malignancy, initial BSA detached >10%,

tachycardia >120 bpm. serum urea >10

mmol/L serum glucose >14 mmol/L,

serum bicarbonate <20mmol/L

Used to determine appropriate clinical

setting:score 0-1can be treated in nonspecialized wards;score >2 should be

transferred to intensive care or bum unit

Score at admission is predictive of

survival: 94% for 0-1,87% for 2.53% for

3.25% for 4, and 17% for zS

Systemic ImmunomodutatingTherapies for

Stevens-Johnson Syndrome and Toxic Epidermal

He crolysis:ASystematicReview and Melaanalysis

JAMA Dermatol 2017:153:514-522

Purpose:To examine possible immunomodulating

treatmentsfor SJS/IEH and estimate mortality effect

compared to suppoHue tare.

Methods:Systematic renew ol randomited

and nonraodomindstudietoflsystemic

mmunomodulating therapies or suppotlnre cere

lot SJS/IEH.

Results: Ninety-six strides with 3248 patients

were included in the final analysis.Glucocorticoids

were associated writha survival benefit for patients

{aggregate - OR Oi.95% Cl 0.3-101).Though findings

were limited In a small number of patients overall,

cyclosporine was associated with significant benefit

(OR 0.1:95% Cl 0.0-0.4).No beneficial effects were

observed with other therapies, including IVIg.

Conclusion:( hough based on limited evidence,

glucocorticoids and cyclosporinewere most promising

as SJS/fEN immunosuppressive therapies.

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, cyclosporine, or etanercept

Other

FIXED DRUG ERUPTION

Clinical Features

• 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)

Epidemiology

• common causative agents:antimicrobials (tetracycline,sulfonamides), anti-inflammatories,

psychoactive agents (barbiturates), phenolphthalein

n

LJ

+

Management

• discontinue offending drug ± prednisone I mg/kg/d x 2 wk for generalized lesions

• potent topical corticosteroids for non-eroded lesions or antimicrobial ointment for eroded lesions

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D27 Dermatology Toronto Notes 2023

PHOTOSENSITIVITY REACTION

Clinical Features

• phototoxic reaction:“exaggerated sunburn” (erythema, edema, vesicles, bullae) confined to sunexposed areas

• photoaliergic reaction: pruritic eczematous eruption with papules, vesicles,scaling,and crusting that

may spread to areas not exposed to light

Pathophysiology

• phototoxic reaction:direct tissue injury

• photoaliergic reaction: type IV delayed hypersensitivity

Epidemiology

• common causative agents:chiorpromazine, doxycycline, thiazide diuretics, procainamide

Management

• sun protection ± topical/oral corticosteroids

Heritable Disorders

Ichthyosis Vulgaris

Clinical Features

• xerosis with fine scaling as well aslarge adherentscales(“fish-scales”)

• affects arms,legs, palms,soles,back,forehead,and cheeks;sparesflexural creases

• improves in summer, with humidity, and asthe child grows into adulthood

Pathophysiology

• genetic deficiency in filaggrin protein leads to abnormal retention of keratinocytes (hyperkeratosis)

• scaling without inflammation

Epidemiology

• 1:300 incidence

• autosomal dominant inheritance

• associated with AD and keratosis pilaris

Investigations

• electron microscopy:keratohvalin granules

Management

• immersion in bath and oilsfollowed by an emollient cream, humectant cream,or creams/otl

containing urea or a- or (5-hydroxv acids

• intermittentsystemic retinoidsfor severe cases

Epidermolysis Bullosa

Clinical Features

• blisters and erosions on skin and mucous membranesfollowing minor trauma

• extracutaneous manifestation may occur in severe disease and include intraoral blistering and

erosions, naii abnormalities, esophagealstrictures, and genitourinary abnormalities

Pathophysiology

• group of rare inherited diseases caused by mutations in genes coding forstructural proteins involved

in basement membrane of skin

Differential Diagnosis

• friction blisters, epidermolysis bullosa acquisita

Investigations

• skin biopsy for immunofluorescence mapping

Management

• symptomatic management

• avoid inducing friction on skin

• place padding on furniture

• wear loose clothing and appropriate footwear

• maintain cool ambient room temperature

n

«. J

+

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D28 Dermatology Toronto Notes 2023

Neurofibromatosis (Type I; von Recklinghausen’s Disease)

Clinical Features

• diagnostic criteria includes 2 or more of the following, if parent not diagnosed with NF1:

1.6 or more cafe-au-lait patches>1.5 cm in an adult or 6 or more cafe-au-lait macules >0.5 cm in

prepubertal individuals

2.axillary or inguinal freckling

3.2 or more iris hamartomas (lisch nodules)

4.optic glioma

5.2 or more neurofibromas of any type or one plexiform neurofibroma

6.distinctive bony lesion (sphenoid wing dysplasia or thinning oflong bone cortex)

7. heterozygous pathogenic NH variant with a variant allele fraction of 50% in normal tissue

• a child of a parent who meets the diagnostic criteria above needs I or more to be diagnosed with NT1

• 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 11 (see Paediatrics. PS9)

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 tumoursuppressor gene)

Epidemiology

• incidence 1 in 3000

Investigations

• Wood'

slamp to detect cafe-au-lait macules in patients with pale skin

Management

• refer to orthopaedics, ophthalmology, plastics, and psychiatry

• follow-up annually for brain tumours (e.g. astrocytoma)

• excise suspicious or painful lesions

• see Paediatrics, PS9

Oculocutaneous Albinism

Clinical Features

• hvpopigmentation ofskin and hair, including eyebrows and eyelashes, compared to family members

and persons ofsame ethnicity

• ocular involvement:decreased retinal pigmentation, impaired vision, photophobia, nystagmus,

strabismus

Pathophysiology

• group of genetic disorders of melanin biosynthesis

• autosomal recessive

•

Epidemiology

1 in 20000

«

• varies across ethnic groups

Investigations

• often clinical diagnosis, may consider molecular testing

Interventions lor Vitiligo

torene D 8 Syst Rev 2315ACK C3263

P urpose:To assessthe effects of eisirg

interceptions used mtte treregeiertcf rttgo.

M ethod:Systematic rerew of 8CTs essessrgthe

effects of vitiligo treatments(tog ce tree—erts.

light therapies, oral treatments,surgcel ceiscds).

Primary outcomes mere goaity of hie and >JSt

re-pigmentation.

Results: Ninety-six RCts wits 4512 pa-tc parts

were deemed el igihle. of nitid only 25 reported

on the pnmary outcoraes and wereSnaly edoded.

8e- pignentation was better msanseasoo

therapy (calcipotnpl ptos PtfVi.than Pintalone,

hydiocortsoreU-P.tyate pineuiaec laser vs.

excimer laser alone:oral mmpaseof prednisolone

(0MP|pins narrowband UVB is. ON?

alone: acathioomeirtt PtfHc.PUUae-e:

8-methos ypsore '

en (8-M0P|ptasst igttvs.

psoralen).Jnoo-signficant increase a pnoortma of

participants with >75% ra-pgirertatic mas noted

n favour nf NB-UVB compared to Finn.Compared to

PUM.the MV-UVB group reported lomer i-utesces of

nausea and erythema.Put not itcheg.

Conclusions:Snnestudiessupport existing

therapies for v tligo menagement t-utfo.om-up s

needed to assess permanence nf re-p gmentanop and

higher quality RCTs need to be condcctel

Management

• sun protection

• close surveillance for skin cancers with whole body skin examinations

Vitiligo

Clinical Features

• primary pigmentary disorder characterized by depigmentation

• acquired destruction of melanocytes characterized by sharply demarcated white patches

• associated with streaks of depigmented hair, chorioretinitis

• sitest extensorsurfaces and periorificial areas (mouth, eyes, anus,genitalia)

• Koebner phenomenon,may be precipitated by trauma

L J

Pathophysiology +

• acquired autoimmune destruction of melanocytes

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P29 Dermatology Toronto Notes 2023

Epidemiology

• 1 in 100 incidence

• 30 in 100 with positive family history

Investigations

• rule out associated autoimmune diseases: thyroid disease, pernicious anemia, Addison’s disease,

TIDM

• Wood’s lamp to detect lesions: illuminates U V light onto skin to detect amelanosis (porcelain white

discolouration)

Management

sun avoidance and protection

• topical calcineurin inhibitor (e.g. tacrolimus, pimecrolimus) or topical corticosteroids

• FUV'A or NB-UVB

• camouflage

•

“bleaching” normal pigmented areas (i.e. monobenzyl ether of hvdroquinone 20%) if widespread loss

of pigmentation

Infections

.2

E Stratum corneum

Impctiijo

iff {Stratum corneum.epidermis)

Erysipolas

M

Upper dermis {Upper dermis& lymphatics only)

Rarely involveslower dermis:

subepidermal oedema underlying

an uninvolved epidermis

E

Lower dermis

Cellulitis

(Lower dermis&subcutaneous lat)

Primarily not raised and demarcation

less distinct than erysipelas

E Subcutaneous fat

Q. Deep fascia

x Muscl

Necrotizing fasciitis

(Subcutaneous lat lascial planes,

and deep muscle)

UAshloy Hui 2016

Figure 11. Layers of skin affected by bacterial infections

Bacterial Infections:Epidermis

IMPETIGO

Clinical Features

• 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

Etiology

• GAS, S. aureus,or both

Epidemiology

• preschool and young adults living in crowded conditions, poor hygiene, neglected minor trauma

Differential Diagnosis

• infected eczema, HSV, VZV r n

cJ

Investigations

• usually clinical diagnosis

• Gram stain and culture of lesion fluid or biopsy

+

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D30 Dermatology Toronto Notes 2023

Management

• remove crusts, use saline compresses, and topical antiseptic soaks BID

• topical antibiotics(e.g.mupirocin 2% or fusidic acid 2% (Canada only)1

'

ID; continue for 7-10 d after

resolution, or ozenaxacin 1% cream BID for 5 d)

• systemic antibiotics (e.g.cloxacillin or cephalexin for 7-10 d)

Staphylococcal Scalded Skin Syndrome

• see Emergency Medicine. ER43

Bacterial Infections:Dermis

Table 17. Comparison of Erysipelas and Cellulitis

Differential

Diagnosis

Clinical Features Etiology Complications Investigations Management

GAS Scarlet lever,

streptococcal

Clinical diagnosis:rarely 1stline:petticilin.

do skin/blood culture cephalexin.cloiacillinor

If suspect necrotizing

fasciitis:do immediate

biopsy and frozen

section,hislopathology

Erysipelas Involves upper dermis

Confluent,erythematous,sharp raisededge,

warm plaque,well demarcated

Very painful("St.Anthony's fire*)

Sites:face and legs

Systemic symptoms:fever,chills,headache,

weakness (if present sign of mote serious

infection)

DVI (less red.less

hoi. smoother),

gangrene,fat necrosis, superficial phlebitis,

coagulopathy

Spreads via lymphatics photosensitivity

reaction,stasis

cefazolin

2nd line:clindamycin

If allergic to penicillin,use

erythromycin

contact dermatitis.

dermatitis,panniculitis,

vasculitis

Cellulitis Involves lower dermiv'subcutaneous fat GAS.S.oureus (large Uncommon

Unilateral erythematous flatlesion,often with sized wounds).

Haemophilus

irrHuenzoe

Same as erysipelas Sameaserysipelas 1st line:cloxacillin«

cefazolm. cephalejin

clindamycin

Hospitalized and HRSA

positive:vancomycin

Children:cefuroiime

If DM (footinfections):IHFi

SMX and raetrorvdazole

vesicles,poorly demarcated,not uniformly

raised

lender

Sites:commonly on legs

Systemic symptoms (uncommon):fever.

leukocytosis,lymphadenopattry

(periorbital).

Posteuiello multocido

(dog 'cat bite)

COMMON HAIR FOLLICLE INFECTIONS

Table 18. Comparison of Superficial Folliculitis,Furuncles, and Carbuncles

Clinical Features Etiology Management

Superficial

Folliculitis

Superficial infection of the hair follicle (versus pseudofoticulitis:

inflammation of follicle due to friction,irritation,or occlusion)

Acute lesion consists of a dome-shaped pustule atthe mouth of hair follicle

Pustule ruptures to form a small crust

Sites:primarily scalp,shoulders,anterior chest,upper back,other hair

-

bearing areas

Red.hot.tender,inflammatory nodules with central yellowish point,which

forms over summit and ruptures

Involves subcutaneous tissue thatarises from a hair follicle

Sites:hair-bearing skin (thigh,neck.face,aullae.perineum,buttocks)

Normal non-pathogenic Antiseptic (Hibiclens:

)

bacteria (Staphylococcus Topicalantibacterial (fusidic acid,mupirocin.erythromycin,or clindamycin)

- most common;

Pseudomonas - hot tub)

Pityrosporum

Oral cloxacillin or cephalexin for 7-10 d

S. oureus Incise and drain large furuncles to relieve pressure and pain

If afebrile:hoi wet packs,topical antibiotic

If febrile/cellulitis:culture blood and aspirate pustules (Gram stain andCAS)

Cloxacillin or cephalexin for1-2 wk (especially forlesions near external

auditory canal/nose,with surrounding cellulitis,andnot responsive to topical

therapy)

Same as lor furuncles

Furuncles

(Boils)

Carbuncles Deep-sealed abscess formed bymultiple coalescing furuncles S.oureus

Usually inareas of thicker skin

Occasionally ulcerates

lesions drain through multiple openings to thesurface

Systemic symptoms may be associated

SKIN ABSCESS

Clinical Features

• painful, fluctuant, erythematous nodule, with or without surrounding cellulitis

• spontaneous drainage or purulent material may be discharged, regional adenopathy may be observed

• may progress to furuncle (deep infection of hair follicle) or carbuncle (collection of furuncles)

• sites:back of the neck, face,axillae,buttocks

Pathophysiology

• one or more pathogens;& aureus with GAS and gram-negative bacilli with anaerobes is common in

the perioral, perirectal, or vulvovaginal areas

• collection of pus within the dermis orsubcutaneous tissue

ri

L.J

Investigations

• clinical diagnosis;laboratory testing with uncomplicated infection in absence of comorbidities or

complications is not required +

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Management

• if drainable abscess, incise and drain

• culture of debrided materials and antibiotics for the following circumstances:

severe local infection,systemic signs of infection, history of multiple/recurrent abscesses,

presence of underlying comorbidities, immunosuppression, failure of initial antibiotic therapy,

extremes of age (i.e. very young or very old),special exposures (e.g. animal bites), prophylaxis

against infective endocarditis

• culture of debrided materials is not required in healthy patients who do not receive antibiotics

Bacterial Infections:Epidermis and Dermis

CUTANEOUS ANTHRAX

Clinical Features

• painless, pruritic, red-brown papule with surrounding edema and erythema

• lesions blister and then ulcerate, developing

• often associated with systemic symptoms: fymphadenopathy,fever, myalgia, nausea, vomiting

a black eschar

Pathophysiology

• caused by Bacillus anthracis

Investigations

• Gram stain and culture

• polymerase chain reaction ( PGR)

• full-thickness punch biopsy

Management

• oral antibiotic: ciprofloxacin, levofloxacin, or doxycycline

LEPROSY

• see Infectious Diseases, ID21

A Placebo-Controlled Trial of Antibioticsfor

Smaller Skin Abscesses

NFJM 2017:376:2545-2555

Purpose: lo determine the appropriate management

of uncomplicated skin abscesses.

Study Multi-centre, piospectne. double-blind

trial involving outpatient adults and children with

abscesses S cm orsmaller,stratified by piesence ol

surgically drainable abscess, abscesssize,number

of sites of skin infection, and presence of nonpurulent cellulitis. Following incision and drainage,

participants were randomly assigned to10 d courses

of clindamycin, TMP-SMX or p 'acebo.Primary outcome

was clinical care 7 to10 d after treatment end.

Intention-to-tieat analyses were conducted.

Results:Seven hundredand eighty sir participants

were enrolled (SOS adults. 281clntdien).10 d

after therapy, the cure rate vrassimiar between

dlndamycin and 1MP-SMI (833% vs.81.7%: P-033),

and was higher than that ol the placebo gmup

(68.9V P-0.001 for both comparisons).Among those

who weie cured, new infections at1mo follow-up

were less common in the clindamycin group than

the TMP-SMX or placebo groups(6.8% vs.11.1V

P-0.03 vs.12.4%; P-0.06).Adverse events were

more frequent with clindamycin than either of the

otber groups(21.9% vs.11.1% n.12.5%).though aII

resolved without sequelae.

Conclusions:Clindamycin or IMP-SMXinconiunebon

with incision and drainage for simple abscesses

improves short-term outcomes compared to incision

and drainage alone, though side effects must be

considered.

PILONIDAL CYST

• see General and llioracic Surgery, < IS

Dermatophytoses

Clinical Features

• 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)

Pathophysiology

• digestion of keratin by dermatophytes resulting in scaly skin, broken hairs, crumbling nails/

onycholysis

Etiology

• Trichophyton, Microsporum, Epidermophyton species ( Pityrosporum is a superficial yeast and not a

dermatophyte)

Investigations

• skin scrapings, hair, and/or nail clippings analyzed with potassium hydroxide ( KOH ) prep to look for

hyphae and mycelia

Management

• topicals asfirst line agents for tinea corporis/cruris and tinea pedis (interdigital type):clotrimazole,

ketoconazole, terbinafine,or ciclopirox olamine cream applied BID

• oral therapy is indicated for onychomycosis and tinea capitis:terbinafine (Lamisil*

-CYP2D6

inhibitor,liver toxicity) or itraconazole (Sporanox* -CYP3A4 inhibitor, liver toxicity)

+

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DJ2 Dermatology Toronto Notes 2023

Table 19. Different Manifestations of Dermatophyte Infection

Clinical Features Differential Diagnosis Investigations Management

Tinea Capitis Round,scaly patches ol alopecia,possibly withbroken oflhairs;pruritic

Sites:scalp,eyelashes, and eyebrows;involving hair shafts and follicles

Kerion (boggy,elevated,purulent inflamed nodule/plaque) maylorm secondary trichotillomania

to infection by bacteria and resullin scarring

May have occipital lymphadenopathy

Affects children (mainly 8lack),immunocompromised adults

Very contagious and may be transmitted from barber,hats,theatre seats,pets

Alopecia areata,psoriasis. Wood's light anamination lerbinafine (lamisil ) n 4 wk

seborrheic dermatitis, of hair:green fluorescence N.B.:oral agents are required

only for Microsporum lo penetrate thehair root where

dermatophyte resides

Culture ofscales/hair shaft Adjunctive antifungal shampoos

Microscopic examination of or lotions may be helpful,and may

KOH preparation of scales prevent spread (e.g.selenium sulfide

or hair shafts 2.5%.ketoconazole,cidopiron)

Topicals:clolnmaiole 1%.

kctoconacole 2%.miconazole 2%,

lerbinafine.or cidopiroxolamme

cream BIO lor 2-4wk

Oral:lerbinafine (Lamisil - ),or

itraconazole (Sporanox% or

fluconazole,or ketoconazole if

extensive

infection

Tinea Corporis Pruritic,scaly,rouncKoval plaque with active erythematous margin.*

central

(Ringworm) clearing

Sites:trunk,limbs, face

Scaly patch/plaque with a well- defined,curved border and central clearing

Pruritic,erythematous,dry/macerated

Sites:starts medial thigh,spreads centrifugally to perineum,gluteal cleft,

buttocks

Pruritic scaling and/or maceration of the web spaces,and powdery scaling of

soles

Acute infection:interdigital (especially 4th web space) red/whitc scales,

vesicles,bullae,often with maceration

Secondary bacterial infection may occur

Chronic:non pruritic,pink,scalingkeratosis on soles,and sidesof feel

May present as flare-up of chronic linea pedis

Predisposing factors:heat,humidity,occlusive footwear

Tinea Manuum Primary fungal infection of the hand is rate;usually associated with tinea pedis

Acute:blisters at edge olred areas on hands

Chronic:single dry scaly patch

Tinea Unguium Crumbling, distally dystrophic nails:yellowish,opaque with subungual

(Onychomycosis) hyperkeratotic debris

Toenail infections usually precede fingernail infections

1.rubium (90% of all toenail infections)

Granuloma annulare. Microscopic examinations

pityriasis rosea,psoriasis, of KOH prep ol scales show

seborrheic dermatitis liyphae

Culture of scales Tinea Cruris

("Jock Itch")

Candidiasis (involvement

of scrotum and satellite

lesions),contact

dermatitis,erythrasma

AD. contact dermatitis,

dyshidrotic dermatitis,

erythrasma,intertiigo.

inverse psoriasis

Tinea Pedis

(Athlete's Foot)

AD, contact dermatitis,

granuloma annulare,

psoriasis

Psoriasis,lichen

planus,contact

dermatitis,traumatic

Microscopic examinations

of KOH prep of scales from

subungual scraping shows

lerbinafine (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:cidopirox (Penlac -

');

nail lacquer (often ineffective),

tfinaconazole (Jublia ) (43 wk)

onychodystrophy,bacterial liyphae

infection Culture of subungual

scraping or naildippings on

Sabouraud'sagar

Periodic acid-Schiff (PAS)

slain of nailclipping by

pathology

Tinea Barbae Superficial inflamed annular lesions:pustules and crusting around hairs

Inflammatory kerion may occur and result in scarring hair loss

Predominantly affects men who workwilh animals

Site:beard area

Folliculitis,malignant

lymphoma,sporotrichosis

Same as for tinea corporis ferbinafme (Lamisil -

) or Itraconazole

(Sporanox -)x 4wk

DIAPER RASH

"

IMPidJliitrlaPI5.1

*44

Parasitic Infections

CUTANEOUS LARVA MIGRANS

Clinical Features

• erythematous pruritic papules at site of initial infection

• larvae migrate under skin causing serpiginous eruption of red pruritic lines

• sites: often feet, legs, buttocks; anywhere skin comes into contact with contaminated sand or soil

Pathophysiology

• parasitic infection caused by hookworm larvae, most commonly from dog or cat feces

Epidemiology

• most common in tropical or subtropical regions

Management

• self-limiting, often resolves without treatment within a few weeks

• consider treatment with anthelmintics, antihistamines

CUTANEOUS LEISHMANIASIS

Clinical Features

• begins as a solitary pink painless papule, enlarges to nodule or plaque-like lesion with central

ulceration

• incubation time typically 2 wk to 6 mo

+

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D33 Dermatology Toronto Notes 2023

Pathophysiology

• transmitted by sandflies infected with Leishmania

Investigations

• histology, culture, and PCR

Management

• most cases resolve spontaneously

• may consider treatment with oral antifungals(e.g.fluconazole,ketoconazole) or parenteral treatment

in severe or complicated cases

SCABIES

Clinical Features

• characterized by superficial burrows, intense pruritus(especially nocturnal), and secondary infecti

• 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)

on

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

Etiology

• Sarcoptes scabici (a mite)

• risk factors:sexual promiscuity, crowding, poverty, nosocomial, immunocompromised

Differential Diagnosis

• asteatotic eczema,dermatitis herpetiformis,lichen simplex chronicus(neurodermatitis)

Investigations

• microscopic examination of root and content of burrow and mineral oil mount for mite, eggs, feces

• skin biopsy may sometimesshow scabies mite

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 requiressecond treatment 7 d after first treatment)

• Ivermectin

• 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 topicalsteroids and antihistaminesfor symptom management after treatment with

permethrin

LICE (PEDICULOSIS)

Clinical Features

• intensely pruritic, red excoriations, morbilliform rash, caused by louse (a parasite)

• scalp lice: nits(i.e.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

Etiology

• Phthirus pubis (pubic), Pcdiculus bumamis capitis (scalp),Pediculus bumamis humanus(body):

attaches to body hair and feeds on the nearby body site

• can transmit infectious agents (e.g. Bartonella quintana, Rickettsia prowazekii)

Differential Diagnosis

• bacterial infection of scalp,seborrheic dermatitis

n

LJ

Diagnosis

• lice visible on inspection of affected area or clothing seams +

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D31Dermatology Toronto Notes 2023

Management

• permethrin 1%: Nix* cream rinse (ovicidal), RC & Cor* shampoo, or Kwellada-P* shampoo

• comb hair with fine-toothed comb using dilute vinegarsolution to remove nits

• repeat in 7 d afier first treatment

• shave hair if feasible, change clothing and linens; wash with detergent in hot water cycle then machine

dry

• children are medically cleared to return to school after first treatment

BED BUGS (HEMIPTERA)

Clinical Features

• 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)

Etiology

• caused by Cimex lectularius,a small insect that feeds mainly at night (hides in crevices in walls and

furniture during the day)

Differential Diagnosis

• dermatitis herpetiformis, drug eruptions, ecthyma,other insect bites,scabies

Investigations

• none required, but lesional biopsy can confirm insect bite reaction

Management

• professional fumigation

• topical steroids and oral H 1-antagonistsfor symptomatic relief

• definitive treatment is removal of clutter in home and application of insecticides to walls and

furniture

Viral Infections

HERPANGINA

Clinical Features

• small vesicles form in mouth after exposure to virus

• lesions evolve into painful shallow oral ulcers, 1 -5 mm in size, yellowish with an erythematous base

• often associated with sore throat, dysphagia, and headache

Pathophysiology

• caused by Coxsackie A viruses, highly contagious

Epidemiology

• most common in children and young adults

Investigations

• typically clinical diagnosis

Management

• self-limited

• symptomatic treatment, acetaminophen for fever and pain

HERPES SIMPLEX VIRUS

Clinical Features

• 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, excesssun exposure, physical trauma, menstruation, emotional

stress, URT1

• complications:dendritic corneal ulcer, EM, herpessimplex encephalitis (infants at risk), HSV

infection on AD causing Kaposi’s varicelliform eruption (eczema herpeticum)

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D35 Dermatology Toronto Notes 2023

• two biologically and immunologically differentsubtypes: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, penisfor 5-7 d

• differential diagnosis of genital ulcers: candidal balanitis, chancroid,syphilitic chancres

Both HSV-1and HSV-2 can occur on face

or genitalia

Investigations

• Tzanck smear with Ciiemsa stain shows multinudeated giant epithelial cells

• viral culture,electron microscopy, P(.

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R, 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

Management

. HSV-1

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