Transcript FUNGAL SKIN INFECTIONS: Candidiasis, Onychomycosis, Tineas

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.
Candiasis
Onychomycosis
Tineas
Tinea 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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TYPES
Common 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 candidiasis
 This 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 candidiasis
 Commonly 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
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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.
Intertrigo
 Keep 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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ONYCHOMYCOSIS
 Fungal 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
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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
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White superficial
onychomycosis
Distal subungual
onychomycosis. Subungual
hyperkeratosis onycholysis
and yellow streak
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Candidal onychomycosis in a
patient with chronic
mucocutaneous candidiasis.
Total onychomycosis and
paronychia
CAUSES
 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.
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RISK FACTORS
 Family history
 Increasing age
 Poor health
 Prior trauma
 Warm climate
 Participation in fitness activities.
 Immunosuppression (eg, HIV, drug induced)
 Communal bathing
 Occlusive footwear
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DIAGNOSIS
 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 MICROSCOPY
A 20% potassium hydroxide (KOH) preparation
in dimethyl sulfoxide (DMSO) is a useful
screening test to rule out the presence of fungi.
CULTURE
To identify the specific pathogen involved in
onychomycosis fungal culture is used.
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TREATMENT
 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.
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TINEA
 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.
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CLASSIFICATION
 Tinea capitis - Scalp
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 Tinea corporis – Body
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 Kerion
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Tinea pedis
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FEATURES
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.
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EXAMINATION
 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
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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
 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 cellmediated immunity and resolves with treatment
of tinea.
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CAUSES
 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.
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LABORATORY INVESTIGATIONS
 Direct microscopic examination: . Skin scrapings,
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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
 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.
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MEDICATIONS
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)
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TINEA INCOGNITO
This is the name given to Tinea when the clinical
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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.
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 margin
Is less scaly
More pustular
More extensive
And more irritable.
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There may also be secondary changes caused by
long-term use of topical steroidAtrophy, purpura, and telengectasia.
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DIAGNOSIS
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.
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TREATMENT
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)
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REFERENCES
1. Sobel JD. Vulvovaginal candidosis. Lancet. 2007 jun 9.
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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