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📚 Superficial Fungal Infections - Study Notes

Superficial Fungal Infections Study Notes

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Here's a summary of what's covered:

What's Included

Part 1 - Dermatophytes

What they are, classification by origin (anthropophilic vs zoophilic vs geophilic)
Hair invasion patterns: endothrix vs ectothrix with organisms
All diagnosis tools (KOH prep, Wood's light fluorescence table, culture media)

Part 2 - Tinea by Location

Tinea pedis (feet), cruris (groin), corporis (body), capitis (scalp), barbae (beard)
Tables comparing each location's presentations, organisms, and treatments
Special forms: Tinea incognito, Majocchi granuloma, Kerion, "Barn itch"

Part 3 - Treatment Reference Tables

Oral antifungal dosages for every condition in one table
Topical antifungal coverage chart (which drugs cover dermatophytes vs yeasts vs bacteria)
Key rule: Allylamines = fungicidal (shorter course) vs Azoles = fungistatic (longer course)

Part 4 - Candidiasis

Risk factors, all locations (VVC, oral thrush, balanitis, skin folds, diaper, perlèche)
Full treatment guide including Recurrent VVC (RVVC) maintenance regimens

Part 5 - Tinea Versicolor + Pityrosporum Folliculitis

"Spaghetti and meatballs" KOH pattern
Which oral drugs DON'T work (griseofulvin, terbinafine)

High-Yield Exam Section

Comparison tables (Tinea cruris vs Candida groin, dermatophyte vs Candida on KOH)
Drug interaction quick-reference
Tinea mnemonics by body location

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ORAL EXAM Study Notes Superficial Fungal

MD File · MD

How these notes are designed for oral assessment:

Q&A Format - Every topic is written as a question an examiner would ask, followed by a full spoken-style answer. Cover the answer, say it out loud, then check yourself.

6 Sections with 40+ questions:

Dermatophyte basics - classification, hair invasion patterns, KOH prep, Wood's light, culture media
Tinea by location - pedis, cruris, corporis, capitis, barbae - with all clinical patterns described
Antifungal drugs - mechanism, key properties, drug interactions for each drug
Candidiasis - every location, what it looks like, the vaginal discharge comparison table, RVVC treatment
Tinea versicolor - triggers, spaghetti-and-meatballs KOH, treatment (with the drugs that DON'T work)
Pityrosporum folliculitis + Pitted keratolysis (the "trick" bacterial one)

Rapid-fire review at the end - 25 short Q&As to test yourself quickly before an exam.

Final summary table - all conditions side by side for a last-minute scan.

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Here are your complete oral exam study notes as text:

SUPERFICIAL FUNGAL INFECTIONS

Oral Assessment & Exam Study Notes

Habif's Clinical Dermatology – Chapter 13

HOW TO USE: Read each question out loud, pause, then say your answer. Cover the answer and practice speaking it. This is how you prepare for oral assessments.

SECTION 1: DERMATOPHYTES - THE BASICS

Q: What are dermatophytes and where can they infect?

Dermatophytes are a group of fungi - also called ringworm fungi - that can ONLY infect dead keratin. That means they infect the top layer of skin (the stratum corneum), the hair, and the nails. They cannot survive on mucous membranes like the mouth or vagina because those surfaces don't have a keratin layer. In very rare cases - mainly in immunosuppressed patients - they can invade deeply and spread to internal organs.

Q: What are the three genera of dermatophytes?

Microsporum
Trichophyton
Epidermophyton (only one species)

Q: How do we classify dermatophytes by their origin?

Three types:

Anthropophilic - parasitic only on humans. Spread from person to person.
Zoophilic - originate from animals but can infect humans.
Geophilic - live in soil but can infect humans.

The important clinical point: zoophilic and geophilic fungi cause a brisk, intense inflammatory response in humans, while anthropophilic fungi cause only mild inflammation.

Q: Is there a genetic component to dermatophyte infections?

Yes. Blood-related family members may share similar manifestations, but spouses do NOT become infected despite prolonged exposure - supporting genetic predisposition over simple contact. Patients with chronic infections have a specific defect in delayed hypersensitivity to Trichophyton, and there is a higher frequency of atopy in chronically infected patients.

Q: What are the two patterns of hair shaft invasion?

Endothrix - fungal hyphae are found INSIDE the hair shaft only. The cuticle remains intact. Caused by: T. tonsurans, T. violaceum, T. soudanense.
Ectothrix - fungal hyphae are found INSIDE and ON THE SURFACE of the hair shaft. The hyphae break through and destroy the cuticle, forming a sheath of spores on the outside. Caused by: M. canis, M. audouinii, T. verrucosum, T. mentagrophytes.

Memory tip: Endo = entirely inside. Ecto = exits to the surface.

Q: What is the single most important test for diagnosing a dermatophyte infection?

The KOH (potassium hydroxide) wet mount preparation. You scrape scale from the active border, place it on a slide, add KOH, gently heat it, and examine under the microscope. KOH dissolves the cellular material but leaves fungal hyphae intact. Dermatophytes appear as translucent, branching, rod-shaped filaments of uniform width with septa at irregular intervals. The uniform width and characteristic branching is what distinguishes hyphae from hair or debris.

Q: Where is the BEST place to scrape for a KOH prep?

From the active border of the lesion - the leading edge - where the highest concentration of hyphae is found. Scrape perpendicular to the border with a number 15 blade.

Q: What is the "mosaic artifact" and why is it important?

Lipid droplets appearing in a single-file line between epidermal cells that can look just like fungal hyphae. Most common in specimens from the palms and soles. The key is that lipid droplets disappear with additional heating and pressure, whereas true hyphae do not.

Q: What does Wood's light tell us about fungal infections?

Blue-green fluorescence of hair = M. canis or M. audouinii
Pale green fluorescence of hair = T. schoenleinii (rare)
Pale yellow-white fluorescence of skin = Tinea versicolor
Coral-red fluorescence = Erythrasma - this is BACTERIAL (Corynebacterium minutissimum), NOT fungal!
No fluorescence = T. tonsurans - very important because T. tonsurans is the most common cause of scalp ringworm in the USA

Always do Wood's light in a dark room with a high-intensity instrument.

Q: What are the three culture media used for dermatophytes?

DTM (Dermatophyte Test Medium) - turns PINK within 6-7 days in the presence of dermatophytes. Quick office test. Good for confirming onychomycosis. Must discard after 2 weeks.
Mycobiotic agar - contains cycloheximide and chloramphenicol to prevent bacteria and saprophytic fungi. Best for hair infections (tinea capitis) because only dermatophytes grow.
Sabouraud's agar - no antibiotics, grows ALL fungi including non-dermatophytes. Best for nail infections where you want to identify saprophytic molds that don't respond to treatment.

SECTION 2: TINEA BY LOCATION

TINEA PEDIS (Athlete's Foot)

Q: What is tinea pedis and who is most affected?

Tinea pedis is a dermatophyte infection of the feet - the MOST COMMON site of dermatophyte infection. It predominantly affects men. It's uncommon in women and rare in prepubertal children. Once established, the person becomes a carrier and is more susceptible to recurrences.

Q: Describe the three main clinical presentations of tinea pedis.

1. Interdigital (toe-web infection): The 4th/5th web space is most commonly involved because tight shoes compress the toes there. Presents as either dry, scaly and fissured - OR white, macerated and soggy. The macerated form results from interaction between the fungus AND bacteria. The fungus damages the stratum corneum and selects for antibiotic-resistant bacteria.

2. Chronic scaly moccasin-type (hyperkeratotic/plantar): The entire sole is covered with fine silvery-white scale. The pattern is typically two feet and one hand. T. rubrum is the usual pathogen and is very difficult to eradicate because it suppresses the immune response.

3. Acute vesicular tinea pedis: A highly inflammatory form - vesicles develop rapidly on the sole or dorsum, may fuse into bullae. Secondary bacterial infection is common. An important complication is the id (dermatophytid) reaction - sterile itchy vesicles at distant sites (arms, chest, fingers) representing an allergic response to the fungus. These resolve when the primary infection is controlled.

Q: What is the two feet-one hand syndrome?

Dermatophyte infection of BOTH feet plus ONE hand (either left or right palm). Nail infection may also be present. Most common in men. The same organism - usually T. rubrum - infects all three areas. The hand used to scratch the feet or pick toenails is typically the one infected.

Q: How do you treat tinea pedis?

Interdigital: Terbinafine 1% cream BID x 1 week (88% cure at 5 weeks). Butenafine BID x 1 week also highly effective.
Moccasin/plantar type: Oral terbinafine 125 mg/day x 4 weeks (95% sustained cure). Topical agents respond slowly.
Acute vesicular: Wet Burow's solution compresses x 30 minutes several times daily + oral antifungal + oral antibiotics if secondary bacterial infection. Topical steroids or prednisone for id reactions.
Oral options: Fluconazole 150 mg once weekly; itraconazole 200 mg daily x 2 weeks; terbinafine 250 mg daily x 2 weeks.

TINEA CRURIS (Jock Itch)

Q: Describe tinea cruris - who gets it and what does it look like?

Much more common in men than women, rare in children. Worse in summer from sweating. Classic appearance: unilateral, half moon-shaped plaque starting in the crural fold and advancing onto the thigh with a well-defined, scaly border. The center becomes red-brown and less scaly. The scrotum is NOT involved - this is a key distinguishing feature from Candida.

Q: What is tinea incognito?

A fungal infection modified by inappropriate treatment with topical steroids. The steroid suppresses inflammation, giving the false impression of improvement - but the fungus flourishes due to cortisone-induced immune suppression. The classic border disappears. The result is diffuse erythema, scattered pustules, and a greatly expanded infection without classic features. Most common sites: groin, face, dorsal hand. Hyphae are still present on KOH prep.

Q: How do you distinguish tinea cruris from Candida groin infection?

Tinea cruris: Unilateral, does NOT involve the scrotum, well-defined scaly advancing border.
Candida groin: Bilateral, MORE extensive, DOES involve the scrotum, has a fringe of scale at the border AND satellite pustules just outside the main lesion.

Q: How do you distinguish tinea cruris from erythrasma?

Erythrasma is caused by a BACTERIUM - Corynebacterium minutissimum. It also forms a half moon-shaped plaque in the groin. The differences: erythrasma is non-inflammatory, uniformly brown and scaly, has NO advancing border, and shows brilliant coral-red fluorescence under Wood's light. Tinea cruris does NOT fluoresce.

TINEA CORPORIS (Ringworm of the Body)

Q: Describe classic tinea corporis.

Begins as a flat scaly spot that develops a raised border expanding outward in all directions. The active border is red and scaly - may have papules or vesicles. As it expands, the center becomes hypopigmented and less scaly - giving the classic "ringworm" ring appearance.

Q: What is Majocchi granuloma?

A form of inflammatory tinea caused mainly by T. rubrum. Originally described in women who shave their legs. The primary lesion is a follicular papulopustule. Granulomatous nodules develop in the dermis and subcutis because infected hair follicles rupture into the dermis, causing a granulomatous reaction with epithelioid cells, giant cells, and lymphocytes. Skin biopsy with special fungal stains is needed for diagnosis.

Q: What is tinea gladiatorum?

Tinea corporis in competitive wrestlers - from close person-to-person contact during wrestling. Most cases caused by T. tonsurans.

TINEA CAPITIS (Scalp Ringworm)

Q: Who gets tinea capitis and what organisms are responsible?

Predominantly prepubertal children aged 3-7 years. Most common in crowded, low socioeconomic settings. In the USA: T. tonsurans accounts for more than 90% of cases. In Europe: M. canis is most common. Farmers acquire T. verrucosum from cattle.

Q: Why can't you treat tinea capitis with topical antifungals alone?

Because the fungus invades deep into the hair follicle - below the cuticle of the hair shaft. Topical agents cannot penetrate to that depth. The fungus gains entry below where the cuticle forms, circumventing any surface treatment. Oral therapy is mandatory.

Q: Describe the four clinical patterns of T. tonsurans tinea capitis.

1. Black dot pattern: Areas of hair loss with hairs broken off at the follicular orifice - the arthrospores weaken the hair so it fractures at or below the scalp surface, leaving black dots. Little to no inflammation.

2. Inflammatory pattern (Kerion): Boggy, tender, indurated, tumor-like mass studded with pustules. Represents an intense hypersensitivity reaction. May have fever and lymphadenopathy. KOH and cultures are often NEGATIVE because inflammation has destroyed fungal structures. Scarring alopecia can occur.

3. Seborrheic dermatitis type: Looks exactly like dandruff - diffuse or patchy fine white scale. This is the most difficult to diagnose - only 29% have a positive KOH. Look closely for perifollicular pustules and broken hair stubs.

4. Pustular type: Discrete pustules or scabbed areas with minimal hair loss. Often gets multiple courses of antibiotics before the correct diagnosis is made.

KEY RULE: Cervical or occipital lymphadenopathy should be present in ALL types. Question the diagnosis if there's no lymphadenopathy and no alopecia.

Q: What are the oral drug options for tinea capitis in children?

Griseofulvin - Drug of choice. Longest safety record. Fungistatic. Take with fatty food. Duration: 6-8 weeks for Trichophyton, 8-12 weeks for Microsporum.
Terbinafine - Fungicidal. BEST for Trichophyton. Efficacy for Microsporum is disputed. 4 weeks duration.
Itraconazole - Good for both types. Take with a full meal and acidic juice. 4-6 weeks. Many drug interactions.
Fluconazole - Effective. Available as a pleasant-tasting liquid. Approved for children over 6 months. 3-6+ weeks.

Q: What adjuvant measures are used in tinea capitis?

Antifungal shampoo (selenium sulfide 2.5%, ketoconazole 2%) 2-3 times per week
Screen ALL family members and close contacts
Clean fomites - combs, brushes, bedding (T. tonsurans spores stay viable for months)
Children can return to school once systemic therapy has started
For asymptomatic carriers with heavy spore counts, consider systemic therapy

TINEA BARBAE (Beard Ringworm)

Q: What is tinea barbae and how is it different from bacterial folliculitis?

Dermatophyte infection limited to the coarse hair-bearing beard/mustache area in men. Usually follows minor trauma from shaving. Frequently mistaken for bacterial folliculitis - patients often receive multiple antibiotic courses before the correct diagnosis. The key clinical difference: hairs in tinea barbae are infected and can be removed painlessly. Hairs in bacterial folliculitis resist removal and removal is painful.

Two patterns:

Superficial - annular lesions like tinea corporis
Deep follicular - boggy, erythematous abscess like a kerion; caused by T. verrucosum (from cattle) and T. mentagrophytes

Treatment: Oral antifungals required (same as tinea capitis) because creams don't penetrate to follicle depth.

SECTION 3: ANTIFUNGAL DRUGS

Q: What is the mechanism of griseofulvin and what are its key properties?

Griseofulvin is fungistatic - works best on actively growing dermatophytes by inhibiting fungal cell wall synthesis. Active ONLY against dermatophytes - Candida and tinea versicolor do NOT respond. Available in microsize and ultramicrosize forms - ultramicrosize is better absorbed. Take with fatty food to enhance absorption.

Side effects: Headache and GI symptoms most common. Rarely: hepatotoxicity, leukopenia, photosensitivity. Drug interactions: Activates hepatic enzymes → decreases levels of warfarin, estrogen, oral contraceptive pills. Alcohol effect is potentiated. Barbiturates reduce griseofulvin activity. Contraindicated in pregnancy and lupus.

Q: What is terbinafine's mechanism and what makes it special?

Terbinafine is an allylamine - inhibits squalene epoxidase, a membrane-bound enzyme NOT part of the cytochrome P-450 family. It is FUNGICIDAL to dermatophytes. Key properties:

Highly lipophilic and keratophilic
Persists in skin, hair, and nails for weeks after stopping therapy
After 6-12 weeks of therapy, still detectable in nails for 30-36 weeks
Delivered to stratum corneum via sebum
Oral terbinafine does NOT work for tinea versicolor

Q: What is the key difference between allylamines and azoles?

Allylamines (terbinafine, naftifine, butenafine) = FUNGICIDAL → shorter treatment duration, higher cure rates, lower relapse rates
Azoles (clotrimazole, miconazole, ketoconazole, econazole, etc.) = FUNGISTATIC → longer treatment needed

Both inhibit ergosterol synthesis, but at different points in the pathway.

Q: What are key properties of itraconazole?

Highly lipophilic with high affinity for keratinizing tissues. Builds up and persists in nail plate for at least 6 months after 3 months of therapy. Sebum levels are FIVE TIMES higher than plasma levels. Absorption is significantly increased by food - take with a full meal and acidic juice. Absorption is reduced by antacids, H2 blockers, and proton pump inhibitors. Many drug interactions because it inhibits cytochrome P-450.

Q: What is special about fluconazole?

Highly water-soluble (unusual for an antifungal). Transported to skin through sweat, where it concentrates by evaporation. Achieves high concentrations in epidermis and nails. Available as a pleasant-tasting liquid for children. Approved for children over 6 months.

Q: Which topical antifungal also covers bacteria?

Econazole - it has activity against several bacterial species in addition to dermatophytes and yeasts. Particularly useful for severely macerated interdigital toe web infections where bacterial overgrowth is a problem.

SECTION 4: CANDIDIASIS

Q: What is Candida and when does it become pathogenic?

C. albicans is normal flora of the mouth, vaginal tract, and gut. It becomes pathogenic and converts from budding yeast to producing pseudohyphae or true hyphae when conditions change. Predisposing factors:

Pregnancy or oral contraceptives
Antibiotic therapy (disrupts normal bacterial flora)
Diabetes mellitus
Skin maceration
Topical steroid therapy
Immunosuppression, HIV
Endocrinopathies (Cushing's, adrenal disorders)

Q: What is the primary lesion of cutaneous candidiasis and what does it produce?

A pustule. The contents dissect horizontally under the stratum corneum and cause it to separate. This produces a red, denuded, glistening surface with a long "cigarette paper-like" scaling advancing border - sometimes called an "ocean wave" fringe. In intertriginous areas, the pustule immediately becomes macerated, so you look for satellite pustules - pinpoint pustules just OUTSIDE the main lesion - as the key diagnostic feature.

Q: Differentiate between the three main causes of vaginal discharge.

Feature	Candida	Bacterial Vaginosis	Trichomoniasis
Discharge	White, clumpy, curdy	Gray, homogeneous, fishy	Profuse, greenish, frothy
Main symptom	Itching	Malodorous discharge	Malodor + itching + dysuria
pH	Less than 4.5 (normal)	Greater than 4.7	4.5
Wet prep	Budding yeast, pseudohyphae	Clue cells	Motile trichomonads
Amine test	Negative	Positive (fishy)	Positive

Q: What is recurrent vulvovaginal candidiasis (RVVC) and how is it treated?

RVVC is defined as 4 or more symptomatic episodes per year. Most women with RVVC have NO apparent underlying condition.

Treatment:

Induction: Fluconazole 150 mg every 72 hours x 3 doses (Day 1, Day 4, Day 7)
Maintenance: Fluconazole 150 mg once weekly x 6 months

Important: 30-50% of women relapse after stopping maintenance therapy. For C. glabrata: boric acid vaginal suppository 600 mg/day x 14 days (azoles are less effective against this species).

Q: Describe oral candidiasis - who gets it and what does it look like?

The tongue is almost always involved. Classic appearance: white, creamy plaques on a red, sore base - you can scrape the plaques off (unlike leukoplakia). Occurs in: diabetes, elderly, cancer (especially leukemia), prolonged steroid or antibiotic use, HIV (more than 90% of AIDS patients develop it). In infants it's called THRUSH - usually self-limited in healthy newborns but should be treated to avoid interference with feeding.

Q: Describe Candida intertrigo - what does it look like and how do you treat it?

Occurs wherever skin touches skin in warm, moist areas - under breasts, between abdominal folds, groin, axillae. Two presentations:

Pustules that macerate → red papules with fringe of moist scale at the border; intact pustules found OUTSIDE the fold
Red, moist, glistening plaque with "ocean wave" fringe of macerated scale at a sharply defined border

Satellite pustules outside the main lesion are the hallmark. Treatment: cool wet compresses to promote dryness + antifungal cream BID + absorbent powder after inflammation resolves.

Q: Describe Candida balanitis.

Yeast infection of the penis - more common in uncircumcised men because the foreskin creates the warm, moist environment yeast needs. Can occur after intercourse with an infected female partner. Presents as tender, pinpoint red papules and pustules on the glans and shaft. White donut-shaped rings appear after pustules break. White exudate may be present. Treatment: miconazole or clotrimazole BID x 7 days, or single oral fluconazole 150 mg.

Q: What is angular cheilitis and what causes it?

Inflammation at the corners of the mouth caused by a moist intertriginous space forming at the mouth angles - capillary action draws saliva into the fold, causing maceration and secondary infection with Candida and/or staphylococci. Caused by: lip licking, thumb sucking, poorly fitting dentures, mouth breathing, advancing age, weight loss. Patients mistakenly think it's a vitamin B deficiency. Treatment: antifungal cream followed in a few hours by a topical steroid, until dry and inflammation-free.

SECTION 5: TINEA VERSICOLOR

Q: What causes tinea versicolor and what triggers it?

Caused by Pityrosporum orbiculare (round form) and Pityrosporum ovale (oval form) - collectively called Malassezia furfur. These are normal skin flora that convert from budding yeast to mycelial form when triggered by:

Endogenous: Cushing's disease, adrenalectomy, pregnancy, malnutrition, burns, corticosteroids, immunosuppression, oral contraceptives
Exogenous: Excess heat and humidity

Most common in adolescents and young adults due to high sebaceous activity. May not be contagious.

Q: Describe the clinical presentation of tinea versicolor.

Multiple small, circular macules that enlarge radially. The color varies - which is why it's called "versicolor":

White/hypopigmented - most noticeable in summer when surrounding skin tans
Pink to red - from inflammatory response
Fawn/tan/brown - from post-inflammatory pigmentation

Hypopigmentation occurs because dicarboxylic acids produced by the yeast are cytotoxic to melanocytes and inhibit the dopa-tyrosinase reaction. Upper trunk is most commonly affected. Facial lesions more common in children. Usually asymptomatic.

Q: How do you diagnose tinea versicolor?

Scrape lightly with a no. 15 blade - reveals powdery scale that may not be visible on inspection
KOH prep shows short broad hyphae intermixed with round spore clusters - the classic "spaghetti and meatballs" appearance
Wood's light - irregular pale yellow-to-white fluorescence (some lesions do NOT fluoresce)
Griseofulvin is NOT active - cannot be used

Q: How do you treat tinea versicolor?

Important patient counseling: Hypopigmented patches will NOT disappear immediately after treatment. Repigmentation takes time. Sunlight accelerates repigmentation. Recurrence rates are HIGH (40-60%).

Topical (first line for limited disease):

Ketoconazole 2% shampoo - FIRST CHOICE. Apply whole body from neck to thighs, leave 5 minutes, rinse. Single application or daily x 3 days.
Selenium sulfide 2.5% - apply for 10 minutes daily x 7 days = 87% cure rate
Any imidazole cream BID x 2-4 weeks

Oral (for extensive or recurrent disease):

Itraconazole 200 mg/day x 7 days
Fluconazole 300 mg/week x 2 doses
Oral terbinafine = NOT effective
Oral griseofulvin = NOT effective
Oral ketoconazole = CONTRAINDICATED (risk of serious liver damage and death)

Recurrence prevention: Ketoconazole 2% shampoo once weekly to trunk/neck.

SECTION 6: PITYROSPORUM FOLLICULITIS

Q: What is Pityrosporum folliculitis and how does it differ from acne?

Infection of hair follicles by Pityrosporum orbiculare - the same organism that causes tinea versicolor. Presents as asymptomatic or mildly itchy follicular papules and pustules on the upper back, chest, upper arms, and neck. FREQUENTLY MISDIAGNOSED AS ACNE. It does not respond to acne antibiotics. In tropical presentations, the face is commonly involved - more lateral (mandible and sides of the face) compared to typical acne which is more central.

Risk factors: Diabetes, broad-spectrum antibiotics, corticosteroids, Hodgkin disease, occlusion, oily skin.

Diagnosis: KOH shows abundant round budding yeast cells and sometimes hyphae.

Treatment: Oral fluconazole combined with topical antifungal. Ketoconazole 2% cream/shampoo. Salicylic acid wash is keratolytic and effective.

BONUS: PITTED KERATOLYSIS (Often confused with tinea!)

Q: What is pitted keratolysis and how do you recognize it?

A BACTERIAL infection (NOT fungal) frequently misinterpreted as tinea pedis. Presents on weight-bearing surfaces of the soles - ventral toe, ball of the foot, and heel. Characteristic finding: circular or longitudinal punched-out pits in the stratum corneum. Key symptoms: hyperhidrosis, malodor, and sliminess of the skin. Little or no inflammation. Caused by bacteria: Dermatophilus congolensis, Corynebacterium species, Streptomyces, Kytococcus sedentarius. These produce keratinases that degrade keratin when skin is hydrated and pH rises above neutral.

Treatment: Promote dryness. Aluminum chloride 20% BID. Topical erythromycin, clindamycin, or mupirocin. Change socks frequently.

RAPID-FIRE REVIEW - TEST YOURSELF

Cover the answers and say them out loud

Q: Tinea versicolor - which two oral drugs do NOT work? Terbinafine and Griseofulvin.

Q: Why must tinea capitis be treated with oral drugs? Topical agents cannot penetrate to the depth of the hair follicle where the fungus resides - below the cuticle.

Q: Which oral antifungal is the drug of choice for tinea capitis in children? Griseofulvin - it has the longest safety record.

Q: Which drug is BETTER for Trichophyton tinea capitis? Terbinafine. Griseofulvin is better for Microsporum.

Q: Which topical antifungal also covers bacteria? Econazole.

Q: What is the KOH pattern for tinea versicolor? "Spaghetti and meatballs" - short hyphae plus round spore clusters.

Q: What does coral-red fluorescence on Wood's light indicate? Erythrasma - a BACTERIAL condition (Corynebacterium minutissimum), NOT fungal.

Q: What are satellite pustules a hallmark of? Candidiasis. Pinpoint pustules appearing just outside the main lesion.

Q: What does "tinea incognito" mean? A fungal infection whose classic features have been masked by inappropriate topical steroid treatment.

Q: What is the "id reaction"? Sterile itchy vesicles at distant sites (arms, chest, fingers) representing an allergic/immune response to a fungal infection elsewhere. They are NOT infective - they resolve when the primary infection is treated.

Q: Tinea cruris vs Candida - does the scrotum get involved? Tinea cruris = NO scrotal involvement. Candida = YES, scrotum is involved.

Q: What organisms cause tinea capitis in the USA vs Europe? USA = T. tonsurans (more than 90%). Europe = M. canis most common.

Q: Does T. tonsurans fluoresce under Wood's light? NO. T. tonsurans does NOT fluoresce - which is why Wood's light has limited value in the USA and UK.

Q: What is a kerion? A boggy, tender, indurated, tumor-like scalp lesion exuding pus - caused by an intense hypersensitivity reaction to a dermatophyte in tinea capitis. Can heal with scarring and hair loss.

Q: What culture medium turns pink in the presence of dermatophytes? DTM - Dermatophyte Test Medium. The phenol red indicator turns pink from alkaline metabolic products in about 6-7 days.

Q: What is moccasin-type tinea and which organism causes it? Chronic diffuse plantar infection covering the entire sole with silvery-white scale. Caused by T. rubrum, which suppresses the immune response and is very difficult to eradicate.

Q: What is the maintenance regimen for recurrent vulvovaginal candidiasis? Fluconazole 150 mg orally once weekly for 6 months.

Q: Which antifungal is contraindicated for tinea versicolor due to liver toxicity? Oral ketoconazole - contraindicated due to risk of serious liver damage, adrenal problems, drug interactions, and death.

Q: What happens if you treat dermatophyte infections with topical steroids? The steroids suppress inflammation temporarily, but the fungus flourishes due to cortisone-induced immune changes. This creates tinea incognito - a modified, expanded, atypical infection without classic features.

Q: What is the two feet-one hand syndrome? Dermatophyte infection of both feet plus one hand, caused by T. rubrum. The infected hand is usually the one used to scratch the feet.

FINAL SUMMARY TABLE

Condition	Organism	Key Feature	Treatment
Tinea pedis	Dermatophytes (T. rubrum)	4th/5th web; moccasin; vesicular; id reaction	Terbinafine cream or oral
Tinea cruris	Dermatophytes	Half-moon plaque; NO scrotum	Topical or oral antifungal
Tinea corporis	Dermatophytes	Ring with active scaly border	Topical; oral if extensive
Tinea capitis	T. tonsurans (USA)	Black dot, kerion, seborrheic, pustular; needs ORAL	Griseofulvin or terbinafine
Tinea barbae	T. verrucosum, T. mentagrophytes	Deep boggy abscess; painless hair removal	Oral antifungal
Tinea incognito	Any dermatophyte + steroids	No classic border; altered appearance	Stop steroids; KOH; oral antifungal
Tinea versicolor	Pityrosporum (Malassezia furfur)	Hypo/hyperpigmented macules; "spaghetti and meatballs" KOH	Ketoconazole shampoo; selenium sulfide; oral itraconazole/fluconazole
Pityrosporum folliculitis	Pityrosporum	Looks like acne; follicular papules on upper back	Oral fluconazole + topical antifungal
Candida (skin folds)	Candida albicans	Satellite pustules; ocean wave fringe of scale	Topical antifungal + wet compresses
Vulvovaginal candidiasis	Candida albicans	Curdy white discharge; pH less than 4.5	Azole cream or oral fluconazole
Oral candidiasis (thrush)	Candida albicans	White plaques on red base; tongue involved	Fluconazole 200 mg/day
Erythrasma	Corynebacterium (BACTERIA)	Coral-red Wood's light; NO advancing border	Erythromycin or clarithromycin
Pitted keratolysis	Bacteria (BACTERIAL)	Punched-out pits; malodor; hyperhidrosis	Dryness; aluminum chloride; antibiotics

Source: Habif's Clinical Dermatology, Chapter 13

Study tip: Read each Q and A out loud, as if speaking to an examiner. Then close the notes and try to say the answer from memory. Repeat until it flows naturally.

I DONT WANT IT IN QUESTIONS FORM

SUPERFICIAL FUNGAL INFECTIONS

Habif's Clinical Dermatology – Chapter 13

SECTION 1: DERMATOPHYTES

What Are Dermatophytes?

Dermatophytes are fungi that can ONLY infect dead keratin - the stratum corneum, hair, and nails. They cannot survive on mucous membranes (mouth, vagina) because those surfaces have no keratin layer. In very rare cases, mainly in immunosuppressed patients, they can invade deeply and spread to internal organs.

There is a genetic component to infection. Blood-related family members share similar infection patterns, but spouses do NOT become infected despite prolonged exposure. Patients with chronic infections have a specific defect in delayed hypersensitivity to Trichophyton, and there is a higher frequency of atopy in chronically infected patients.

Three Genera of Dermatophytes

Microsporum
Trichophyton
Epidermophyton (only one species)

Classification by Origin

Anthropophilic - parasitic only on humans; spread person to person; cause MILD inflammation
Zoophilic - originate from animals; can infect humans; cause BRISK, intense inflammation
Geophilic - live in soil; can infect humans; cause BRISK, intense inflammation

The degree of inflammation is important: zoophilic and geophilic organisms provoke a strong inflammatory response, while anthropophilic organisms tend to cause only mild reactions.

Hair Invasion Patterns

Endothrix - fungal hyphae are INSIDE the hair shaft only. The cuticle remains intact. Hyphae fragment into arthrospores inside the shaft.

Organisms: T. tonsurans, T. violaceum, T. soudanense

Ectothrix - fungal hyphae are INSIDE and ON THE SURFACE of the hair shaft. The hyphae break through and destroy the cuticle, forming a sheath of spores on the outside.

Organisms: M. canis, M. audouinii, T. verrucosum, T. mentagrophytes

Memory tip: Endo = entirely inside. Ecto = exits to the surface.

Diagnosis

KOH Wet Mount - The Most Important Test

Scrape scale from the active border with a no. 15 blade (perpendicular to the lesion). Place on a slide, add potassium hydroxide, gently heat, and examine under the microscope. KOH dissolves cellular material but leaves fungal hyphae intact.

Dermatophytes appear as translucent, branching, rod-shaped filaments of uniform width with septa at irregular intervals. The uniform width and characteristic branching distinguishes hyphae from hair or debris.

Only branching hyphae are seen in dermatophyte infections. Short, non-branching hyphae plus spores are seen in Candida and tinea versicolor.

Mosaic artifact - lipid droplets in a single-file line between cells that mimic hyphae. Most common in specimens from palms and soles. They disappear with additional heating and pressure. True hyphae do not disappear.

Wood's Light

Appearance	Organism/Condition
Blue-green fluorescence of hair	M. canis or M. audouinii
Pale green fluorescence of hair	T. schoenleinii (rare)
Pale yellow-white fluorescence of skin	Tinea versicolor
Coral-red fluorescence	Erythrasma - BACTERIAL (Corynebacterium minutissimum), NOT fungal
No fluorescence	T. tonsurans - most common cause of scalp ringworm in USA

Always perform Wood's light examination in a dark room with a high-intensity instrument.

Culture Media

DTM (Dermatophyte Test Medium) - turns PINK within 6-7 days in the presence of dermatophytes. The phenol red indicator turns pink from alkaline metabolic products. Quick office test. Must discard after 2 weeks. Good for confirming onychomycosis.

Mycobiotic agar - contains cycloheximide and chloramphenicol to suppress bacteria and saprophytic fungi. Best for hair infections (tinea capitis) because only dermatophytes grow.

Sabouraud's agar - no antibiotics; grows ALL fungi including non-dermatophytes. Best for nail infections where identifying saprophytic molds (that don't respond to treatment) is important.

SECTION 2: TINEA BY LOCATION

Tinea Pedis (Athlete's Foot)

Tinea pedis is the MOST COMMON site of dermatophyte infection. It predominantly affects men. It is uncommon in women and rare in prepubertal children. Once established, the person becomes a carrier and is more susceptible to recurrences. Shoes promote warmth and sweating, which encourage fungal growth.

Three Clinical Types

1. Interdigital (Toe-Web Infection) The 4th/5th web space is most commonly involved because tight shoes compress the toes there, creating warmth and moisture ideal for fungal growth. The web presents in two ways:

Dry, scaly, and fissured
White, macerated, and soggy

The macerated form results from interaction between the fungus AND bacteria. The fungus damages the stratum corneum and selects for antibiotic-resistant bacteria including Staphylococcus aureus, Gram-negative organisms, and Corynebacterium minutissimum.

2. Chronic Scaly Moccasin-Type (Hyperkeratotic/Plantar) The entire sole is covered with fine silvery-white scale. The skin may be pink and tender. The typical pattern is two feet and one hand - never both hands and both feet simultaneously. T. rubrum is the usual pathogen. This is particularly difficult to eradicate because T. rubrum produces substances that suppress the immune response and inhibit stratum corneum turnover.

3. Acute Vesicular Tinea Pedis A highly inflammatory form, often originating from a chronic web infection. Vesicles develop rapidly on the sole or dorsum. They may fuse into bullae. Secondary bacterial infection is common after bullae rupture. An important complication is the id (dermatophytid) reaction - sterile itchy vesicles appearing at distant sites (arms, chest, sides of fingers) representing an allergic immune response to the fungus. These are NOT infectious. They resolve once the primary infection is controlled.

Two Feet-One Hand Syndrome

Dermatophyte infection of both feet plus one hand (left or right palm). Nail infection often accompanies it. Most common in men. The same organism - usually T. rubrum - infects all three areas. The infected hand is typically the one used to scratch the feet or pick toenails.

Treatment

Interdigital: Terbinafine 1% cream BID x 1 week (88% mycologic cure at 5 weeks). Butenafine BID x 1 week also highly effective. Econazole is useful when bacterial overgrowth is significant.
Moccasin/plantar: Oral terbinafine 125 mg/day x 4 weeks (95% sustained cure rate). Topical agents respond slowly.
Vesicular: Wet Burow's solution compresses x 30 minutes several times daily + oral antifungal + oral antibiotics for secondary bacterial infection. Topical steroids or prednisone 20 mg BID x 8-10 days for id reactions.
Oral options: Fluconazole 150 mg once weekly x 3-4 weeks; itraconazole 200 mg BID x 1 week; terbinafine 250 mg daily x 2 weeks.
Prevention: Wider shoes, lamb's wool between toes, absorbent powder on feet (not shoes), change wet socks.

Tinea Cruris (Jock Itch)

Tinea cruris is a dermatophyte infection of the groin. It is much more common in men than women, rare in children. It is worse in summer from sweating, and in winter from wearing multiple layers. The predisposing factor is a warm, moist environment in the intertriginous area.

Clinical Appearance

Classic appearance is a unilateral, half moon-shaped plaque starting in the crural fold and advancing onto the thigh with a well-defined, scaly border. The skin inside the border turns red-brown and less scaly. Occasionally red papules appear at the edges. The infection may migrate to the buttocks and gluteal cleft. Importantly, the scrotum is NOT involved - this distinguishes tinea cruris from Candida infection.

Tinea Incognito

When tinea is treated inappropriately with topical steroids, the classic features become masked - this is called tinea incognito. The steroid suppresses inflammation and gives the false impression of improvement, but the fungus flourishes due to cortisone-induced immune changes. When steroids stop, the rash returns and the patient reapplies them, creating a cycle. The result is diffuse erythema, scattered pustules, a greatly expanded infection, and no classic border. Hyphae are still present on KOH prep. Most common sites: groin, face, dorsal hand.

Differential Diagnosis

vs. Candida groin infection:

Tinea cruris: Unilateral, NO scrotal involvement, scaly advancing border
Candida: Bilateral, more extensive, INVOLVES scrotum, satellite pustules at the border

vs. Erythrasma (Corynebacterium minutissimum - BACTERIAL):

Erythrasma: Non-inflammatory, uniformly brown and scaly, NO advancing border, coral-red fluorescence under Wood's light
Tinea cruris: Advancing scaly border, does NOT fluoresce

vs. Intertrigo:

Intertrigo extends equally onto the groin AND thigh; no advancing border; painful longitudinal fissures in crease

Treatment

Topical antifungal cream BID for at least 10 days. Allylamines (terbinafine, naftifine, butenafine) need a shorter duration than fungistatic azoles. Oral when needed: fluconazole 150 mg once weekly x 2-3 weeks; itraconazole 100 mg/day x 2 weeks; terbinafine 250 mg/day x 1-2 weeks.

Tinea Corporis (Ringworm of the Body)

Tinea corporis affects the face (excluding beard), trunk, and limbs. It can occur at any age and is more common in warm climates.

Classic Appearance

Begins as a flat scaly spot that develops a raised border expanding outward in all directions. The active border is red, scaly, and may have papules or vesicles. As it expands, the center becomes hypopigmented and less scaly - giving the classic "ringworm" ring appearance.

Special Forms

Tinea Gladiatorum - tinea corporis in competitive wrestlers. Common due to close person-to-person contact. Most cases caused by T. tonsurans.

Majocchi Granuloma - caused mainly by T. rubrum. Originally described in women who shave their legs; also seen in men and children at other sites. Primary lesion is a follicular papulopustule or nodule. Intracutaneous and subcutaneous granulomatous nodules develop because infected follicles rupture into the dermis, producing a granulomatous reaction with epithelioid cells, giant cells, and lymphocytes. Skin biopsy with special fungal stains is needed for diagnosis.

T. verrucosum ("Barn Itch") - zoophilic fungus from cattle. Produces a very intensely inflamed, boggy, pustular lesion. The pustules are follicular. The process heals with brown hyperpigmentation and scarring. Common in farmers.

Treatment

Topical antifungal cream BID x 2 weeks (continue 1 week after resolution). Oral therapy for extensive or papular lesions: fluconazole, itraconazole, or terbinafine (see drug dosage table).

Tinea Capitis (Scalp Ringworm)

Tinea capitis predominantly affects prepubertal children aged 3-7 years. It is most common in areas of poverty and crowded living. In the USA, T. tonsurans accounts for more than 90% of cases. In Europe, M. canis is the most common. Farmers can acquire T. verrucosum from cattle.

Why Topical Treatment Fails

The fungus invades deep into the hair follicle - below the level of the cuticle of the hair shaft. It gains entry into the hair below where the cuticle forms, meaning it cannot be reached by anything applied to the surface. Oral therapy is mandatory.

Four Clinical Patterns of T. tonsurans

1. Black Dot Pattern Areas of hair loss with hairs broken off at the follicular orifice. The arthrospores inside the hair shaft weaken the hair so it fractures at or below the scalp surface, leaving characteristic black dots (red dots if the patient's hair is red). Little to no inflammation. Mild to moderate scalp scale. Occipital adenopathy may be present.

2. Inflammatory Pattern (Kerion) A boggy, tender, indurated, tumor-like mass studded with pustules. Represents an intense hypersensitivity reaction to the fungus. May have fever, occipital adenopathy, leukocytosis, and even a morbilliform rash. KOH and cultures are often NEGATIVE because inflammation has destroyed the fungal structures - treatment may need to be started on clinical appearance alone. Scarring alopecia can result.

3. Seborrheic Dermatitis Type Looks exactly like dandruff - diffuse or patchy fine white scale. The most difficult pattern to diagnose. Only 29% have a positive KOH examination. Look closely for tiny perifollicular pustules and broken hair stubs.

4. Pustular Type Discrete pustules or scabbed areas without significant hair loss. Strongly suggests bacterial infection, and patients often receive multiple antibiotic courses before the correct diagnosis is made.

KEY RULE: Cervical or occipital lymphadenopathy should be present in ALL types of tinea capitis. The diagnosis should be questioned if there is no lymphadenopathy and no alopecia.

Diagnosis Methods

Toothbrush technique - rub a sterile toothbrush over the affected scalp, then inoculate bristles onto Mycosel medium. Superior to scalp scrapings.
Cotton swab technique - moistened sterile swab rubbed over affected area, then inoculated onto Mycosel. Easier in young children.
KOH prep of plucked hairs
Wood's light - only useful for M. canis/M. audouinii (blue-green fluorescence). T. tonsurans does NOT fluoresce.

Treatment - Oral Drugs for Tinea Capitis

Drug	Dose	Duration	Key Points
Griseofulvin	15-25 mg/kg/day	6-8 wks (Trichophyton); 8-12 wks (Microsporum)	Drug of choice in children; take with fatty food; longest safety record; fungistatic
Terbinafine	62.5-250 mg/day (weight-based)	4 weeks	Fungicidal; BEST for Trichophyton; efficacy for Microsporum disputed
Itraconazole	5 mg/kg/day	4-6 weeks	Take with full meal and acidic juice; many drug interactions
Fluconazole	6 mg/kg/day	3-6+ weeks	Available as pleasant-tasting liquid; approved for children over 6 months

Adjuvant Measures

Antifungal shampoo (selenium sulfide 2.5%, ketoconazole 2%, zinc pyrithione) used 2-3 times per week to reduce spore load
Screen ALL family members and close contacts
Clean all fomites - combs, brushes, bedding, furniture (T. tonsurans spores remain viable for months on inanimate objects)
Children may return to school once systemic therapy has started - no need for extended exclusion
For asymptomatic carriers with heavy spore counts, systemic therapy may be justified

Tinea Barbae (Beard Ringworm)

Dermatophyte infection limited to the coarse hair-bearing beard and mustache areas in men. Usually follows minor trauma such as shaving. Frequently mistaken for bacterial folliculitis - patients typically receive multiple antibiotic courses before the correct diagnosis is made.

Key distinguishing feature from bacterial folliculitis: In tinea barbae, hairs are infected and can be removed painlessly. In bacterial folliculitis, removal is painful and hairs resist removal.

Two patterns:

Superficial - annular lesions resembling tinea corporis; hair is usually infected
Deep follicular - boggy, erythematous, tumor-like abscess with dense crust, similar to a kerion; caused by T. verrucosum (from cattle) and T. mentagrophytes

Treatment: Oral antifungals required because creams cannot penetrate to the depth of the hair follicle.

SECTION 3: ANTIFUNGAL DRUGS

Griseofulvin

Griseofulvin is fungistatic. It works best on actively growing dermatophytes by inhibiting fungal cell wall synthesis. It diffuses into the stratum corneum from extracellular fluid and sweat. It is active ONLY against dermatophytes - Candida and tinea versicolor do NOT respond.

Available in microsize and ultramicrosize forms. Ultramicrosize is better absorbed and requires only 50-70% of the microsize dose. Take with fatty food to enhance absorption.

Side effects: Headache and GI symptoms most common. Rarely: hepatotoxicity, leukopenia, photosensitivity.

Drug interactions: Activates hepatic enzymes that decrease levels of warfarin, estrogen, and oral contraceptive pills. Alcohol effect is potentiated. Barbiturates reduce griseofulvin activity.

Contraindications: Pregnancy, lupus erythematosus, porphyria, severe liver disease.

Terbinafine

Terbinafine is an allylamine that inhibits squalene epoxidase - a membrane-bound enzyme NOT part of the cytochrome P-450 family. It is FUNGICIDAL to dermatophytes.

Key pharmacokinetic properties:

Highly lipophilic and keratophilic
Distributed throughout adipose tissue, dermis, epidermis, and nails
Persists in skin, hair, and nails for weeks after stopping therapy
After 6-12 weeks of therapy, still detectable in nails for 30-36 weeks
Delivered to stratum corneum via sebum (NOT found in eccrine sweat)
Metabolized in the liver; dose adjustment needed in liver and renal dysfunction

Important: Oral terbinafine does NOT work for tinea versicolor.

Allylamines vs. Azoles - The Key Distinction

Allylamines (terbinafine, naftifine, butenafine) = FUNGICIDAL → shorter treatment, higher cure rates, lower relapse rates

Azoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole) = FUNGISTATIC → longer treatment needed

Both groups inhibit ergosterol synthesis, but at different points in the pathway.

Itraconazole

Highly lipophilic with a high affinity for keratinizing tissues. Progressively builds up in the nail plate and persists for at least 6 months after 3 months of therapy. Sebum levels are FIVE TIMES higher than plasma levels.

Absorption is significantly increased by food - take with a full meal and acidic juice. Absorption is reduced by antacids, H2 blockers, and proton pump inhibitors.

Has many drug interactions because it inhibits cytochrome P-450. Contraindicated with cisapride, astemizole, triazolam, lovastatin, simvastatin, and midazolam.

Fluconazole

Highly water-soluble - unusual for an antifungal. Transported to skin through sweat, where it concentrates by evaporation. Achieves high concentrations in the epidermis and nails. Persists for long periods. Available as a pleasant-tasting liquid for children. Approved for children over 6 months.

Econazole - The Special One

Econazole covers dermatophytes + yeasts + BACTERIA. Particularly useful for severely macerated interdigital toe web infections where bacterial overgrowth is a significant problem.

Topical Antifungal Coverage Summary

Class	Drug	Dermatophytes	Yeasts	Bacteria
Allylamine	Terbinafine, Naftifine, Butenafine	YES	No	No
Imidazole	Clotrimazole	YES	YES	No
Imidazole	Econazole	YES	YES	YES
Imidazole	Ketoconazole, Miconazole, Oxiconazole	YES	YES	No

Oral Antifungal Dosage Reference

Condition	Griseofulvin	Fluconazole	Itraconazole	Terbinafine
Tinea corporis/cruris	500 mg/day x 2-4 wks	150 mg weekly x 2-4 wks	100 mg/day x 2 wks	250 mg/day x 1-2 wks
Tinea capitis	15-25 mg/kg/day x 6-8 wks	6 mg/kg/day x 4-6 wks	5 mg/kg/day x 4-6 wks	Weight-based x 2-4 wks
Onychomycosis	Not recommended	150 mg weekly x 9 months	200 mg/day - pulse dosing	250 mg/day: fingers 6 wks; toes 12 wks
Tinea pedis	500 mg/day x 6-12 wks	50 mg weekly x 3-4 wks	200 mg BID x 1 week	250 mg/day x 2 wks
Tinea versicolor	NOT effective	300 mg x 1-2 doses	200 mg/day x 7 days	NOT effective (oral)

SECTION 4: CANDIDIASIS

Key Facts

C. albicans is normal flora of the mouth, vaginal tract, and gut. It infects only the outer layers of the epithelium - the stratum corneum. The primary lesion is a pustule. Its contents dissect horizontally under the stratum corneum, producing a red, denuded, glistening surface with a "cigarette paper-like" scaling advancing border.

Yeast grows best in warm, moist environments - so infection is confined to mucous membranes and intertriginous areas. The advancing border stops when it reaches dry skin.

When Does Candida Become Pathogenic?

Pregnancy, oral contraceptives
Antibiotic therapy (disrupts normal bacterial flora)
Diabetes mellitus
Skin maceration
Topical steroid therapy
Immunosuppression, HIV
Cushing's disease, adrenal disorders
Inhalant steroid use (oral candidiasis)

Candida on KOH vs. Dermatophytes

Candida shows both pseudohyphae AND budding spores. Dermatophytes show only branching hyphae. Since pseudohyphae are indistinguishable from dermatophyte hyphae in a KOH prep, culture must be interpreted carefully - Candida is also part of normal flora in many areas.

Vulvovaginal Candidiasis (VVC)

Presentation: Pruritus, vaginal soreness, dyspareunia, external dysuria, thick curdy white vaginal discharge. Signs include vulvar edema, fissures, excoriations.

Diagnosis: KOH or saline wet prep showing yeasts, hyphae, or pseudohyphae. Vaginal pH is NORMAL (less than 4.5) - pH testing is NOT useful here. Identifying Candida on culture without symptoms is NOT an indication for treatment, because 10-20% of women normally carry Candida.

Vaginal Discharge Comparison

Feature	Candida	Bacterial Vaginosis	Trichomoniasis
Discharge	White, clumpy, curdy	Gray, homogeneous, fishy	Profuse, greenish, frothy
Main symptom	Itching	Malodorous discharge	Malodor + itching + dysuria
pH	Less than 4.5	Greater than 4.7	4.5
Wet prep	Budding yeast, pseudohyphae	Clue cells with adherent bacteria	Motile trichomonads
Amine test	Negative	Positive (fishy odor)	Positive

Treatment of VVC

Uncomplicated: OTC topical azoles (clotrimazole, miconazole) x 1-7 days, OR single oral fluconazole 150 mg. Topical azoles are more effective than nystatin.

Recurrent VVC (RVVC = 4 or more episodes per year):

Induction: Fluconazole 150 mg every 72 hours x 3 doses (Day 1, Day 4, Day 7)
Maintenance: Fluconazole 150 mg once weekly x 6 months

Note: 30-50% of women relapse after stopping maintenance therapy.

Severe VVC: 7-14 days topical, OR fluconazole 150 mg x 2 doses taken 72 hours apart.

C. glabrata (causes 10-20% of RVVC; azole-resistant): Boric acid vaginal suppository 600 mg/day x 14 days, or nystatin suppository.

Oral Candidiasis (Thrush)

The tongue is almost always involved. Classic presentation: white, creamy plaques on a red, sore base. The plaques can be scraped off (unlike leukoplakia).

Occurs in: diabetes, elderly, cancer (especially leukemia), prolonged steroid/antibiotic use, HIV (more than 90% of AIDS patients develop it), inhalant steroid use.

In infants, it is called THRUSH. It is self-limited in healthy newborns but should be treated to avoid interference with feeding. The mother should be examined for vaginal candidiasis.

Drug	Dose
Fluconazole	200 mg/day x 1 week (FIRST LINE)
Itraconazole	200 mg/day x 1-3 weeks
Clotrimazole troche	Dissolve slowly x 5 times/day x 14 days
Nystatin suspension	4-6 mL QID for adults; 2 mL QID for infants

Candida Balanitis

More common in uncircumcised men because the foreskin creates the warm, moist environment yeast needs. Can occur after intercourse with an infected female partner. Presents as tender, pinpoint red papules and pustules on the glans and shaft. White donut-shaped rings form after pustules break. White exudate may be present. Presence of pustules is highly suggestive of candidiasis.

Treatment: Miconazole or clotrimazole BID x 7 days, or single oral fluconazole 150 mg.

Candida Intertrigo (Large Skin Folds)

Occurs wherever skin touches skin: under pendulous breasts, between abdominal folds, in the groin, axillae, and rectal area. Hot humid weather, tight underclothing, poor hygiene, and inflammatory conditions in skin folds make infection more likely.

Two presentations:

Pustules that macerate under opposing skin surfaces → red papules with a fringe of moist scale at the border; intact pustules found OUTSIDE the fold
Red, moist, glistening plaque with an "ocean wave" fringe of macerated scale at a sharply defined border

Satellite pustules - pinpoint pustules just outside the main lesion - are the hallmark diagnostic feature. There is a tendency for painful fissuring in the skin creases.

Treatment: Cool wet compresses x 20-30 minutes several times daily to promote dryness + antifungal cream BID + absorbent powder after inflammation resolves.

Candidiasis of Small Skin Folds

Finger/Toe Web Spaces: White, tender, macerated skin erodes to reveal a pink moist base. Toe web candidiasis most common in the 4th/5th interspace where it may coexist with dermatophytes and Gram-negative bacteria. Treatment: topical antifungal cream or lotion.

Angular Cheilitis (Perlèche): Inflammation at the corners of the mouth. Caused by saliva pooling via capillary action into the skin fold at the mouth angles, causing maceration and secondary infection with Candida and/or staphylococci. Causes include lip licking, thumb sucking, poorly fitting dentures, mouth breathing, advancing age, weight loss. Patients mistakenly believe they have a vitamin B deficiency. Treatment: antifungal cream followed in a few hours by a topical steroid until the area is dry and inflammation-free, then thick lip balm to protect.

Diaper Candidiasis: The wet diaper creates an artificial intertriginous area. Presents as a red base with satellite pustules. Change diapers frequently. Antifungal cream BID x 10 days.

SECTION 5: TINEA VERSICOLOR

What It Is

Tinea versicolor is caused by dimorphic lipophilic yeasts - Pityrosporum orbiculare (round form) and Pityrosporum ovale (oval form), collectively called Malassezia furfur. These are normal skin flora that live in the stratum corneum and hair follicles, feeding on free fatty acids and triglycerides. They convert from their normal budding yeast form to a mycelial (hyphal) form when triggered by certain conditions.

The disease is most common in adolescents and young adults due to higher sebaceous activity. May not be contagious.

Triggers (Yeast Converts to Pathogenic Mycelial Form)

Endogenous: Cushing's disease, adrenalectomy, pregnancy, malnutrition, burns, corticosteroids, immunosuppression, oral contraceptives

Exogenous: Excess heat and humidity

Clinical Presentation

Lesions begin as multiple small, circular macules that enlarge radially. The color varies - hence "versicolor":

White/hypopigmented - most obvious in summer when surrounding skin tans
Pink to red - from an inflammatory/hyperemic response
Fawn/tan/brown - post-inflammatory pigmentation

The upper trunk is most commonly affected, along with upper arms, neck, and abdomen. Facial lesions are more common in children (forehead is the usual site). Lesions may be asymptomatic or mildly itchy.

Why hypopigmentation occurs: Dicarboxylic acids produced by the yeast are cytotoxic to melanocytes and inhibit the dopa-tyrosinase reaction. There is a reduction in number, size, and aggregation of melanosomes.

The lesions are worst/most noticeable in summer because unaffected skin tans while the lesions remain white.

Diagnosis

Scrape lightly with a no. 15 blade to reveal powdery scale that may not be visible on inspection. KOH prep shows the classic "spaghetti and meatballs" pattern - short broad hyphae (spaghetti) intermixed with round spore clusters (meatballs). Wood's light shows pale yellow-to-white fluorescence (some lesions do not fluoresce). Culture is possible but rarely necessary.

Griseofulvin is NOT active against tinea versicolor.

Treatment

Important patient counseling: Hypopigmented patches will NOT disappear immediately after treatment. Repigmentation takes time. Sunlight accelerates repigmentation. Confirm eradication by scraping - when no powdery scale is produced, the fungus has been cleared. Recurrence rates are high (40-60%).

Topical (First Line for Limited Disease)

Ketoconazole 2% shampoo - FIRST CHOICE. Apply to entire body from neck to thighs, leave 5 minutes, rinse. Single application or daily x 3 days. Also wash scalp.
Selenium sulfide 2.5% - apply for 10 minutes daily x 7 days = 87% cure rate. Apply from lower posterior scalp to thighs.
Any imidazole cream (miconazole, clotrimazole, econazole) BID x 2-4 weeks.
Zinc pyrithione shampoo is the most effective non-imidazole topical agent.

Oral (For Extensive or Recurrent Disease)

Itraconazole 200 mg/day x 7 days
Fluconazole 300 mg/week x 2 doses
Oral terbinafine = NOT effective
Oral griseofulvin = NOT effective
Oral ketoconazole = CONTRAINDICATED - risk of serious liver damage, adrenal problems, drug interactions, and death

Recurrence Prevention

Ketoconazole 2% shampoo applied once weekly to trunk, neck, and proximal extremities, 5-10 minutes before showering. Repeat full treatment before the summer months.

SECTION 6: PITYROSPORUM FOLLICULITIS

Pityrosporum folliculitis is an infection of hair follicles by Pityrosporum orbiculare - the same organism that causes tinea versicolor. It presents as asymptomatic or mildly itchy follicular papules and pustules on the upper back, chest, upper arms, and neck. It is frequently misdiagnosed as acne and does not respond to acne antibiotics.

In tropical presentations, the face is commonly involved - more lateral (mandible and sides of the face) compared to typical acne, which is more central.

Risk factors: Diabetes, broad-spectrum antibiotics, corticosteroids, Hodgkin disease, occlusion, oily skin.

Diagnosis: KOH shows abundant round budding yeast cells and sometimes hyphae.

Treatment: Oral fluconazole combined with topical antifungal. Ketoconazole 2% cream/shampoo. Salicylic acid wash is keratolytic and effective.

BONUS: PITTED KERATOLYSIS

Pitted keratolysis is a BACTERIAL infection (NOT fungal) that is frequently misinterpreted as tinea pedis. It affects the weight-bearing surfaces of the soles.

Characteristic features: Circular or longitudinal punched-out pits in the stratum corneum, hyperhidrosis, malodor, and sliminess of the skin. There is little or no inflammation.

Caused by: Dermatophilus congolensis, Corynebacterium species, Streptomyces, Kytococcus sedentarius. These bacteria produce keratinases that degrade keratin when the skin is hydrated and the pH rises above neutral.

Treatment: Promote dryness. Aluminum chloride 20% BID for rapid clearing. Topical erythromycin, clindamycin, or mupirocin. Change socks frequently.

RAPID-FIRE SUMMARY - KEY FACTS TO KNOW

Dermatophytes infect dead keratin only - NOT mucous membranes
The single most important diagnostic test = KOH wet mount
Best place to scrape for KOH = active border
Mosaic artifact disappears with heat; true hyphae do not
T. tonsurans (USA) does NOT fluoresce under Wood's light
Coral-red Wood's light = Erythrasma = BACTERIAL, not fungal
DTM turns PINK in 6-7 days with dermatophytes
Tinea capitis MUST be treated orally - topical agents cannot reach the follicle
Griseofulvin = drug of choice in children for tinea capitis
Terbinafine = BEST for Trichophyton; griseofulvin = BETTER for Microsporum
Tinea cruris does NOT involve the scrotum; Candida groin DOES
Tinea incognito = dermatophyte infection masked by steroid use
Id reaction = sterile vesicles at distant sites; allergic response; NOT infectious
Two feet-one hand syndrome = T. rubrum; the opposite hand is the infected one
Satellite pustules = hallmark of Candidiasis
Tinea versicolor KOH = "spaghetti and meatballs"
Oral terbinafine and oral griseofulvin do NOT work for tinea versicolor
Oral ketoconazole is CONTRAINDICATED for tinea versicolor (liver toxicity/death)
RVVC maintenance = fluconazole 150 mg weekly x 6 months
Pitted keratolysis = bacterial, NOT fungal; treat with dryness and antibiotics
Pityrosporum folliculitis is frequently misdiagnosed as acne

COMPLETE AT-A-GLANCE TABLE

Condition	Organism	Key Feature	Treatment
Tinea pedis	Dermatophytes (T. rubrum)	4th/5th web; moccasin type; vesicular with id reaction	Terbinafine cream or oral
Tinea cruris	Dermatophytes	Half-moon plaque; NO scrotum; does not fluoresce	Topical or oral antifungal
Tinea corporis	Dermatophytes	Ring with active scaly border; expands outward	Topical; oral if extensive
Tinea capitis	T. tonsurans (USA)	Black dot, kerion, seborrheic, pustular; lymphadenopathy in ALL types	ORAL mandatory - griseofulvin or terbinafine
Tinea barbae	T. verrucosum, T. mentagrophytes	Boggy abscess; painless hair removal	Oral antifungal
Tinea incognito	Any dermatophyte + steroids	No classic border; expanded infection	Stop steroids; KOH; oral antifungal
Tinea versicolor	Pityrosporum (Malassezia furfur)	Hypo/hyperpigmented macules; spaghetti and meatballs KOH	Ketoconazole shampoo; selenium sulfide; oral itraconazole/fluconazole
Pityrosporum folliculitis	Pityrosporum	Looks like acne; follicular papules on upper back	Oral fluconazole + topical antifungal
Candida skin folds	Candida albicans	Satellite pustules; ocean wave fringe of scale	Topical antifungal + wet compresses
VVC	Candida albicans	Curdy white discharge; pH less than 4.5	Azole cream or oral fluconazole
Oral candidiasis	Candida albicans	White plaques on red base; tongue involved	Fluconazole 200 mg/day
Erythrasma	Corynebacterium (BACTERIAL)	Coral-red Wood's light; NO advancing border	Erythromycin or clarithromycin
Pitted keratolysis	Mixed bacteria (BACTERIAL)	Punched-out pits; malodor; hyperhidrosis	Dryness; aluminum chloride; antibiotics

Source: Habif's Clinical Dermatology, Chapter 13 - Superficial Fungal Infections

WHY IS TREATMENT FOR SOME PARTS MISSING

EDIT THE FULL TEXT , DOSES IS NOT IMPORTANT JUST MENTION TREATMENT FOR ALL DISEASES

SUPERFICIAL FUNGAL INFECTIONS

Habif's Clinical Dermatology – Chapter 13

SECTION 1: DERMATOPHYTES

What Are Dermatophytes?

Three Genera of Dermatophytes

Microsporum
Trichophyton
Epidermophyton (only one species)

Classification by Origin

Anthropophilic - parasitic only on humans; spread person to person; cause MILD inflammation
Zoophilic - originate from animals; can infect humans; cause BRISK, intense inflammation
Geophilic - live in soil; can infect humans; cause BRISK, intense inflammation

Hair Invasion Patterns

Endothrix - fungal hyphae are INSIDE the hair shaft only. The cuticle remains intact. Hyphae fragment into arthrospores inside the shaft. Organisms: T. tonsurans, T. violaceum, T. soudanense

Ectothrix - fungal hyphae are INSIDE and ON THE SURFACE of the hair shaft. The hyphae break through and destroy the cuticle, forming a sheath of spores on the outside. Organisms: M. canis, M. audouinii, T. verrucosum, T. mentagrophytes

Memory tip: Endo = entirely inside. Ecto = exits to the surface.

Diagnosis

KOH Wet Mount - The Most Important Test

Scrape scale from the active border with a no. 15 blade perpendicular to the lesion. Place on a slide, add potassium hydroxide, gently heat, and examine under the microscope. KOH dissolves cellular material but leaves fungal hyphae intact.

Dermatophytes appear as translucent, branching, rod-shaped filaments of uniform width with septa at irregular intervals. The uniform width and characteristic branching distinguishes hyphae from hair or debris.

Only branching hyphae are seen in dermatophyte infections. Short non-branching hyphae plus spores are seen in Candida and tinea versicolor.

Wood's Light

Appearance	Organism / Condition
Blue-green fluorescence of hair	M. canis or M. audouinii
Pale green fluorescence of hair	T. schoenleinii (rare)
Pale yellow-white fluorescence of skin	Tinea versicolor
Coral-red fluorescence	Erythrasma - BACTERIAL (Corynebacterium minutissimum), NOT fungal
No fluorescence	T. tonsurans - most common cause of scalp ringworm in USA

Always perform Wood's light examination in a dark room with a high-intensity instrument.

Culture Media

Mycobiotic agar - contains cycloheximide and chloramphenicol to suppress bacteria and saprophytic fungi. Best for hair infections (tinea capitis) because only dermatophytes grow.

Sabouraud's agar - no antibiotics; grows ALL fungi including non-dermatophytes. Best for nail infections where identifying saprophytic molds is important.

SECTION 2: TINEA BY LOCATION

Tinea Pedis (Athlete's Foot)

Three Clinical Types

1. Interdigital (Toe-Web Infection) The 4th/5th web space is most commonly involved because tight shoes compress the toes there, creating warmth and moisture. The web presents in two ways:

Dry, scaly, and fissured
White, macerated, and soggy

3. Acute Vesicular Tinea Pedis A highly inflammatory form, often originating from a chronic web infection. Vesicles develop rapidly on the sole or dorsum and may fuse into bullae. Secondary bacterial infection is common after bullae rupture. An important complication is the id (dermatophytid) reaction - sterile itchy vesicles at distant sites (arms, chest, sides of fingers) representing an allergic immune response to the fungus. These are NOT infectious and resolve once the primary infection is controlled.

Two Feet-One Hand Syndrome

Dermatophyte infection of both feet plus one hand. The same organism - usually T. rubrum - infects all three areas. The infected hand is typically the one used to scratch the feet or pick toenails.

Treatment

Interdigital: Topical terbinafine or butenafine cream for 1 week. Econazole is useful when bacterial overgrowth is significant because it also covers bacteria.
Moccasin/plantar type: Requires oral antifungal therapy (terbinafine, itraconazole, or fluconazole). Topical agents alone respond too slowly.
Acute vesicular: Wet Burow's solution compresses several times daily to dry the blisters + oral antifungal + oral antibiotics if secondary bacterial infection occurs. Topical or oral steroids are used to control id reactions.
Prevention: Wider shoes, lamb's wool between toes, absorbent powder on feet, change wet socks.

Tinea Cruris (Jock Itch)

Tinea cruris is a dermatophyte infection of the groin. It is much more common in men than women, rare in children. It is worse in summer from sweating, and in winter from wearing multiple layers.

Clinical Appearance

Classic appearance is a unilateral, half moon-shaped plaque starting in the crural fold and advancing onto the thigh with a well-defined, scaly border. The skin inside the border turns red-brown and less scaly. The infection may migrate to the buttocks and gluteal cleft. Importantly, the scrotum is NOT involved - this distinguishes tinea cruris from Candida infection.

Tinea Incognito

When tinea is treated inappropriately with topical steroids, the classic features become masked. The steroid suppresses inflammation giving the false impression of improvement, but the fungus flourishes due to cortisone-induced immune changes. The classic border disappears and the result is diffuse erythema, scattered pustules, and a greatly expanded infection. Hyphae are still present on KOH prep. Most common sites: groin, face, dorsal hand.

Differential Diagnosis

vs. Candida groin infection:

Tinea cruris: Unilateral, NO scrotal involvement, scaly advancing border
Candida: Bilateral, more extensive, INVOLVES scrotum, satellite pustules at the border

vs. Erythrasma (Corynebacterium minutissimum - BACTERIAL):

Erythrasma: Non-inflammatory, uniformly brown and scaly, NO advancing border, coral-red fluorescence under Wood's light
Tinea cruris: Advancing scaly border, does NOT fluoresce

vs. Intertrigo:

Extends equally onto the groin AND thigh, no advancing border, painful longitudinal fissures in the crease

Treatment

Topical antifungal cream applied twice daily for at least 10 days. Allylamines (terbinafine, naftifine, butenafine) need a shorter treatment duration than fungistatic azoles (clotrimazole, miconazole, econazole). When the area is moist and macerated, cool wet compresses are applied first to dry the skin. Oral antifungal therapy (fluconazole, itraconazole, or terbinafine) is used for resistant or extensive infections.

Tinea Corporis (Ringworm of the Body)

Tinea corporis affects the face (excluding beard), trunk, and limbs. It can occur at any age and is more common in warm climates.

Classic Appearance

Special Forms

Tinea Gladiatorum - tinea corporis in competitive wrestlers. Common due to close person-to-person skin contact. Most cases caused by T. tonsurans.

Majocchi Granuloma - caused mainly by T. rubrum. Originally described in women who shave their legs; also seen in men and children at other sites. Primary lesion is a follicular papulopustule or nodule. Granulomatous nodules develop in the dermis and subcutis because infected follicles rupture into the dermis, producing a reaction with epithelioid cells, giant cells, and lymphocytes. Skin biopsy with special fungal stains is needed for diagnosis.

T. verrucosum ("Barn Itch") - zoophilic fungus acquired from cattle. Produces a very intensely inflamed, boggy, pustular lesion. Heals with brown hyperpigmentation and scarring. Common in farmers.

Treatment

Superficial lesions: Topical antifungal cream applied twice daily for 2 weeks, continued for 1 week after the infection has resolved.
Extensive lesions or those with red papules: Oral antifungal therapy (fluconazole, itraconazole, or terbinafine) because topical agents alone are less reliable.
Deep inflammatory lesions (e.g. Majocchi granuloma, T. verrucosum): Oral antifungal therapy for 1-3 months or more. Wet Burow's compresses reduce inflammation. Bacterial infection is treated with oral antibiotics. A short course of oral prednisone may be considered for highly inflamed kerions to reduce swelling and discomfort.

Tinea Capitis (Scalp Ringworm)

Tinea capitis predominantly affects prepubertal children aged 3-7 years. Most common in areas of poverty and crowded living. In the USA, T. tonsurans accounts for more than 90% of cases. In Europe, M. canis is most common. Farmers acquire T. verrucosum from cattle.

Why Topical Treatment Fails

The fungus invades deep into the hair follicle - below the level of the cuticle. Topical agents cannot penetrate to that depth. Oral therapy is mandatory.

Four Clinical Patterns of T. tonsurans

1. Black Dot Pattern Areas of hair loss with hairs broken off at the follicular orifice. The arthrospores inside the hair shaft weaken it so it fractures at or below the scalp surface, leaving characteristic black dots. Little to no inflammation. Mild to moderate scalp scale.

2. Inflammatory Pattern (Kerion) A boggy, tender, indurated, tumor-like mass studded with pustules. Represents an intense hypersensitivity reaction to the fungus. May have fever and lymphadenopathy. KOH and cultures are often NEGATIVE because inflammation has destroyed the fungal structures. Scarring alopecia can result.

4. Pustular Type Discrete pustules or scabbed areas with minimal hair loss. Often receives multiple antibiotic courses before the correct diagnosis is made.

KEY RULE: Cervical or occipital lymphadenopathy should be present in ALL types. Question the diagnosis if there is no lymphadenopathy and no alopecia.

Diagnosis Methods

Toothbrush technique - rub a sterile toothbrush over the affected scalp then inoculate bristles onto Mycosel medium. Superior to scalp scrapings.
Cotton swab technique - moistened sterile swab rubbed over affected area then inoculated onto Mycosel medium. Easier in young children.
KOH prep of plucked hairs
Wood's light - only useful for M. canis/M. audouinii (blue-green fluorescence). T. tonsurans does NOT fluoresce.

Treatment

Oral therapy is mandatory - topical alone is never sufficient.

Drug options:

Griseofulvin - Drug of choice in children. Fungistatic. Longest safety record. Take with fatty food. Best for Microsporum.
Terbinafine - Fungicidal. Best for Trichophyton species. Efficacy for Microsporum is disputed.
Itraconazole - Good for both Trichophyton and Microsporum. Take with a full meal and acidic juice.
Fluconazole - Effective for both. Available as a pleasant-tasting liquid. Approved for children over 6 months.

Adjuvant measures:

Antifungal shampoo (selenium sulfide 2.5%, ketoconazole 2%, zinc pyrithione) used 2-3 times per week to reduce spore load and transmission
Screen ALL family members and close contacts
Clean all fomites - combs, brushes, bedding (T. tonsurans spores remain viable for months)
Children may return to school once systemic therapy has started
For kerions, a short course of oral corticosteroids may be added to reduce severe inflammation
For asymptomatic carriers with heavy spore counts, systemic therapy may be justified

Tinea Barbae (Beard Ringworm)

Key distinguishing feature from bacterial folliculitis: In tinea barbae, hairs are infected and can be removed painlessly. In bacterial folliculitis, removal is painful and hairs resist removal.

Two patterns:

Superficial - annular lesions resembling tinea corporis with infected hairs
Deep follicular - boggy, erythematous, tumor-like abscess with dense crust, similar to a kerion. Caused by T. verrucosum (from cattle) and T. mentagrophytes.

Treatment

Oral antifungal therapy is required because topical creams cannot penetrate to the depth of the hair follicle. This is treated the same way as tinea capitis. For deep infections with secondary bacterial involvement, oral antibiotics are added. Wet compresses help reduce inflammation.

SECTION 3: ANTIFUNGAL DRUGS

Griseofulvin

Griseofulvin is fungistatic. It works best on actively growing dermatophytes by inhibiting fungal cell wall synthesis. It diffuses into the stratum corneum from extracellular fluid and sweat. Active ONLY against dermatophytes - Candida and tinea versicolor do NOT respond. Take with fatty food to enhance absorption.

Side effects: Headache and GI symptoms most common. Rarely: hepatotoxicity, leukopenia, photosensitivity.

Drug interactions: Activates hepatic enzymes - decreases levels of warfarin, estrogen, and oral contraceptive pills. Alcohol effect is potentiated. Barbiturates reduce griseofulvin activity.

Contraindications: Pregnancy, lupus erythematosus, porphyria, severe liver disease.

Terbinafine

Terbinafine is an allylamine that inhibits squalene epoxidase - a membrane-bound enzyme NOT part of the cytochrome P-450 family. It is FUNGICIDAL to dermatophytes.

Key properties:

Highly lipophilic and keratophilic
Persists in skin, hair, and nails for weeks after stopping therapy
After 6-12 weeks of therapy, still detectable in nails for 30-36 weeks
Delivered to stratum corneum via sebum (NOT found in eccrine sweat)
Metabolized in the liver; dose adjustment needed in liver and renal dysfunction
Oral terbinafine does NOT work for tinea versicolor

Allylamines vs. Azoles - The Key Distinction

Allylamines (terbinafine, naftifine, butenafine) = FUNGICIDAL - shorter treatment, higher cure rates, lower relapse rates

Azoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole) = FUNGISTATIC - longer treatment needed

Both groups inhibit ergosterol synthesis, but at different points in the pathway.

Itraconazole

Highly lipophilic with a high affinity for keratinizing tissues. Builds up progressively in the nail plate and persists for at least 6 months after 3 months of therapy. Sebum levels are FIVE TIMES higher than plasma levels. Take with a full meal and acidic juice to enhance absorption. Many drug interactions because it inhibits cytochrome P-450.

Fluconazole

Highly water-soluble - unusual for an antifungal. Transported to skin through sweat, where it concentrates by evaporation. Achieves high concentrations in the epidermis and nails. Available as a pleasant-tasting liquid for children. Approved for children over 6 months.

Econazole - The Special One

Econazole covers dermatophytes + yeasts + BACTERIA. Particularly useful for severely macerated interdigital toe web infections where bacterial overgrowth is significant.

Topical Antifungal Coverage

Class	Drug	Dermatophytes	Yeasts	Bacteria
Allylamine	Terbinafine, Naftifine, Butenafine	YES	No	No
Imidazole	Clotrimazole	YES	YES	No
Imidazole	Econazole	YES	YES	YES
Imidazole	Ketoconazole, Miconazole, Oxiconazole	YES	YES	No

SECTION 4: CANDIDIASIS

Key Facts

Yeast grows best in warm, moist environments - so infection is confined to mucous membranes and intertriginous areas. The advancing border stops when it reaches dry skin.

When Does Candida Become Pathogenic?

Pregnancy, oral contraceptives
Antibiotic therapy (disrupts normal bacterial flora)
Diabetes mellitus
Skin maceration
Topical steroid therapy
Immunosuppression, HIV
Cushing's disease, adrenal disorders
Inhalant steroid use

Candida on KOH vs. Dermatophytes

Candida shows both pseudohyphae AND budding spores. Dermatophytes show only branching hyphae. Since pseudohyphae look similar to dermatophyte hyphae in a KOH prep, culture results must be interpreted carefully - Candida is also part of normal flora in many areas.

Vulvovaginal Candidiasis (VVC)

Presentation: Pruritus, vaginal soreness, dyspareunia, external dysuria, thick curdy white vaginal discharge. Signs include vulvar edema, fissures, excoriations.

Vaginal Discharge Comparison

Feature	Candida	Bacterial Vaginosis	Trichomoniasis
Discharge	White, clumpy, curdy	Gray, homogeneous, fishy	Profuse, greenish, frothy
Main symptom	Itching	Malodorous discharge	Malodor + itching + dysuria
pH	Less than 4.5	Greater than 4.7	4.5
Wet prep	Budding yeast, pseudohyphae	Clue cells with adherent bacteria	Motile trichomonads
Amine test	Negative	Positive (fishy odor)	Positive

Treatment of VVC

Uncomplicated VVC: Short-course topical azole creams or suppositories (clotrimazole, miconazole, butoconazole, tioconazole) applied intravaginally. Single-dose oral fluconazole is equally effective and more convenient. Topical azoles are more effective than nystatin.

Recurrent VVC (4 or more episodes per year):

First, an induction course of oral fluconazole taken on days 1, 4, and 7 to achieve mycologic remission
Then a maintenance course of oral fluconazole once weekly for 6 months
30-50% of women relapse after stopping maintenance therapy
If not feasible, intermittent topical treatments can be used as maintenance

Severe VVC: Longer course of topical azole therapy (7-14 days) OR oral fluconazole given as two doses taken 72 hours apart.

C. glabrata (azole-resistant species): Boric acid vaginal suppository daily for 14 days, or nystatin vaginal suppository.

Oral Candidiasis (Thrush)

The tongue is almost always involved. Classic presentation: white, creamy plaques on a red, sore base. The plaques can be scraped off (unlike leukoplakia). Occurs in: diabetes, elderly, cancer patients, prolonged steroid or antibiotic use, HIV (more than 90% of AIDS patients develop it), inhalant steroid use.

In infants it is called THRUSH. It is self-limited in healthy newborns but should be treated to avoid interference with feeding. The mother should be examined for vaginal candidiasis.

Treatment

First-line: Oral fluconazole for one week. Effective, well tolerated, suitable for most patients.
Alternative: Itraconazole oral solution, especially for fluconazole-resistant cases in HIV patients.
Topical options: Clotrimazole troches dissolved slowly in the mouth, or nystatin oral suspension - useful for infants but less effective for adults.
Ketoconazole is a second-line oral drug for oropharyngeal candidiasis.
In HIV patients who develop fluconazole resistance from long-term prophylaxis, itraconazole oral solution is the next step.

Candida Balanitis

Treatment

Topical miconazole or clotrimazole applied twice daily for 7 days gives almost immediate relief, though the full 7-day course must be completed. A single oral dose of fluconazole is comparable in efficacy to topical treatment. Preparations containing topical steroids give temporary relief but the eruption rebounds and worsens.

Candida Intertrigo (Large Skin Folds)

Occurs wherever skin touches skin in warm, moist areas - under pendulous breasts, between abdominal folds, in the groin, axillae, and rectal area. Hot humid weather, tight underclothing, poor hygiene, and inflammatory skin diseases in the folds make infection more likely.

Two presentations:

Pustules that macerate under opposing skin surfaces → red papules with a fringe of moist scale at the border; intact pustules found outside the fold
Red, moist, glistening plaque with an "ocean wave" fringe of macerated scale at a sharply defined border

Satellite pustules - pinpoint pustules just outside the main lesion - are the hallmark diagnostic feature. There is a tendency for painful fissuring in the skin creases.

Treatment

The key principle is eradication of the yeast infection PLUS maintaining dryness of the area.

Cool wet compresses (Burow's solution, water, or saline) applied several times daily to promote dryness
Topical antifungal cream (miconazole, econazole, clotrimazole) applied twice daily until the rash clears
Absorbent non-medicated powder (e.g. Z-Sorb) applied after inflammation has resolved to keep the area dry and prevent recurrence
Any residual inflammation from intertrigo after the yeast is cleared is treated with a mild topical steroid (e.g. desonide or hydrocortisone) for a limited time

Intertrigo (Without Candida)

Intertrigo is an inflammatory condition of skin folds of the axillae, breasts, abdomen, groin, or buttocks. Obese people are at greatest risk. The folds retain moisture, become warm, macerated, and inflamed. Itching, burning, and stinging are the most common symptoms.

Treatment

A short 1-2 week course of a mild topical steroid (desonide or hydrocortisone) may be all that is needed
Cool water compresses applied for 1 hour two or three times a day for a few days rapidly control moisture and suppress inflammation
Add topical antifungal cream if Candida infection is suspected - alternate with the topical steroid
0.1% tacrolimus cream can be used as an anti-inflammatory instead of steroids for cases requiring long-term treatment (avoids the risk of atrophy and striae)
Castellani's paint (carbolfuchsin paint) and "Greer's goo" (nystatin + hydrocortisone + zinc oxide paste) are effective compounded preparations

Candidiasis of Small Skin Folds

Finger and Toe Web Spaces

White, tender, macerated skin erodes to reveal a pink moist base. Toe web candidiasis most common in the 4th/5th interspace where it may coexist with dermatophytes and Gram-negative bacteria.

Treatment

Any topical antifungal cream or lotion. Strands of lamb's wool can be placed between the toe webs to separate them and promote dryness.

Angular Cheilitis (Perlèche)

Inflammation at the corners of the mouth caused by saliva pooling into the skin fold at the mouth angles, causing maceration and secondary infection with Candida and/or staphylococci. Causes include lip licking, thumb sucking, poorly fitting dentures, mouth breathing, advancing age, and weight loss. Patients mistakenly believe they have a vitamin B deficiency.

Treatment

Apply antifungal cream (to cover Candida) followed in a few hours by a topical steroid cream with a nongreasy base to reduce inflammation. Continue until the area is dry and inflammation-free.
After resolution, apply a thick protective lip balm frequently to prevent recurrence.
For culture-resistant cases where both yeast and bacteria are involved, mupirocin ointment applied several times daily is effective for both organisms.
Cosmetic fillers injected at the mouth angles can correct the anatomic fold causing the problem in recurrent cases.

Diaper Candidiasis

The wet diaper creates an artificial intertriginous area, predisposing the area to yeast infection. Presents as a red base with satellite pustules in the diaper area.

Treatment

Change diapers frequently or leave the diaper off for short periods to maintain dryness
Apply topical antifungal cream twice daily until the eruption is clear (approximately 10 days)
Any residual erythema from irritation after 10 days can be treated by alternating a mild hydrocortisone cream with an antiyeast cream
Baby powders help prevent recurrence by absorbing moisture
Mupirocin ointment applied several times daily is effective for severe Candida and bacterial diaper dermatitis
For severe refractory cases, cholestyramine 5% in Aquaphor (must be compounded) neutralizes bile acids and is applied after each diaper change with stool
Steroid combination creams should be used cautiously as the cortisone component can alter the clinical presentation and prolong the disease

SECTION 5: TINEA VERSICOLOR

What It Is

Tinea versicolor is caused by Pityrosporum orbiculare (round form) and Pityrosporum ovale (oval form), collectively called Malassezia furfur. These are normal skin flora that live in the stratum corneum and hair follicles, feeding on free fatty acids and triglycerides. They convert from their normal budding yeast form to a pathogenic mycelial form when triggered by certain conditions.

The disease is most common in adolescents and young adults due to higher sebaceous activity. May not be contagious.

Triggers

Endogenous: Cushing's disease, adrenalectomy, pregnancy, malnutrition, burns, corticosteroids, immunosuppression, oral contraceptives

Exogenous: Excess heat and humidity

Clinical Presentation

Lesions begin as multiple small, circular macules that enlarge radially. The color varies - hence "versicolor":

White/hypopigmented - most obvious in summer when surrounding skin tans
Pink to red - from an inflammatory/hyperemic response
Fawn/tan/brown - post-inflammatory pigmentation

The upper trunk is most commonly affected, along with upper arms, neck, and abdomen. Facial lesions are more common in children. Lesions may be asymptomatic or mildly itchy.

Why hypopigmentation occurs: Dicarboxylic acids produced by the yeast are cytotoxic to melanocytes and inhibit the dopa-tyrosinase reaction. There is a reduction in the number, size, and aggregation of melanosomes.

The lesions are most noticeable in summer because unaffected skin tans while the lesions stay white or discoloured.

Diagnosis

Treatment

Topical (First Line for Limited Disease)

Ketoconazole 2% shampoo - FIRST CHOICE. Apply to entire body from neck to thighs, leave 5 minutes, rinse. Single application or a few days of daily use is highly effective. Also wash the scalp at the same time.
Selenium sulfide 2.5% - Apply for 10 minutes daily for 7 consecutive days. Apply from lower posterior scalp down to the thighs. Results in 87% cure rate.
Any imidazole cream (miconazole, clotrimazole, econazole, ciclopirox) applied once or twice daily for 2-4 weeks.
Zinc pyrithione shampoo is the most effective non-imidazole topical agent.
Sulfur salicylic acid shampoo is also effective.

Oral (For Extensive or Recurrent Disease)

Itraconazole is effective
Fluconazole is effective
Oral terbinafine = NOT effective
Oral griseofulvin = NOT effective
Oral ketoconazole = CONTRAINDICATED - risk of serious liver damage, adrenal problems, drug interactions, and death

Recurrence Prevention

Ketoconazole 2% shampoo applied once weekly to trunk, neck, and proximal extremities before showering. Itraconazole taken twice a day for one day per month for 6 consecutive months is effective prophylaxis. Repeat full treatment before the summer months.

SECTION 6: PITYROSPORUM FOLLICULITIS

What It Is

In tropical presentations, the face is commonly involved - more lateral (mandible and sides of the face) compared to typical acne which is more central. Both young men and women are equally affected.

Risk factors: Diabetes, broad-spectrum antibiotics, corticosteroids, Hodgkin disease, occlusion, oily skin.

Diagnosis: KOH shows abundant round budding yeast cells and sometimes hyphae.

Treatment

Oral fluconazole combined with a topical antifungal - oral antifungal is important because topical agents alone fail in the majority of cases
Ketoconazole 2% cream and shampoo - some response shown in studies
Salicylic acid wash - keratolytic and effective; helps clear follicular plugs
Topical econazole and miconazole fail in approximately 90% of patients with this condition

BONUS: PITTED KERATOLYSIS

Pitted keratolysis is a BACTERIAL infection (NOT fungal) that is frequently misinterpreted as tinea pedis. It affects the weight-bearing surfaces of the soles.

Characteristic features: Circular or longitudinal punched-out pits in the stratum corneum, hyperhidrosis, malodor, and sliminess of the skin. There is little or no inflammation.

Treatment

Wash feet daily with soap or antibacterial cleanser
Promote dryness - change socks frequently, avoid occlusive footwear
Aluminum chloride 20% applied twice daily gives rapid clearing
Lazerformalyde solution (10% formaldehyde) is a potent antiperspirant and is useful
Topical erythromycin solution or clindamycin solution applied twice daily is curative
Mupirocin ointment or cream is also effective
Oral erythromycin is an alternative for more resistant cases
The application of alcohol-based benzoyl peroxide twice daily may also be useful

RAPID-FIRE SUMMARY - KEY FACTS

Dermatophytes infect dead keratin only - NOT mucous membranes
The single most important diagnostic test = KOH wet mount
Best place to scrape for KOH = active border
Mosaic artifact disappears with heat; true hyphae do not
T. tonsurans (USA) does NOT fluoresce under Wood's light
Coral-red Wood's light = Erythrasma = BACTERIAL, not fungal
DTM turns PINK in 6-7 days with dermatophytes
Tinea capitis MUST be treated orally - topical agents cannot reach the follicle
Griseofulvin = drug of choice for tinea capitis in children; best for Microsporum
Terbinafine = BEST for Trichophyton tinea capitis
Tinea cruris does NOT involve the scrotum; Candida groin DOES
Satellite pustules = hallmark of Candidiasis
Tinea incognito = dermatophyte infection masked by steroid use
Id reaction = sterile vesicles at distant sites; allergic response; NOT infectious
Two feet-one hand syndrome = T. rubrum
Tinea versicolor KOH = "spaghetti and meatballs"
Oral terbinafine and oral griseofulvin do NOT work for tinea versicolor
Oral ketoconazole is CONTRAINDICATED for tinea versicolor
RVVC maintenance = oral fluconazole once weekly for 6 months
Pityrosporum folliculitis is frequently misdiagnosed as acne; treat with oral fluconazole + topical antifungal
Pitted keratolysis = BACTERIAL; treat with dryness, aluminum chloride, and topical antibiotics
Econazole is the only topical antifungal that also covers bacteria
Allylamines are FUNGICIDAL (shorter treatment); Azoles are FUNGISTATIC (longer treatment)

COMPLETE AT-A-GLANCE TABLE

Condition	Organism	Key Feature	Treatment
Tinea pedis	Dermatophytes (T. rubrum)	4th/5th web; moccasin; vesicular; id reaction possible	Topical terbinafine (interdigital); oral antifungal (moccasin); compresses + oral (vesicular)
Tinea cruris	Dermatophytes	Half-moon plaque; NO scrotal involvement; does not fluoresce	Topical antifungal cream; oral antifungal for resistant cases
Tinea corporis	Dermatophytes	Ring with active scaly border	Topical antifungal; oral for extensive or deep lesions
Tinea capitis	T. tonsurans (USA)	Black dot, kerion, seborrheic, pustular; lymphadenopathy in ALL types	ORAL mandatory (griseofulvin preferred in children); antifungal shampoo as adjunct
Tinea barbae	T. verrucosum, T. mentagrophytes	Boggy abscess; hairs removed painlessly	Oral antifungal (same as tinea capitis)
Tinea incognito	Any dermatophyte + steroid use	No classic border; expanded atypical infection	Stop steroids; confirm with KOH; oral antifungal
Tinea versicolor	Pityrosporum (Malassezia furfur)	Hypo/hyperpigmented macules; spaghetti and meatballs KOH	Ketoconazole shampoo or selenium sulfide (topical); oral itraconazole or fluconazole for extensive disease
Pityrosporum folliculitis	Pityrosporum	Looks like acne; follicular papules on upper back	Oral fluconazole + topical antifungal; ketoconazole shampoo; salicylic acid wash
Candida skin folds (intertrigo)	Candida albicans	Satellite pustules; ocean wave fringe of scale	Wet compresses to dry area + topical antifungal cream + mild topical steroid for residual inflammation
Vulvovaginal candidiasis	Candida albicans	Curdy white discharge; pH less than 4.5; itching	Topical azole cream or single oral fluconazole; 6-month fluconazole maintenance for recurrent cases
Oral candidiasis (thrush)	Candida albicans	White plaques on red base; tongue involved	Oral fluconazole (first line); clotrimazole troches or nystatin suspension (topical)
Candida balanitis	Candida albicans	Red papules/pustules on glans and shaft; white exudate	Topical miconazole or clotrimazole BID x 7 days; OR single oral fluconazole
Angular cheilitis	Candida + Staphylococcus	Fissures at mouth angles; erythema and scale	Antifungal cream + topical steroid; mupirocin for resistant cases
Diaper candidiasis	Candida albicans	Red base + satellite pustules in diaper area	Maintain dryness; topical antifungal cream; mild hydrocortisone for residual irritation
Erythrasma	Corynebacterium minutissimum (BACTERIAL)	Coral-red Wood's light; NO advancing border	Oral erythromycin or clarithromycin; topical miconazole or clotrimazole
Pitted keratolysis	Mixed bacteria (BACTERIAL)	Punched-out pits; malodor; hyperhidrosis; soles only	Promote dryness; aluminum chloride; topical erythromycin or clindamycin; mupirocin
Intertrigo (no Candida)	Inflammatory + mixed flora	Skin fold erythema; painful fissures; obesity risk factor	Mild topical steroid; cool wet compresses; add antifungal if Candida suspected

Source: Habif's Clinical Dermatology, Chapter 13 - Superficial Fungal Infections

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PSORIASIS AND OTHER PAPULOSQUAMOUS DISEASES

Habif's Clinical Dermatology - Chapter 8 Study Notes

PSORIASIS

Overview and Pathogenesis

Psoriasis is a common, chronic, immune-mediated inflammatory skin disease driven by activation of dendritic cells that stimulate aberrant T-cell pathways. IL-12 and IL-23 produced by antigen-presenting cells drive differentiation of Th1 and Th17 cells, which release inflammatory cytokines (including IL-17A, IL-17F, TNF-alpha, IL-22) that trigger keratinocyte hyperproliferation and the characteristic plaques.

Psoriasis affects extensor more than flexor surfaces and usually spares the palms, soles, and face (though exceptions occur). Favoured sites that should always be examined are: elbows, knees, scalp, gluteal cleft, fingernails, and toenails.

The Koebner phenomenon - new lesions appearing at sites of trauma or injury - is characteristic.

Comorbidities are common and increase with age. Psoriasis patients have elevated rates of cardiovascular disease, metabolic syndrome, diabetes, hypertension, obesity, Crohn disease, ulcerative colitis (3.8-7.5 times more likely), depression (up to 60%), anxiety, low vitamin D (25-OHD), and alcohol abuse.

Clinical Presentations / Subtypes

Chronic Plaque Psoriasis

The most common form. Irregular, round to oval, noninflamed, well-defined plaques with silvery surface scale. Symmetrically distributed, predilection for elbows and knees. Plaques enlarge then remain stable for months or years. A temporary brown, white, or red macule remains when plaques subside.

Guttate Psoriasis (Acute Eruptive)

More than 30% of psoriasis patients have their first episode before age 20, and guttate psoriasis is often the very first presentation. Streptococcal pharyngitis or a viral URTI may precede the eruption by 1-2 weeks. Scaling papules suddenly appear on the trunk and extremities (not palms and soles). Lesions range from pinpoint to 1 cm. May resolve spontaneously in weeks or months. More responsive to treatment than chronic plaque disease. Treat streptococcal infection: penicillin or amoxicillin for 10 days; if penicillin-allergic, use first-generation cephalosporin, clindamycin, clarithromycin, or azithromycin.

Generalized Pustular Psoriasis (Von Zumbusch Type)

A rare, serious, potentially fatal multisystem disorder. Erythema suddenly appears in flexural areas and spreads. Numerous tiny sterile pustules evolve from an erythematous base and coalesce into lakes of pus. Patients are weak and febrile (up to 40°C) with arthralgia and myalgia. Labs show leukocytosis with neutrophilia, elevated CRP, and elevated liver enzymes. Complications include osteoarthritis, uveitis, neutrophilic cholangitis, ARDS, and cardiovascular shock. IL36R gene mutations are found in familial cases.

Precipitants: infection, emotional stress, withdrawal from topical or systemic steroids, pregnancy, tar or anthralin in unstable psoriasis.

Treatment: Wet dressings and group V topical steroids provide initial control. First-line: acitretin, cyclosporine (CS), methotrexate (MTX), and infliximab (rapid relief within days). Second-line: adalimumab, etanercept, PUVA.

Erythrodermic Psoriasis

Generalized erythrodermic psoriasis is a severe, unstable, labile disease. May be the initial manifestation but usually occurs in patients with previous disease. Precipitants include: systemic corticosteroids, excessive topical steroid use, overzealous irritating topical therapy, phototherapy complications, severe emotional stress, preceding infection, and discontinuation of CS, MTX, or ixekizumab.

Treatment: Bed rest, avoid all UV light initially, Burow's solution compresses or colloidal oatmeal baths, emollients, increased protein and fluid intake, antihistamines for pruritus, avoid potent topical steroids. In severe cases, hospitalization. Fastest-acting agents: cyclosporine and infliximab. Acitretin and MTX are also first-line. Tar and anthralin should be avoided.

Light-Sensitive Psoriasis

Some patients benefit from sun exposure (summer clearance) but overexposure causing sunburn triggers the Koebner phenomenon with guttate lesions or diffuse inflammatory plaques in sunburned areas.

Psoriasis of the Scalp

A favoured site; may be the only site affected. Scale is more readily retained, anchored by hair. Extension onto the forehead is common. Hair is not permanently lost even in severe disease (unless scale is chronically removed along with the hair). Persistent and often recalcitrant to therapy.

Psoriasis of the Palms and Soles

May be part of a generalized eruption or the only manifestation. Presentations include: superficial red plaques with thick brown scale (indistinguishable from chronic eczema), or smooth deep red plaques similar to flexural disease.

Pustular Psoriasis of the Palms and Soles

Deep pustules first appear on the middle portion of palms and insteps of soles. Pustules do not rupture but turn dark brown and scaly. Surrounding skin becomes pink, smooth, and tender. Course is chronic, lasting years. Higher prevalence of smoking in these patients.

Treatment: Acitretin, MTX, PUVA, NB-UVB, and intermittent courses of topical steroids under plastic occlusion.

Keratoderma Blennorrhagicum (Reiter Syndrome)

A reactive immune response in genetically susceptible individuals (60-90% HLA-B27 positive), triggered by infections (Yersinia, chlamydia) causing dysentery or urethritis. Psoriasiform skin lesions develop 1-2 months after arthritis onset. Distinctive lesions (keratoderma blennorrhagica) on soles and toes - scaly, scalloped-edged plaques from coalescence of papulovesicular plaques with thick yellow scale. Nail dystrophy, thickening, and destruction occur. Also involves: conjunctivitis (25%), urethritis/cervicitis, peripheral arthritis. Balanitis circinata on the penis is highly characteristic (erosions with scale forming a winding pattern on corona and glans). Treatment: MTX, acitretin, ketoconazole.

Psoriasis of the Penis

Typical white-scaled plaques on circumcised penis. Scale does not form on covered foreskin.

Pustular Psoriasis of the Digits (Acrodermatitis Continua of Hallopeau)

A severe localized variant limited to one or more fingers for years. Vesicles rupture leaving tender, eroded, fissured surface. Loosely adherent crust shed but recurs. Very resistant to therapy.

HIV-Induced Psoriasis

Psoriasis may be the first sign of HIV infection. Can be mild, moderate, or severe. Atypical and unusually severe with involvement of groin, axilla, scalp, palms, and soles. An explosive onset with erythroderma or pustules that rapidly become confluent should lead to suspicion of HIV.

Treatment is challenging because depleted T cells in HIV may be worsened by systemic immunosuppressive therapies. Topical steroids and vitamin D analogues for mild disease. Phototherapy (NB-UVB) and antiretroviral therapy are first-line for moderate-to-severe. Acitretin may be used next. Third-line: CS, MTX, and TNF-alpha inhibitors. Apremilast has also been used.

Psoriasis Inversus (Flexural/Intertriginous Psoriasis)

Involves gluteal fold, axillae, groin, submammary folds, retroauricular fold, glans of uncircumcised penis. Deep red, smooth, glistening plaques that stop at the junction of skin folds. Moist surface, macerated white debris. Pustules beyond the plaque border suggest secondary yeast infection. Treatment: weaker topical steroids and calcineurin inhibitors (tacrolimus, pimecrolimus). Hydrocortisone-iodoquinol is often effective for gluteal cleft.

Psoriasis of the Nails

Nail changes are characteristic of psoriasis and occur in 30% of uncomplicated psoriasis but in over 80% of patients with psoriatic arthritis.

Onycholysis: Separation of the nail from the nail bed. The nail plate turns yellow, simulating fungal infection. Unlike pressure-induced onycholysis, psoriatic separation is irregular.
Subungual debris: Nail bed scale is retained, forcing distal nail to separate from nail bed.
Pitting: The best known and possibly most frequent nail abnormality. Tiny, punched-out depressions on the nail plate surface from loss of parakeratotic cells. Many other conditions also cause pitting (eczema, fungal infections, alopecia areata).
Oil spot lesion: Localized separation of nail plate with accumulation of serum and debris visible as a translucent yellow-red discoloration (looks like a drop of oil).
Nail deformity: Extensive matrix involvement leads to fragmentation and crumbling.

Psoriatic Arthritis (PsA)

PsA is a chronic inflammatory arthropathy of peripheral joints, spine, and entheses; associated with psoriasis; usually RF and anti-CCP negative. Affects 5-42% of psoriasis patients. In approximately 15% of patients with PsA, arthritis precedes the skin manifestations. Prevalence is higher with more severe cutaneous disease. Peak onset ages 20-40; women and men equally affected.

Key features distinguish PsA from RA:

PsA: RF negative, anti-CCP negative, DIP joint involvement common, asymmetric distribution, DIP-predominant, axial involvement (50%), dactylitis, enthesitis, nail lesions common, psoriasis always present
RA: RF positive, anti-CCP positive, MCP and PIP involvement, symmetric, no DIP, rarely axial, no dactylitis, rheumatoid nodules, no psoriasis

Dactylitis: "Sausage digit" - diffuse swelling of an entire digit.

Enthesitis: Inflammation at ligament/tendon insertion sites; characteristic of all HLA-B27-associated spondyloarthropathies.

Moll and Wright Classification (5 subtypes):

Oligoarticular asymmetric arthritis (30-50%): Sausage fingers/toes, most common
Polyarticular symmetric (RA-like) (30-50%): RF negative; small joints of hands/feet, wrists, ankles, knees, elbows
DIP-predominant (25%): Mild, chronic; associated with nail disease; most characteristic presentation
Destructive polyarthritis / Arthritis mutilans (5%): Most severe; osteolysis of small bones; "opera glass" deformity from digital telescoping
Ankylosing spondylitis and sacroiliitis (30-35%): Strong HLA-B27 association; asymmetric sacroiliitis; spinal involvement

CASPAR Criteria (score 3+ for diagnosis): Current psoriasis (2 points), history of psoriasis (1), family history (1); nail dystrophy (1); negative RF (1); current dactylitis (1), history of dactylitis (1); radiographic evidence of juxtaarticular new bone formation (1). Sensitivity 91.4%, specificity 98.7%.

Lab tests: No specific test for PsA. ESR is best lab guide to disease activity. 4.6% RF positive, 7.6% anti-CCP positive. HLA-B27 positive in 15-70%.

Treatment of PsA:

Mild disease: NSAIDs and low-dose prednisone as adjunctive therapy; intraarticular corticosteroid injections
Conventional DMARDs (csDMARDs): MTX (preferred), leflunomide, sulfasalazine - first-line for peripheral arthritis, do not prevent structural damage
Methotrexate: Effective second-line agent; given as single weekly oral dose or divided; improves pain and function within 2-6 weeks
Cyclosporine: Impressive relief at daily doses 1.5-5 mg/kg
Apremilast: Oral PDE4 inhibitor; effective for moderate-to-severe plaque psoriasis and PsA
TNF-alpha inhibitors (biologics): Etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), golimumab (Simponi); highly effective for PsA; often combined with MTX; used when csDMARDs fail
IL-12/23 inhibitors, IL-17 inhibitors, IL-23 inhibitors: Used for peripheral, axial, and entheseal disease when TNF inhibitors fail

Drugs that Precipitate or Exacerbate Psoriasis

Major culprits and their latency periods:

Beta-blockers (propranolol, metoprolol, atenolol): Variable latency (up to 48 weeks); causes psoriasiform dermatitis and lichenoid changes; antipsoriatic medications generally not effective unless beta-blocker is discontinued
Lithium: Latency average 20 weeks (up to 48); alters cAMP; affects plaque, pustular, scalp, nail, and erythrodermic psoriasis
Antimalarials (chloroquine, hydroxychloroquine): Intermediate latency; inhibit transglutaminase; causes pustular psoriasis; lesions resolve on average within 1 month of discontinuation
NSAIDs (naproxen, ibuprofen, indomethacin): Short latency (average 1.6 weeks); inhibit COX pathway, accumulate leukotrienes
ACE inhibitors / ARBs (captopril, losartan): Intermediate latency 4.1-8.4 weeks; increase bradykinin
Interferons (IFN-alpha, beta, gamma): Variable latency 1 week to 6 months; all forms can cause de novo psoriasis
Systemic corticosteroids (prednisone): Can trigger generalized pustular psoriasis and erythrodermic exacerbations on withdrawal
TNF-alpha inhibitors (adalimumab, etanercept, infliximab): Paradoxical psoriasis more common in females and smokers
Terbinafine (allylamines): Latency 1.8-3 weeks; plaque, pustular, inverse psoriasis
Imiquimod: Plaque psoriasis and erythroderma

Treatment of Psoriasis

Topical Therapy

Topical Corticosteroids - First-line for limited disease

Antiinflammatory, antiproliferative, immunosuppressive, vasoconstrictive
Lower potency for face, intertriginous areas, infants
Mid-high potency (group I-II) for thick chronic plaques
Pulse dosing preferred (2 weeks on, 1 week lubrication only)
Plastic occlusion dramatically enhances effectiveness (but not used for group I steroids or intertriginous areas)
Tachyphylaxis (tolerance) occurs with continued use
Intralesional triamcinolone acetonide (5-10 mg/mL) for small, few plaques: clears completely with months of remission
Side effects: atrophy, telangiectasia, striae, purpura; systemic HPA axis suppression possible

Vitamin D Analogues (Calcipotriene/Dovonex, Calcitriol/Vectical)

Inhibit epidermal cell proliferation, enhance differentiation
No tachyphylaxis (unlike steroids)
Most effective: calcipotriene morning + group I corticosteroid evening for 2 weeks, then maintenance with corticosteroid on weekends and calcipotriene twice daily on weekdays - 60-70% improvement in 6-8 weeks
Calcipotriene hydrate + betamethasone dipropionate combination is superior to either alone (once daily)
Hypercalcemia if >100 g/week applied over large areas
Not effective as adjunct to UVB or PUVA

Topical Calcineurin Inhibitors (Tacrolimus, Pimecrolimus)

Block synthesis of inflammatory cytokines
Useful for facial and intertriginous psoriasis (no atrophy risk)
Only effective for plaque psoriasis if occluded
Main side effect: burning and itching

Tazarotene (Tazorac) - Retinoid

Available 0.05% and 0.1% gel and cream
Effective, induces long remissions, but irritating
Combine with topical steroids to control irritation and enhance effectiveness
Short contact (5-30 min) minimizes irritation
Causes thinning of stratum corneum - reduce UV doses by at least one third if using with phototherapy
Teratogenic - category X

Halobetasol + Tazarotene (Duobril lotion): Once-daily application; 36-45% clear/almost clear at 8 weeks

Coal Tar

Suppresses DNA synthesis (Goeckerman regimen: coal tar + UVB)
Moderately effective; stains clothes and hair
Most effective combined with UVB
Poor cosmetic acceptability

Anthralin (Dritho Cream)

Short contact: applied 30 minutes, then washed off
More effective combined with phototherapy
Irritating; avoid face and intertriginous areas; stains

Nonmedicated Moisturizers

Applied 1-3 times daily
Often effective especially for maintenance
Patients frustrated with expensive prescriptions often turn to moisturizers with gratifying results

Phototherapy

NB-UVB (Narrowband UVB)

Delivered to office; requires many visits
Effective in 70% of patients for plaque and guttate psoriasis
Can be combined with MTX or acitretin for enhanced effectiveness
Significant positive correlation between sunbathing response and UVB phototherapy response

PUVA (Psoralen + UVA)

Oral methoxypsoralen 2 hours before carefully measured UVA
Major advantage: controls severe psoriasis with relatively few maintenance treatments; outpatient
Substantial PUVA exposure increases risk of nonmelanoma skin cancer and melanoma
Used less frequently in era of biologic therapy

Scalp Treatment

Remove scale first (tar shampoos containing salicylic acid; Baker's P&S liquid for thick scale; 10% LCD in Nivea oil at bedtime)
Mild-moderate: tar shampoos every other day; corticosteroid solutions/gels; fluocinolone acetonide 0.01% oil
Calcipotriene 0.005% + betamethasone dipropionate 0.064% suspension: once daily for 2-8 weeks
Betamethasone valerate foam and clobetasol foam: very effective through hair
Small plaques: intralesional triamcinolone 5-10 mg/mL
Resistant disease: systemic immunosuppressives or biologics

Inverse/Intertriginous and Genital Psoriasis Treatment

Weaker topical steroids (penetration enhanced by moist opposing skin surfaces)
Topical calcineurin inhibitors (tacrolimus, pimecrolimus)
Avoid potent topical steroids (increased atrophy risk)

Systemic Therapy

Indicated for >5% BSA involvement or unresponsive to topical therapy.

Methotrexate (MTX)

Used >40 years; effective for plaque, erythrodermic, generalized pustular, and psoriatic arthritis
Mechanism: folic acid antagonist; inhibits dihydrofolate reductase; suppresses epidermal cell reproduction; antiinflammatory and immunomodulatory
Dosing: single weekly oral dose or three doses at 12-hour intervals weekly; start with test dose then repeat labs at 7 days; usual range 7.5-25 mg/week
Folic acid supplementation (1-5 mg/day, not on MTX day) reduces side effects without reducing efficacy
Major side effects: bone marrow toxicity (most serious short-term), hepatotoxicity (most common long-term), nausea, oral ulcerations, leukopenia, macrocytic anemia, interstitial pneumonitis
Methotrexate is excreted mainly via the kidney - reduce dose in renal insufficiency
Liver biopsy: first biopsy at 3.5-4 g cumulative dose in low-risk patients; earlier in high-risk patients (obesity, DM, alcohol, abnormal LFTs, prior liver disease)
Contraindicated in pregnancy (category X), nursing, alcoholism, immunodeficiency, bone marrow hypoplasia, active infection

Acitretin (Soriatane)

Oral retinoid; one of the safest systemic psoriasis therapies
Most effective as monotherapy for pustular and erythrodermic psoriasis; less effective for plaque psoriasis alone
Combined with PUVA or UVB is more effective for plaque psoriasis (lower UV doses required)
Start at low dose (10-25 mg/day), escalate gradually
Major side effects: cheilitis, alopecia, xerosis, xerophthalmia, hypertriglyceridemia, abnormal LFTs, paresthesias, myalgia, headache (pseudotumor cerebri risk)
Teratogenic (category X). CRITICAL: In presence of ethanol, acitretin converts to etretinate which persists in tissues for years. Therefore acitretin is NOT prescribed to women of childbearing potential who may become pregnant within 3 years
Generally ineffective for psoriatic arthritis

Cyclosporine (CS)

Rapidly effective; indicated for severe, recalcitrant plaque psoriasis in immunocompetent adults
Also effective for pustular, erythrodermic, and nail psoriasis
Dosing: 2.5-5 mg/kg/day in two divided doses; adjust by 0.5-1 mg/kg increments
Most serious side effects: nephrotoxicity and hypertension
Monitor creatinine monthly; elevations >25% above baseline on two occasions prompt dose reduction 25-50%
Hypertension: often resolves after short courses; treat with calcium channel blockers (avoid nifedipine); avoid ACE inhibitors and potassium-sparing diuretics
Intermittent short courses (12-week courses) significantly reduce nephrotoxicity risk vs. continuous therapy
Contraindicated with: concurrent PUVA or UVB, MTX, other immunosuppressives, coal tar, history of >200 PUVA treatments or radiation, abnormal renal function, uncontrolled hypertension, malignancy, live vaccinations
No live vaccines; avoid grapefruit juice

Apremilast (Otezla)

Oral PDE4 inhibitor; elevates intracellular cAMP, reduces proinflammatory mediators
Indicated for moderate-to-severe plaque psoriasis and psoriatic arthritis
Principal side effects: GI (nausea, diarrhea, vomiting), weight loss; depression reported in trials
No monitoring requirements
Strong CYP450 inducer - do not use with rifampin, phenobarbital, carbamazepine, phenytoin

Isotretinoin

Highly effective for pustular psoriasis; beneficial combined with PUVA or UVB for plaque psoriasis

Biologic Therapy

Biologic therapies are indicated for moderate-to-severe plaque psoriasis (and other types). Pre-screening: chemistry screen, LFTs, CBC, hepatitis panel, tuberculosis testing (PPD or QuantiFERON-Gold). No live vaccines once started.

TNF-alpha Inhibitors

Adalimumab (Humira): Humanized monoclonal IgG1 antibody against TNF-alpha. Approved for RA, juvenile RA, PsA, AS, adult and pediatric Crohn disease, ulcerative colitis, plaque psoriasis, hidradenitis suppurativa, uveitis. 70% of patients achieve PASI 75 at 12 weeks.
Etanercept (Enbrel): Dimeric fusion protein (human p75 TNF receptor + Fc portion of IgG1). Approved for moderate-to-severe plaque psoriasis, PsA, RA, polyarticular juvenile RA, AS. No rebound on discontinuation. Loss of efficacy over time may occur. Biosimilar: etanercept-szzs.
Infliximab (Remicade): Chimeric IgG1kappa monoclonal antibody specific for TNF-alpha. Fastest onset of action of all biologics. Administered by IV infusion. 80% achieve PASI 75 at week 10. Continuous therapy preferred to prevent infusion reactions and anti-infliximab antibodies. Low-dose concurrent MTX reduces antibody formation. Biosimilar: infliximab-dyyb.
Certolizumab pegol (Cimzia): PEGylated anti-TNF IgG1 antibody fragment.

IL-12/23 Inhibitors

Ustekinumab (Stelara): Human monoclonal IgG1 antibody targeting p40 subunit shared by IL-12 and IL-23. Approved for plaque psoriasis, PsA, and Crohn disease. More effective than adalimumab, etanercept, and apremilast but less effective than ixekizumab, brodalumab, infliximab, and secukinumab. Stable response with no rebound on withdrawal. Dose: 45 mg for weight ≤100 kg; 90 mg for >100 kg; week 0, week 4, then every 12 weeks. PsA may worsen in some patients.

IL-17 Inhibitors (among the most effective biologics for psoriasis)

Secukinumab (Cosentyx): IgG1 monoclonal antibody binding IL-17A and blocking its interaction with the IL-17A receptor. Approved for plaque psoriasis, PsA, and AS. At 12 weeks: PASI 75 in 77% (300 mg) and 67% (150 mg). Durable with 93% maintaining PASI 90 at 52 weeks. Patients with inflammatory bowel disease may worsen.
Ixekizumab (Taltz): IgG4 monoclonal antibody neutralizing IL-17A. Approved for moderate-to-severe plaque psoriasis and PsA. At 12 weeks, 90% of patients achieve PASI 75 - one of the most effective biologic agents for psoriasis. Fast-acting with results within 4 weeks.
Brodalumab (Siliq): IgG2 monoclonal antibody against IL-17A receptor. At 12 weeks, 86% achieve PASI 75. Concern about suicidal ideation in clinical trials - available only through REMS program (SILIQ REMS). Analysis of 5 trials did not show brodalumab causing suicide.

IL-23 Inhibitors

Guselkumab (Tremfya): IgG1 lambda monoclonal antibody selectively blocking IL-23. At week 16, 73.1% achieve PASI 90 - highly effective.
Tildrakizumab-asmn (Ilumya), Risankizumab-rzaa (Skyrizi): Additional anti-IL-23 agents.

Network Meta-Analysis Ranking (PASI 90 response, Table 8.15): Ixekizumab > Brodalumab > Infliximab > Secukinumab 300 mg > Ustekinumab > Adalimumab > Etanercept > Apremilast > Placebo

Rotational Therapy

Rotating between UVB, MTX, retinoids, biologic agents, and CS at intervals of approximately 1-2 years limits cumulative toxicity. Cyclosporine immediately before or especially after PUVA should be avoided (synergistic skin cancer risk).

Treatment in Pregnancy

Emollients and low-to-moderate potency topical steroids are first-line. Second-line: NB-UVB phototherapy or broadband UVB. TNF-alpha inhibitors (adalimumab, etanercept, infliximab), CS, and systemic steroids (second and third trimesters) may be used.

PITYRIASIS RUBRA PILARIS (PRP)

Overview

PRP is a rare, chronic disease of unknown etiology with a unique combination of features. It often has a devastating impact on patients. Most cases occur in the first and fifth or sixth decades of life.

Griffiths Classification (6 Types)

Type	% Cases	Onset/Features	Course
I - Classic adult	50%	Adults 5th-6th decade; erythroderma, islands of sparing, salmon-colored keratoderma, follicular hyperkeratosis; cephalocaudal spread	80% remission in 3 years
II - Atypical adult	5%	Ichthyosiform/psoriasiform lesions; more persistent; eczematous changes, alopecia	20+ years
III - Classic juvenile	10%	First 2 years of life; similar to type I; generalized coalescent hyperkeratotic follicular papules with islands of spared skin; cephalocaudal spread	Remission average 1-2 years
IV - Circumscribed juvenile	25%	Prepubertal; focal follicular hyperkeratotic papules and plaques on elbows/knees/palms/soles; disseminated papules on face, trunk, extremities	Acute form resolves 6 months; can progress to erythrodermic form
V - Atypical juvenile	5%	First year of life; follicular hyperkeratosis; scleroderma-like changes of palms/soles; most familial cases	Chronic, intractable
VI - HIV-associated	Increasing	Face and upper trunk; nodulocystic/pustular acneiform lesions; lichen spinulosus-type lesions	Refractory; may respond to antiretroviral therapy

Clinical Manifestations

Classic adult PRP begins insidiously with a small, indolent, red scaling plaque on the face or upper body that slowly enlarges. Palms and soles begin to thicken, then bright red-orange follicular papules appear on dorsal proximal phalanges, elbows, knees, and trunk. The follicular keratotic papules coalesce on the trunk to produce a complex pattern of discrete papules and sharply bordered red plaques with islands of normal skin ("skip spots") - pathognomonic. Scaling is coarse on the lower half of the body and fine and powdery on the upper half. Ectropion with facial involvement. Nails: distal yellow-brown discoloration, subungual hyperkeratosis, thickening, splinter hemorrhages. Little or no itching. 80% are clear within 3 years.

Childhood PRP: Begins on scalp/face, simulating seborrheic dermatitis. More widespread with follicular keratotic papules. Childhood form tends to recur for years. Circumscribed form: red-orange plaques on elbows and knees with follicular hyperkeratosis. 3-year remission rate: 32%.

Diagnosis: Distinctive clinical picture is most valuable. Looks like psoriasis when localized. Biopsy shows thick scale, dense keratotic follicular plugs, increased granular cell layer, acantholysis.

Treatment

No standard protocol exists.

Lubricants/Emollients: Frequent use of ammonium lactate 12%, Eucerin, Aquaphor, or Vaseline. 40% urea cream to feet with plastic bag at bedtime removes scale. Heavy moisturizers with occlusion in plastic suit.
Vitamin D analogues (calcipotriene/calcipotriol): May be effective
Retinoids: Effective systemic agents. Isotretinoin provides symptomatic improvement in 4 weeks, significant improvement/clearing in 16-24 weeks. Acitretin with or without light therapy may be superior for adult-onset disease. Combined oral retinoids + low-dose weekly MTX resulted in 25-75% improvement in 17/24 patients after 16 weeks.
Methotrexate: Daily MTX (2.5 mg/day) may be more effective than standard weekly psoriasis regimen. Improvement noted in 2nd-3rd week; marked improvement in 10-12 weeks.
Cyclosporine: Should be considered for classic adult-type PRP.
TNF-alpha inhibitors (etanercept, adalimumab, infliximab): Partial to marked clinical response; mean interval to notable response was 5.7 weeks.
Tazarotene gel twice daily for localized PRP.
Many patients with PRP are photosensitive and may worsen with PUVA and UVB. Isolated case reports of NB-UVB improvement.

SEBORRHEIC DERMATITIS (SD)

Overview

SD is a common, chronic, inflammatory disease with characteristic patterns for different age groups. The yeast Malassezia ovalis is probably a causative factor, but genetic and environmental factors also influence course. In adults, tends to persist with periods of remission and exacerbation. It is one of the most common cutaneous manifestations of HIV infection, seen in 85% of HIV patients (worsens with lower CD4 counts).

Clinical Presentations by Age Group

Infants (Cradle Cap)

Greasy, adherent scale on the vertex of the scalp. May accumulate and become thick and adherent over much of the scalp with inflammation. Secondary infection can occur.

Young Children

Tinea amiantacea: Characteristic eruption of unknown etiology (may be eczema or psoriasis). Dense patches of scale anywhere on scalp, with temporary hair loss. Distinctive large, oval, yellow-white plates of scale firmly adhered to scalp and hair shafts (scale binds and is drawn up with growing hair). Patches 2-10 cm. Resembles fungal disease.

Seborrheic blepharitis: White scale adherent to eyelashes and lid margins with variable erythema. Persists for years and is resistant to treatment.

Adolescents and Adults (Classic SD)

Most individuals periodically experience fine, dry, white scalp scaling with minor itching (dandruff). In more severe forms: fine, dry, white or yellow scale on an inflamed base. Distribution in seborrheic areas: scalp and scalp margins, eyebrows, base of eyelashes, nasolabial folds, external ear canals, posterior auricular fold, presternal area. Axillae, inframammary folds, groin, and umbilicus affected less frequently. Older patients and those with Parkinson disease have more chronic and extensive disease. Occasional extensive involvement of entire face.

The "petaloid" or "flower-like" pattern (discrete round papules and plaques) is a recognized variant.

HIV and SD: SD is one of the most common cutaneous manifestations of HIV. Worsens with lower CD4 counts; can involve face, chest, back, axillae, and groin.

Treatment

Shampoos: Frequent washing with antiseborrheic shampoos. Options include: zinc shampoos, selenium shampoos, ketoconazole 1% or 2%, ciclopirox 1% shampoo, tar shampoo, or salicylic acid shampoo.

Topical Antifungal Agents (mainstay of treatment):

Ketoconazole, bifonazole, ciclopirox in creams, gels, foams, or shampoos
Effective for face, ears, chest, and upper back
Minor SD of face may need addition of group V-VII topical steroids or pimecrolimus cream for control

Topical Steroids:

Group V through VII topical steroid creams for inflamed areas - respond quickly
Steroid lotions applied to scalp twice daily
Fluocinolone acetonide 0.01% lotion (peanut oil, mineral oil) applied to entire scalp and occluded with shower cap; very effective
Not for long-term maintenance

Calcineurin Inhibitors:

Both pimecrolimus and tacrolimus effective for SD
Tacrolimus 0.1% ointment: very effective; discontinue once control is obtained
Relapse of facial SD observed 3-8 weeks after stopping pimecrolimus
A rosacea-form dermatitis may occur as complication of treating facial SD with pimecrolimus 1%

Oral Antifungals:

Oral itraconazole: initially 200 mg/day for 1 week, then maintenance 200 mg every 2 weeks; beneficial for moderate-to-severe SD
Fluconazole 300 mg single dose weekly for 2 weeks: marginal benefit; daily 50 mg/day for 2 weeks also used
Oral terbinafine: NOT effective for SD

Cradle Cap Treatment: Group VI or VII topical steroid creams or lotions. Dense, thick adherent scale removed with warm mineral oil, olive oil, or fluocinolone acetonide 0.01% oil. Ketoconazole 2% cream and 1% hydrocortisone cream: similar efficacy for infantile SD.

Tinea Amiantacea Treatment: Fluocinolone acetonide 0.01% (peanut oil, mineral oil) applied to scalp nightly, washed out in morning for 1-3 weeks until clear; then tar shampoos for maintenance. 10% LCD in Nivea oil for thick scale.

Blepharitis: Scale suppressed by frequent washing with zinc- or tar-containing antidandruff shampoos. Avoid prolonged topical steroids around eyes (glaucoma risk). Ketoconazole once daily in resistant cases. Sulfacetamide ointment may control inflammation and scale.

Oral Treatment (severe/unresponsive):

Itraconazole 200 mg/day first week of month, then 200 mg/day first 2 days for 2-11 months
Fluconazole 50 mg/day for 2 weeks or 200-300 mg weekly for 2-4 weeks
Ketoconazole 200 mg daily for 4 weeks
Pramiconazole single 200-mg dose

PITYRIASIS ROSEA (PR)

Overview

PR is a common, benign, usually asymptomatic, distinctive, self-limiting skin eruption of unknown etiology. Human herpesvirus 6 (HHV-6) may be involved. Small epidemics have occurred. More than 75% of patients are between ages 10 and 35 (mean age 23). Higher incidence in colder months. 20% have preceding acute infection history (fatigue, headache, sore throat, lymphadenitis, fever). 2% have recurrence.

IMPORTANT: During pregnancy, PR may foreshadow premature delivery with neonatal hypotonia and fetal demise, especially if it develops within 15 weeks of gestation.

Clinical Manifestations

Herald patch (precedes eruption in ~74% of cases): A single 2-10 cm round to oval lesion that abruptly appears, most frequently on trunk or proximal extremities. Retains same features as subsequent oval lesions. Patients often think it's ringworm at this stage.

Eruptive phase (7-14 days later): Smaller lesions appear and reach maximum number in 1-2 weeks. Typically limited to trunk and proximal extremities; extensive cases develop on arms, legs, and face. Lesions are concentrated in the lower abdominal area.

Individual lesion: Salmon pink in white patients, hyperpigmented in black patients. Typical 1-2 cm oval plaques with collarette scale - a fine, wrinkled, tissue-like scale attached within the border of the plaque. Long axis of oval plaques oriented along skin lines.

Christmas-tree distribution: Numerous lesions on the back oriented along skin lines give the appearance of drooping pine-tree branches.

Variant forms: Papular variety more common in young children, pregnant women, and Black patients. Vesicular and purpuric lesions in infants and children. Inverse distribution (mainly extremities) in 6% of cases, more common in children.

Course: Mostly asymptomatic; mild transient itching in most; severe itching in extensive inflammatory eruptions. Clears spontaneously in 1-3 months. Postinflammatory hyperpigmentation especially in Black patients.

Diagnosis

Experienced observers diagnose clinically. KOH examination rules out tinea. Secondary syphilis may be indistinguishable from PR (especially if herald patch absent) - serologic test for syphilis if diagnosis uncertain. Biopsy useful in atypical cases (extravasated erythrocytes in dermal papillae, dyskeratotic cells in dermis). PR also mimicked by guttate psoriasis and nummular eczema.

Treatment

Disease is benign and self-limited; does not affect the fetus. Isolation is unnecessary.

Group V topical steroids and oral antihistamines for itching
Oral acyclovir (400 mg 5x daily for 1 week): reduces erythema and shortens duration in one study
Oral erythromycin for 2 weeks: effective in some studies, ineffective in others
Direct sun exposure hastens resolution of individual lesions (protected areas persist)
UVB (5 consecutive daily erythemogenic exposures): decreased pruritus and hastens involution; most beneficial in first week of eruption
Severe extensive cases with intense itching: 1-2 week course of prednisone (20 mg twice daily)

LICHEN PLANUS (LP)

Overview

LP is a unique inflammatory cutaneous and mucous membrane reaction pattern of unknown etiology. Mean age of onset: 40.3 years in males, 46.4 years in females. Main eruption clears within 1 year in 68%; 49% recur. Rare in children under 5. About 10% have a positive family history.

Pathogenesis: Basal keratinocytes in LP show increased ICAM-1 expression, interacting with CD4+ and especially CD8+ T lymphocytes (T-helper-1 arm). This leads to basal keratinocyte apoptosis.

Association with hepatitis C: Cutaneous and oral LP may be associated with HCV-related chronic active hepatitis. Some evidence HCV may induce cytokine/chemokine changes leading to LP development. However, one study showed no clear association between OLP and chronic HCV.

Malignancy risk: Patients with cutaneous LP are NOT at increased risk for cutaneous cancer. However, oral LP and vulvar LP are at increased risk for SCC.

Lichenoid eruptions (similar appearance to LP) can be caused by: drugs (gold, chloroquine, methyldopa, penicillamine), chemical exposure (film processing), bacterial infections (secondary syphilis), and post-bone marrow transplants (graft-versus-host reaction).

Clinical Subtypes

The 5 Ps of Lichen Planus: Pruritic, Planar (flat-topped), Polyangular (polygonal), Purple papules

Primary lesion: 2-10 mm flat-topped papule with irregular angulated border. Surface shows Wickham striae - lacy, reticular pattern of crisscrossed whitish lines (accentuated by a drop of immersion oil). Histologically, Wickham striae = areas of focal epidermal thickening. Initially pink-white, then develop distinctive violaceous/purple hue with waxy luster.

Localized Papular LP

Most common form. Papules on flexor surfaces of wrists and forearms, legs above ankles, lumbar region. Itching variable (20% no pruritus). Chronic, average ~4 years.

Generalized LP and Lichenoid Drug Eruptions

Abrupt onset of intensely pruritic eruption. Initially pinpoint, numerous, isolated papules. May remain discrete or become confluent as large, red, eczematous-like thin plaques. Characteristic diffuse dark brown postinflammatory pigmentation when disease clears. Untreated generalized LP continues approximately 8 months. Lichenoid drug eruptions frequently of this diffuse type. Disease seldom on face or scalp; rare on palms/soles.

Hypertrophic LP

Second most common pattern. Typically on pretibial areas and ankles. Papules lose characteristic features and become confluent as reddish brown or purplish, thickened, band-like plaques with rough or verrucous surface. Severe itching. Average ~8 years duration. May be perpetuated by scratching.

LP of Palms and Soles

Usually isolated phenomenon. Papules larger and aggregate into semitranslucent plaques with globular waxy surface. Intolerable itching. Ulceration may occur; feet may require surgical excision and grafting. May last indefinitely.

Follicular LP (Lichen Planopilaris)

Lesions localized to hair follicles; may occur alone or with papular LP. Pinpoint hyperkeratotic follicular projections. Most common form on the scalp (papular lesions rarely on scalp). Hair loss occurs and may be permanent if disease causes scarring. LP of the scalp is a cause of scarring alopecia. Direct immunofluorescence abnormalities differ from those of LP, suggesting lichen planopilaris and LP may be two different diseases.

Oral Mucous Membrane LP (OLP)

Occurs without cutaneous disease in 23% of LP patients
Less likely to spontaneously remit than cutaneous LP
Mean age of onset in sixth decade; women > men 2:1
Most common location: buccal mucosa (80-90%), followed by tongue (30-50%)
Mucous membrane involvement in >50% of patients with cutaneous LP - oral cavity should always be examined when LP is suspected
Two stages: Nonerosive (most common) - asymptomatic dendritic/lacy white network on buccal mucosa - strong supporting evidence for cutaneous LP diagnosis. Erosive - localized or extensive ulcerations, any area of the oral cavity.
Candida infection found in 17-25% of ulcerated and non-ulcerated LP cases
Oral SCC developed in 0.8% of patients at sites of erosive/erythematous OLP - important malignancy risk

Erosive Vaginal LP

First sign of LP in some patients; lichen planus may be the most common cause of desquamative vaginitis
No tendency for complete remission; flares and partial remissions
Marked vaginal mucosal fragility and erythema; agglutination of labia minora; vaginal adhesions
Unknown whether it predisposes to SCC
Vulvovaginal-gingival syndrome: variant with erosions and desquamation of vulva, vagina, and gingiva

LP on the Penis

Lacy white pattern identical to buccal mucosa pattern. Superficial and erosive lesions on glans penis.

Nail LP

Accompanies generalized LP or may be only manifestation. Approximately 25% of nail LP patients have LP in other sites before or after nail lesions. Appears in fifth or sixth decade. Changes include: proximal to distal linear depressions or grooves, and partial or complete destruction of the nail plate. Long-term permanent damage is rare even with diffuse matrix involvement.

Diagnosis

Usually clinical. Skin biopsy eliminates doubt. Direct immunofluorescence: ovoid globular deposits of IgG, IgM, IgA, and complement. Basement membrane zone deposits of fibrin and fibrinogen present in a linear pattern in both cutaneous and oral lesions in almost all patients. Indirect immunofluorescence is negative (no circulating antibodies).

Treatment

Cutaneous LP

Topical steroids: Group I or II topical steroids (cream or ointment twice daily) are initial treatment for localized disease. Relieve itching but lesions slow to clear. Plastic occlusion enhances effectiveness.

Intralesional steroids: Triamcinolone acetonide 5-10 mg/mL for hypertrophic lesions on wrists and lower legs; repeat every 3-4 weeks.

Systemic steroids: For generalized, severely pruritic LP. Prednisone 20 mg twice daily for 2-4 weeks, then gradually decrease over 3 weeks.

Acitretin: One large study: 30 mg/day acitretin showed 64% remission or marked improvement vs. 13% placebo. During subsequent open phase, 83% of prior placebo patients responded to acitretin.

Azathioprine: Effective steroid-sparing treatment for generalized LP.

Cyclosporine: Successful treatment with oral CS (6 mg/kg/day); response within 4 weeks, complete clearing after 6 weeks; remission up to 10 months after therapy.

Antihistamines: Hydroxyzine 10-25 mg every 4 hours for itching.

Light therapy: PUVA and broadband and NB-UVB are effective for generalized, symptomatic LP. Maintenance may not be required once complete clearance is attained.

Tacrolimus ointment: Ulcerative LP of the sole may respond to topical tacrolimus 0.1%.

Oral/Mucosal LP

Most patients asymptomatic and do not need treatment. Most symptomatic forms are erosive and atrophic types, which may need systemic therapy.

Topical corticosteroids: Initial treatment. Clobetasol propionate, fluocinonide, fluocinolone acetonide, triamcinolone acetonide in an adhesive base (Orabase). Apply on lesions; do NOT rub in. Fluocinolone acetonide gel 0.1% is a safe and effective alternative.

Intralesional steroids: Single submucosal injection of methylprednisolone acetate (Depo-Medrol 40 mg/mL) may heal erosive OLP within 1 week.

Prednisone: Rapidly and effectively controls disease, but recurrences may occur when dosage is tapered.

Tacrolimus 0.1% and pimecrolimus (Elidel): Effective for erosive OLP; long-term treatment may be required. Monitor closely due to malignant transformation risk of OLP and immunosuppressive nature of calcineurin inhibitors.

Aloe vera gel: Induces clinical and symptomatologic improvement of OLP.

Dapsone (50-150 mg/day): If conservative treatment fails.

Hydroxychloroquine sulfate (Plaquenil) 200-400 mg daily: Useful for oral LP. Pain relief and reduced erythema after 1-2 months; erosions require 3-6 months.

Mycophenolate mofetil 1000-2000 mg/day: Effective in cases of oral erosive LP.

Azathioprine: Very effective for controlling OLP; considered for resistant, debilitating cases.

High-dose curcuminoids (6000 mg/day): May control signs and symptoms of OLP.

Vulvovaginal LP: Topical and oral steroids most effective; tacrolimus or pimecrolimus may be effective; some respond to dapsone; aloe vera gel safe and effective for vulval LP. Estrogens not effective.

LICHEN SCLEROSUS (LS)

Overview

LS is an uncommon but distinctive chronic cutaneous disease. An autoimmune inflammatory process. Some evidence for Borrelia burgdorferi or similar strains as a trigger. Cases in females outnumber males by 10:1. Predilection for the vulva, perianal area, and groin, though trunk and extremities may be affected. Some lesions induced by trauma or radiation (Koebner phenomenon).

Clinical Appearance

Early lesions: Small, smooth, pink or ivory, flat-topped, slightly raised papules. White to brown horny follicular plugs on surface = "delling" (not seen in lichen planus or morphea). Over time, clusters coalesce to form small oval plaques with dull or glistening, smooth, white, atrophic, wrinkled surface (like wrinkled tissue paper).

Anogenital LS in Females

Distinctive patterns (may coexist):

White atrophic plaque in hourglass or inverted keyhole shape encircling vagina and rectum - highly characteristic
Deep red, smooth plaque pattern
Intertrignous lesions with fissures, hemorrhagic erosion

Symptoms: Vulvar pruritus and dyspareunia most common. Dysuria and pain on defecation common.

Prepubertal LS

May occur in infants; resolves without sequelae in about 2/3 of cases at or just before menarche (leaving brown hyperpigmented area). Disease persists in approximately 1/3. IMPORTANT: Purpura of the vulva mimics sexual abuse - has led to false accusations and investigations. Vitiligoid LS can overlap with features of vitiligo in darker-skinned children.

Adult LS (Vulvar)

Typically appears after menopause; lengthy duration. Fragile, atrophic, thin, parchment-like tissue erodes, becomes macerated, heals slowly. Repeated cycles of erosion and healing induce contraction/stenosis of vaginal introitus, atrophy, and shrinkage of clitoris and labia minora. SCC of vulva has been reported in approximately 3% of patients with chronic LS - biopsy lesions that are white and raised (leukoplakia), fissured/ulcerated, or unresponsive to medical therapy.

LS of the Penis (Balanitis Xerotica Obliterans)

May present as recurrent balanitis intensified by intercourse; shaft rarely involved. White atrophic plaques on glans and prepuce that erode and heal with contraction. Most patients uncircumcised (LS may be caused by chronic occlusion). Encroachment into urinary meatus may cause stricture. Neoplastic changes in 2.3-8.4% of LS patients. 50% of penile SCC patients had clinical/histologic evidence of LS.

In boys: Ages 4-12 most common; nearly all have severe phimosis; purpura occasional.

Management

Topical Steroids - First-Line for Vulvar and Penile LS

Clobetasol ointment 0.05%: Remarkable relief of symptoms (itching, burning, pain, dyspareunia); improves and reverses atrophy, hyperkeratosis, sclerosis.

Adult vulvar treatment schedule: Apply twice daily for 1 month, then once daily for 1 month, then taper to twice weekly maintenance. Typical 30-g tube should last ~3-6 months. Follow-up examinations important.

Complete remission in 54% of patients; probability significantly associated with age (72% in women < 50; 23% in women 50-70; 0% in women >70). Relapse rate 50% at 16 months and 84% at 4 years.

Alternative steroids: Mometasone furoate 0.1% and triamcinolone acetonide 0.1% ointment: very effective; may be alternatives to clobetasol for long-term therapy with higher safety and tolerability. Biweekly maintenance with mometasone furoate reduces relapse rate.

Pediatric vulvar LS: Clobetasol ointment 0.05% for 2-4 weeks, then taper to less potent steroid.

Calcineurin Inhibitors

Tacrolimus 0.1% ointment and pimecrolimus 1% cream: clinical and subjective improvement in extragenital and genital LS. May reduce flare-ups, improve long-term disease control, especially in postmenopausal women. Concern about malignant transformation risk - use in patients unresponsive to potent topical steroids.

Other Systemic Options

Methotrexate: May be considered for widespread cutaneous LS
Cyclosporine: Oral CS 3-4 mg/kg/day for 3 months for refractory vulvar LS
Acitretin (20-30 mg/day for 16 weeks): Effective for severe vulvar LS
Antibiotics: Some evidence for infectious etiology from Borrelia; patients failing potent steroids treated with IM penicillin, oral penicillin/amoxicillin, or ceftriaxone; all showed significant response within weeks
Light therapy: NB-UVB and PUVA effective for widespread extragenital LS; patients warned skin may appear "deteriorated" during phototherapy because healthy skin tans more strongly than LS lesions
Photodynamic therapy (PDT) with 5-aminolevulinic acid: may be considered for unresponsive cases
Topical androgens and progesterone: NOT effective

Surgery

High recurrence rate makes surgery suitable only when medical treatment fails. Options for male genital LS: circumcision, meatotomy, one-stage penile oral mucosal graft urethroplasty. Carbon dioxide laser ablation to 1-2 mm depth: acceptable for LS of penis or vulva refractory to other measures; healing complete 6 weeks postoperatively.

PITYRIASIS LICHENOIDES

Pityriasis lichenoides (PL) is a rare disease with two variants: PLEVA (pityriasis lichenoides et varioliformis acuta, Mucha-Habermann disease) - acute, and PLC (pityriasis lichenoides chronica) - chronic. The terms "acute" and "chronic" refer to characteristics of individual lesions, not to the overall disease course.

PL and lymphomatoid papulosis share clinical and immunohistologic features, suggesting they are part of a spectrum of clonal T-cell cutaneous lymphoproliferative disorders. Most cases occur in first three decades; more common in males. History of infection or drug intake preceded skin manifestations in 30% (PLC) and 11.2% (PLEVA). More common in winter (35%) and fall (30%).

In children, PL is more likely to run an unremitting course, with greater lesional distribution, more dyspigmentation, and poorer response to conventional treatment.

PLEVA (Mucha-Habermann Disease)

A clonal T cell-mediated lymphoproliferative disorder. Usually benign and self-limited. Most cases in second and third decades.

Clinical features: Insidious onset, few symptoms other than mild itching or low-grade fever. Crops of round or oval reddish-brown papules, usually 2-10 mm, appearing singly or in clusters. Typical locations: trunk, thighs, and upper arms; face, scalp, palms, and soles in approximately 10% of cases. Papules may develop violaceous center and surrounding erythema with micaceous scale. Lesions can become vesicular or pustular, then undergo hemorrhagic necrosis within 2-5 weeks, often leaving postinflammatory hyperpigmentation and sometimes scars. Acute exacerbations common; may wax and wane for months or years. Mean duration 1.6-18 months.

Febrile ulceronecrotic Mucha-Habermann disease (FUMHD): Rare, serious variant in children - sudden widespread eruption of purpuric-black ulceronecrotic plaques with systemic signs and symptoms. Potential lethality of up to 25% - dermatologic emergency. Treatment: systemic corticosteroids, MTX, IVIg, oral antimicrobials, PUVA, dapsone, consider biologics.

Differential: Varicella, arthropod bites, impetigo, pityriasis rosea, scabies, lymphomatoid papulosis, viral exanthems.

PLC (Pityriasis Lichenoides Chronica, Juliusberg Type)

Gradually developing, very small, red-to-brown, flattened macules and papules with centrally adherent, micalike, shiny scales. Can start de novo or evolve from PLEVA lesions. PLEVA and PLC can coexist. Lesions flatten with time and resolve with hypo- or hyperpigmentation without scarring. Each lesion lasts weeks to months. Median disease duration: 20 months (range 3-132 months); may persist for years. Systemic symptoms rare.

Differential: Guttate psoriasis, pityriasis rosea, postinflammatory hypopigmentation, secondary syphilis, tinea corporis.

Histology

PLEVA: perivascular and diffuse lymphocytic and histiocytic infiltration at dermoepidermal junction; erythrocyte extravasation, epidermal necrosis, edema, basal vacuolar degeneration. PLC: similar but to a lesser extent.

Treatment

Erythromycin: Produced remission in 73% of cases; often took 2 months before significant therapeutic effect; frequently took as long as 2 months before a significant effect was noted; tapered over several months; disease usually recurred if tapered too rapidly. Dosage: 30-50 mg/kg/day.
Azithromycin: Effective (500 mg day 1, 250 mg days 2-5, on weeks 1 and 3 monthly); may clear in 3 weeks and remain clear for 6 months.
PUVA, UVB, NB-UVB phototherapy
Tetracycline, gold, MTX, oral corticosteroids, dapsone
Bromelain (crude aqueous extract of pineapple stems): 40 mg 3x daily for 1 month, then 40 mg twice daily for 1 month, then 40 mg/day for 1 month; all patients showed complete recovery in one series
Children with PL in particular: rule out diagnosis of lymphomatoid papulosis with follow-up

GROVER DISEASE (Transient Acantholytic Dermatosis)

Overview

Grover disease is most common in men older than age 60. Significant association with atopy and dry skin; peak incidence in winter.

Clinical Features

Pruritic papules and vesicles on the chest, back, and thighs. Itching may be transient and minimal. Persistent truncal, asymptomatic papules often localized to the submammary area in men (simulating folliculitis) is a very common presentation. Lesions last days to weeks, sometimes years. Lesions are initiated or exacerbated by sunlight. Diagnosis confirmed by finding focal acantholysis on skin biopsy.

Treatment

Disease is often transient and resolves without treatment
Avoid strenuous exercise and excessive sun exposure
Group II-V topical steroids: may control itch but may not clear eruption
Soothing baths with emollient bath oils or colloidal oatmeal
UVB phototherapy may help
A 1-month course of isotretinoin or acitretin may be effective

QUICK COMPARISON TABLES

Psoriatic Arthritis vs. Rheumatoid Arthritis vs. Osteoarthritis vs. Gout

Feature	PsA	RA	OA	Gout
DIP involvement	Common	Uncommon	Common	Uncommon
Symmetry	Less common	Common	Uncommon	Uncommon
Erythema of joint	Common	Uncommon	Uncommon	Common
Tenderness	Mild	Severe	Mild	Severe
Back involvement	Common	Uncommon	Uncommon	Uncommon
Skin lesions	Always	Uncommon	Uncommon	Uncommon
Nail lesions	Common	Uncommon	Uncommon	Uncommon
Dactylitis	Common	Uncommon	Uncommon	Uncommon
Enthesitis	Common	Uncommon	Uncommon	Uncommon
Rheumatoid nodules	Never	Common	Uncommon	Uncommon
RF	Uncommon	Common	Uncommon	Uncommon
Sacroiliitis	50%, asymmetric	Rare	Uncommon	Uncommon
Female:male	1:1	3:1	Hand/foot more in females	1:3.6

Psoriasis vs. Seborrheic Dermatitis vs. Pityriasis Rosea - Key Distinguishing Features

Feature	Psoriasis	Seborrheic Dermatitis	Pityriasis Rosea
Scale	Silvery, adherent	Greasy, yellowish	Fine, collarette scale
Distribution	Extensor surfaces, scalp, nails	Seborrheic areas (nasolabial folds, brows, ears)	Trunk, proximal limbs, "Christmas tree"
Herald patch	No	No	Yes (in 74%)
Nail changes	Yes (pitting, onycholysis, oil spots)	No	No
Arthritis	Yes (PsA)	No	No
Malassezia role	No	Yes	No
Course	Chronic	Chronic, relapsing	Self-limiting 1-3 months

PLEVA vs. PLC Comparison

Feature	PLEVA	PLC
% cases	57.3%	37%
Clinical	Acute polymorphic papules, vesicles, pustules, ulcers, necrosis	Gradual brownish papules/macules with micalike shiny scales
Median age	60 months (peaks 2-3 yr and 5-7 yr)	72 months (same peaks)
Median duration	18 months	20 months
Histopathology	Dense wedge-shaped CD8+ T-cell infiltrate, epidermal spongiosis, necrosis, ulceration	Superficial CD4+ T-cell bandlike infiltrate, slight parakeratotic scale
Treatment	Erythromycin, azithromycin, phototherapy, topical or systemic corticosteroids, MTX, dapsone, cyclosporine, acitretin	Phototherapy, erythromycin, azithromycin, topical corticosteroids, antihistamines, MTX, acitretin, cyclosporine, bromelain

Study Notes based on Habif's Clinical Dermatology, Chapter 8: Psoriasis and Other Papulosquamous Diseases

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