FUNGAL INFECTIONS

Keratomycoses

Tinea versicolor is a common, benign, superficial cutaneous fungal infection usually

characterized by hypopigmented or hyperpigmented macules and patches on the chest and the
back. In patients with a predisposition, the condition may chronically recur. The fungal infection
is localized to the stratum corneum.

Tinea versicolor is caused by the dimorphic, lipophilic organism, Malassezia furfur,

Pityrosporon orbiculare, Pityrosporon ovale, and Malassezia ovalis are synonyms for M furfur.
M furfur is a member of normal human cutaneous flora, and it is found in 18% of infants and 90-
100% of adults.

Tinea versicolor occurs more frequently in areas with higher temperatures and higher relative
humidities. The national prevalence of this condition is 2-8% of the population.

Tinea versicolor occurs worldwide, with prevalence reported to be as high as 50% in the humid,
hot environment of Western Samoa and as low as 1.1% in the colder temperatures of Sweden.

Tinea versicolor is a benign skin disease that causes scaly macules or papules on the skin.
As the name implies (versi means several), the condition can lead to discoloration of the
skin, with colors ranging from white to red to brown. The condition is not considered to
be contagious because the causative fungal pathogen is a normal inhabitant of the skin.
The skin of an individual who is affected may be either hypopigmented or
hyperpigmented. In the case of hypopigmentation, tyrosinase inhibitors (resulting from
the inhibitory action of tyrosinase of dicarboxylic acids formed through the oxidation of
some unsaturated fatty acids of skin surface lipids) competitively inhibit a necessary
enzyme of melanocyte pigment formation. In hyperpigmented macules in tinea
versicolor, the organism induces an enlargement of melanosomes made by melanocytes at
the basal layer of the epidermis

Tinea versicolor can present in 3 forms.

Form 1
o The most common appearance of the disease is as numerous, well-marginated,
finely scaly, oval-to-round macules scattered over the trunk and/or the chest, with
occasional extension to the lower part of the abdomen, the neck, and the proximal
extremities.
o The macules tend to coalesce, forming irregularly shaped patches of pigmentary
alteration. As the name versicolor implies, the disease characteristically reveals a
variance in skin hue. The involved areas can be either darker or lighter than the
surrounding skin.
o The condition is more noticeable during the summer months when the
discrepancy in color from the normal skin becomes more apparent.
o Light scraping of the involved skin with a scalpel blade characteristically yields a
copious amount of keratin.
 Form 2
o An inverse form of tinea versicolor also exists in which the condition has an
entirely different distribution, affecting the flexural regions, the face, or isolated
areas of the extremities. This form of tinea versicolor is more often seen in hosts
who are immunocompromised.
o This form of the disease can be confused with candidiasis, seborrheic dermatitis,
psoriasis, erythrasma, and dermatophyte infections.
Form 3
o The third form of M furfur infections of the skin involves the hair follicle. This
condition is typically localized to the back, the chest, and the extremities.
o This form can be clinically difficult to differentiate from bacterial folliculitis. The
presentation of Pityrosporum folliculitis is a perifollicular, erythematous papule or
pustule.
o Predisposing factors include diabetes, high humidity, steroid or antibiotic therapy,
and immunosuppressant therapy. Additionally, several reports reveal that M furfur
also plays a role in seborrheic dermatitis.
Tinea versicolor can be successfully treated with various agents. Effective topical agents
include selenium sulfide, sodium sulfacetamide, ciclopiroxolamine, as well as azole and
allylamine antifungals. Various regimens can be used. Selenium sulfide lotion is liberally
applied to affected areas of the skin daily for 2 weeks; each application is allowed to
remain on the skin for at least 10 minutes prior to being washed off. In resistant cases,
overnight application can be helpful. Topical azole antifungals can be applied every night
for 2 weeks. Weekly application of any of the topical agents for the following few months
may help prevent recurrence. In patients with widespread disease, topical antifungal
therapy can be expensive. Topical allylamines have been demonstrated to be clinically
and mycologically effective.
Oral therapy is also effective for tinea versicolor and is often preferred by patients
because it is more convenient and less time consuming. Of course, oral therapy can be
used in consort with topical regimens. Ketoconazole, fluconazole, and itraconazole are
the preferred oral agents. Various dosing regimens have been used. With ketoconazole, a
10-day 200-mg daily therapy and as a single-dose 400-mg treatment are popular, both
with comparable results. Fluconazole has been offered as a single 150- to 300-mg weekly
dose for 2-4 weeks. Itraconazole is usually given at 200 mg/d for 7 days.

ERYTHRASMA is a chronic superficial infection of the intertriginous areas of the skin. The
incriminated organism is Corynebacterium minutissimum, which usually is present as a normal
human skin inhabitant. The incidence of erythrasma is reported to be around 4%. This infection
is observed all over the world; the widespread form is found more frequently in the subtropical
and tropical areas than in other parts of the world.

The typical appearance is well-demarcated, brown-red macular patches. The skin has a
wrinkled appearance with fine scales.
Infection commonly is located over inner thighs, crural region, scrotum, and toe webs.
Axillae, submammary area, periumbilical region, and intergluteal fold are less commonly
involved.
Toe web lesions appear as maceration.

Predisposing factors include the following:

o Excessive sweating/hyperhidrosis
o Delicate cutaneous barrier
o Obesity
 o Diabetes mellitus
o Warm climate
o Poor hygiene
o Advanced age

Antibacterial and/or antifungal agents are used to eradicate C minutissimum and possible
concomitant infection. Erythromycin is the DOC. Infection may be treated with topical and/or
oral agents. Therapy must be comprehensive and cover all likely pathogens in the context of this
clinical setting. C minutissimum is generally susceptible to penicillins, first-generation
cephalosporins, erythromycin, clindamycin, ciprofloxacin, tetracycline, and vancomycin.
However, multiresistant strains have been isolated.

Dermatomycosis
Tinea Corporis

Tinea corporis is a superficial dermatophyte infection characterized by either inflammatory or

noninflammatory lesions on the glabrous skin (ie, skin regions except the scalp, groin, palms,
and soles). Three anamorphic (asexual or imperfect) genera cause dermatophytoses:
Trichophyton, Microsporum, and Epidermophyton. Dermatophytes may infect humans
(anthropophilic), infect nonhuman mammals (zoophilic), or reside primarily in the soil
(geophilic).

Tinea corporis is a common infection more often seen in typically hot, humid climates. T rubrum
is the most common infectious agent in the world and is the source of 47% of tinea corporis
cases. Trichophyton tonsurans is the most common dermatophyte to cause tinea capitis, and
people with an anthropophilic tinea capitis infection are more likely to develop associated tinea
corporis. Therefore, the prevalence of tinea corporis caused by T tonsurans is increasing.
Microsporum canis is the third most common causative organism and associated with 14% of
tinea corporis infections.

Tinea corporis can manifest in a variety of ways.

o Typically, the lesion begins as an erythematous, scaly plaque that may rapidly
worsen and enlarge.
o Following central resolution, the lesion may become annular in shape.
o Scale, crust, vesicles, and papules often develop, especially in the advancing
border.
o Infections due to zoophilic or geophilic dermatophytes may produce a more
intense inflammatory response than those caused by anthropophilic microbes.
o Rarely, HIV-positive or immunocompromised patients can present with deep
abscesses or dissemination.
Majocchi granuloma manifests as perifollicular, granulomatous nodules typically in a
distinct location, which is the lower two thirds of the leg in females.
Tinea corporis gladiatorum often manifests on the head, neck, and arms, which is a
distribution consistent with the areas of skin-to-skin contact in wrestling.
Tinea imbricata is recognized clinically by its distinct scaly plaques arranged in
concentric rings.

Topical therapy is recommended for a localized infection because dermatophytes rarely

invade living tissues. Topical therapy should be applied to the lesion and at least 2 cm
beyond this area once or twice a day for at least 2 weeks, depending on which agent is used.
 Topical azoles and allylamines show high rates of clinical efficacy. These agents inhibit the
synthesis of ergosterol, a major fungal cell membrane sterol.

Systemic therapy may be indicated for tinea corporis that is extensive, involves
immunocompromised patients, or is refractory to topical therapy. Use of oral agents requires
attention to potential drug interactions and monitoring for adverse effects.

Tinea capitis

Tinea capitis is a disease caused by superficial fungal infection of the skin of the scalp,
eyebrows, and eyelashes, with a propensity for attacking hair shafts and follicles. The disease is
considered to be a form of superficial mycosis or dermatophytosis. Several synonyms are used,
including ringworm of the scalp and tinea tonsurans. In the United States and other regions of the
world, the incidence of tinea capitis is increasing.

Clinical presentation of tinea capitis varies from a scaly noninflamed dermatosis resembling
seborrheic dermatitis to an inflammatory disease with scaly erythematous lesions and hair loss or
alopecia that may progress to severely inflamed deep abscesses termed kerion, with the potential
for scarring and permanent alopecia. The type of disease elicited depends on interaction between
the host and the etiologic agents. Tinea capitis is predominantly a disease of preadolescent
children. It accounts for up to 92.5% of dermatophytoses in children younger than 10 years. The
disease is rare in adults, although occasionally, it may be found in elderly patients.

A variety of clinical presentations of tinea capitis are recognized as being inflammatory or

noninflammatory and are usually associated with patchy alopecia. However, the infection may be
widespread, and the clinical appearances can be subtle. In urban areas, tinea capitis should be
considered in the differential diagnosis of children older than 3 months with a scaly scalp until
proven negative by mycological examination. Infection may also be associated with painful
regional lymphadenopathy, especially in the inflammatory variants.

Pertinent physical findings are limited to the skin of scalp, eyebrows, and eyelashes.

Primary skin lesions

o Lesions begin as red papules with progression to grayish ring-formed patches
containing perifollicular papules.
o Pustules with inflamed crusts, exudate, matted infected hairs, and debris may be
seen.
o Black dot tinea capitis refers to an infection with fracture of the hair, leaving the
infected dark stubs visible in the follicular orifices.
o Kerion celsi may progress to a patchy or diffuse distribution and to severe hair
loss with scarring alopecia
Id reaction: Dermatophyte idiosyncratic or id reactions are manifestations of the immune
response to dermatophytosis.
o Id reactions occur at a distant site, and the lesions are devoid of organisms.
o Id reactions may be triggered by antifungal treatment.
o The most common type of id reaction is an acute vesicular dermatitis of the hands
and feet. The grouped vesicles are tense, pruritic, and sometimes painful. Id
reactions are noted in patients with inflammatory ringworm of the feet, primarily
resulting from infection by Trichophyton mentagrophytes. Similar lesions may
occur on the trunk in tinea capitis.
o Vesicular lesions may evolve into a scaly eczematoid reaction or a follicular
papulovesicular eruption.
 o Other less common types of id reactions include annular erythema and erythema
nodosum. These patients have a strong delayed-type hypersensitivity reaction to
intradermal trichophytin.
Distribution of lesions: Skin lesions appear on the scalp with extension to the eyebrows
and/or eyelashes.
Regional lymph nodes: Cervical lymphadenopathy may develop in patients with severe
inflammation associated with kerion formation.

Choice of treatment is determined by the species of fungus concerned, the degree of

inflammation, and in some cases, by the immunologic and nutritional status of the patient.

Systemic administration of griseofulvin provided the first effective oral therapy for tinea
capitis.
Topical treatment alone usually is ineffective and is not recommended for the
management of tinea capitis.
Newer antifungal medications, such as ketoconazole, itraconazole, terbinafine, and
fluconazole, have been reported as effective alternative therapeutic agents for tinea
capitis. Of these agents, itraconazole and terbinafine are used most commonly.
Selenium sulfide shampoo may reduce the risk of spreading the infection early in the
course of therapy by reducing the number of viable spores that are shed.

Tinea pedis

Tinea pedis is the term used for a dermatophyte infection of the soles of the feet and the
interdigital spaces. It is most commonly caused by Trichophyton rubrum, a dermatophyte
initially endemic only to a small region of Southeast Asia and in parts of Africa and Australia.
Interestingly, tinea pedis was not noted in these areas then, possibly because these populations
did not wear occlusive footwear. The colonization of the T rubrumendemic regions by
European nations helped to spread the fungus throughout Europe. Wars with accompanying mass
movements of troops and refugees, the general increase in available means of travel, and the rise
in the use of occlusive footwear have all combined to make T rubrum the world's most prevalent
dermatophyte. Patients with tinea pedis have the following 4 possible clinical presentations:

Interdigital
o The interdigital presentation is the most characteristic type of tinea pedis, with
erythema, maceration, fissuring, and scaling, most often seen between the fourth
and fifth toes. This type is often accompanied by pruritus.
o The dorsal surface of the foot is usually clear, but some extension onto the plantar
surface of the foot may occur.
o This type can be associated with the dermatophytosis complex, which is an
infection with fungi followed by an infection with bacteria.
Chronic hyperkeratotic
o The hyperkeratotic type of tinea pedis is characterized by chronic plantar
erythema with slight scaling to diffuse hyperkeratosis. This type can be
asymptomatic or pruritic.
o This type is also called moccasin tinea pedis, after its moccasinlike distribution.
Both feet are usually affected.
o Typically, the dorsal surface of the foot is clear, but, in severe cases, the condition
may extend onto the sides of the foot.
Inflammatory/vesicular
o Painful, pruritic vesicles or bullae, most often on the instep or anterior plantar
surface, characterize the inflammatory/vesicular type.
 o The lesions can contain either clear or purulent fluid; after they rupture, scaling
with erythema persists.
o Cellulitis, lymphangitis, and adenopathy can complicate this type of tinea pedis.
o The inflammatory/vesicular type can be associated with an eruption called the
dermatophytid reaction, which develops on the palmar surface of one or both
hands and/or the sides of the fingers. Papules, vesicles, and occasionally bullae or
pustules may occur, often in a symmetrical fashion, and it may mimic dyshidrosis
(pompholyx). This is an allergy or hypersensitivity response to the infection on
the foot, and it contains no fungal elements. The specific explanation of this
phenomenon is still unclear. Distinguishing between a dermatophytid reaction and
dyshidrosis can be difficult. Dermatophytid reactions are associated with vesicular
tinea pedis; therefore, a close inspection of the feet is necessary in patients with
vesicular hand dermatoses. The dermatophytid reaction resolves when the tinea
pedis infection is treated, and treatment of the hands with topical steroids can
hasten resolution.
Ulcerative
o The ulcerative variety is characterized by rapidly spreading vesiculopustular
lesions, ulcers, and erosions, typically in the web spaces, and is often
accompanied by a secondary bacterial infection.
o Cellulitis, lymphangitis, pyrexia, and malaise can accompany this infection.
o Occasionally, large areas, even the entire sole, can be sloughed.
o This type is commonly seen in immunocompromised and diabetic patients.

Patients may have other associated dermatophyte infections, such as onychomycosis, tinea
cruris, and tinea manuum. Tinea manuum is often unilateral and associated with moccasin-type
tinea pedis (two feetone hand syndrome).

Tinea pedis can be treated with topical or oral antifungals or a combination of both. Topical
agents are used for 1-6 weeks, depending on manufacturers' recommendations. A patient with
chronic hyperkeratotic (moccasin) tinea pedis should be instructed to apply medication to the
bottoms and sides of his or her feet. For interdigital tinea pedis, even though symptoms may not
be present, a patient should apply the topical agent to the interdigital areas and to the soles
because of the likelihood of plantar-surface infection.

Recurrence of the infection is often due to a patient's discontinuance of medication after

symptoms abate. A simple strategy to increase a patient's compliance is to prescribe a large
quantity of topical medicine, which may motivate a patient to continue use until the entire tube is
empty.

Moccasin-type tinea pedis is often recalcitrant to topical antifungals alone, owing to the
thickness of the scale on the plantar surface. The concomitant use of topical urea or other
keratolytics with topical antifungals should improve the response to topical agents. In addition,
for moccasin tinea pedis caused by Scytalidium species, Whitfield solution, containing benzoic
and salicylic acids, can be beneficial. However, patients with extensive chronic hyperkeratotic
tinea pedis or inflammatory/vesicular tinea pedis usually require oral therapy, as do patients with
concomitant onychomycosis, diabetes, peripheral vascular disease, or immunocompromising
conditions.

CUTANEOUS CANDIDIASIS

Yeasts are unicellular fungi that typically reproduce by budding, a process that entails a progeny
pinching off of the mother cell. Candidosis is an infection caused by the yeast Candida albicans
or other Candida species. C albicans, the principal infectious agent in human infection, is an
oval yeast 2-6 m in diameter. C albicans (as well as most medically significant fungi) has the
ability to exist in both hyphal and yeast forms (termed dimorphism). If pinched cells do not
separate, a chain of cells is produced and is termed pseudohyphae.

Superficial infections of skin and mucous membranes are the most common types of candidal
infections of the skin. Common types of candidal skin infection include intertrigo, diaper
dermatitis, erosio interdigitalis blastomycetica, perianal dermatitis, and candidal balanitis. In
certain subpopulations, candidal infection of the skin has increased in prevalence in recent years,
principally because of the increased numbers of patients who are immunocompromised.

Candidal vulvovaginitis: Clinical examination reveals erythema of the vaginal mucosa

and vulval skin with curdy white flecks within the discharge. Erythema may spread to
include the perineum and groin, with satellite pustules. Alternatively, the vaginal mucosa
may appear red and glazed. A patient presenting with symptoms of vulvovaginitis with
identification of yeasts in the vaginal discharge has a diagnosis of candidosis.
Congenital candidosis: In 2004, Diana et al13 reported that cutaneous congenital
candidiasis (CCC) is a rare disease of term or premature infants. It typically manifests as
an erythematous maculopapular eruption affecting the trunk and extremities; it resolves
after extensive desquamation. Pustules and vesicles usually are superficial and resolve
spontaneously or with topical treatment The presence of white microabscesses on the
placenta and umbilical cord of an infant with such an eruption must suggest the diagnosis
of CCC. It is always secondary to candidal chorioamnionitis, but it may pass
unrecognized.
OPC in the infant: Lesions become visible as pearly white patches on the mucosal
surfaces. Buccal epithelium, gums, and the palate commonly are involved with extension
to the tongue, pharynx, or esophagus in more severe cases. If the lesions are scraped
away, an erythematous base is exposed. Lesions may progress to symptomatic erosion
and ulceration.
Candidal diaper dermatitis: The eruption of CDD usually starts in the perianal area,
spreading to involve the perineum and, in severe cases, the upper thighs, lower abdomen,
and lower back. Maceration of the anal mucosa and the perianal skin often is the first
clinical manifestation. The typical eruption begins with scaly papules that merge to form
well-defined, weeping, eroded lesions with a scalloped border. A collar of overhanging
scales and an erythematous base may be demonstrated. Satellite flaccid vesicopustules
around the primary intertriginous plaque also are characteristic of CDD and represent the
primary lesions.
Oral candidiasis in elderly persons: The most common clinical appearance of OPC
(pseudomembranous candidosis or oral thrush) in the adult population occurs as white
plaques that are present on the buccal, palatal, or oropharyngeal mucosa overlying areas
of mucosal erythema. Typically, the lesions are removed easily and may demonstrate
areas with tiny ulcerations. In addition, some patients may develop soreness and cracks at
the lateral angles of the mouth (angular cheilitis). Denture stomatitis presents as chronic
mucosal erythema typically beneath the site of a denture.
Intertrigo: Intertrigo typically presents with erythema, cracking, and maceration with
soreness and pruritic symptoms. Lesions typically have an irregular margin with
surrounding satellite papules and pustules. Web spaces of affected fingers or toes are
macerated and have the appearance of soft white skin, which is a condition termed erosio
interdigitalis blastomycetica (interdigital candidosis).
Paronychia: The nailfold becomes erythematous, swollen, and tender, with an occasional
discharge. Loss of the cuticle occurs, along with nail dystrophy and onycholysis with
discoloration around the lateral nailfold. A greenish color with hyponychial fluid
 accumulation may occur that results entirely from Candida, and not Pseudomonas,
infection. A potassium hydroxide (KOH) preparation is helpful and is likely to show
yeast organisms.
Candidal vulvovaginitis: Topical antifungal agents including miconazole nitrate (Micatin,
Monistat-Derm) or clotrimazole (Lotrimin, Mycelex) creams 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.
Candidal 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.
Congenital candidosis: Topical preparations usually are effective. Some authors
recommend the use of oral nystatin in conjunction with topical agents to lower the risk of
systemic infection.
OPC in the infant: Most patients can be treated with nystatin oral suspension. Treat for
10-14 days or until 48-72 hours after resolution of symptoms. Dosage for preterm infants
is 0.5 mL (50,000 U) to each side of mouth 4 times/day; dosage for infants is 1 mL
(100,000 U) to each side of the mouth 4 times/d.
Candidosis of the nipple: Treat nipple candidosis for 2 weeks using an antifungal cream
after each feeding. The baby must be treated simultaneously with nystatin swabbed on all
4 gum lines and in the oral cavity, along with a few ingested drops, for 2 weeks. Babies
may have no symptoms of OPC and still be reinfecting their mothers. Careful hygiene is
also important. Frequent changing and washing of bras in boiling water (along with
anything the baby puts in its mouth, eg, pacifiers) is necessary. Gentian violet is not used
because it stains badly and may irritate the infant's mouth. If candidosis of the nipple
goes untreated, it may extend, and oral treatment for the mother may be necessary.
Cultures often are not pure and usually are not helpful.
Candidal diaper dermatitis: Treatment for CDD includes 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. For topical therapy of CDD, nystatin, amphotericin B,
miconazole, and clotrimazole are effective and almost equivalent in efficacy.
Oral candidiasis in adults
o Treatment with a topical agent such as nystatin (1:100,000 U/mL, 5 mL oral rinse
and swallow qid) or clotrimazole troches (10 mg 5 times/d) usually is effective. In
most patients, extend the duration of antifungal therapy at least twice as long as
the termination of clinical signs and symptoms of candidosis. Reserve oral
fluconazole, 100 mg once daily for 2 weeks, for patients with more severe
disease.
o With denture stomatitis, improved oral hygiene with removal of dentures at night,
vigorous brushing to remove plaque, and disinfecting (swish and spit) with
chlorhexidine gluconate (Peridex) usually is adequate treatment. Topical therapy
with clotrimazole troches or nystatin may be used for lesions that do not respond
to the above measures. For more resistant cases oral fluconazole, 100 mg/day for
several weeks, in addition to the above measures, may prove effective.
Intertrigo
o Treatment is targeted to keeping the skin dry, with the addition of topical nystatin
powder, clotrimazole, or miconazole twice daily. 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). Many anecdotally based remedies exist
for intertrigo that have been used in dermatology offices for years with success.
The remedies have focused on both drying the moist inflamed area and treating
 the candidosis. The treatments are adjusted based on whether the inflammation is
acute (wet and red), subacute (red +/- maceration), or chronic (red and dry).
o For acute intertrigo, use vinegar/water (1 tablespoon vinegar per quart of room
temperature water) applied twice per day for 5-10 minutes for 3-5 days as needed.
Dry the area with a hair dryer (no heat). Apply a shake lotion twice per day
(mixture: 40 g USP talc, 40 g zinc oxide, 10 g glycerin; mix into slurry or
milkshake consistency, add distilled water up to 120 mL, dispense in 180-mL [6
oz] bottle). Place a large bath towel under breasts or in pendulous areas twice per
day. Castellani paint (carbol fuchsin) is messy, but nightly painting may help
when nothing else does.
o For subacute intertrigo, benzoyl peroxide wash may be used to cleanse the area
instead of application of vinegar or Castellani paint. A topical anticandidal cream
of choice is applied twice per day, with or without a mild hydrocortisone cream
(no refills for the latter).
o For chronic intertrigo, the zinc-talc shake lotion may be used once or twice daily,
and the hydrocortisone cream/antifungal mixture may be applied at night. Local
hyperhidrosis may be treated with antiperspirants (ie, Arrid Extra Dry Unscented,
Dry Idea) on a long-term basis. These products, along with the more concentrated
Drysol (aluminum chloride 20%), may sting macerated skin. Nystatin in talc
(100,000 U/g or 15 g) may be applied twice per day for a few days, then tapered
and replaced with unscented baby powder as a powder-approach alternative.
o Sundaram et al14 noted that candidal intertrigo can be treated with filter paper
soaked in Castellani paint.
Paronychia: Treatment with topical agents usually is not effective but should be tried for
chronic candidal paronychia. Drying solutions or antifungal solutions are used. Oral
therapy with either itraconazole (pulse dosing with 200 mg bid for 1 wk of each of 3
consecutive mo) or terbinafine (250 mg qd for 3 mo) is recommended.
Candidosis and HIV: Topical therapy with agents such as nystatin and clotrimazole
require a minimum of 20-30 minutes of drug contact with the oral mucosa. Treatment
with topical therapies may be effective in the early stages of HIV infection, and it
becomes less effective with disease progression. Oral treatment with a 2-week course of
antifungal therapy (itraconazole, fluconazole, ketoconazole) is indicated in more
refractory cases. In patients who are significantly immunocompromised, maintenance
therapy on an intermittent (alternate days to twice weekly dosing of ketoconazole 200 mg
or fluconazole 100 mg) or continuous basis may be required to provide symptomatic
relief. In general, the goal is the cessation of therapy once clinical symptoms have
subsided, since prolonged therapy increases the likelihood of the development of drug-
resistant organisms.