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Black Piedra Pathophysiology

Anatomy: Black piedra is a superficial infection involving the hair shaft. The scalp is not affected.

What: It presents as multiple small black nodules that are firmly attached to the hair shaft. Hair breakage is a less prominent feature with black piedra than with white piedra. Typically, there are no other symptoms.

Where: Hair of the scalp.

Who: It is a rare disease in the U.S., and affects primarily people in tropical climates.

The Diagnosis: Examination of an affected hair under light microscopy with KOH prep.

The Differential: Lice, white piedra.

White Piedra Pathophysiology

Anatomy: In white piedra, the fungus initially invades the cuticle of the hair. Over time, the growth extends outside of the hair shaft, resulting in the characteristic nodule of the disease. The organism does not invade the skin in white piedra, but it is capable of invasive disease, primarily in immunosupressed patients.

Interesting Facts:

Humans can be colonized with T. beigelii

The organism is closely related to Cryptococcus.

What: Soft, loose white nodules on the hair shaft. The smaller (0.5mm) nodules can coalesce to cover large areas of the shaft. The fungal infection weakens the hair, and breakage is common. Pruritus and pain are uncommon, but do occur.

Where: Hairs of (groin, axilla, beard) > (scalp, torso).

Who: Young men develop white piedra of the groin more commonly. It occurs in tropical areas and in the southeastern U.S. No other identified risk factors.

The Diagnosis: KOH prep of the hair shaft.

The Differential: Trichomycosis, black piedra, lice.

Shaving the area affected
and
Topical amphotericin B or azole x 1 to 4 months.

Oral antifungals are not effective.

Tinea Capitis Pathophysiology

Changing epidemiology: In the U.S. the most common organism causing tinea capitis is T. tonsurans (an anthropophilic organism), surpassing M. canis (a zoophilic organism) about a half century ago. The change in epidemiology is attributed, in part, to differences in antimicrobial sensitivity (M. canis is more susceptible to griseofulvin than T. tonsurans) and also to immigration trends (T. tonsurans is endemic in areas of Mexico and Central America).

Anatomy: There are 3 basic types of infections of the hair shaft. In ectothrix infections, the fungus invades the cuticle of the hair shaft but never penetrates further than the fully keritinized layer. The arthroconidia are transported to the surface of the hair shaft and can be visualized via KOH prep. However, in endothrix infections, the organism invades more deeply into the hair shaft. With light microscopy, large numbers of arthroconidia seem to be packed inside the hair. Favus will be discussed further in the section Tinea Favosa.

The surrounding inflammatory response can vary from a mild perifollicular mixed infiltrate to a very inflammatory dermal reaction with a predominance of neutrophils. In the latter, abscesses within the hair follicle and dermis can occur. (Figure HI 4)

Interesting Facts:

Studies have shown that organisms that cause tinea capitis, particularly T. tonsurans, can exist in a carrier state. The cited carriage numbers vary from 6 to 30% (from studies done primarily in children).

Infection in the U.S. is primarily spread from person to person or, on occasion, from pet to child. Dermatophytes can be cultured from fomites (such as hair brushes, combs, barrettes and pillows), but their significance in the spread of infection is unclear.

What: Most lesions begin as erythematous, scaling patches that slowly enlarge and result in alopecia. Four generally recognized clinical patterns exist.

Gray-Patch or Non-inflammatory. Ectothrix organisms such as M. canis and M. audouinii are typically the cause, but T. tonsurans can also be a culprit. Involved hairs typically break off just above (not at) the level of the scalp, and the areas of alopecia are characteristically gray due to a coating of arthrospores. Areas of scale and mild erythema are also common, and the disease can resemble seborrheic dermatitis. (Figure HI 5)

Black-Dot. Can be used to describe a number of clinical presentations in which the hairs break off just at the surface of the scalp, leaving a characteristic "black dot" appearance. The endothrix fungi T. tonsurans and T. violaceum are most commonly involved. This type of infection can vary from non-inflammatory (with scale and minimal hair loss) to inflammatory (with pustules, faruncles or frank kerions). Scarring alopecia is common. (Figure HI 6)

Inflammatory. Severe inflammation is more likely to occur with zoophilic or geophilic organisms (e.g. M. canis and M. gypseum). The spectrum of disease can vary from a pustular folliculitis to kerion. Kerion are boggy, painful, masses usually with marked alopecia and often with purulent drainage. Pruritis, pain, and regional lymphadenopathy can be seen even without superinfection. (Figures HI 7 & 8)

Favus. Will be discussed under the section Tinea Favosa.

Where: Hair of the scalp

Who: Tinea capitis is primarily a disease of children. In the U.S. it is more common in the African American population and in the urban poor. It is endemic in some regions of the world due to overcrowding, poor hygiene and little access to healthcare.

The Diagnosis: Wood's lamp exam may reveal fluorescence for some Microsporum species. KOH prep examination of an infected hair shaft can often demonstrate arthroconidia in the typical ectothrix or endothrix patterns. Definitive diagnosis is made through culture. A sterile toothbrush or damp sterile cotton swab rubbed over the area can be used to directly inoculate fungal culture plates. Biopsy may be needed to establish the diagnosis in very inflammatory lesions (e.g. kerion) in which organisms are sparse.

The Differential: Alopecia areata, seborrheic dermatitis (including tinea amiantacea), atopic dermatitis, trichotillomania, discoid lupus erythematosus.

First line

Good safety profile

0.5 grams per day for adults

10-15mg/kd for children

20mg/kg for T. tonsurans

6-8 weeks

M. canis and some others may require 12 weeks

Not yet officially approved in the U.S. for tinea capitis in children.

May not be as effective for Microsporum sp.

4 weeks

May be shorter for T. violaceum

Shorter treatment periods

Resistance uncommon

Pulse doses can be used

4-6 weeks for daily dose

2-3 cycles of pulse therapy

• Topical treatments have no role in disease cure. However, if used in conjunction with oral therapies, they can limit the shedding of organisms and allow children to return to school. Selenium or ketoconazole shampoos are both good options.
• Kerions may require up to 16 weeks of oral therapy.
• Some small studies have suggested that oral steroids do not change the disease course of inflammatory disease. However, several sources still recommend a short course of oral steroids in kerion to help to prevent hair loss and scarring. Topical or oral steroids may also have a role in severe pruritus.
• In anthropophilic infections, other children in the household should be examined and potentially cultured.
• In zoophilic infections pets should be examined and, if necessary, treated.

Tinea Favosa Pathophysiology

Anatomy: Invasion by the organism might be characterized as endothrix, but the fungus undergoes autolysis, leaving characteristic empty tunnels within the hair shaft (favus is Latin for honeycomb). A scutula is formed on the surface of the hair follicle composed of hyphae and keratinous debris. The center of the scutula is usually composed of necrotic debris, while the periphery contains viable organisms. Epithelium is atrophic with acanthosis at the periphery. Chronic dermal infiltration is common, with either plasma cells or granulomas. After longstanding infection, the dermis may simply show fibrous change.

What: The scutula, a small mass of hyphae and debris around a hair follicle, can coalesce with other scutula to form a large adherent crust over the scalp (generally also referred to as a scutula). Hair loss and scarring are also common.

On the glabrous skin, favus commonly appears like tinea corporis, but can occasionally form a scutula. Nail infections are impossible to differentiate from other types of onychomycosis.

Where: Most common on the scalp, but can also affect glabrous skin and nails.

Who: The infection is common in the Middle East and Mediterranean. It can occur in families, although it is difficult to tell if this is a genetic predisposition or shared environment (poor nutrition and hygiene are risk factors).

The Diagnosis: KOH exam and culture (see tinea capitis) are recommended. Wood's lamp exam shows a subtle pale green fluorescence.

The Differential: Seborrheic dermatitis, psoriasis, tinea amiantacea, cicatrizing alopecia from radiation or chemotherapy or other causes of scarring alopecia.

Treat as you would for TINEA CAPITIS.

Tinea Barbae Pathophysiology

Anatomy: Is dependent on the type of infection. In circinate tinea barbae pathology is similar to tinea corporis. With superficial and inflammatory types, pathology is more similar to tinea capitis.

What: The disease can take on 3 different morphologies.

1. Circinate tinea barbae. An infection analogous to tinea corporis of glabrous skin with erythematous, scaling plaques with well demarcated, advancing borders.

2. Superficial (follicular) tinea barbae. Tends to be less inflammatory and is primarily caused by anthropophilic organisms. Perifollicular papules or pustules with surrounding erythema are common, resembling a bacterial folliculitis. (Figure HI 9)

3. Inflammatory tinea barbae. Analogous to inflammatory tinea capitis. Pustules, faruncles or kerion formation can be observed, and infection may result in alopecia and eventual scarring. This type of inflammation is more common with zoophilic organisms.

Where: Chin, neck, submandibular areas. Upper lip involvement is less frequent.

Who: Men. Now commonly ranchers, dairy farmers or vetrinarians due to exposure to infected animals.

The Diagnosis: KOH prep and culture, as in tinea capitis.

The Differential: Bacterial folliculitis, acneform dermatitis, perioral dermatitis, carbuncles, candidal dermatitis, herpes zoster or simplex, pseudofolliculitis.

Treat for circinate tinea barbae as you would for TINEA CORPORIS.

Treat for follicular and inflammatory tinea barbae as you would for TINEA CAPITIS.

Pityrosporum Folliculitis Pathophysiology

Anatomy: In biopsy samples, budding yeast and occasional hyphae can be seen in the hair follicle. The follicle ostium can be quite dilated due to the presence of fungal elements and cellular debris. Dermal infiltrate is more common with follicular rupture (and can result in giant cell formation).
(Figure HI 11)

Other:

• The organism also causes TINEA VERSICOLOR.
• Occlusive clothing and greasy skin may contribute to the disease.

What: 2-3mm perifollicular papules and pustules are typical. Lesions are small but can be very pruritic, so excoriations are often seen. (Figure HI 12)

Where: Commonly occurs on the chest, back, neck, and upper arms. Facial involvement is more common in the tropics.

Who: Women>men. Most patients are younger or middle aged adults. Common in tropical climates. There is increased prevalence among patients undergoing immunosuppressive therapy and those with diabetes or HIV.

The Diagnosis: KOH examination and culture are recommended. Sometimes biopsy may be needed.

The Differential: Acne, bacterial folliculitis, scabes, pustular drug eruption, scabies.

Treat as you would for TINEA VERSICOLOR.