Skin Infections and Infestations Flashcards
Give 6 examples of vesicular or vesiculobullous eruptions
- Herpes Simplex I and II
- Varicella
- Herpes Zoster
- Impetigo
- Bullous Insect Bite Reaction
- Primary Skin Bullous Disorder (e.g. pemphigus)
For HSV I and II describe: the morphology, how to diagnose, spread.
Morphology: grouped vesicles on erythematous base
Dx: Mostly based on morphology (however, cannot tell apart type I and 2 by morph).
Ancillary tests include Tzanck Smear, viral culture, antibody testing and skin biopsy
Spread: Virus can be shed in presence or absence of a visible lesion. Most of the adult population has been exposed
Where does latent HSV reside and what can precipitate a recurrent infection?
Latent virus persists in sensory ganglia.
Can be ppt’d by menses, fever, URTI, immunodeficiency.
Prevalence of labialis vs urogenital HSV 1 and 2
Labialis: 70-80% HSV 1, 10-20% HSV 2
Urogenital: 70-90% HSV 2, 10-30% HSV 1
Describe the appearance of varicella (aka chicken pox)
‘Dewdrop on rose petal’ appearance
Initial lesions are papules which develop into vesicles
Vesicles eventually crust over
May heal with scarring
Crops of lesions in all stages of evolution
‘Christmas tree’ distribution due to hematogenous spread
Etiology of varicella and testing options.
Caused by varicella zoster virus.
Testing: viral culture, Tzanck smear or skin biopsy
Describe the onset and appearance of Herpes Zoster
Prodrome of neuritic pain for days to weeks.
Acute vesicles then crusted papules.
Distribution is unilateral and dermatomal.
Morphology of grouped vesicles on erythematous base.
Etiology and testing options for herpes zoster
Etiology: reactivation of latent varicella zoster-virus
Testing: viral culture, Tzanck smear or skin bx
Re: Tzanck smear: shows multinucleated keratinocytes or acantholytic keratinocytes. Can be used to diagnose herpes infections but won’t tell you what type of herpes.
Re: skin biopsy: there are identical histological changes in HSV, varicella and herpes zoster.
Describe nonbullous impetigo.
Scaling, honey crusted lesions.
Superficial infection of epidermis caused by GAS or staph aureus.
Dx by gram stain and culture
Describe bullous impetigo.
Vesicles and bullae form and are clear or slightly yellow.
Shallow erosions may be present if bullae break.
Caused by staph aureus
Dx with gram stain and culture
Describe the general appearance of arthropod bites
Grouped into papules or vesicles.
‘Breakfast-lunch-dinner’ pattern.
Pruritic or urticarial papules that may be painful.
Can occur minutes to days after bite.
Impossible to differentiate the cause of the biting organism.
Potential sources of arthropod bites
Mites, ticks, spiders, centipedes, millipedes, mosquitoes, black flies, sand flies, bedbugs, ants, bees, wasps, hornets, fleas.
When should you suspect a bedbug infection in a patient?
- Well-traveled patients (no association with socio-economic status)
- note that often only one person will be bitten
Appearance:
- Erythematous papules, vesicles and nodules
- Red-brown colour the size of a ladybug
- Will often bite on body, neck and head areas
Information about bedbug environment, disease risk and follow up for patients.
Know their environment: nocturnal but not limited to beds, often under mattresses, in appliances, behind pictures.
Bedbugs are not disease vectors.
Pt will need to call in an exterminator.
Give 4 examples of follicular eruptions
- Pityrosporum folliculitis (yeast)
- Pseudomonas folliculitis (think hot tubs!)
- Staphylococcal folliculitis
- Acne
How to differenitate follicular eruptions:
- Pseudomonas: Ask about history of exposure to hot tub or other people with similar disorder.
- Distribution of folliculitis.
- Acne will have comedones, papules, nodules and cysts.
- Staph and pseudomonas infections tend to be more inflammatory than Pityrosporum
- KOH and cultures are helpful
Describe pityrosporum folliculitis
What it is: condition where yeast (pityrosporum) get into the hair follicles and multiply, causing an itchy, acne-like eruption.
Apperance:
- monomorphous papules without comedones
- Often sweaty individuals
- culture negative but KOH positive
Describe pseudomonas folliculitis
Community-acquired skin infection, which results in pseudomonas colonization of hair follicles after exposure to contamined water.
- Ask about Hhx of hot tub exposure
- often greater than one person affected
- Inflammatory follicular-based papules and pustules
- Involves exposed areas
- Culture +ve for pseudomonas
- self-limited so treated not necessary
- hot tub needs to be cleaned and pH adjusted
Staphylococcal folliculitis
- Inflammatory pustules
- Gram stain and culture positive for staph aureus
5 examples of annular (ring shaped) and scaling eruptions
- Tinea corporis (ring worm)
- Tinea versicolour
- Secondary syphilis
- Psoriasis
- Nummular eczema (discoid eczema)
Approach to scaling eruptions
- Scrap the scaling edge for KOH (used to Dx fungal infections) and culture
- Look at distribution: psoriasis is symmetrical and on extensor surfaces
- Tinea versicolour: non-inflammatory brown and white scaling patches
- Tinea corporis: few lesions with central clearing
What is tinea corporis and what does it look like?
Aka ringworm. Superficial fungal (dermatophyte) infection with predilection for arms and legs.
- Annular, sealing edge
- well demarcated plaques
- Central clearing
- Single or multiple lesions
- usual asymmetrical
Etiology and diagnosis of tinea corporis
Dx: scrap scaling edge for KOH and culture
Trichophyton rubrum: most common (may be innoculated from other body sites)
Microsporum canis: if exposed to animals
Ringworm/Dermatophytosis: look for fungal hyphae on PAS stain
Describe appearance of tinea versicolour (Pityriasis Versicolor)
Well marginated round scaling brown or light macules
Etiology of tinea versicolour
Caused by Malassezia furfur or Pityrosporum versicolour
Risk factors for tinea versicolour
Common in young adults
Risk factors: warm and humid climates, oily skin, hyperhidrosis (aka increased sweating)
Appearance of tinea versiclour on KOH stain
positive KOH microscopy will show scale with ‘spaghetti and meatballs’ spores and hyphae (do not culture suspected tinea versicolour)
DDx for tinea versicolour
Vitiligo, pityriasis alba, post-inflammatory hypopigmentation
Describe the onset/appearance of secondary syphillis skin manifestations
Occurs 2-6 months post-primary infection
+/- Hx of painless ulcer from primary syph
Great mimic: look for involvement of palms and soles.
First eruption is macular then can be papulosquamous, pustular or acneiform.
Condylomata lata: flat-topped papules in moist areas, especially mouth and ano-genital.
Etiology and diagnosis of secondary syph
Etiology: treponema pallidum infection
Diagnosis: serological testing or skin Bx
Describe the appearance of verruca vulgaris
Firm, hyperkeratotic papules with clefted surface and vegetations
Red or brown dots are caused by thrombosed capillary loops
Etiology and transmission of verruca vulgaris
Verruca vulgaris: aka common wart. Benign growth caused by HPV infection in the skin.
Transmitted by skin-skin contact.
Breaks in stratum corneum facilitate epidermal infection.
Describe the appearance of molluscum contagiosum.
Skin coloured umbilicated papules.
Gentle pressure can cause the central keratotic plug to extrude.
Mollusca undergoing spotaneous regression may have an erythematous halo.
Etiology and spread of molluscum contagiosum
Caused by pox virus and spread through skin-skin contact.
Aka water waters.
Common in children, sexually active adults and HIV+ pts.
Describe the appearance (morphological, distributive and temporal) of scabies
Widespread pruritic eczematous eruption.
Spares heads and neck except in infants and elderly
Eruption caused by hypersensitivity to mite so can take 6 weeks from exposure to develop.
Pruritis is often nocturnal
Burrows: serpiginous (skin lesion with wavy margin) track with spot at end (scrape burrow for Dx)
Nodules: red-brown nodules in axillary area and groin, can persist after infection is clear
Describe Norwegian scabies
Refers to heavy infestation of scabies in an immunocompromised host. Highly contagious and requires repeated treatments
Describe pediculosis corporis
An eczematous eruption with no primary lesion, secondary infections are common. Aka BODY LICE.
Seen in crowded conditions and associated with poverty
Etiology: peduculosis humanus humanus (body louse)
Transmit infections: trench fever, epidemic typhus
Louse: look in seams of clothing for louse and nits
Differentiate ectothrix, endothrix and kerion tinea capitus infections
All caused by infection of hair by dermatophyte.
Ectothrix: Infection OUTSIDE of hair shaft. May present as partial alopecia with broken hair shafts. Microsporum spp
Endothirx: Infection WITHIN hair shaft. Black dot tinea capitus. Hair breaks off near surface. Trichophyton spp
Kerion: inflammatory mass with boggy plaques
Describe pediculosis capitis
Pruritis of the scalp caused by head lice/nits.
Bite reactions include: eczema, excoriation and lichenification.
Caused by: pediculosis humanis capitis
Transmitted by shared hats, brushes, head-head contact
Describe Tinea cruris appearance
Well marginated, scaling red plaques with central clearing
Papules and pustules may present at margins
Occurs in inguinal area and thighs
Describe candida intertrigo
Erythematous plaque with satellite papules and pustules
Found in moist environments
Risk factors: immunocompromised, topical steroid use, DM
DDx: contact dermatitis, seborrheic dermatitis, inverse psoriasis, dermatophyte infection
Dx: swab for gram stain and culture
Describe erythrasma
Sharply marginated patch
Prediliction for folds: toe web spaces, groin, axillae, intergluteal, inframammary
Etiology: cornybacterium minutissimum
Epidemiology: adults, humid weather, obesity, tight clothes
Dx: coral red fluorescence of Wood’s light, bacterial culture +ve for minutissimum, absence of fungi on KOH
Describe Inverse Psoriasis
Well marginated erythematous plaques.
Check for psoriasis elsewhere, scalp, fingernails.
Tends not to scale like psoriasis elsewhere.
KOH negative.
Describe cellulitis
Skin infection extending into the subQ tissue.
Presents as painful firm area of erythema.
Malaise, fever, chills may be present.
May form bullae or undergo necrosis with epidermal sloughing.
Common causes: Staph aureus or GAS. Also Hib in children.
DDx: DVT, stasis dermatitis, contact dermatitis, erysipelas
Risk factors: interdigital tinea, IVDU if arm, operative wound site
Dx: clinical, wound cultures if exudative
What is folliculitis?
Pusutues that are pierced by a hair follicle.
Superficial infection of the hair follicle.
Acute lesion: dome-shaped pustule at the mouth of hair follicle.
Late lesion: pustules rupture, crust forms
Sites: scalp, shoulders, anterior chest, upper back
Localized infection may spread deeper and wider
What are furuncles (boils)?
Follicular staph infection that spreads and involves the tissue around the hair follicle.
Firm erythematous nodule early on. Later fluctuant erythematous nodule.
Very tender and painful
Common sites: face, neck, axilla, buttoks, perineum, thighs
Course: red, tender, nodule points –> ruptures
What is a carbuncle?
Forms as several furuncles connect subcutaneously.
Larger and deeper than furuncles.
Typically caused by staph aureus.
Sites: hair bearing skin, prefer back of neck in men.
Lesions drain through multiple sites to the skin surface.
Diabetes predisposes to carbuncles.
What is an abscess?
Forms when furuncles/carbuncles are not treated adequately.
Subcutenaous tissue liquefies, forms granulomatous ‘pus pocket’
Signs: tender, swollen areas of reddened skin, hot and tender to touch
Can progress via hematogenous or lyphatic spread –> ultimately seed to other end organs.
Sepsis, pneumonia, arthritis, osteomyelitis and endocarditis can subsequently develop.
Describe a flat wart
‘Verruca plana’
Sharply defined flat skin coloured or brown papules, 1-2 mm thick
DDx: seborrheic keratoses, skin tags
Hard to spread but can be spread by shaving
Describe a plantar wart
Has multiple capillary loops- these distinguish warts from calluses.
Plantar warts are very common, often acquired at swimming pools.
Mosaic warts.
Describe HPV condylomata
Perianal condylomata are caused by HPV
Transmission is primarily sexual
Etiology: HPV6, 11 most common
HPV types 16,18,31,35 associated with cancer
HPV vax can decrease incidence of infection.
DDx: condylomata lata of secondary syph, seborrheic keratosis, skin tags
Dx: clinical, Bx can differentiate if clinically challenging
Describe tinea unguium
Causes thick, yellow, dystrophic toenails or fingernails
Toenails more commonly involved.
Genetic predisposition to infection and often associated with tinea pedis
Etiology: Trichophyton rubrum most common.
DDx: psoriasis, traumatic changes
Dx: scrape under toe for KOH and culture
Describe tinea pedis (what are the 3 types?)
Aka Athlete’s foot
Interdigital type: area of scaling, maceration and fissures. Often between 4th/5th toes
Moccasin type: well-marginated erythema with fine scale and hyperkeratosis
Inflammatory or bullous type: vesicles filled with clear fluid
Transmitted by walking barefoot on contaminated ground (e.g. pool).
Etiology: trichophyton, microsprum, epidermophyton
Dx: hyphae on KOH, culture +ve for dermatophyte
DDx: erythrasma, psorasis, eczema
