# 🍄 Superficial Fungal Infections - Study Notes
### *Based on Habif's Clinical Dermatology, Chapter 13*

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## QUICK OVERVIEW

| Category | Organisms | Key Locations |
|----------|-----------|---------------|
| **Dermatophytes** (ringworm) | Microsporum, Trichophyton, Epidermophyton | Skin, hair, nails |
| **Candidiasis** | Candida albicans (mainly) | Moist areas, mucous membranes, skin folds |
| **Tinea Versicolor** | Pityrosporum orbiculare/ovale (Malassezia furfur) | Upper trunk, arms, neck |

---

## PART 1: DERMATOPHYTES

### What are Dermatophytes?
- Fungi that infect **dead keratin only** (stratum corneum, hair, nails)
- Cannot survive on mucous membranes (no keratin layer there)
- Rarely invade deeply EXCEPT in immunosuppressed patients
- Genetic susceptibility exists - family members share patterns, but spouses don't get infected

### Classification by Origin
| Type | Source |
|------|--------|
| **Anthropophilic** | Human skin/hair/nails only |
| **Zoophilic** | Animals - can infect humans |
| **Geophilic** | Soil - can infect humans |

> **Remember:** Zoophilic + Geophilic = **BRISK inflammation**; Anthropophilic = **mild inflammation**

### Hair Invasion Patterns
| Pattern | Location of Fungus | Organisms |
|---------|-------------------|-----------|
| **Endothrix** | INSIDE hair shaft only | T. tonsurans, T. violaceum |
| **Ectothrix** | Inside + OUTSIDE hair shaft | M. canis, M. audouinii, T. verrucosum |

---

## DIAGNOSIS TOOLS

### 1. KOH Wet Mount (MOST IMPORTANT TEST)
- **Purpose:** Direct visualization of hyphae
- **Appearance:** Translucent, branching, rod-shaped filaments of **uniform width** with septa
- Only branching hyphae = dermatophytes; short non-branching hyphae = Candida/tinea versicolor
- **Mosaic artifact:** Lipid droplets that look like hyphae - disappear with heating

### 2. Wood's Light
| Finding | Organism |
|---------|---------|
| Blue-green fluorescence (hair) | M. canis or M. audouinii |
| Pale green fluorescence (hair) | T. schoenleinii |
| Pale yellow-white fluorescence (skin) | Tinea versicolor |
| Coral-red fluorescence | Erythrasma (bacterial, NOT fungal!) |
| **No fluorescence** | T. tonsurans (most common US scalp fungus!) |

### 3. Culture Media
| Media | Use |
|-------|-----|
| **DTM** (Dermatophyte Test Medium) | Turns PINK with dermatophytes in 6-7 days; quick office test |
| **Mycobiotic agar** | Best for hair infections (selective for dermatophytes) |
| **Sabouraud's agar** | Grows all fungi including non-dermatophytes (good for nails) |

---

## PART 2: TINEA BY LOCATION

### Tinea Pedis (Athlete's Foot) - Most Common Site

**Who gets it?** Men > Women; uncommon in prepubertal children

| Clinical Type | Description | Organism |
|--------------|-------------|---------|
| **Interdigital** | 4th/5th web space most common; dry/scaly OR wet/macerated | Various |
| **Moccasin-type** | Entire sole, silvery-white scale, chronic, hard to treat | T. rubrum |
| **Vesicular** | Acute, blisters on sole/dorsum, can get id reaction | T. rubrum |

**Two Feet-One Hand Syndrome:** Both feet + one hand (usually dominant). Caused by T. rubrum.

**Treatment - Tinea Pedis:**
- Interdigital: Terbinafine 1% cream BID x 1 week (88% clear at 5 weeks)
- Moccasin-type: Oral terbinafine 125 mg/day x 4 weeks (95% cure)
- Vesicular: Wet Burow's compresses + oral antifungal; treat secondary bacterial infection

---

### Tinea Cruris (Jock Itch)

**Who gets it?** Men >> Women; rare in children; common in summer

**Classic Appearance:**
- Unilateral, half-moon shaped plaque from crural fold onto thigh
- Well-defined SCALY border
- Does NOT involve scrotum (unlike Candida!)

**Differential Diagnosis:**
| Condition | Difference from Tinea Cruris |
|-----------|------------------------------|
| **Candida** | Bilateral, involves scrotum, satellite pustules |
| **Intertrigo** | Extends equally to groin AND thigh, no advancing border |
| **Erythrasma** | Uniform brown, no advancing border, coral-red Wood's light |
| **Tinea Incognito** | History of steroid use, altered appearance |

**Treatment:** Topical azoles x 10+ days; terbinafine/butenafine (faster); oral: fluconazole, itraconazole, or terbinafine

---

### Tinea Corporis (Ringworm of the Body)

**Classic appearance:**
- Flat scaly spot → raised border that expands outward
- Active border: red, raised, may have vesicles/papules
- Center: hypopigmented, less scaly

**Special Forms:**
- **Tinea Gladiatorum:** From wrestling (T. tonsurans); person-to-person contact
- **Majocchi Granuloma:** Caused by T. rubrum; follicular papulopustules; occurs on legs of women who shave; granulomatous nodules in dermis/subcutis
- **T. verrucosum ("Barn itch"):** From cattle; intensely inflamed, boggy, pustular; causes hyperpigmentation + scarring

**Tinea Incognito:** Fungal infection modified by topical steroid use
- Loses characteristic features; diffuse erythema, scattered pustules, no border
- Most common sites: groin, face, dorsal hand
- Hyphae still present - do KOH prep!

**Treatment:** Topical antifungal cream x 2 weeks BID (continue 1 week post-resolution); oral for extensive disease

---

### Tinea Capitis (Scalp Ringworm)

**Who gets it?** Prepubertal children 3-7 years; more in crowded/low socioeconomic settings

**USA:** T. tonsurans > 90% of cases (does NOT fluoresce)
**Europe:** M. canis most common

#### Four Clinical Patterns of T. tonsurans:

| Pattern | Description | Distinguishing Feature |
|---------|-------------|----------------------|
| **Black Dot** | Areas of alopecia with broken hairs at follicular orifice | Black dots at scalp surface |
| **Inflammatory (Kerion)** | Boggy, tender, purulent mass; fever, lymphadenopathy | Hypersensitivity reaction |
| **Seborrheic Dermatitis Type** | Diffuse/patchy fine white scale; looks like dandruff | Perifollicular pustules + broken hairs |
| **Pustular Type** | Discrete pustules/scabbed areas, minimal hair loss | Often mistaken for bacterial infection |

> **Key Rule:** Cervical/occipital lymphadenopathy should be present in ALL types of tinea capitis!

**Diagnosis:**
- Toothbrush technique (superior) or cotton swab technique
- KOH prep of plucked hairs
- Wood's light (only useful for M. canis/M. audouinii - blue-green fluorescence)
- Culture on Mycosel medium

**Treatment (Oral is REQUIRED - topical alone fails because it can't reach hair follicle):**

| Drug | Dose | Duration | Notes |
|------|------|----------|-------|
| **Griseofulvin** | 15-25 mg/kg/day | 6-8 wks (Trichophyton); 8-12 wks (Microsporum) | Drug of choice in children; take with fatty food |
| **Terbinafine** | Weight-based (62.5-250 mg/day) | 4 weeks | Best for Trichophyton; disputed for Microsporum |
| **Itraconazole** | 5 mg/kg/day | 4-6 weeks | Good alternative |
| **Fluconazole** | 6 mg/kg/day | 3-6+ weeks | Available as pleasant liquid |

**Adjuvant measures:**
- Antifungal shampoo (selenium sulfide 2.5%, ketoconazole 2%) 2-3x/week
- Screen family members (especially T. tonsurans - very infectious)
- Clean fomites (combs, brushes, bedding)

---

### Tinea Barbae (Beard Ringworm)

- Only in coarse hair-bearing areas of men (beard/mustache)
- Often follows minor trauma (shaving)
- Often mistaken for bacterial folliculitis/impetigo

| Type | Description |
|------|-------------|
| **Superficial** | Annular lesions like tinea corporis |
| **Deep Follicular** | Boggy, erythematous abscess; like kerion |

**Organisms:** T. mentagrophytes and T. verrucosum (from cattle)
**Treatment:** Same as tinea capitis (oral agents required)

---

## PART 3: TREATMENT REFERENCE TABLES

### Oral Antifungal Dosage Summary

| 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 | 5-6 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 x 6 wks (fingers) / 12 wks (toes) |
| 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) |

### Topical Antifungal Coverage

| Class | Drug | Dermatophytes | Yeasts | Bacteria |
|-------|------|---------------|--------|----------|
| Allylamine | Terbinafine, Naftifine, Butenafine | ✓ | - | - |
| Imidazole | Clotrimazole | ✓ | ✓ | - |
| Imidazole | Econazole | ✓ | ✓ | ✓ |
| Imidazole | Ketoconazole, Miconazole, Oxiconazole | ✓ | ✓ | - |

> **Rule:** Allylamines (terbinafine, naftifine, butenafine) are **FUNGICIDAL** - shorter treatment
> Azoles (clotrimazole, etc.) are **FUNGISTATIC** - longer treatment needed

---

## PART 4: CANDIDIASIS

### Key Facts
- C. albicans - normal flora of mouth, vagina, gut
- Infects only outer epithelial layers (stratum corneum)
- Primary lesion = pustule → red, denuded, glistening surface with "cigarette paper" scaling border
- Grows best in warm, moist environments

### Risk Factors (When Does Candida Become Pathogenic?)
- Pregnancy, oral contraceptives
- Antibiotics (disrupts normal flora)
- Diabetes
- Skin maceration
- Topical steroid therapy
- Immunosuppression, HIV
- Cushing's disease / corticosteroid use

### Candida by Location

| Location | Presentation | Key Features |
|----------|--------------|--------------|
| **Vulvovaginitis** | Pruritus, thick curdy white discharge, dyspareunia | pH < 4.5; KOH shows pseudohyphae |
| **Oral (Thrush)** | White plaques on red base; tongue most common | Infants, immunocompromised, elderly |
| **Balanitis** | Red papules/pustules on glans and shaft | Uncircumcised > circumcised |
| **Large skin folds** | Red plaque + "ocean wave" fringe of scale at border; satellite pustules | Under breasts, groin, axillae |
| **Small skin folds** | Macerated white skin → pink moist base | Between fingers, toes, mouth angles |
| **Angular cheilitis (Perlèche)** | Fissures at mouth angles; erythema, scale, crust | Saliva pooling; Candida + staph |
| **Diaper candidiasis** | Red base + satellite pustules in diaper area | Artificial intertriginous environment |

### Vulvovaginal Candidiasis (VVC) Treatment

**Uncomplicated:**
- OTC topical azoles (clotrimazole, miconazole) x 1-7 days
- Single oral fluconazole 150 mg

**Recurrent VVC (RVVC = 4+ episodes/year):**
1. Induce: Fluconazole 150 mg every 72 hours x 3 doses (Days 1, 4, 7)
2. Maintain: Fluconazole 150 mg weekly x 6 months

**Severe VVC:** 7-14 days topical OR fluconazole 150 mg x 2 doses (72 hours apart)

**Non-albicans Candida (C. glabrata):**
- Boric acid vaginal suppository 600 mg/day x 14 days
- Nystatin suppository 100,000 U x 14 days
- Azole-resistant: Amphotericin B or flucytosine cream

### Oral Candidiasis Treatment
| Drug | Dose |
|------|------|
| Fluconazole | 200 mg/day x 1 week (FIRST LINE) |
| Itraconazole | 200 mg/day x 1-3 weeks |
| Clotrimazole troche | 5x/day x 14 days |
| Nystatin suspension | 4-6 mL QID (for infants: 2 mL QID) |

---

## PART 5: TINEA VERSICOLOR

### What is it?
- Caused by Pityrosporum orbiculare/ovale (= Malassezia furfur)
- Normal skin flora that becomes pathogenic
- More common in adolescents/young adults (high sebaceous activity)
- Not known to be contagious

### Triggers (Yeast → Mycelial Form)
- Cushing's disease, adrenalectomy, pregnancy
- Malnutrition, burns
- Corticosteroids, immunosuppression
- Heat and humidity (exogenous)

### Clinical Presentation
- Multiple small CIRCULAR macules that enlarge radially
- **Colors vary:** White (hypopigmented), pink/red, fawn/brown
- Upper trunk most common; upper arms, neck, abdomen
- Hypopigmentation mechanism: Dicarboxylic acids from Pityrosporum are cytotoxic to melanocytes
- Lesions are WORSE/more obvious in summer (unaffected skin tans, lesions stay white)
- Facial lesions more common in children (forehead)

### Diagnosis
- Scrape with no. 15 blade → powdery white scale
- KOH: **"Spaghetti and meatballs"** = short hyphae + round spore clusters
- Wood's light: Pale yellow-white fluorescence
- Griseofulvin is NOT effective

### Treatment
**Topical (first line for limited disease):**
- Ketoconazole 2% shampoo x 1 application or 3 days (FIRST CHOICE)
- Selenium sulfide 2.5% x 10 min/day x 7 days = 87% cure rate
- Any imidazole cream BID x 2-4 weeks

**Oral (for extensive/recurrent disease):**
| Drug | Regimen |
|------|---------|
| Itraconazole | 200 mg/day x 7 days |
| Fluconazole | 300 mg/week x 2-4 weeks |
| Terbinafine (oral) | NOT effective |
| Griseofulvin | NOT effective |

**Recurrence Prevention:** Weekly ketoconazole 2% shampoo to trunk/neck; repeat treatment before summer

> **Important:** Hypopigmented patches DO NOT disappear immediately after treatment - repigmentation takes time; sunlight accelerates it.

---

## PART 6: PITYROSPORUM FOLLICULITIS

- Caused by same organism as tinea versicolor (P. orbiculare)
- **Typical patient:** Young woman with itchy follicular papules/pustules on upper back, chest, upper arms
- Often **misdiagnosed as acne**
- Risk factors: Diabetes, antibiotics, corticosteroids, Hodgkin disease, occlusion, oily skin

### Treatment
- Same as tinea versicolor
- Oral antifungals (fluconazole) + topical antifungal
- Ketoconazole 2% cream/shampoo
- Salicylic acid wash (keratolytic, effective)

---

## PITTED KERATOLYSIS (Bacterial, NOT Fungal!)

- Often misdiagnosed as tinea pedis
- Weight-bearing surfaces of soles (toes, ball of foot, heel)
- Circular/longitudinal punched-out depressions (pits) in stratum corneum
- Associated with hyperhidrosis and malodor
- Caused by bacteria: Dermatophilus congolensis, Corynebacterium, Streptomyces
- **Treatment:** Dry the feet; aluminum chloride 20%; antibiotics (erythromycin, clindamycin, mupirocin)

---

## HIGH-YIELD COMPARISONS FOR EXAMS

### Tinea Cruris vs. Candida Groin Infection
| Feature | Tinea Cruris | Candida Groin |
|---------|-------------|---------------|
| Pattern | Unilateral, half-moon | Bilateral, more extensive |
| Scrotum | NOT involved | INVOLVED |
| Border | Scaly, advancing | Fringe of scale + satellite pustules |
| Wood's light | No fluorescence | No fluorescence |

### Dermatophyte vs. Candida on KOH
| Feature | Dermatophyte | Candida |
|---------|-------------|---------|
| Hyphae type | Branching hyphae ONLY | Short hyphae + pseudohyphae + spores |
| Appearance | Long branching filaments | Shorter, less regular |

### Key Drug Rules
| Remember This | Detail |
|---------------|--------|
| Tinea versicolor: 2 drugs DON'T work orally | Terbinafine, Griseofulvin |
| Tinea capitis: must use oral (not topical) | Topical can't reach hair follicle below cuticle |
| Tinea incognito | Steroids suppress signs while fungus grows |
| Allylamines = fungicidal | Shorter course vs. azoles (fungistatic) |
| Econazole is special | Covers dermatophytes + yeasts + BACTERIA |
| Griseofulvin: drug interactions | Warfarin, OCP, barbiturates |
| Itraconazole: take with food | Fatty meal + acidic juice enhances absorption |
| Terbinafine: alter taste | 2.8% get taste disturbance |

---

## QUICK MNEMONIC AID

**"TINEA = The Infected Nooks Every Anatomy"**
- **T**inea pedis = feet
- **T**inea cruris = crotch/groin
- **T**inea corporis = body
- **T**inea capitis = cap (scalp)
- **T**inea barbae = beard
- **T**inea manuum = manual (hands)
- **T**inea unguium (= onychomycosis) = nails

**For Tinea Capitis organisms:**
- **"BLACK DOT"** = T. tonsurans (most common USA)
- **"GRAY PATCH"** = M. audouinii (pre-1950s, fluoresces GREEN)
- **"KERION"** = any, but especially M. canis, T. verrucosum
- **"BARN ITCH"** = T. verrucosum (from cattle)

---

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

# SUPERFICIAL FUNGAL INFECTIONS
## Oral Assessment & Exam Study Notes
### *Habif's Clinical Dermatology – Chapter 13*

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> **HOW TO USE THESE NOTES:**
> Read the question out loud, pause, then say your answer out loud.
> The answer is written the way you should speak it in an oral exam.
> Cover the answer with your hand or a piece of paper and practice!

---

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# SECTION 1: DERMATOPHYTES - THE BASICS

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**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?**

The three genera are:
1. **Microsporum**
2. **Trichophyton**
3. **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 here is that zoophilic and geophilic fungi cause a **brisk, intense inflammatory response** in humans, while anthropophilic fungi usually cause only **mild inflammation**.

---

**Q: Is there a genetic component to dermatophyte infections?**

Yes. Studies show that blood-related family members may share similar manifestations - so if several siblings are infected, it's likely due to shared genetic susceptibility. Interestingly, spouses do NOT become infected despite prolonged exposure, which supports the idea of a specific genetic predisposition rather than just close contact. Patients with chronic infections also tend to have a specific defect in delayed hypersensitivity to Trichophyton, and there's a higher frequency of atopy in chronically infected patients.

---

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

1. **Endothrix** - fungal hyphae are found INSIDE the hair shaft only. The cuticle remains intact. The hyphae break into spores (arthrospores) inside the shaft.
   - Caused by: *T. tonsurans*, *T. violaceum*, *T. soudanense*

2. **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 the fungal hyphae intact. Under the microscope, 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. That's 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?**

The mosaic artifact is produced by lipid droplets that appear in a single-file line between epidermal cells - they can look just like fungal hyphae. It's most common in specimens from the palms and soles. It's important because you don't want to misdiagnose a fungal infection based on artifact. The key is that the lipid droplets **disappear with additional heating and pressure**, whereas true hyphae do not.

---

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

Wood's light emits UV rays at over 365 nm. Key findings:

- **Blue-green fluorescence of hair** = *M. canis* or *M. audouinii* (ectothrix organisms)
- **Pale green fluorescence of hair** = *T. schoenleinii* (rare)
- **Pale yellow-white fluorescence of skin** = Tinea versicolor
- **Coral-red fluorescence** = Erythrasma (this is BACTERIAL, caused by *Corynebacterium minutissimum*, NOT fungal!)
- **No fluorescence** = *T. tonsurans* - which is very clinically relevant because T. tonsurans is the most common cause of scalp ringworm in the USA and does NOT fluoresce

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

---

**Q: What are the three culture media used for dermatophytes and when do you use each?**

1. **DTM (Dermatophyte Test Medium)** - turns PINK/red within 6-7 days in the presence of dermatophytes (due to alkaline metabolic products turning phenol red indicator). Quick and good for office diagnosis. Must discard after 2 weeks. Good for confirming onychomycosis.

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

3. **Sabouraud's agar** - no antibiotics, so grows ALL fungi including non-dermatophytes. Best for **nail infections** where you might want to identify saprophytic molds that don't respond to treatment.

---

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# SECTION 2: TINEA BY LOCATION

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## TINEA PEDIS (Athlete's Foot)

---

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

Tinea pedis is a dermatophyte infection of the feet - also known as athlete's foot. It is the MOST COMMON site of dermatophyte infection overall. It predominantly affects men. It's uncommon in women and rare in prepubertal children, though tinea should be considered in children with foot dermatitis. 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 tinea pedis (toe-web infection):**
The web between the 4th and 5th toes is most commonly involved because tight shoes compress the toes there and create a warm, moist environment. The web can present in two ways: either dry, scaly, and fissured - OR white, macerated, and soggy. The macerated form results from an interaction between the fungus AND bacteria. The fungus damages the stratum corneum and selects for antibiotic-resistant bacteria like Staph aureus and Gram-negative organisms.

**2. Chronic scaly moccasin-type (hyperkeratotic/plantar):**
The entire sole is infected, covered with fine silvery-white scale. The skin may be pink and tender. The pattern is typically two feet and one hand (or two hands and one foot), never both hands and both feet simultaneously. *T. rubrum* is the usual pathogen. This pattern is very difficult to eradicate because T. rubrum produces substances that suppress the immune response.

**3. Acute vesicular tinea pedis:**
A highly inflammatory form, often starting 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 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"?**

It describes dermatophyte infection of BOTH feet plus ONE hand (either left or right palm). Nail infection of hands and feet may also be present. It's most common in men. The same organism - usually *T. rubrum* - infects all three areas. Typically, tinea pedis/onychomycosis develops first, followed by tinea of the hand used to scratch the feet or pick toenails.

---

**Q: How do you treat tinea pedis?**

- **Interdigital type:** Terbinafine 1% cream BID x 1 week - gives 88% mycologic cure at 5 weeks. Butenafine BID x 1 week is also highly effective. Econazole has extra activity against the bacteria in macerated interdigital infections.
- **Moccasin/plantar type:** Oral terbinafine 125 mg/day x 4 weeks gives 95% sustained cure. This responds slowly to topical agents alone.
- **Acute vesicular type:** Wet Burow's solution compresses x 30 minutes several times daily; oral antifungal for the acute infection; oral antibiotics if secondary bacterial infection; topical steroids or prednisone for id reactions.
- Oral options include: fluconazole 150 mg once weekly, itraconazole 200 mg daily x 2 weeks, terbinafine 250 mg daily x 2 weeks.
- Prevention: Wider shoes, lamb's wool between toes, absorbent powder on feet (not shoes).

---

## TINEA CRURIS (Jock Itch)

---

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

Tinea cruris, or "jock itch," is a dermatophyte infection of the groin. It's much more common in men than women, and rare in children. It's worse in summer from sweating, and in winter from wearing multiple layers. The classic appearance is a **unilateral, half moon-shaped plaque** that starts in the crural fold and advances onto the thigh with a **well-defined, scaly border**. The skin inside the border turns red-brown and less scaly. The scrotum is NOT involved - this is an important distinguishing feature. For KOH examination, scrape from the advancing scaly border.

---

**Q: What is tinea incognito and how does it happen?**

Tinea incognito is a fungal infection that has been modified by inappropriate treatment with topical steroids. What happens is: the steroid suppresses the inflammation and gives the false impression that the rash is improving - but the fungus is actually flourishing because of the cortisone-induced immune suppression. When treatment stops, the rash returns, the patient reapplies the steroid, and a cycle is created. The characteristic border disappears. The patient ends up with diffuse erythema, scattered pustules, and a greatly expanded infection without the classic features. The most common sites are the groin, face, and dorsal hand. The diagnosis is confirmed by KOH prep - hyphae are still present.

---

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

This is a classic comparison:
- Tinea cruris is typically **unilateral**, does NOT involve the scrotum, and has a scaly advancing border.
- Candida groin infection is typically **bilateral**, MORE extensive, DOES involve the scrotum, has a fringe of scale at the border AND **satellite pustules** - those pinpoint pustules beyond the main border are a hallmark of Candida.

---

**Q: How do you distinguish tinea cruris from erythrasma?**

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

---

**Q: How is tinea cruris treated?**

Topically: Any antifungal cream BID for at least 10 days. Allylamines (terbinafine, naftifine, butenafine) need shorter duration than fungistatic azoles.
Systemically when needed: Fluconazole 150 mg once weekly x 2-3 weeks; itraconazole 100 mg/day x 2 weeks or 200 mg/day x 7 days; terbinafine 250 mg/day x 1-2 weeks.

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## TINEA CORPORIS (Ringworm of the Body)

---

**Q: Describe classic tinea corporis.**

Tinea corporis begins as a flat, scaly spot that develops a raised border expanding in all directions. The border is red and scaly - it may have papules or vesicles. As it expands, the center becomes hypopigmented and less scaly - giving the classic "ringworm" appearance of a ring with a clearing center. The disease can occur at any age and is more common in warm climates.

---

**Q: What is Majocchi granuloma?**

Majocchi granuloma is a distinctive form of inflammatory tinea caused mainly by *T. rubrum*. It was originally described in women who shave their legs, but also occurs in men and children at other sites. The primary lesion is a follicular papulopustule or nodule. Intracutaneous and subcutaneous granulomatous nodules develop. These form because infected hair follicles rupture into the dermis, causing a granulomatous reaction with epithelioid cells, giant cells, and lymphocytes. A skin biopsy with special fungal stains is needed for diagnosis if you can't find hyphae in scale or hair.

---

**Q: What is tinea gladiatorum?**

Tinea gladiatorum is tinea corporis occurring in competitive wrestlers. It's become common because of close person-to-person contact in wrestling. Most cases are caused by *T. tonsurans*. Asymptomatic carriers may play a role in transmission.

---

## TINEA CAPITIS (Scalp Ringworm)

---

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

Tinea capitis predominantly affects prepubertal children aged 3-7 years. It's most common in areas of poverty and crowded living conditions. In the USA, *Trichophyton tonsurans* accounts for more than 90% of cases. In Europe, *Microsporum canis* is more common. Farmers can 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. The topical agent cannot penetrate to that depth. The fungus gains entry to the hair below where the cuticle forms, which is why it cannot be reached from the skin surface. 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 spores inside the shaft weaken the hair so it fractures at or below the scalp surface, leaving "black dots." Little to no inflammation. Occipital lymphadenopathy may be present.

2. **Inflammatory pattern (Kerion):** The most dramatic form - a boggy, tender, indurated, tumor-like mass studded with pustules. Represents an intense hypersensitivity reaction to the fungus. There may be fever, occipital lymphadenopathy, and even a morbilliform rash. KOH and cultures are often NEGATIVE because inflammation has destroyed the fungal structures. Scarring alopecia can occur.

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

4. **Pustular type:** Discrete pustules or scabbed areas without much hair loss. Often gets several 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: How do you take samples for tinea capitis diagnosis?**

The **toothbrush technique** is superior - rub a sterile toothbrush over the affected scalp, then inoculate the bristles onto Mycosel medium. Alternatively, a moistened sterile cotton-tipped applicator rubbed over the affected area can be inoculated onto Mycosel medium. KOH prep of plucked hairs confirms the pattern of invasion. Culture on Mycosel allows accurate species identification.

---

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

| Drug | Key Points |
|------|-----------|
| **Griseofulvin** | Drug of choice; longest history of safety; fungistatic; take with fatty food; 6-8 weeks for Trichophyton, 8-12 weeks for Microsporum |
| **Terbinafine** | Fungicidal; BEST for Trichophyton; efficacy for Microsporum is disputed; 4 weeks |
| **Itraconazole** | Good for both; take with a full meal and acidic juice; 4-6 weeks; many drug interactions |
| **Fluconazole** | Effective; available as pleasant liquid; 3-6+ weeks; approved for children >6 months |

---

**Q: What adjuvant measures are used in tinea capitis?**

- Antifungal shampoo (selenium sulfide 2.5%, ketoconazole 2%, zinc pyrithione) 2-3 times/week - reduces spore load and transmission risk
- Topical antifungal to hair/scalp once daily x 1 week reduces infectious load
- Screen ALL family members and close contacts
- Clean fomites - combs, brushes, bedding, furniture (T. tonsurans spores remain viable for months)
- Children can return to school once systemic therapy has started - no need for extended exclusion
- For asymptomatic carriers with heavy spore counts, consider systemic therapy

---

## TINEA BARBAE (Beard Ringworm)

---

**Q: What is tinea barbae?**

Tinea barbae is a dermatophyte infection limited to the coarse hair-bearing areas of the beard and mustache in men. It usually follows minor trauma such as shaving. It's frequently mistaken for bacterial folliculitis, and patients often receive multiple courses of antibiotics before the correct diagnosis is made. The hairs in tinea are almost always infected and can be removed painlessly - this is an important distinction because hairs in bacterial folliculitis resist removal and removal is painful.

---

**Q: What are the two patterns of tinea barbae?**

1. **Superficial infection:** Annular lesions resembling tinea corporis with infected hairs.

2. **Deep follicular infection:** Boggy, erythematous, tumor-like abscess covered with dense crust - similar to a kerion. Caused by zoophilic organisms like *T. verrucosum* (from cattle) and *T. mentagrophytes*.

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

---

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# SECTION 3: ANTIFUNGAL DRUGS

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

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. It is 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. Contraindicated in pregnancy and lupus erythematosus.

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

---

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

Terbinafine is an **allylamine** - it inhibits squalene epoxidase, a membrane-bound enzyme that is 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 discontinuation
- After 6-12 weeks of therapy, detectable in nail plate for 30-36 weeks
- Delivered to stratum corneum via sebum
- NOT found in eccrine sweat
- Metabolized in liver; dose adjustment needed in liver and renal dysfunction

Notably: Terbinafine taken orally 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** → need longer treatment to maintain suppression

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

---

**Q: What is special about itraconazole's pharmacokinetics?**

Itraconazole is highly lipophilic with a very high affinity for keratinizing tissues. It adheres to keratinocytes in the nail plate - building up progressively and persisting 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 fruit juice. Absorption is reduced by antacids, H2 blockers, and proton pump inhibitors.

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

---

**Q: What is special about fluconazole?**

Fluconazole is much more specific for fungal cytochrome P-450 than imidazoles. It is highly water-soluble (unusual for an antifungal) and is transported to skin through sweat, where it concentrates by evaporation. It achieves high concentrations in the epidermis and nails. It persists for long periods. Available in pleasant-tasting liquid for children. Approved for children over 6 months.

---

**Q: What antifungal covers bacteria as well as fungi?**

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

---

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# SECTION 4: CANDIDIASIS

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

*Candida albicans* is a yeast-like fungus that lives as normal flora in the mouth, vaginal tract, and gut - it's normally harmless. It becomes pathogenic and converts from budding yeast to producing pseudohyphae or true hyphae when conditions change. Predisposing factors are:
- 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 does Candida look like on KOH prep?**

Short, non-branching hyphae AND spores. Both pseudohyphae and hyphae are present, and they are indistinguishable from dermatophytes in a KOH prep. That's why culture is important - the yeast is also part of normal flora, so culture must be interpreted carefully.

---

**Q: What is the primary lesion of cutaneous candidiasis?**

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. The characteristic pustule is seen at the margins. In intertriginous areas, the pustule immediately becomes macerated, so you look for **satellite pustules** - pinpoint pustules just OUTSIDE the main lesion - as a key diagnostic feature.

---

**Q: How does Candida vulvovaginitis present and how is it diagnosed?**

Symptoms: Pruritus, vaginal soreness, dyspareunia, external dysuria, abnormal discharge.
Signs: Vulvar edema, fissures, excoriations, thick curdy white vaginal discharge.
Diagnosis: Wet prep or KOH showing yeasts, hyphae, or pseudohyphae - OR positive culture. pH is NORMAL (<4.5) - so pH testing is NOT useful here (unlike bacterial vaginosis where pH >4.5).

Identifying Candida on culture WITHOUT symptoms is NOT an indication for treatment, because 10-20% of women normally carry Candida.

---

**Q: Differentiate between the three main causes of vaginal discharge: Candida, bacterial vaginosis, and trichomoniasis.**

| Feature | Candida | Bacterial Vaginosis | Trichomoniasis |
|---------|---------|---------------------|----------------|
| Discharge | White, clumpy, curdy | Gray, homogeneous, fishy | Profuse, greenish, frothy |
| Main symptom | Itching | Malodorous discharge | Malodor + itching + dysuria |
| pH | <4.5 (normal) | >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. It affects less than 5% of women.

Treatment strategy:
1. **Induction:** Fluconazole 150 mg every 72 hours x 3 doses (Day 1, Day 4, Day 7) to achieve mycologic remission
2. **Maintenance:** Fluconazole 150 mg once weekly x 6 months - this is first-line maintenance.

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

For *C. glabrata* (which causes up to 20% of RVVC): Boric acid vaginal suppository 600 mg/day x 14 days, or nystatin. Azoles are less effective.

---

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

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

The oral cavity may alternatively appear red, swollen and sore with LITTLE OR NO white exudate - this is the erythematous form, and pseudohyphae can be hard to find in this presentation.

---

**Q: What is angular cheilitis (perlèche) and what causes it?**

Angular cheilitis is inflammation at the angles (corners) of the mouth. It's 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. Causes include: lip licking, thumb sucking, malocclusion from poorly fitting dentures, excessive salivation, advancing age causing skin folds at the mouth, and weight loss with sagging. Patients mistakenly think it's a vitamin B deficiency. Treatment: antifungal cream followed in a few hours by a topical steroid, until the area is dry and inflammation-free.

---

**Q: Describe Candida intertrigo - where does it occur and what does it look like?**

Candida intertrigo occurs wherever skin touches skin in warm, moist areas: under pendulous breasts, between abdominal folds, in the groin, axillae, and rectal area. The skin folds retain heat and moisture - ideal for yeast. There are TWO presentations:

1. Pustules that become macerated → red papules with a fringe of moist scale at the border (pustules intact OUTSIDE the fold)
2. Red, moist, glistening plaque extending to/just beyond the apposing skin folds, with an "ocean wave" fringe of macerated scale at a sharply defined border.

Satellite pustules OUTSIDE the main lesion are the hallmark diagnostic feature.

Treatment: Cool wet compresses to promote dryness + antifungal cream BID + absorbent powder after inflammation resolves.

---

**Q: What is Candida balanitis and how does it present?**

Candida balanitis is yeast infection of the penis - more common in uncircumcised men because the foreskin creates the warm, moist environment that yeast needs. It 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 similar to vaginal candidiasis may be present. The presence of pustules is highly suggestive. Treatment: Miconazole or clotrimazole BID x 7 days, or a single 150 mg dose of fluconazole.

---

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# SECTION 5: TINEA VERSICOLOR

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**Q: What causes tinea versicolor and what triggers it?**

Tinea versicolor is caused by dimorphic lipophilic yeasts - *Pityrosporum orbiculare* (round form) and *Pityrosporum ovale* (oval form), collectively known as *Malassezia furfur*. These are normal skin flora. They 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:
- **Endogenous factors:** Cushing's disease, adrenalectomy, pregnancy, malnutrition, burns, corticosteroids, immunosuppression, oral contraceptives
- **Exogenous factors:** Excess heat and humidity

The disease is most common in adolescents and young adults because of higher sebaceous activity. It may not be contagious.

---

**Q: Describe the clinical presentation of tinea versicolor.**

Lesions begin as 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 an inflammatory/hyperemic response
- **Fawn/tan/brown** - from post-inflammatory pigmentation

The hypopigmentation is caused by dicarboxylic acids produced by the yeast that are cytotoxic to melanocytes and inhibit the dopa-tyrosinase reaction. The upper trunk is most commonly affected; also upper arms, neck, abdomen. The face is more commonly involved in children. The lesions may be asymptomatic or mildly itchy. It may fluctuate for years.

---

**Q: How do you diagnose tinea versicolor?**

1. Scrape lightly with a no. 15 blade - this reveals **powdery scale** that may not be visible on inspection.
2. KOH prep of the scale shows **short broad hyphae intermixed with round spore clusters** - the classic **"spaghetti and meatballs"** appearance.
3. Wood's light - irregular, pale yellow-to-white fluorescence. NOTE: Some lesions do NOT fluoresce.
4. Griseofulvin is NOT active and cannot be used for diagnosis or treatment.

---

**Q: How do you treat tinea versicolor?**

Important patient counseling point: **Hypopigmented patches will NOT disappear immediately after treatment.** Repigmentation takes time. Sunlight accelerates repigmentation. You confirm eradication by scraping with a no. 15 blade - when no more powdery scale is produced, the fungus has been eradicated. Recurrence rates are HIGH (40-60%).

**Topical (for limited disease):**
- **Ketoconazole 2% shampoo** - FIRST CHOICE. Apply to the whole body from neck to thighs, leave 5 minutes, rinse. Single application or daily x 3 days is highly effective.
- **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.

**Oral (for extensive/recurrent disease):**
- Itraconazole 200 mg/day x 7 days
- Fluconazole 300 mg/week x 2 doses
- **Terbinafine oral = NOT effective**
- **Griseofulvin oral = NOT effective**
- Oral ketoconazole = CONTRAINDICATED (risk of serious liver damage and death)

**Recurrence prevention:** Ketoconazole 2% shampoo once weekly to trunk/neck. Repeat treatment before summer.

---

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# SECTION 6: PITYROSPORUM FOLLICULITIS

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

Pityrosporum folliculitis is an infection of the hair follicle 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. Key differences from acne: it doesn't respond to acne antibiotics, and in tropical Pityrosporum folliculitis the face is commonly involved (mandible and sides of the face) - more lateral than 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: Same as tinea versicolor - oral fluconazole combined with topical antifungal. Ketoconazole 2% cream/shampoo. Salicylic acid wash is keratolytic and effective.

---

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# BONUS: PITTED KERATOLYSIS (Often confused with tinea!)

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

Pitted keratolysis is a BACTERIAL infection (NOT fungal) that is frequently misinterpreted as tinea pedis. It presents on the weight-bearing surfaces of the soles - the ventral toe, ball of the foot, and heel. The characteristic finding is many **circular or longitudinal punched-out depressions (pits)** in the stratum corneum. Key symptoms: **hyperhidrosis, malodor, and sliminess of the skin**. There is little or no inflammation. Caused by bacteria: *Dermatophilus congolensis*, *Corynebacterium* species, *Streptomyces*, *Kytococcus sedentarius*. These bacteria produce keratinases that degrade keratin when the skin is hydrated and the pH rises.

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

---

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# RAPID-FIRE REVIEW QUESTIONS

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

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

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

**Q: Which antifungal is BETTER for Trichophyton tinea capitis?**
Terbinafine is more effective for Trichophyton species. 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 + 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. They are 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 lesions - 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* (>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 is of limited value in the USA/UK where T. tonsurans predominates.

**Q: What is a kerion?**
A boggy, tender, indurated, tumor-like scalp lesion that exudes pus, caused by an intense hypersensitivity reaction to a dermatophyte (especially in tinea capitis). It can heal with some 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 due to alkaline metabolic products in about 6-7 days.

**Q: What is the 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 risk?**
Oral ketoconazole - contraindicated for skin and nail fungal infections due to risk of serious liver damage, adrenal problems, drug interactions, and death.

**Q: What is the two feet-one hand syndrome?**
Dermatophyte infection of both feet AND one hand (but not both hands) - caused by T. rubrum. The infected hand is usually the one used to scratch the feet.

**Q: What happens if you treat dermatophyte infections with topical steroids?**
The steroids suppress inflammation and temporarily improve the appearance, but the fungus flourishes due to cortisone-induced immune changes. This creates tinea incognito - a modified, expanded, atypical infection.

---

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# FINAL SUMMARY TABLE

| Condition | Organism | Location | Key Feature | Treatment |
|-----------|---------|----------|-------------|-----------|
| Tinea pedis | Dermatophytes (T. rubrum) | Feet | 4th/5th web; or moccasin; or vesicular | Terbinafine cream/oral |
| Tinea cruris | Dermatophytes | Groin | Half-moon plaque; NO scrotum | Topical/oral antifungal |
| Tinea corporis | Dermatophytes | Body | Ring with active scaly border | Topical; oral if extensive |
| Tinea capitis | T. tonsurans (USA) | Scalp | Black dot, kerion, seborrheic, pustular | ORAL mandatory (griseofulvin, terbinafine) |
| Tinea barbae | T. verrucosum, T. mentagrophytes | Beard | Deep boggy abscess; painless hair removal | Oral antifungal |
| Tinea incognito | Any dermatophyte + steroids | Any site | Modified, atypical appearance; no classic border | Stop steroids; KOH; oral antifungal |
| Tinea versicolor | Pityrosporum (Malassezia furfur) | Upper trunk | Hypo/hyperpigmented circular macules; "spaghetti and meatballs" KOH | Ketoconazole shampoo; selenium sulfide; oral itraconazole/fluconazole |
| Pityrosporum folliculitis | Pityrosporum | Upper back/chest | Looks like acne; doesn't respond to antibiotics | Oral fluconazole + topical antifungal |
| Candida (skin folds) | Candida albicans | Moist folds | Satellite pustules; fringe of scale | Topical antifungal + wet compresses |
| VVC | Candida albicans | Vagina | Curdy white discharge; pH < 4.5 | Azole cream or oral fluconazole |
| Oral candidiasis | Candida albicans | Mouth | White plaques on red base; tongue involvement | Fluconazole 200 mg/day |
| Erythrasma | Corynebacterium minutissimum (BACTERIA) | Groin/toe webs | Brown uniform scale; CORAL-RED Wood's light | Erythromycin/clarithromycin |
| Pitted keratolysis | Bacteria (Dermatophilus, Corynebacterium) | Soles | Punched-out pits; malodor; hyperhidrosis | Dryness; aluminum chloride; antibiotics |

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*Source: Habif's Clinical Dermatology, Chapter 13 — Superficial Fungal Infections*
*Study tip: Read each Q&A out loud, as if speaking to an examiner. Practice explaining concepts in your own words after reading.*