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Lecture 4 & 8 Minor Skin Infections Klassen & Watson Impetigo: superficial skin infection Commonly S. aureus, occasionally S. pyogenes o S. aureus: production of exotoxins and coagulase causes cytotoxic damage Innate immune response results in cytotoxic degranulation & inflammation Commonly occurs on face (nostrils) or extremities after trauma Impetigo Contagiosa: nonbullous impetigo Most common type of impetigo > 2 years old Very contagious Begins with red sores around nose & mouth Sores weeping, red rash crusted Rash may be itchy but NOT PAINFUL Bullous impetigo Most common in infants – 2 years old Bulla appear first on torso, arms, legs Bullas initially appear turn cloudy Blisters tend to last longer than other types Areas around blisters may be red & itchy Ecythma: most serious form of impetigo DERMAL INVOLVEMETN Blisters tend to be PAINFUL May turn into ulcers or open sores Folliculitis etc Types Folliculitis: superficial infection of hair follicle o Erythematous, follicular-based papules & pustules Furuncles: deeper infections of hair follicle o Inflammatory nodules with pustular drainage Carbuncles: collections of furuncles that form draining nodules Classifications Superficial: very mild & self-limiting o Multiple small papules & pustules on an erythematous base that are pierced by a central hair Deep: painful, erythematous, often fluctuant, nodules with suppurative drainage o Persistent or recurrent lesions scarring and permanent hair loss o Commonly S. aureus infection Aggravating factors Pseudofolliculitis: shaving & other hair removal Occlusion folliculitis: on back and buttocks o Sitting down for long periods o Hot environments + protective clothing Medications: corticosteroids, androgens, lithium Likely pathogens S. aureus P. aeruginosa “hot-tub folliculitis” Goals of therapy Treat causative organisms Relieve sx and resolve lesions Prevent further spread of infection Prevent recurrence Treatment Smaller furuncles: may spontaneously rupture & drain o Apply moist, warm compresses x 20 min TID-QID Larger furuncles, all carbuncles: I & D key +/- C & S of pus Add systemic antibiotics when: o Moderate (systemic signs of infection) Empiric: PO TMP/SMX or doxycycline Defined: cloxacillin, cephalexin (MSSA) clindamycin (pen-allergy) TMP/SMX, clindamycin (MRSA) o Severe (prior txt failure or SIRS or immunocompromised) Empiric or MRSA: vancomycin Defined: cefazolin IV, cloxacillin IV clindamycin IV (pen-allergy) Antibacterial OTC products: NOT for treatment of bacterial skin infections!! Polysporin

Lecture 4 & 8 Minor Skin Infections Klassen & Watson · Tinea Pedis Contributing Factors Poor foot hygiene Tight -fitting and/or non -breathable footwear Hot, humid weather Hyperhidrosis

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Lecture 4 & 8 Minor Skin Infections Klassen & Watson

Impetigo: superficial skin infection

Commonly S. aureus, occasionally S. pyogenes

o S. aureus: production of exotoxins

and coagulase causes cytotoxic damage

Innate immune response results in cytotoxic

degranulation & inflammation

Commonly occurs on face (nostrils) or extremities

after trauma

Impetigo Contagiosa: nonbullous impetigo

Most common type of impetigo > 2 years old

Very contagious

Begins with red sores around nose & mouth

Sores weeping, red rash crusted

Rash may be itchy but NOT PAINFUL

Bullous impetigo

Most common in infants – 2 years old

Bulla appear first on torso, arms, legs

Bullas initially appear turn cloudy

Blisters tend to last longer than other types

Areas around blisters may be red & itchy

Ecythma: most serious form of impetigo

DERMAL INVOLVEMETN

Blisters tend to be PAINFUL

May turn into ulcers or open sores

Folliculitis etc

Types

Folliculitis: superficial infection of hair follicle

o Erythematous, follicular-based papules &

pustules

Furuncles: deeper infections of hair follicle

o Inflammatory nodules with pustular

drainage

Carbuncles: collections of furuncles that form

draining nodules

Classifications

Superficial: very mild & self-limiting

o Multiple small papules & pustules on an

erythematous base that are pierced by a

central hair

Deep: painful, erythematous, often fluctuant,

nodules with suppurative drainage

o Persistent or recurrent lesions

scarring and permanent hair loss

o Commonly S. aureus infection

Aggravating factors

Pseudofolliculitis: shaving & other hair removal

Occlusion folliculitis: on back and buttocks

o Sitting down for long periods

o Hot environments + protective clothing

Medications: corticosteroids, androgens, lithium

Likely pathogens

S. aureus

P. aeruginosa

“hot-tub

folliculitis”

Goals of therapy

Treat causative

organisms

Relieve sx and resolve

lesions

Prevent further

spread of infection

Prevent recurrence Treatment

Smaller furuncles: may spontaneously rupture & drain

o Apply moist, warm compresses x 20 min TID-QID

Larger furuncles, all carbuncles: I & D key +/- C & S of pus

Add systemic antibiotics when:

o Moderate (systemic signs of infection)

Empiric: PO TMP/SMX or doxycycline

Defined: cloxacillin, cephalexin (MSSA)

clindamycin (pen-allergy)

TMP/SMX, clindamycin (MRSA)

o Severe (prior txt failure or SIRS or immunocompromised)

Empiric or MRSA: vancomycin

Defined: cefazolin IV, cloxacillin IV

clindamycin IV (pen-allergy)

Antibacterial OTC

products: NOT for

treatment of bacterial

skin infections!!

Polysporin

Lecture 8 Minor Skin Infections Watson

Dermatophyte infections: fungal infection by

organisms with high affinity for keratinized tissue

(skin, nails, hair)

DO not infect mucosal surfaces

Inflammation = redness/scaling at edge

o AKA RINGWORM

General pathophysiology

1. Fungal hyphae grow in stratum corneum

2. Fungus grows deeper into hair follicle

3. Devours keratin in skin and hair as it is formed

4. Impact zone – extends upwards as hair grows

Visible above skin surface by days 12-14

Infected hairs are brittle

Week 3: broken hairs are evident

(alopecia)

Goals of therapy of Tinea infections

Relieve symptoms

Cure infection

Prevent recurrence

Prevent transmission

Tinea Pedis

Contributing Factors

Poor foot hygiene

Tight-fitting and/or non-breathable footwear

Hot, humid weather

Hyperhidrosis

Populations at increased risk

Elderly, teenagers, males

Diabetics

Immunocompromised

Patients with PVD

Types

Interdigital

Intensely pruritic, usually

malodorous

Uni or bilateral

Usually starts with 4th-5th

toe web

Moist, pale white scaly,

white macerated areas

Fissures of toe web

Commonly due to T.

Mentagrophytes

Moccasin

Occurs along soles (generally

bilateral)

o Heels, sides of both feet

also affected (thickened,

cracked)

o Often affects toe nails

Possibly involves palms

Fine scale & diffuse erythema

(tender, sore)

Usually due to T. rubrum

Vesicular

Sudden onset

Usually at instep, may

affect toe webs, soles,

dorsa of feet

Patches of erythema,

scaling, painful vesicles,

malodorous

Commonly due to T.

Mentagrophytes

o Chronic interdigital

tinea

Refer

Diabetes

Peripheral vascular disease

Peripheral neuropathy

Immunocompromised

> 65 yo or < 12 yo

Extensive lesions

(mocassion)

Toenail involved

May have bacterial

infection

Non-drug measures

Shoes: breathable material (leather, canvass)

o Keep separate pairs for sports

o Clean shoes & allow to dry between wearings

o Avoid bare feet in public places

Socks: breathable material (cotton, silk, wool); avoid nylons

o Change daily or when sweaty

avoid sharing towels

bathe feet daily, dry thoroughly, talcum powder, antifungal

powder

Lecture 8 Minor Skin Infections Watson

Tinea Pedis Treatment

All antifungal drugs within a class are equi-efficacious

o Most to least effective: allylamines (Rx) > azoles > undecylenic acid > tolnaftate

Azoles first-line in pregnancy & lactation

To dry weepy lesions: Burow’s solution may be used TID (max 3 days)

General product application tips

Wash and dry the affected area pre-application

Apply product in a thin layer & extend 2 cm beyond infection borders

May take several days to see initial improvement

o Refer to MD if no improvement after 1 week or not resolved by 6 weeks of therapy

Use product for a further 7-14 days after disappearance of sx

Tinea Corporis & Cruris

Tinea Corporis Symptoms

Initial Plaque on neck, trunk, limbs

Round or oval shape

Expands outward centrifugally (centre clears)

PRURITIC, ERYTHEMATOUS

Chronic Annular lesion

Circumference varies

Raised, scaly, erythematous border o Border may have bumps or blisters

Centre clear

Several lesions may be close together

ITCHING, BURNING

Tinea Cruris Symptoms

Involves groin area; may extend to

involve inner leg, buttocks, anal

cleft, stomach

Usually bilateral, symmetrical

Does not affect genitalia

Presentation

o Large, well-defined, red or

brown round plaques

o Bumpy, scaly margins

Referral

Large lesions ( > 10 cm circumference)

Multiple lesions over a widespread area

Genitalia infected

No improvement after 1 week of

appropriate txt

Immunocompromised

Sx of systemic illness, bacterial infection

If unsure of diagnosis

Non-drug measures

Keep skin dry: non-medicated powders; blow drying

area; loose-fitting, breathable clothing

Wash clothing, bedding, towels frequently

Bathe and dry feet, put on socks before putting on

undergarments if they have tinea pedis

Inspect pets as source of infection

Antifungal infection: clean & dry area then

apply a thin layer of product to cover the

lesion as well as a “halo” extending 2-3 cm

beyond the lesion border

Treat for 1-2 weeks post-sx resolution

Duration of therapy

OTC topicals

o Tinea corporis: BID x 4 weeks

o Tinea cruris: BID x min 2 wks (tolnaftate 4 wks)

Terbinafine 1% cream: OD x 1 week

Oral terbinafine 250 mg: OD x 2-4 weeks

Ketoconazole 2% cream: daily-BID x 2-4 weeks

Corticosteroids or corticosteroids + antifungal combination: AVOID DUE TO…

Potential deleterious effect on clinical appearance

Potential to exacerbate the infection

Potential SEs

Lecture 4 Minor Skin Infections Klassen

Candida infections

Candidiasis refers to a diverse group of infections caused

by genus Candida = YEAST INFECTION

o Candida albicans – 70-80%

Infects skin, nails, MUCOUS MEMBRANES, and GIT

o Can cause systemic disease

Candida virulence

Surface molecules that permit adherence of the

organism to extracellular matrix

Acid proteases and phospholipases that involve

penetration and damage of cell envelopes

Ability to convert to a hyphal (growth form) –

phenotype switching

Elicit innate and then acquired immune response