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