks after first exposure to drug; persists weeks after withdrawal of drug
Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) epidemiology
- rare: incidence varies considerably depending on drug
- common causative agents: aniconvulsants (e.g. phenytoin, phenobarbital, carbamazepine, lamotrigine), sulfonamides, and allopurinol
- 10% mortality if severe, undiagnosed, and untreated
Drug induced hypersensitivity syndrome (DIHS)/Drug reaction with eosinophilia and systemic symptoms (DRESS) management
- discontinue offending drug ± prednisone 0.5mg/kg per day, consider cyclosporine in severe cases
- may progress to generalized exfoliative dermatitis/erythroderma if drug is not discontinued
Diagnosis of a drug reaction
Classification by Naranjo et. al has 4 criteria:
- Temporal relationship between drug exposure and reaction
- Recognized response to suspected drug
- Improvement after drug withdrawal
- Recurrence of reaction on re-challenge with the drug
Definite drug reaction requires all 4 criteria to be met
Probable drug reaction requires #1-3 to be met
Possible drug reaction requires only #1
Drug hypersensitivity syndrome triad
Fever
exanthematous eruption
internal organ involvement
Drug induced urticaria and angioedema clinical presentation
morphology: wheals lasting >24 h unlike non drug induced urticaria, angioedema (face and mucous membranes)
- systemic features: may be associated with systemic anaphylaxis (bronchospasm, laryngeal edema, shock)
- time course: hours to days after exposure depending on the mechanism
Drug induced urticaria and angioedema epidemiology
- second most common cutaneous drug reaction
* common causative agents: penicillins, ACEI, analgesics/anti-inflammatories radiographic contrast media
Drug induced urticaria and angioedema management
• discontinue offending drug, treatment with antihistamines, steroids, epinephrine if anaphylactic
Serum sickness like reaction clinical presentation
- morphology: symmetrical cutaneous eruption (usually urticarial)
- systemic features: malaise, low grade fever, arthralgia, lymphadenopathy
- time course: appears 1-3 wk after drug initiation, resolve 2-3 wk after withdrawal
Serum sickness like reaction epidemiology
- more prevalent in kids 0.02-0.2%
* common causative agents: cefaclor in kids; bupropion in adults
Serum sickness like reaction management
• discontinue offending drug ± topical/oral corticosteroids
Acute generalized exanthematous pustulosis (AGEP) clinical presentation
- morphology: erythematous edema and sterile pustules prominent in intertriginous areas
- systemic features: high fever, leukocytosis with neutrophilia
- spread: starts in face and intertriginous areas and spread to trunk and extremities
- time course: appears 1 wk after drug initiation, resolve 2 wk after withdrawal
Acute generalized exanthematous pustulosis (AGEP) epidemiology
- rare: 1-5/million
* common causative agents: aminopenicillins, cephalosporins, clindamycin, calcium channel blockers
Acute generalized exanthematous pustulosis (AGEP) management
Discontinue offending drug and systemic corticosteroids
Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) clinical presentation
• morphology: prodromal rash (morbilliform/targetoid lesions ± purpura, or diffuse erythema), confluence of flaccid blisters, positive Nikolsky sign (epidermal detachment with shear stress), full thickness epidermal loss; dusky tender skin, bullae, desquamation/skin sloughing, atypical targets
• classification: BSA with epidermal detachment:
<10% in SJS
10-30% in SJS/TEN overlap
>30% in TEN
- spread: face and extremities; may generalize; scalp, palms, soles relatively spared; erosion of mucous membranes (lips, oral mucosa, conjunctiva, GU mucosa)
- systemic features: fever (higher in TEN), cytopenias, renal tubular necrosis/AKI, tracheal erosion, infection, contractures, corneal scarring, phimosis, vaginal synechiae
- time course: appears 1-3 wk after drug initiation; progression <4 d; epidermal regrowth in 3 wk
- can have constitutional symptoms: malaise, fever, hypotension, tachycardia
Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) epidemiology
- SJS: 1.2-6/million; TEN: 0.4-1.2/million
- risk factors SLE, HIV/AIDS, HLA-B1502 (associated with carbamazepine), HLA-B5801 (associated with allopurinol)
- common causative agents: drugs (allopurinol, anti-epileptics, sulfonamides, NSAIDs, cephalosporins) responsible in 50% of SJS and 80% of TEN; viral or mycoplasma infections
- prognosis: 5% mortality in SJS, 30% in TEN due to fluid loss and infection
Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) differential diagnosis
• scarlet fever, phototoxic eruption, GVHD, SSSS, exfoliative dermatitis, AGEP, paraneoplastic pemphigus
Steven Johnson Syndrome (SJS)/Toxic epidermal necrolysis (TEN) management
- discontinue offending drug
- admit to intermediate/intensive care/burn unit
- supportive care: IV fluids, electrolyte replacement, nutritional support, pain control, wound care, sterile handling, monitor for and treat infection
- IVIg or cyclosporine or etanercept
SCORTEN Score for TEN PROGNOSIS
One point for each of: age ≥40 malignanc body surface area detached ≥10% tachycardia ≥120 bpm serum urea >10 mmol/L serum glucose >14 mmol/L serum bicarbonate <20 mmol/L
Used to determine appropriate clinical setting:
score 0-1 can be treated in non-specialized wards
score ≥2 should be transferred to intensive care or burn unit
Score at admission is predictive of survival: 94% for 0-1, 87% for 2, 53% for 3, 25% for 4, and 17% for ≥5
Effect of IVIG IV at dosages over 2+ g/kg for SJS or TEN
Significantly decreased mortality in patients with SJS or TEN
Fixed drug eruption clinical presentation
- morphology: sharply demarcated erythematous oval patches on the skin or mucous membranes
- spread: commonly face, mucosa, genitalia, acral; recurs in same location upon subsequent exposure to the drug (fixed location)
Fixed drug eruption epidemiology
• common causative agents: antimicrobials (tetracycline, sulfonamides), anti-inflammatories, psychoactive agents (barbiturates), phenolphthalein
Fixed drug eruption management
• discontinue offending drug ± prednisone 1mg/kg/d x 2 wk for generalized lesions ± potent topical corticosteroids for non-eroded lesions or antimicrobial ointment for eroded lesions
Photosensitivity reaction clinical presentation
- phototoxic reaction: “exaggerated sunburn” (erythema, edema, vesicles, bullae) confined to sun-exposed areas
- photoallergic reaction: pruritic eczematous eruption with papules, vesicles, scaling, and crusting that may spread to areas not exposed to light
Photosensitivity reaction pathophysiology
- phototoxic reaction: direct tissue injury
* photoallergic reaction: type IV delayed hypersensitiviy
Photosensitivity reaction epidemiology
common causative agents: chlorpromazine, doxycycline, thiazide diuretics, procainamide
Photosensitivity reaction management
sun protection +/- topical/oral corticosteroids
Ichthyosis vulgaris clinical presentation
- xerosis with fine scaling as well as large adherent scales (“fish-scales”)
- affects arms, legs, palms, soles, back, forehead, and cheeks; spares flexural creases
- improves in summer, with humidity, and as the child grows into adulthood
Ichthyosis vulgaris pathophysiology
- genetic deficiency in filaggrin protein leads to abnormal retention of keratinocytes (hyperkeratosis)
- scaling without inflammation
Ichthyosis vulgaris epidemiology
- 1:300 incidence
- autosomal dominant inheritance
- associated with AD and keratosis pilaris
Ichthyosis vulgaris investigations
electron microscopy keratohyalin granules
Ichthyosis vulgaris management
- immersion in bath and oils followed by an emollient cream, humectant cream, or creams/oil containing urea or α or β-hydroxy acids
- intermittent systemic retinoids for severe cases
Neurofibromatosis (Type I; von Recklinghausen’s Disease) clinical presentation
• diagnostic criteria includes 2 or more of the following
- more than 5 café-au-lait patches >1.5 cm in an adult or more than 5 café-au-lait macules >0.5 cm in a child <5 yr
- axillary or inguinal freckling
- iris hamartomas (Lisch nodules)
- optic gliomas
- neurofibromas
- distinctive bony lesion (sphenoid wing dysplasia or thinning of long bone cortex)
- first degree relative with neurofibromatosis type 1
- associated with pheochromocytoma, astrocytoma, bilateral acoustic neuromas, bone cysts, scoliosis, precocious puberty, developmental delay, and renal artery stenosis
- skin lesions less prominent in neurofibromatosis Type II
Neurofibromatosis (Type I; von Recklinghausen’s Disease) pathophysiology
- autosomal dominant disorder with excessive and abnormal proliferation of neural crest elements (Schwann cells, melanocytes), high incidence of spontaneous mutation
- linked to absence of neurofibromin (a tumour suppressor gene)
Neurofibromatosis (Type I; von Recklinghausen’s Disease) epidemiology
incidence 1: 3000
Neurofibromatosis (Type I; von Recklinghausen’s Disease) investigations
Wood’s lamp examination to detect cafe-au-lait macules in patients with pale skin
Neurofibromatosis (Type I; von Recklinghausen’s Disease) management
- refer to orthopedics, ophthalmology, plastics, and psychology for relevant management
- follow-up annually for brain tumours such as astrocytoma
- excise suspicious or painful lesions
Vitiligo clinical presentation
- primary pigmentary disorder characterized by depigmentation
- acquired destruction of melanocytes characterized by sharply marginated white patches
- associated with streaks of depigmented hair, chorioretinitis
- sites: extensor surfaces and periorificial areas (mouth, eyes, anus, genitalia)
- Koebner phenomenon, may be precipitated by trauma
Vitiligo pathophysiology
acquired autoimmune destruction of melanocytes
Vitiligo epidemiology
- 1% incidence, polygenic
* 30% with positive family history
Vitiligo investigations
- rule out associated autoimmune diseases: thyroid disease, pernicious anemia, Addison’s disease, Type I DM
- Wood’s lamp to detect lesions: illuminates UV light onto skin to detect amelanosis (porcelain white discolouration)
Vitiligo management
- sun avoidance and protection
- topical calcineurin inhibitor (e.g. tacrolimus, pimecrolimus) or topical corticosteroids
- PUVA or Narrow band UVB
- make-up
- “bleaching” normal pigmented areas (i.e. monobenzyl ether of hydroquinone 20%) if widespread loss of pigmentation
Level of skin that impetigo affects
Stratum corneum of the epidermis
Level of skin that erysipelas effects
Upper dermis and lymphatics only
Rarely involves the lower dermis
Subepidermal edema underlying an uninvolved epidermis
Level of skin that cellulitis effects
lower dermis and subcutaneous fat
primarily not raised and demarcation less distinct than erisypelas
Level of skin that necrotizing fasciitis effects
subcutaneous fat, fascial planes and deep muscle
Dermatological group A strep infections
Impetigo - just below stratum corneum
Erysipelas - epidermis and upper dermis only
cellulitis - primarily lower dermis and subcutis (primarily not raised, and demarcation less distinct than erysipelas)
Nec fasciitis - deep fascia and mucle
Impetigo clinical presentation
- acute purulent infection which appears vesicular; progresses to golden yellow “honey-crusted” lesions surrounded by erythema
- can present with bullae
- common sites: face, arms, legs, and buttocks
Impetigo etiology
GAS, S. aureus or both
Impetigo epidemiology
Preschool and young adults living in crowded conditions, poor hygiene, neglected minor trauma
Impetigo differential diagnosis
infected eczema
HSV
VZV
Impetigo investigations
Gram stain and culture of lesion fluid or biopsy
Impetigo management
remove crusts, use saline compresses and topical antiseptic soaks bid
topical antibacterials such as 2% mupirocin or fusidic acid (Canada only) tid; continue for 7-10 days after resolution
systemic antibiotics such as cloxacillin or cephalexin for 7-10 days
Erysipelas clinical presentation
Involves upper dermis
Confluent, erythematous, sharp raised edge, warm plaque, well demarcated
Very painful (“St. Anthony’s fire”)
Sites: face and legs
Systemic symptoms: fever, chills, headache, weakness (if present, sign of more serious infection)
Erysipelas etiology
GAS
Erysipelas complications
Scarlet fever, streptococcal gangrene, fat necrosis, coagulopathy
Spreads via lymphatics
Erysipelas differential diagnosis
DVT (less red, less hot, smoother),
superficial phlebitis,
contact dermatitis,
photosensitivity reaction,
stasis dermatitis,
panniculitis,
vasculitis
Erysipelas investigations
Clinical diagnosis: rarely do skin/blood culture
If suspect necrotizing fasciitis: do immediate biopsy and frozen section, histopathology
Erysipelas management
1st line: penicillin, cloxacillin or cefazolin
2nd line: clindamycin or cephalexin
If allergic to penicillin, use erythromycin
Cellulitis clinical presentation
Involves lower dermis/subcutaneous fat
Unilateral erythematous flat lesion, often with vesicles poorly demarcated, not uniformly raised
Tender
Sites: commonly on legs
Systemic symptoms (uncommon): fever, leukocytosis, lymphadenopathy
Cellulitis etiology
GAS
S. aureus (large sized wounds)
H. influenzae (periorbital)
Pasteurella multocida (dog/ cat bite)
Cellulitis complications
Uncommon
Cellulitis ddx
Same as erysipelas
Cellulitis investigations
Same as erysipelas
Cellulitis management
1st line: cloxacillin or cefazolin/cephalexin
2nd line: erythromycin or clindamycin Children: cefuroxime
If DM (foot infections): TMP/SMX and metronidazole
Common hair follicle infections
Superficial folliculitis
Furuncles (Boils)
Carbuncles
Superficial folliculitis clinical presentation
Superficial infection of the hair follicle (versus pseudofolliculitis: inflammation of follicle due to friction, irritation, or occlusion)
Acute lesion consists of a dome-shaped pustule at the mouth of hair follicle
Pustule ruptures to form a small crust
Sites: primarily scalp, shoulders, anterior chest, upper back, other hair-bearing areas
Superficial folliculitis etiology
Normal non-pathogenic bacteria (Staphylococcus – most common; Pseudomonas – hot tub)
Pityrosporum
Superficial folliculitis management
Antiseptic (Hibiclens)
Topical antibacterial (fusidic acid, mupirocin, erythromycin or clindamycin)
Oral cloxacillin for 7-10 d
Furuncles (boils) clinical presentation
Red, hot, tender, inflammatory nodules with central yellowish point, which forms over summit and ruptures
Involves subcutaneous tissue that arises from a hair follicle
Sites: hair-bearing skin (thigh, neck, face, axillae, perineum buttocks)
Furuncles (boils) etiology
S. aureus
Furuncles (boils) management
Incise and drain large furuncles to relive pressure and pain
If afebrile: hot wet packs, topical antibiotic
If febrile/cellulitis: culture blood and aspirate pustules (Gram stain and C&S)
Cloxacillin for 1-2 wk (especially for lesions near external auditory canal/ nose, with surrounding cellulitis, and not responsive to topical therapy)
Carbuncles clinical presentation
Deep-seated abscess formed by multiple coalescing furuncles
Usually in areas of thicker skin
Occasionally ulcerates
Lesions drain through multiple openings to the surface
Systemic symptoms may be associated
Carbuncles etiology
S. aureus
Carbuncles management
Same as for furuncles
Dermatophytoses clinical presentation
• infection of skin, hair, and nails caused by dermatophytes (fungi that live within the epidermal keratin or hair follicle and do not penetrate into deeper structures)
Dermatophytoses pathophysiology
• digestion of keratin by dermatophytes results in scaly skin, broken hairs, crumbling nails/onycholysis
Dermatophytoses etiology
Trichophyton, Microsporum, Epidermophyton species (Pityrosporum is a superficial yeast and not a dermatophyte)
Dermatophytoses investigations
• skin scrapings, hair, and/or nail clippings analyzed with potassium hydroxide (KOH) prep to look for hyphae and mycelia
Dermatophytoses management
- topicals as first line agents for tinea corporis/cruris and tinea pedis (interdigital type): clotrimazole, or terbinafine or ciclopirox olamine cream applied bid
- oral therapy is indicated for onychomycosis or tinea capitis: terbinafine (Lamisil® – liver toxicity, CYP2D6 inhibitor) or itraconazole (Sporanox® – CYP3A4 inhibitor, liver toxicity)
Tinea capitis clinical presentation
Round, scaly patches of alopecia, possibly with broken off hairs; pruritic
Sites: scalp, eyelashes, and eyebrows; involvng hair shafts and follicles
Kerion (boggy, elevated, purulent inflamed nodule/ plaque) may form secondary to infection by bacteria and result in scarring
May have occipital lymphadenopathy
Affects children (mainly black), immunocompromised adults
Very contagious and may be transmitted from barber, hats, theatre seats, pets
Tinea capitis ddx
Aloecia areata
psoriasis
seborrheic dermatitis
trichotillomania
Tinea capitis investigations
Wood’s light examination of hair: green fluorescence only for Microsporum infection
Culture of scales/hair shaft
Microscopic examination of KOH preparation of scales or hair shaft
Tinea capitis management
Terbinafine (Lamisil) x 4 weeks
NB: oral agents are required to penetrate the hair root where dermatophyte resides
Adjunctive antifungal shampoos or lotions may be helpful, and may prevent spread (e.g. selenium sulfide, ketoconozole, ciclopirox)
Tinea corporis (ringworm) clinical presentation
Pruritic, scaly, round/oval plaque with active erythematous margin, and central clearing
Site: trunk, limbs, face
Tinea corporis (ringworm) ddx
Granuloma annulare, pityriasis rosea, psoriasis, seborrheic dermatitis
Tinea corporis (ringworm) investigations
Microscopic examinations of KOH prep of scales shows hyphae
Culture of scales
Tinea corporis (ringworm) management
Topicals: 1% clotrimaole, 2% ketoconazole 2% miconazole, terbinafine or ciclopirox olamine cream bid for 2-4 wk
Oral terbinafine, or itraconazole, or fluconazole, or ketoconazole if extensive
Tinea Cruris (“jock itch”) clinical presentation
Scaly patch/plaque with a well-defined, curved border and central clearing
Pruritic, erythematous, dry/macerated
Site: medial thigh
Tinea Cruris (“jock itch”) ddx
Candidiasis (involvement of scrotum and satellite lesions), contact dermatitis, erythrasma
Tinea Cruris (“jock itch”) investigations
Same as for tinea corporis
Tinea Cruris (“jock itch”) management
Same as for tinea corporis
Tinea pedis (athlete’s foot) clinical presentation
Pruritic scaling and/or maceration of the web spaces, and powdery scaling of soles
Acute infection: interdigital (especially 4th web space) red/white scales, vesicles, bullae, often with maceration
Secondary bacterial infection may occur
Chronic: non-pruritic, pink, scaling keratosis on soles and sides of feet
May present as flare-up of chronic tinea pedis
Predisposing factors: heat, humidity, occlusive footwear
Tinea pedis (athlete’s foot) ddx
AD, contact dermatitis, dyshidrotic dermatitis, erythrasma, intertrigo, inverse psoriasis
Tinea pedis (athlete’s foot) investigations
same as for tinea corporis
Tinea pedis (athlete’s foot) management
same as for tinea corporis
Tinea manuum clinical presentation
Primary fungal infection of the hand is rare; usually associated with tinea pedis
Acute: blisters at edge of red areas on hands
Chronic: single dry scaly patch
Tinea manuum ddx
AD, contact dermatitis, granuloma annulare, psoriasis
Tinea manuum investigations
same as for tinea corporis
Tinea manuum management
same as for tinea corporis
Tinea unguium (onychomycosis) clinical presentation
Crumbling, distally dystrophic nails; yellowish, opaque with subungual hyperkeratotic debris
Toenail infections usually precede fingernail infections
T. rubrum (90% of all toenail infections)
Tinea unguium (onychomycosis) ddx
Psoriasis, lichen planus, contact dermatitis, traumatic onychodystrophies, bacterial infections
Tinea unguium (onychomycosis) investigations
Microscopic examinations of KOH prep of scales from subungual scraping shows hyphae Culture of subungual scraping or nail clippings on Sabouraud’s agar PAS stain of nail clipping by patholog
Tinea unguium (onychomycosis) management
Terbinafine (Lamisil) (6 wk for fingernails, 12 wk for toenails)
Itraconazole (Sporanox®) 7 d on, 3 wk off (2 pulses for fingernails 3 pulses for toenails)
Topical: ciclopirox (Penlac®); nail lacquer (often ineffective), Efinaconazole (Jublia®) (48 wk)
Scabies clinical presentation
- characterized by superficial burrows, intense pruritus (especially nocturnal), and secondary infection
- primary lesion: superficial linear burrows; inflammatory papules and nodules in the axilla and groin
- secondary lesion: small urticarial crusted papules, eczematous plaques, excoriations
- common sites: axillae, groin, buttocks, hands/feet (especially web spaces), sparing of head and neck (except in infants)
Scabies pathophysiology
- scabies mite remains alive 2-3 d on clothing/sheets
- incubation of 1 mo, then pruritus begins
- re-infection followed by hypersensitivity in 24 h
Scabies etiology
- Sarcoptes scabiei (a mite)
* risk factors: sexual promiscuity, crowding, poverty, nosocomial, immunocompromised
Scabies differential diagnosis
• asteatotic eczema, dermatitis herpetiformis, lichen simplex chronicus (neurodermatitis)
Scabies investigations
- microscopic examination of root and content of burrow and mineral oil mount for mite, eggs, feces
- skin biopsy may sometimes show scabies mite
Scabies management
- bathe, then apply permethrin 5% cream (i.e. Nix®) from neck down to soles of feet (must be left on for 8-14 h and requires second treatment 7 d after first treatment)
- change underwear and linens; wash twice with detergent in hot water cycle then machine dry
- treat family and close contacts
- pruritus may persist for 2-3 wk after effective treatment due to prolonged hypersensitivity reaction
- mid potency topical steroids and antihistamines for symptom management
Lice (pediculosis) clinical presentation
- intensely pruritic red excoriations, morbilliform rash, caused by louse (a parasite)
- scalp lice: nits (ie louse eggs) on hairs; red, excoriated skin with secondary bacterial infection, lymphadenopathy
- pubic lice: nits on hairs; excoriations
- body lice: nits and lice in seams of clothing; excoriations and secondary infection mainly on shoulders, belt-line and buttocks
Lice (pediculosis) etiology
- Phthirus pubis (pubic), Pediculus humanus capitis (scalp), Pediculus humanus humanus (body): attaches to body hair and feeds
- can transmit infectious agents such as Bartonella quintana and Rickettsia prowazekii
Lice (pediculosis) differential diagnosis
bacterial infection of scalp
seborrheic dermatitis
Lice (pediculosis) diagnosis
lice visible on inspection of affected area or clothing seams
Lice (pediculosis) management
- permethrin 1% (Nix® cream rinse) (ovicidal) or permethrin 1% (RC & Cor®, Kwellada-P® shampoo)
- comb hair with fine-toothed comb using dilute vinegar olution to remove nits
- repeat in 7 d after first treatment
- shave hair if feasible, change clothing and linens; wash with detergent in hot water cycle then machne dry
Bed bugs (hemiptera) clinical presentation
burning wheals, turning to firm papules, often in groups of three – “breakfast, lunch and dinner” – in areas with easy access (face, neck, arms, legs, hands)
Bed bugs (hemiptera) etiology
• caused by Cimex lectularius, a small insect that feeds mainly at night (hide in crevices in walls and furniture during the day)
Bed bugs (hemiptera) differential diagnosis
dermatitis herpetiformis, drug eruptions, ecthyma, other insect bites, scabies
Bed bugs (hemiptera) investigations
none required, but lesional biopsy can confirm insect bite reaction
Bed bugs (hemiptera) management
- professional fumigation
- topical steroids and oral H1-antagonists for symptomatic relief
- definitive treatment is removal of clutter in home and application of insecticides to walls and furniture
Herpes simplex clinical presentation
- herpetiform (i.e. grouped) vesicles on an erythematous base on skin or mucous membranes
- transmitted via contact with erupted vesicles or via asymptomatic viral shedding
• primary
■ children and young adults
■ usually asymptomatic; may have high fever, regional lymphadenopathy, malaise
■ followed by antibody formation and latency of virus in dorsal nerve root ganglion
• secondary
■ recurrent form seen in adults; much more common than primary
■ prodrome: tingling, pruritus, pain
■ triggers for recurrence: fever, excess sun exposure, physical trauma, menstruation, emotional stress, URTI
• complications: dendritic corneal ulcer, EM, herpes simplex encephalitis (infants at risk), HSV infection on AD causing Kaposi’s varicelliform eruption (eczema herpeticum)
• two biologically and immunologically different subtypes: HSV-1 and HSV-2
■ HSV-1
◆ typically “cold sores” (grouped vesicles at the mucocutaneous junction which quickly burst)
◆ recurrent on face, lips and hard palate, but NOT on soft, non-keratinized mucous membranes (unlike aphthous ulcers)
■ HSV-2
◆ usually sexually transmitted; incubation 2-20 d
◆ gingivostomatitis: entire buccal mucosa involved with erythema and edema of gingiva
◆ vulvovaginitis: edematous, erythematous, extremely tender, profuse vaginal discharge
◆ urethritis: watery discharge in males
◆ recurrent on vulva, vagina, penis for 5-7 d
Herpes simplex investigations
- Tzanck smear with Giemsa stain shows multinucleated giant epithelial cells
- viral culture, electron microscopy, and direct fluorescence antibody test of specimen taken from the base of a relatively new lesion
- serologic testing for antibody for current or past infection if necessary
Herpes simplex management HSV 1
■ treat during prodrome to prevent vesicle formation
■ topical antiviral (Zovirax®/Xerese®) cream, apply 5-6x/d x 4-7 d for facial/genital lesions
■ oral antivirals (e.g. acyclovir, famciclovir, valacyclovir) are far more effective and have an easier dosing schedule than topicals
Differential diagnosis of genital ulcers
Candida balanitis, chancroid syphilitic chancres
Herpes simplex HSV 2 management
■ rupture vesicle with sterile needle if you wish to culture it
■ wet dressing with aluminum subacetate solution, Burow’s compression, or betadine solution
■ 1st episode: acyclovir 200 mg PO 5x/d x 10 d
◆ maintenance: acyclovir 400 mg PO bid
■ famciclovir and valacyclovir may be substituted and have better enteric absorption and less frequent dosing
■ in case of herpes genitalis, look for and treat any other sexually-transmitted infections STIs
■ for active lesions in pregnancy, see Obstetrics
Erythema Multiforme etiology
most often HSV or mycoplasma pneumoniae, rarely drugs
Erythema multiforme morphology
macules/papules with central vesicles; classic bull’s-eye pattern of concentric light and dark rings (typical target lesions)
Erythema multiforme management
symptomatic treatment (oral antihistamines, oral antacids)
corticosteroids in severely ill (controversial)
prophylactic oral acyclovir for 6-12 mo for HSV-associated EM with frequent recurrences
Herpes zoster (shingles) clinical presentation
- unilateral dermatomal eruption occurring 3-5 d after pain and paresthesia of that dermatome
- vesicles, bullae, and pustules on an erythematous, edematous base
- lesions may become eroded/ulcerated and last days to weeks
- pain can be pre-herpetic, synchronous with rash, or post-herpetic
- severe post-herpetic neuralgia often occurs in elderly
- Hutchinson’s sign: shingles on the tip of the nose signifies ocular involvement. Shingles in this area involves the nasociliary branch of the ophthalmic branch of the trigeminal nerve (V1)
- distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV
Herpes zoster (shingles) etiology
- caused by reactivation of VZV
* risk factors: immunosuppression, old age, occasionally associated with hematologic malignancy
Herpes zoster (shingles) differential diagnosis
- before thoracic skin lesions occur, must consider other causes of chest pain
- contact dermatitis, localized bacterial infection, zosteriform HSV (more pathogenic for the eyes than VZV)
Herpes zoster (shingles) investigations
• none required, but can do Tzanck test, direct fluorescence antibody test, or viral culture to rule out HSV
Herpes zoster (shingles) management
- compress with normal saline, Burow’s, or betadine solution
- analgesics (NSAIDs, amitriptyline)
- famciclovir, valacyclovir, or acyclovir for 7 d; must initiate within 72 h to be of benefit
- gabapentin 300-600 mg PO tid for post-herpetic neuralgia
Herpes zoster distribution
Herpes zoster typically involves a single dermatome; lesions rarely cross the midline
Molluscum contagiosum clinical presentation
- discrete dome-shaped and umbilicated pearly, white papul s caused by DNA Pox virus (Molluscum contagiosum virus)
- common sites: eyelids, beard (likely spread by shaving), neck, axillae, trunk, perineum, buttocks
Molluscum contagiosum etiology
- virus is spread via direct contact, auto-inoculation, sexual contact
- common in children and sexually active young adults (giant molluscum and severe cases can be seen in the setting of HIV)
- virus is self-limited and can take 1-2 yr to resolve
Molluscum contagiosum investigations
none required, however can biopsy to confirm diagnosis
Molluscum contagiosum management
- topical cantharidin (a vesicant)
- cryotherapy
- curettage
- topical retinoids
- Aldara® (imiquimod): immune modulator that produces a cytokine inflammation
Manifestations of HPV infection
Verruca vulgaris (common warts)
Verruca plantaris (plantar warts) and verruca palmaris (palmar warts)
Verruca planae (flat warts)
Condyloma acuminata (genital warts)
Verruca vulgaris (common warts) definition and clinical features
Hyperkeratotic, elevated discrete epithelial growths with papillated surface caused by HPV
Paring of surface reveals punctate, red-brown specks (thrombosed capillaries)
Verruca vulgaris (common warts) differential diagnosis
molluscum contagiosum
seborrheic keratosis
Verruca vulgaris (common warts) distribution
located at trauma sites: fingers, hands, knees of children and teens
Verruca vulgaris (common warts) hpv type
at least 80 types are known
Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) definition and clinical features
Hyperkeratotic, shiny, sharply marginated growths Paring of surface reveals red-brown specks (capillaries), interruption of epidermal ridges
Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) differential diagnosis
May need to scrape (“pare”) lesions to differentiate wart from callus and corn
Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) distribution
Located at pressure sites: metatarsal heads, heels, toes
Verruca plantaris (plantar warts) and verruca palmaris (palmar warts) hpv type
commonly HPV 1, 2, 4, 10
Verruca planae (flat warts) definition and clinical features
Multiple discrete, skin coloured, flat topped papules grouped or in linear configuration
Common in children
Verruca planae (flat warts) differential diagnosis
Syringoma, seborrheic keratosis, molluscum contagiosum, lichen planus
Verruca planae (flat warts) distribution
Sites: face, dorsa of hands, shins, knees
Verruca planae (flat warts) hpv type
commonly HPV 3, 10
Condyloma acuminata (genital warts) definition and clinical features
Skin-coloured pinhead papules to soft caulflower like masses in clusters
Often occurs in young adults, infants, children
Can be asymptomatic, lasting months to years
Highly contagious, transmitted sexually and non-sexually (e.g. Koebner phenomenon via scratching, shaving), and can spread without clinically apparent lesions
Condyloma acuminata (genital warts) ddx
Condyloma lata (secondary syphilitic lesion, dark field strongly +ve), molluscum contagiosum
Condyloma acuminata (genital warts) distribution
Sites: genitalia and perianal areas
Condyloma acuminata (genital warts) hpv type
Commonly HPV 6 and 11
HPV 16, 18, 31, 33 cause cervical dysplasia, SCC and invasive cancer
Condyloma acuminata (genital warts) investigations
acetowhitening (subclinical lesions seen with 5% acetic acid x 5 min and hand lens)
Condyloma acuminata (genital warts) complications
fairy-ring warts (satellite warts at periphery of treated area of original warts)
Treatment for warts
• first line therapies
■ salicylic acid preparations (patches, solutions, creams ointments), cryotherapy, topical cantharone
• second line therapies
■ topical imiquimod, topical 5-fluorouracil, topical tretinoin, podophyllotoxin
• third line therapies
■ curettage, cautery, surgery for non plantar warts, CO2 laser, oral cimetidine (particularly children), intralesional bleomycin (plantar warts), trichloroacetic acid, diphencyprone
• other viruses associated with skin changes, such as measles, roseola, fifth disease, etc.
Candidiasis etiology
- many species of Candida (70-80% of infections are from Candida albicans)
- opportunistic infection in those with predisposing factors (e.g. trauma, malnutrition, immunodeficiency)
Candidal paronychia clinical presentation
painful red swellings of periungual skin
Candidal paronychia management
topical agents not as effective; oral antifungals recommended
Candidal intertrigo clinical presentation
■ macerated/eroded erythematous patches that may be covered with papules and pustules, located in intertriginous areas often under breast, groin, or interdigitally
■ peripheral “satellite” pustules
■ starts as non-infectious maceration from heat, moisture, and friction
Candidal intertrigo predisposing factors
obesity, DM, systemic antibiotics, immunosuppression, malignancy
Candidal intertrigo management
keep area dry, terbinafine, ciclopirox olamine, ketoconazole/clotrimazole cream bid until rash clears
Why is oral Terbinafine not used for candidiasis intertrigo
Oral Terbinafine (Lamisil®) is not effective because it is not secreted by sweat glands
Pityriasis (tinea) versicolour clinical presentation
- asymptomatic superficial fungal infection with brown/white scaling macules
- affected skin darker than surrounding skin in winter, lighter in summer (does not tan)
- common sites: upper chest and back
Pityriasis (tinea) versicolour pathophysiology
- microbe produces azelaic acid → inflammatory reaction inhibiting melanin synthesis yielding variable pigmentation
- affinity for sebaceous glands; require fatty acids to survive
Pityriasis (tinea) versicolour etiology
- Pityrosporum ovale (Malassezia furfur)
- also associated with folliculitis and seborrheic dermatitis
- predisposing factors: summer, tropical climates, excessive sweating, Cushing’s syndrome, prolonged corticosteroid use
Pityriasis (tinea) versicolour investigations
clinical dagnosis but can perform microscopic examination, KOH prep of scales for hyphae and spores
Pityriasis (tinea) versicolour management
- ketoconazole shampoo or cream daily
- topical terbinafine or ciclopirox olamine bid
- systemic fluconazole or itraconazole for 7 d if extensive
Syphilis clinical presentation
- characterized initially by a painless ulcer (chancre)
* following inoculation, systemic infection with secondary and tertiary stages
Syphilis etiology
- Treponema pallidum
* transmitted sexually, congenitally, or rarely by transfusion
Primary syphilis clinical presentation
Single red, indurated, painless chancre, that deveops into painless ulcer with raised border and scanty serous exudate
Chancre develops at site of inoculation after 3 wk of incubation and heals in 4-6 wk; chancre may also develop on lips or anus
Regional non-tender lymphadenopathy appears <1 wk after onset of chancre
Primary syphilis investigations
CANNOT be based on clinical presentation alone
VDRL negative – repeat weekly for 1 mo
Fluorescent treponemal antibody-syphilis (FTA-ABS) test has greater sensitivity and may detect disease earlier in course
Dark field examination – spirochete in chancre fluid or lymph node aspirate
Primary syphilis management
Penicillin G, 2.4 million units IM, single dose
Primary syphilis ddx
chancroid (painful), HSV (multiple lesions)
Natural history of untreated syphilis
- Inoculation
- Primary syphilis (10-90 d after infection)
- Secondary syphilis (simultaneous to primary syphilis or up to 6 mo after healing of primary lesion)
- Latent syphilis
- Tertiary syphilis (2-20 yr)
Secondary syphilis clinical presentation
Presents 2-6 mo after primary infection (patient may not recall presence of primary chancre)
Associated with generalized lymphadenopathy, splenomegaly, headache, chills, fever, arthralgias, myalgias, malaise, photophobia
Lesions heal in 1-5 wk and may recur for 1 yr
3 types of lesions:
- Macules and papules: flat top, scaling nonpruritic, sharply defined, circular/annular rash (DDx: pityriasis rosea, tinea corporis, drug eruptions, lichen planus)
- Condyloma lata: wart-like moist papules around genital/perianal region
- Mucous patches: macerated patches mainly found in oral mucosa
Secondary syphilis investigations
VDRL positive
FTA-ABS +ve; –ve after 1 yr following appearance of chancre
Dark field +ve in all secondary
Secondary syphilis management
same as primary syphilis
Tertiary syphilis clinical presentation
Extremely rare 3-7 yr after secondary
Main skin lesion: ‘Gumma’ – a granulomatous nontender nodule
Tertiary syphilis investigations
As in primary syphilis, VDRL can be falsely negative
Tertiary syphilis management
Treatment: penicillin G, 2.4 million units IM weekly x 3 wk
Latent syphilis
70% of untreated patients will remain in this stage for the rest of their lives and are immune to new primary infection
Gonococcemia clinical presentation
- disseminated gonococcal infection
- hemorrhagic, tender, pustules on a purpuric/petechial background
common sites: distal aspects of extremities
- associated with fever, arthritis, urethritis, proctitis, pharyngitis, and tenosynovitis
- neonatal conjunctivitis if infected via birth canal
Gonococcemia etiology
Neisseria gonorrhoeae
Gonococcemia investigations
- requires high index of clinical suspicion plays because tests are often negative
- bacterial culture of blood, joint fluid, and skin lesions
- joint fluid cell count and Gram stain
Gonococcemia management
- notify Public Health authorities
- screen for other STIs
- cefixime 400 mg PO (drug of choice) or ceftriaxone 1 g IM
