FUNGAL SKIN INFECTIONS: Candidiasis, Onychomycosis, Tineas and Tinea Incognito. By Dr S. L. Pitmang Dept of Family Medicine JUTH, Jos.

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OUTLINE

Introduction.CandiasisOnychomycosisTineasTinea incognito.Conlusion.References.

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CANDIDIASIS

Cutaneous candidiasis and other forms of candidiasis are infections caused by the yeast Candida albicans or other Candida species.

Yeasts are unicellular fungi that typically reproduce by budding.

Candida Albicans is an oval yeast 2-6 µm in diameter.

Superficial infections of skin and mucous membranes are the most common types of candida infections of the skin.

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TYPESCommon types of candida skin

infection include Vulvovaginal candidiasis Intertrigo Diaper dermatitis Erosion interdigitalis blastomycetica Perianal dermatitis Candida balanitis.

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Humans carry yeast fungi, including candida species, throughout the gastrointestinal tract (mouth through anus) as part of the normal commensal flora.

The vagina also commonly is colonized by yeast (13% of women), most commonly by C albicans and C glabrata.

The commensal oral isolation of candida species ranges from 30-60% in healthy adults.

Candida species are not part of the normal flora of the skin; however, they may colonize fingers or body folds transiently.

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Vulvovaginal candidiasisThis common condition in women presents

with itching, soreness, and a thick creamy white discharge.

Candida infections occur more frequently with advancing age, vulvovaginitis is unusual in older women. In the absence of estrogen stimulation, the vaginal mucosa becomes thin and atrophic, producing less glycogen.

Candida colonization of vaginal mucosa is estrogen dependent and subsequently decreases sharply after menopause.

In contrast, the likelihood of colonization increases during pregnancy (25-33%).

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Candidal BALANITIS

Signs and symptoms of this candida infection vary but may include tiny papules, pustules, vesicles, or persistent ulcerations on the glans penis.

Exacerbations following intercourse are common.

Dry, red, superficially scaly, pruritic macules and patches .

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Oropharyngeal candidiasisCommonly as oral thrush, considered by

many to be a minor problem of little significance that may clear spontaneously.

However, without appropriate treatment this can lead to a chronic condition that can result in discomfort and anorexia.

Rarely, oropharyngeal infection leads to systemic candidiasis.

Use of broad-spectrum antibiotics and inhaled corticosteroids, diminished cell-mediated immunity, and xerostomia are all risk factors for candidiasis.

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In Adults when it occurs with no obvious cause should raise suspicion for immuno-suppression.

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Intertrigo

Most cases of cutaneous candidiasis occur in skin folds where occlusion (by clothing or shoes) produces abnormally moist conditions.

Candida infection of the skin under the breasts or pannus occurs when those areas become macerated

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Erythema, maceration, and satellite pustules in the axilla, accompanied by soreness and pruritus result in a form of intertrigo.

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Candida diaper dermatitis 

Infants with oropharyngeal candidiasis invariably harbor C albicans in the intestine and feces (85-90%).

Candida diaper dermatitis is the result of progressive colonization from oral and gastrointestinal candidiasis and infected stools represent the most important focus for cutaneous infection.

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Moist macerated skin is particularly susceptible to invasion by C albicans.

Additional factors that predispose infants to candida diaper dermatitis include local irritation of the skin by friction; ammonia from bacterial breakdown of urea, intestinal enzymes, and stool; detergents; and disinfectants.

Diaper dermatitis candidiasis can result in an a generalized eruption known as an Id reaction, also known as autosensitization or an autoeczematization reaction 13

Lab studies

KOH preparation is the easiest and most cost-effective method for diagnosing cutaneous candidiasis.

Culture from an intact pustule, skin biopsy tissue, or desquamated skin can help to support the diagnosis.

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Microscopic examination of skin scrapings prepared with calcofluor white stain.

A skin biopsy specimen stained with a periodic acid-Schiff stain reveals nonseptated hyphae. The presence of nonseptated hyphae allows cutaneous candidiasis to be distinguished from tinea.

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Treatment.Candidal Vulvovaginitis:Topical antifungal agents including

miconazole nitrate (Micatin, Monistat-Derm) or clotrimazole (Lotrimin, Mycelex) creams/pessaries are curative.

One-time oral therapy with fluconazole (150 mg) or itraconazole (600 mg) is effective and may be a more attractive alternative to some patients, but it is more costly.

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Candida Balanitis:

Topical therapy is sufficient in most patients. Evaluate asymptomatic sexual partners and treat them if they are affected.

If persistent lesions spread beyond the genitalia, consider the possibility of diabetes, and assess for the disease.

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Oropharyngeal candidiasis in the infant:

Nystatin oral suspension. Treat for 10-14 days or until 48-72 hours after resolution of symptoms. For preterm infants is 0.5 mL (50,000 IU), for infants is 1 mL (100,000 IU) to each side of the mouth 4 times/day.

Candidal diaper dermatitis:Practical measures that reduce the amount of

time the diaper area is exposed to hot and humid conditions.

Air drying, frequent diaper changes, and generous use of baby powders and zinc oxide paste are adequate preventive measures.

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For topical therapy- Nystatin, amphotericin B, miconazole, and clotrimazole are effective and almost equivalent in efficacy.

Oral candidiasis in adults:Nystatin (1:100,000 U/mL, 5 mL oral rinse

and swallow qid) or clotrimazole troches (10 mg 5 times/d) usually is effective.

Extend the duration of antifungal therapy at least twice as long as the termination of clinical signs and symptoms of candidiasis.

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Reserve oral fluconazole, 100 mg once daily for 2 weeks, for patients with more severe disease.

IntertrigoKeep the skin dry, with the addition of

topical nystatin powder, clotrimazole, or miconazole twice daily, often in conjunction with a mild potency corticosteroid.

Patients with extensive infection may require the addition of fluconazole (100 mg PO qd for 1-2 wk) or itraconazole (100 mg PO qd for 1-2 wk).

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ONYCHOMYCOSISFungal infection of the toenails or

fingernails that may involve any component of the nail unit, including the matrix, bed, or plate.

Can cause pain, discomfort, and disfigurement and may produce serious physical and occupational limitations, as well as reducing quality of life (psychosocial and emotional effects).

Accounts for half of all nail disorders.Most common nail disease in adults.M>F 21

MAIN SUBTYPES:

Distal lateral subungual onychomycosis (DLSO)

White superficial onychomycosis (WSO)

Proximal subungual onychomycosis (PSO)

Endonyx onychomycosis (EO) Candidal onychomycosis.Total dystrophic onychomycosis.

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Proximal subungual onychomycosis. Proximal leukonychia

White superficial onychomycosis

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Distal subungual onychomycosis. Subungual hyperkeratosis onycholysis and yellow streak

Candidal onychomycosis in a patient with chronic mucocutaneous candidiasis. Total onychomycosis and paronychia

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CAUSES

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Caused by 3 main classes of fungi: dermatophytes, yeasts, and nondermatophyte molds.

Dermatophytes are by far the most common cause of onychomycosis.

Two major pathogens are responsible for approximately 90% of all onychomycosis cases. Trichophyton rubrum accounts for 70% and Trichophyton mentagrophytes accounts for 20% of all cases.

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Onychomycosis caused by nondermatophyte molds (Fusarium species, Scopulariopsis brevicaulis,Aspergillus species) is becoming more common worldwide, accounting for up to 10% of cases.

 Onychomycosis due to Candida is rare.

RISK FACTORS

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Family historyIncreasing agePoor healthPrior traumaWarm climateParticipation in fitness activities.Immunosuppression (eg, HIV, drug

induced)Communal bathingOcclusive footwear

DIAGNOSIS

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Features of onychomycosis may mimic a large number of other nail disorders.

Laboratory diagnosis of onychomycosis must be confirmed before beginning a treatment regimen.

A negative mycological result does not rule out onychomycosis (microscopy may be negative in up to 10% of cases and culture in up to 30% of cases).

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DIRECT MICROSCOPYA 20% potassium hydroxide (KOH)

preparation in dimethyl sulfoxide (DMSO) is a useful screening test to rule out the presence of fungi.

CULTURETo identify the specific pathogen

involved in onychomycosis fungal culture is used.

TREATMENT

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Depends on the type, number of nails and severity.

Combination of systemic and topical treatment increases cure rate.

Recurrence is high.Topical: ciclopirox olamine 8%,

efinaconazole 10% nail solutions, Amorolfine and bifonazole/urea.

Oral therapy: Itraconazole, terbinafine, Fluconazole and the new triazole posaconazole.

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Continuous Therapy- The FDA-labelled dosage of Itraconazole is 200mg daily taken continuously for 12 weeks and 6 weeks for toenail and fingernail infections resp.

Pulse Therapy- Itraconazole 200mg taken bd for a week per month; repeated for two to three months (ie two or three ‘pulses’) for fingernail infections.

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Shown to be effective for toenail infections when given in three to four pulses.

Liver enzyme monitoring is recommended before continuous therapy is initiated and every four to six weeks during treatment.

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Surgical Care:Laser- Nd:YAG lasers and diode

lasers.Photodynamic therapy.Mechanical, chemical or surgical

nail avulsion.

TINEA

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Several species of dermatophytes commonly invade human keratin, and these belong to the Epidermophyton,Microsporum, and Trichophyton

 genera. Grow outwards on skin, producing a ring like

pattern, hence the term "ringworm". Very common and affect different parts of the

body. Dermatophytosis infections, also known as

tinea, are classified according to the body regions involved.

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May spread from person to person (anthropophilic), animal to person (zoophilic), or soil to person (geophilic).

The most common of these organisms are 

Trichophyton rubrum. Trichophyton tonsurans. Trichophyton

interdigitale/mentagrophytes. Microsporum canis. Epidermophyton floccosum.

CLASSIFICATION

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Tinea capitis - Scalp

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Tinea corporis – Body

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Kerion

Tinea pedis

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FEATURES

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About 2 weeks elapse from inoculation to subsequent clinically visible skin changes.

Tinea pedis often follow activities that cause the feet to sweat.

Pruritus (itching) is the main symptom in most forms of tinea.

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Hair loss, infected hairs are brittle and break easily.

Ask patient about participation in sports, such as judo, karate, wrestling, and other contact sports, is important. Likewise, asking the patient about military enrollment and any contacts with similar skin disease is important.

EXAMINATION

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Tinea capitis: scaling of the scalp or circumscribed alopecia with broken hair at the scalp.

Tinea corporis: on exposed skin of the trunk and extremities. It is characterized by annular scaly plaques with raised edges, pustules, and vesicles. This is usually tinea imbricata (T concentricum).

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Tinea pedis: Toe webs and plantar surface and often affects only one foot. Toe-web scaling, fissuring, and maceration; scaling of soles and lateral surfaces; erythema; vesicles; pustules; and bullae may be present.

Tinea manuum: Palms and finger webs that usually occurs in association with tinea pedis. Similarly, often only one hand is involved. Scaling and erythema may be present.

Tinea cruris: Groin and pubic region. Characterized by erythematous lesions with central clearing and raised borders. Tinea cruris often co-occurs with tinea pedis or tinea unguium

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Tinea barbae: The beard and neck area. Erythema, scaling, and pustules are present.

Tinea unguium: also called onychomycosis.It is characterized by onycholysis (nail plate separation from nail bed) and thickened, discolored (white, yellow, brown, black), broken, and dystrophic nails.

Tinea incognito: This is a common difficult diagnosis to make without history. As a result of prior treatment with hydrocortisone, causing atypical appearance

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Autoeczematization reactions: (also known as id reactions) are secondary dermatitic eruptions that occur in association with primary, often inflammatory, skin disorders. It is secondary to a tinea infection at another site. It is due to cell-mediated immunity and resolves with treatment of tinea.

CAUSES

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Caused chiefly by species of the genera Microsporum,Trichophyton, and Epidermophyton

Risk factors:Moist conditions.Communal baths.

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Immunocompromised states (including the use of immunosuppressive drugs).

Atopy.Genetic predisposition.Athletic activity that causes skin

tears abrasions, or trauma such as wrestling, judo, or soccer.

LABORATORY INVESTIGATIONS

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Direct microscopic examination: . Skin scrapings, nail specimens, or plucked hairs are treated with potassium hydroxide and examined. Hyphae and spores.

Fungal cultures.Wood light (UV light) examination:

mainly for tinea capitis.Histology is not needed, but biopsy

findings would show spongiosis, parakeratosis (that may alter with orthokeratosis), and a superficial inflammatory infiltrate.

TREATMENT

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A common practice that is highly discouraged is the prescribing of combined steroid/antifungal creams.

Tinea corporis infections may be treated with topical agents or with oral antifungals in extensive or recalcitrant disease.

For tinea capitis and nail infections, topical therapy is ineffective.

Use of oral medications requires baseline liver function testing and repeat laboratory testing half way through the typical 3-month course.

MEDICATIONS

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Ketoconazole topical (Nizoral)Clotrimazole

1% cream or lotion (Lotrimin, Mycelex)Miconazole topical (Monistat, Daktarin)Terbinafine (Lamisil)Naftifine 1% cream (Naftin)Griseofulvin (Gris-PEG, Grifulvin V,

Fulvicin, Griseofulvin)Itraconazole (Sporanox)Fluconazole (Diflucan)Sertaconazole nitrate cream (Ertaczo)

TINEA INCOGNITO

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This is the name given to Tinea when the clinical appearance has been altered by inappropriate treatment, usually a topical steroid cream.

The result is that the original infection slowly extends.

Often the patient and/or their doctor believe they have a dermatitis, hence the use of steroid cream.

The steroid dampens inflammation so the condition feels less irritable.

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Itch gets worse if the cream is stopped for a few days, hence promptly used again.

The more steroid applied, the more extensive the fungal infection becomes.

Compared with an untreated Tinea Coporis, tinea incognito:

Has a less raised marginIs less scalyMore pustularMore extensiveAnd more irritable.

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There may also be secondary changes caused by long-term use of topical steroid-

Atrophy, purpura, and telengectasia.

DIAGNOSIS

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Made by taking skin scrapings for microscopy and culture.

Few days after stopping the steroid cream, the rash becomes very inflamed and more fungal elements may be seen on microscopy.

TREATMENT

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The topical steroid should be discontinued.

Bland anti-pruritic lotions can be applied.Standard antifungal treatment should be

used.Treatment is usually with topical

antifungal agents, but if unsuccessful, oral antifungals may be considered (Terbinafine, Itraconazole)

REFERENCES

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1. Sobel JD. Vulvovaginal candidosis. Lancet. 2007 jun 9. 369(9577):1961-71

2. Pappas PG, rex Jh, Lee J. A prospective observational study of candidemia: epidemiology, therapy, and influence on mortality in hospitalized adult and paediatric patients.Clin infect Dis.2003 sep1. 37(5):634-43

3. Yang YL. Virulence factors of candida specie. J microbiol immunol infect. 2003Dec. 36(4):223-8

4. Alexander BD, Pfaller MA. Contemporary tools for the diagnosis and management of invasive mycoses. Clin infect Dis. 2006.43:s15-s27