Julia Chen

-

http://www.telemedicine.org/common/common.htm

Superficial

Tinea Versicolor

Tinea versicolor is caused by
the Malassezia furfur. It seems to be increasingly common, especially in people
who habitually lie on sandy beaches in the Caribbean. It usually affects the
upper trunk and produces a variegated hyper-or hypopigmentation. Selenium
sulfide shampoo, using 2% selenium sulfide two or three time a week and leaving
it on overnight, is very helpful; and if the areas are localized, Whitfield's
ointment, 3% sulfur-sal and Whitfield's"ointment" in an alcoholic
solution are effective preparations. Twenty percent or a saturated solution of
sodium hyposulfite (or sodium thiosulfate) is a classical remedy, but has an
unpleasant odor. When people perspire in hot communities, it is unpleasant for
their friends.

 

Ketoconazole 200 mg per day for
two days in an adult is effective. Efficacy should be improved by ingestion
with a carbonated beverage, followed by engaging in a sweat producing activity
without an ensuing shower. This approach will leave a residue in the sweat.
Caution should be taken as ketoconazole has a potent inhibitory effect on
microsomal P-450 hydroxylation, thereby producing derangements in the
metabolism of lipophilic drugs and endogenous molecules. The short duration of
treatment makes the fatal hepatic necrosis occasionally seen with this drug of
little or no consequence.

 

The problem of cure is largely
due to the fact that the small fungus can get down into the hair follicles, and
when a clinical cure appears to have been achieved, the infection may still be
present in the depths of the hair follicles. Then, when the patient perspires
excessively, the organism comes back up onto the surface again and reinfects,
and the clinical infection is obvious. The patient therefore may need to
continue to treat himself intermittently for years with anti-dandruff shampoos
containing mild antimycotic agents such as selenium sulfide

-

Erythrasma

Erythrasma is caused by a
gram-positive bacteria, Corynebacterium minutissimum, occurring in humid
climates. It fluoresces with a coral red color and responds to systemic
antibiotics, especially erythromycin, tetracycline and chloromycetin;
and occasionally in widespread cases, this is the only way you can cure them. Penicillin
and griseofulvin do not help, and generally keratolytic ointments are
sufficient to clear them.

--------------

http://www.hkmj.org.hk/skin/skinfect.htm

3.9. Candidiasis

 

Candida infections caused by
yeast-like fungi Candida albicans commonly occur in moist, flexural sites. It
is more common at the extremes of age and during pregnancy. Predisposing
factors include diabetes mellitus, pregnancy, broad-spectrum antibiotics,
obesity, Cushing disease, uraemia, malignant disease and immunodeficiency. It
can present as 10 clinical patterns, depending on the site of involvement. They
are the oral thrush, angular cheilitis, genital candidiasis (vulvovaginitis),
candida balanitis, candida intertrigo, chronic paronychia, chronic onychia,
pruritus ani, erosio interdigitalis and candida granuloma. The diagnosis is
arrived clinically and confirmed by fungal culture.

 

Treatment

 

1) Topical treatment

    Nystatin, imidazole cream, amphotericin
lozenges (in oral candidiasis)

 

2) Systemic treatment

    Oral fluconazole, itraconazole,
ketoconazole

 

-

3. COMMON FUNGAL DISEASES OF
SKIN

 

3.1. Pityriasis Versicolor

 

It is caused by yeasts
(Pityrosporum orbiculare and P. ovale) providing widespread fine scaly macules
on the upper trunk and back. The colour of the lesions varies. The lesions are
pale in dark skin and darker in fair skin. Recurrent attacks are common. The
diagnosis is established clinically and can be supported by the faint yellow
fluorescence under Wood's  light in the
affected areas.

 

Treatment

 

1) Topical treatment

 

a) Imidazoles cream e.g.
clotrimazole, miconazole, isoconazole

 

b) Ketoconazole shampoo

 

c) 2.5% selenium sulphide
shampoo

 

d) 3% salicylic (a.得自水楊酸的;水楊酸的) acid in spirit

 

e) 20% sodium thiosulphate in
spirit

 

2) Systemic treatment

 

a) Oral ketoconazole 200 mg
daily for 5 days

 

b) Oral itraconazole 100 mg
daily for 5 days

 

-

 

http://www.hkmj.org.hk/skin/skinfect.htm

 

1.7.
Erythrasma

 

Erythrasma
is a superficial bacterial skin infection due to Corynebacterium minutissimum.
The lesions are reddish-brown, scaly and finely wrinkled macular (a.有斑點的;有污點的)
patches, usually involve the intertriginuous areas. Axillary (a.腋窩的;葉腋的;腋生的 n.腋窩的羽翼)
and genitocrural areas are commonly involved. The diagnosis is supported by the
characteristic "coral-red" fluorescence under wood's  light.

 

Treatment

 

1) Oral
erythromycin 250 mg QID for 1 week. The lesions usually clear within
several weeks.

 

2)
Topical therapy includes aqueous clindamycin solution, whitfield's ointment or miconazole
cream

 

-------------------------------------------------------

 

  

Superficial
fungal infection of the skin

Where
and how it appears help determine therapy

Thomas
J. Zuber, MD; Kavitha Baddam, MD

 

VOL 109
/ NO 1 / JANUARY 2001 / POSTGRADUATE MEDICINE

 

CME
learning objectives

 

To
become familiar with the various presentations of superficial cutaneous fungal
infections

To
recognize the many nonfungal infections that make up differential diagnosis

To
understand the most effective treatment approaches to superficial fungal
infections

The
authors disclose no financial interests in this article.

 

 

This
page is best viewed with a browser that supports tables.

 

Preview:
What people gain in warmth and protection from use of occlusive clothing and
shoes they may pay for in the form of cutaneous fungal infections. Warm, moist
conditions can promote growth of numerous organisms or allow fungal infection
to develop over another disorder of the skin or nails. In this article, the
authors describe the usual appearance of tinea pedis, tinea corporis, tinea
cruris, tinea versicolor, tinea capitis, tinea faciei, tinea manuum, cutaneous
candidiasis, and onychomycosis. They also summarize differential diagnosis of
similar-appearing lesions and discuss management options for each of the fungal
infections.

Zuber
TJ, Baddam K. Superficial fungal infection of the skin: where and how it
appears help determine therapy. Postgrad Med 2001;109(1):117-132

 

 

 

--------------------------------------------------------------------------------

 

Superficial
fungal infections of the skin are some of the most common dermatologic
conditions seen in clinical practice, so recognition is important for primary
care physicians. How- ever, making the correct diagnosis can be difficult,
because these infections can have an atypical presentation or be confused with
similar-appearing conditions.

 

Superficial
fungal infections can be divided into three broad categories: dermatophytic
infections, tinea versicolor, and cutaneous candidiasis (1). Up to 20% of the
US population is believed to be infected with dermatophytes alone (2). Dividing
infections into the body region most often affected can help in identification
of the problem.

 

Tinea
pedis

Tinea
pedis is the most common dermatophytosis and may affect up to 70% of adults
worldwide (2). Also referred to as athlete's foot or ringworm of the foot, it
involves the plantar surface and interdigital spaces of the foot and can
include inflammatory and noninflammatory lesions. Tinea pedis appears to be a
disease of civilized humans, having evolved in the late 19th and early 20th
centuries (3). It occurs throughout the United States but is most prevalent in
warm, humid climates.

 

Trichophyton
rubrum accounts for most dermatophytic foot infections. Epidermophyton floccosum
and Trichophyton mentagrophytes have also been reported to be causative agents
(4). In addition, fungi (eg, Scytalidium hyalinum), yeasts (eg, Candida
albicans), and bacteria (eg, Corynebacterium minutissimum) may be isolated in
tinea pedis infections (4). The three most common clinical forms of tinea pedis
are interdigital (figure 1: not shown), moccasin type (figure 2: not shown),
and vesiculobullous (figure 3: not shown) (3,4).

 

Interdigital
infection often presents as white, macerated skin between the fourth and fifth
toes (3), but it may appear in any web space. This type of tinea pedis often
develops in persons with hyperhidrosis, and it typically produces itching and a
foul smell from bacterial superinfection with diphtheroids or Pseudomonas species
(3).

 

Moccasin-type,
or hyperkeratotic, tinea pedis usually presents as silvery white scales on a
red, thickened base (3). Distribution is over the sole, heel, and sides of the
foot, or what would be covered by a moccasin. Occasionally, a single hand may
also be involved: the so-called two-foot, one-hand presentation (3).
Onychomycosis often is present and may be asymptomatic. Typically,
moccasin-type tinea pedis is a chronic condition (3).

 

Vesiculobullous
tinea pedis usually presents as vesicles or pustules on the sole (3). With each
flare of infection, the sole becomes thicker, and maceration, itching, or
secondary infection can develop. Cellulitis or lymphangitis is a potential
complication of vesiculobullous tinea pedis (3).

 

Dry-type
interdigital infection can mimic psoriasis (4). Moccasin-type tinea pedis may
appear similar to long-standing contact dermatitis of the foot. Vesiculobullous
infection can mimic pompholyx (dyshidrotic eczema), pustular psoriasis, contact
dermatitis, or nummular eczema (4). Differential diagnosis of tinea pedis is
summarized in table 1.

 

Table
1. Differential diagnosis of tinea pedis 

Acrodermatitis
continua

Candidiasis

Contact
dermatitis

Eczema

   Dyshidrotic

   Nummular

Erythrasma

Psoriasis

   Pustular

   White

Pustular
bacterids

Pyoderma

Secondary
syphilis

 

 

--------------------------------------------------------------------------------

 

 

 

Most
cases of tinea pedis respond to topical agents, such as econazole nitrate
(Spectazole), ketoconazole (Nizoral), and terbinafine hydrochloride (Lamisil).
Recurrence is common, especially if untreated onychomycosis serves as a
reservoir for reinfection.

 

Tinea
corporis

Tinea
corporis is dermatophytosis of the glabrous skin of the trunk and extremities
(2). Commonly referred to as ringworm of the body, this infection consists of a
round, scaly patch that has a prominent, enlarging border and a relatively
clear central portion (figure 4: not shown) (5). The prominent edge often
contains pustules or follicular papules, and multiple lesions can be present.
Itching is variable and not diagnostic. T rubrum is the most common cause of
tinea corporis.

 

A deep
form of tinea corporis known as Majocchi's (or trichophytic) granuloma can
develop when the fungus is driven down into the hair follicles (5). It
typically develops after inappropriate topical corticosteroid therapy (5).

 

When
the diagnosis of tinea corporis is being considered, the annular scaling margin
with follicular prominence that suggests a dermatophyte infection should be
sought. Conditions that may appear similar to the infection include nummular
eczema, plaque psoriasis, contact dermatitis, granuloma annulare, and erythema
nodosum.

 

Tinea
corporis usually responds to topical therapy.

 

Tinea
cruris

Tinea
cruris is dermatophytosis of the proximal medial thigh and buttock (2). It
often is characterized by invasion of the hair follicles and can be confused
with candidal infection at the same site (2). Also known as jock itch, the
infection is most commonly caused by T rubrum or E floccosum. It is more common
in summer months and in persons who wear tight-fitting clothing.

 

Tinea
cruris is found primarily in young men (5). The lesion on the leading edge of
the thigh is prominent, with follicular papules and pustules (5,6). A ringed
lesion typically extends from the crural fold over the adjacent upper inner
thigh. Lesions can be superinfected with bacteria or Candida.

 

Differential
diagnosis includes mechanical intertrigo (chafing), which often has sharp
demarcation from the normal skin and no scaling in the center of the lesion
(6). Candidiasis can be differentiated from tinea cruris by its irregular
border with satellite lesions and scrotal involvement (which often appears
bright red and shiny).

 

Tinea
cruris often responds to topical therapy.

 

Tinea
versicolor

Tinea
versicolor (figure 5: not shown) is common, primarily in young and middle-aged
adults. The condition is caused by the lipophilic yeasts Pityrosporum
orbiculare and Pityrosporum ovale (7,8). In the mycelial phase, P orbiculare is
known as Malassezia furfur, (8) which many experts consider to be the preferred
nomenclature (9). Tinea versicolor is also referred to as pityriasis versicolor
(9,10). Predisposing factors are listed in table 2.

 

Table
2. Factors predisposing to development of tinea versicolor 

Exogenous

Application
of oils

High
ambient temperature

High
relative humidity

Occlusion
(eg, by clothing)

 

Endogenous

Greasy
skin

Hereditary
predisposition

Hyperhidrosis

Immunodeficiency

Malnutrition

Systemic
steroid treatment

 

 

--------------------------------------------------------------------------------

 

 

 

Tinea
versicolor is typically found in regions of the body that have sebaceous
glands, such as the upper trunk, neck, and arms (8,9). The characteristic
finding is skin depigmentation, but lesions can range from red to hypopigmented
to hyperpigmented (9). Hyperpigmentation is often found in dark-skinned
patients (9). The depigmentation of tinea versicolor is believed to be due to
the inhibitory effect of the organism on pigmentation and tanning (7).

 

Usually,
tinea versicolor does not clear spontaneously and may persist for many years
(7). "Spotty body" often presents in adolescence (7) and is
associated with itching in up to one third of patients. Unfortunately, tinea
versicolor has a high rate of recurrence (80% after 2 years), and periodic
retreatment may be needed (10).

 

Differential
diagnosis includes vitiligo (figure 6: not shown), tinea corporis, pityriasis
rosea, pityriasis alba, and secondary syphilis (9). A condition that is
uncommon but often confused with tinea versicolor is confluent and reticulate
papillomatosis (8), which is characterized by grayish-brown pigmented papules,
most often found in the interscapular and inframammary areas in postpubertal
adolescents.

 

Tinea
versicolor responds to topical therapies, such as terbinafine, econazole,
ketoconazole, and selenium sulfide lotion or shampoo (Exsel, Head &
Shoulders, Selsun). Recurrences may be less frequent if a short course of oral
therapy with itraconazole (Sporanox) or ketoconazole is instituted.

 

Tinea
capitis

Tinea
capitis (figure 7: not shown) is a dermatophytic infection of the head and
scalp, usually found in infants, children, and young adolescents (11-14). Most
infections occur in preschool-aged children in African-American or Hispanic
minority populations (11,12). Infection can be spread from child to child or
from animals to humans (13).

 

Before
1960, most tinea capitis infections in the United States were caused by
Microsporum audouinii (13). Today, the great majority of infections are caused
by Trichophyton tonsurans (13). Up to 30% of children may be asymptomatic
carriers of T tonsurans (12,13).

 

Tinea
capitis can have a wide range of clinical presentations (11-14). Initially, the
condition may be asymptomatic and have a subtle appearance. As the inflammatory
response to infection increases, inflammatory alopecia may develop. Breakage of
hairs at the roots may result in "black-dot" alopecia (figure 8: not
shown) (13). Scaling that resembles seborrheic dermatitis may occur on the
scalp (11). With an increase in cell-mediated immune response, nodular, boggy
swellings known as kerions may develop (figure 9: not shown) (14). An unusual
scaling reaction known as favus may give the scalp a waxy or doughy appearance
(14).

 

Tinea
capitis should be considered in any prepubertal child over the age of 6 months
who has scalp scaling (14). Cervical lymphadenopathy is common in symptomatic
children, and examination for nodes should be performed whenever the diagnosis
is considered (13). Because T tonsurans does not produce fluorescence on Wood's
lamp examination, this test is not positive in most tinea capitis infections,
so laboratory evaluation for fungi should be performed (13). Laboratory testing
usually can differentiate tinea capitis from other conditions.

 

Differential
diagnosis of tinea capitis includes seborrheic dermatitis, dandruff, scalp
psoriasis (figure 10: not shown), atopic dermatitis, bacterial furunculosis,
trichotillomania, and alopecia areata (13). The finding of large areas of
alopecia that have early pustule formation favors a diagnosis of tinea capitis
over alopecia areata (14).

 

Successful
treatment of the condition in children almost always requires use of an oral
agent, such as griseofulvin. Other oral antifungal agents have been used
successfully but as yet do not have approval by the US Food and Drug
Administration. Ketoconazole cream and shampoo can be added as adjunctive
therapy to reduce fungal shedding.

 

Tinea
faciei

Tinea
faciei (figure 11: not shown), also known as tinea incognito because of its
subtle appearance, is dermatophytosis of the nonbearded areas of the face (2).
The condition may present as itchy, red skin without a discernible border, or
it may have a raised border as seen with tinea corporis (15). Common causative
organisms are T rubrum and T mentagrophytes (15).

 

Tinea
faciei should be considered in all erythematous eruptions of the face (16).
Differential diagnosis of tinea faciei includes discoid lupus erythematosus,
lymphocytic infiltration, seborrheic dermatitis, rosacea, and contact
dermatitis (16).

 

The
infection often responds to topical therapy.

 

Tinea
manuum

Tinea
manuum is an unusual dermatophytic infection of the interdigital and palmar
surfaces (2), usually of one hand but sometimes of both (17). It may coexist
with other fungal infections, such as tinea pedis (17). The palmar surface
often has diffuse areas of dry, hyperkeratotic skin (figure 12: not shown)
(17). Involvement on the dorsum of the hand can appear similar to tinea
corporis.

 

Differential
diagnosis should include pompholyx, eczema, secondary syphilis, and callus
formation. Infection with nondermatophytic fungi, such as S hyalinum or
Scytalidium dimidiatum, can also resemble tinea manuum (2).

 

The
condition often responds to topical therapy, although it may recur if untreated
onychomycosis is present.

 

Cutaneous
candidiasis

Cutaneous
candidiasis is skin infection caused by C albicans and other species (18).
Other conditions encompassed in this general term include angular cheilitis
(perlèche), erosio interdigitalis blastomycetica, and
candidal intertrigo, balanitis, vaginitis, and paronychia (1). Involvement of
the skinfolds and mucous membranes is most common (18), but any area of the
skin with increased moisture is susceptible.

 

C albicans is a ubiquitous organism, and about 18% of healthy people
carry the yeast in their oral flora (18). Host factors (eg, wearing of
occlusive clothing, obesity) or disorders affecting the immune system (eg,
diabetes, AIDS, Cushing's syndrome, Addison's disease) may increase
susceptibility to candidal infection (18).

 

Candidal skin infection often presents with erythema, cracking, or
maceration (18). When maceration develops in the web spaces of the fingers, the
skin can become soft and white. Important clues to the presence of candidal
skin infection are irregular (serrated) edges, tissue erythema, and the
presence of satellite lesions. Differential diagnosis includes dermatophytosis,
seborrheic dermatitis, bacterial intertrigo, and flexural psoriasis (18).
Superinfection with Candida can accompany any of these conditions.

 

In patients with normal immunity, candidiasis is most often treated with
topical therapy. Commonly used topical agents include nystatin (Mycostatin,
Nilstat, Nystex), ketoconazole, miconazole nitrate, and clotrimazole. When
clinically indicated, systemic therapy with oral fluconazole (Diflucan) is
highly effective.

 

Onychomycosis

Onychomycosis is fungal infection of the nail unit, including the nail
plate and nail bed. There are four types of onychomycosis: proximal subungual,
distal subungual (figure 13: not shown), superficial white (figure 14: not
shown), and candidal (19). Dermatophytes usually cause the first three types,
although Candida can be present in all types (1,18,19). Patients with
onychomycosis often have concomitant fungal infections at other sites (1).

 

The incidence of onychomycosis has been increasing worldwide, and at
present it accounts for almost half of all nail disorders (19). The increase is
believed to be due to many factors, including the aging population, the growing
number of immunocompromised patients, and the widespread use of occlusive
clothing and shoes (19).

 

Fungal nail infections can cause a wide variety of clinical
presentations. The nail may become hyperkeratotic and markedly dystrophic (in
proximal subungual onychomycosis) or exhibit white crumbling of the surface (in
superficial white onychomycosis). Differential diagnosis includes almost all
conditions that affect the nails, including psoriasis (figure 15: not shown),
lichen planus, alopecia areata, subungual tumors and warts, and bacterial
infection. A sample of infected cellular debris should be collected from
beneath the nail and sent for confirmatory laboratory examination (19).

 

Topical therapies penetrate poorly to the nail bed and in general are
believed to be successful in less than 20% of patients. Oral agents that are
commonly used to treat onychomycosis are terbinafine, itraconazole, and
fluconazole.

 

Treatment approaches

As noted, treatment of cutaneous fungal infections may consist of
topical or systemic agents, used singly or in combination. Usually, treatment
is not started until the diagnosis has been confirmed.

 

Topical agents

Topical treatment alone may be sufficient for noninflammatory tinea
corporis, tinea cruris, tinea faciei, tinea manuum, and tinea pedis. Topical
agents can be divided into three major categories: imidazoles, allylamines, and
polyenes.

 

Imidazoles: Imidazole derivatives act by binding to the cytochrome P-450
system and blocking synthesis of ergosterol, a vital component of cell
membranes (17). At higher concentrations, imidazoles can have bactericidal as
well as fungicidal action. The following are four of the most commonly used
topical imidazoles:

 

Econazole 1% is indicated for treatment of tinea pedis, tinea cruris,
and tinea corporis caused by T rubrum, T mentagrophytes, T tonsurans,
Microsporum canis, Microsporum gypseum, M audouinii, and E floccosum as well as
for treatment of cutaneous candidiasis and tinea versicolor (4,20). In addition
to its antimycotic properties, econazole has been found to have useful effects
in treatment of severe interdigital bacterial infections complicated by
dermatophyte colonization (4).

Miconazole 2% is indicated for treatment of tinea pedis, tinea cruris,
and tinea corporis caused by T rubrum, T mentagrophytes, and E floccosum and
also cutaneous candidiasis and tinea versicolor (20). Like econazole,
miconazole is also effective against certain gram-positive cocci and bacilli.
It is available in cream, ointment, powder, and spray formulations (4).

Ketoconazole 2% is indicated for treatment of tinea corporis, tinea
cruris, and tinea pedis caused by T rubrum, T mentagrophytes, and E floccosum.
It also is effective for tinea versicolor, cutaneous candidiasis, and
seborrheic dermatitis (20).

Clotrimazole is used mainly to treat vaginal candidiasis (20).
Historically, it has been used against cutaneous mycoses (20), but now it is
often replaced by other agents with broader coverage.

Allylamines: The mechanism of action of the allylamines is inhibition of
squalene epoxidase synthesis (20). These agents are effective in treatment of
dermatophytes and Candida, (4) but they have no known antibacterial properties.
The following are three of the most commonly used topical allylamines:

 

Terbinafine 1% is approved for treatment of tinea pedis, tinea cruris,
and tinea corporis caused by T rubrum, T mentagrophytes, and E floccosum (4).
Terbinafine seems to be more potent than naftifine hydrochloride (Naftin) in
eliminating dermatophytosis (20).

Butenafine hydrochloride (Mentax) has demonstrated fungicidal activity
against T rubrum, T mentagrophytes, M canis, and Candida parapsilosis (5,21).

Naftifine 1% has fungicidal activity against T rubrum, T tonsurans, T
mentagrophytes, E floccosum, M canis, M audouinii, and M gypseum. It is also
effective against Candida species (4).

 

Polyenes: These agents act by binding to the fungal cell membrane
sterols, causing changes in permeability, leakage of contents and, finally,
death of the cell. Polyenes are useful in topical treatment of candidiasis
(18), but they have no efficacy against dermatophytes (20).

 

Amphotericin B (Fungizone) is an older polyene that is currently used
infrequently in superficial fungal infections (18).

Nystatin powder (eg, Pedi-Dri) provides drying as well as antifungal
action against candidiasis in intertriginous areas (eg, perineum, under
breasts) (18). The efficacy of nystatin is similar to that of clotrimazole.

Additional topical agents: The following antifungal medications have
various classifications and actions and may be of value in certain clinical
situations.

 

Ciclopirox olamine (Loprox) interferes with synthesis of cell membrane
proteins, thus disrupting formation of fungal cell membranes (4,17). It is
effective against cutaneous candidiasis, tinea versicolor, tinea pedis, and
tinea cruris (20).

Tolnaftate is a thiocarbamide, used principally in tinea pedis (17),
although it appears to be less effective than miconazole for this condition. It
is active against T rubrum, T mentagrophytes, T tonsurans, E floccosum, and
Pityrosporum species (17) but has no activity against Candida.

Haloprogin (Halotex) is a halogenated phenol and is used for tinea
pedis, tinea corporis, tinea cruris, tinea manuum, and tinea versicolor
(17,20). Results of comparative clinical studies suggest that it is superior to
tolnaftate in efficacy.

Undecylenic acid is used primarily for dermatophyte infections, most
commonly tinea pedis (17).

 

Corticosteroid and antifungal combinations: In certain clinical
situations, topical corticosteroids have been used in combination with topical
antifungal agents to add an anti-inflammatory effect (2,20). Although
corticosteroids can produce initial symptomatic relief, they also reduce the
body's natural immunologic response and defenses. Corticosteroid therapy
requires restrictions on duration of use, location of application, and age of
patient (with children usually eliminated from consideration) (2). Because of
potential side effects of corticosteroid therapy (figure 16: not shown), use of
combination therapy is typically discouraged.

 

Systemic agents

In general, systemic therapy is indicated for treatment of tinea
capitis, onychomycoses, and recalcitrant cutaneous mycoses (20,21). Systemic
therapy often is needed in treatment of moccasin-type tinea pedis (4).

 

Griseofulvin: This agent acts at the cellular level by inhibiting fungal
cell-wall synthesis, cellular microtubules, DNA synthesis, and RNA binding (5).
Its bioavailability is increased in microcrystalline formulations (1). It is
active against Trichophyton, Epidermophyton, and Microsporum species but
ineffective against yeasts and nondermatophytes (4). Griseofulvin is considered
first-line therapy for tinea capitis (13). A dosage of 15 to 25 mg/kg daily of
the liquid microsized formula (Grifulvin V) is recommended (13).

 

Some of the commonly seen side effects associated with griseofulvin
therapy are rash, hives, headache, nausea, vomiting, arthralgia, peripheral
neuritis, confusion, insomnia, and memory lapse (4,5,17).

 

Ketoconazole: This agent acts by binding to the heme moiety of the
cytochrome P-450 system and interferes with certain mixed oxidase functions
(8). It is effective against dermatophytes, yeasts, and some systemic mycoses
(4,5). A dosage of 200 mg once daily for 2 to 4 weeks is often effective for
tinea cruris, tinea capitis, and tinea pedis. In addition, oral ketoconazole
therapy for 1 week may eradicate tinea versicolor (8).

 

Use of oral ketoconazole is limited by the potential for hepatotoxicity
(5,17). Other potential side effects include nausea, vomiting, abdominal pain,
diarrhea, headache, pruritus, insomnia, leukopenia, hemolytic anemia, decreased
libido, and impotence (4,5,17).

 

Itraconazole: Of all the oral antifungal agents, itraconazole has the
broadest spectrum of activity. It is effective against dermatophytes, Candida
species, some molds, and P ovale (5,8,18). It is effective in treatment of
tinea corporis, tinea cruris, tinea pedis, tinea manuum, and onychomycoses
(5,21). Because of the lipophilic tendencies of itraconazole, concentration of
the drug in keratinous tissues remains high for months after cessation of
therapy (5).

 

Possible side effects of itraconazole therapy include diarrhea,
headache, rhinitis, dyspepsia, nausea, dry skin, rash, weakness, pruritus,
dizziness, hypertension, and loss of libido (4,5). Itraconazole also has
numerous interactions with medications metabolized by the cytochrome P-450 system,
such as terbinafine, astemizole (Hismanal), triazolam (Halcion), and midazolam
hydrochloride (Versed) (5).

 

Terbinafine: This agent acts by inhibiting squalene epoxidase, an
essential step in fungal ergosterol synthesis. Oral terbinafine has shown efficacy
in treatment of tinea pedis, tinea cruris, tinea corporis, and onychomycoses
(4,5,11,13,21). A dosage of 250 mg daily for 6 weeks for fingernail
onychomycosis and 12 weeks for toenail onychomycosis is highly effective (5).
Terbinafine is not effective for cutaneous candidiasis or tinea versicolor (8).

 

The most common side effects of terbinafine therapy include diarrhea,
pruritus, dyspepsia, rash, taste disturbance, abdominal pain, and toxic effects
on the liver (5,21).

 

Fluconazole: This agent is effective treatment for oral and esophageal
candidiasis (4), and it is also beneficial in selected superficial cutaneous
fungal infections (5) at a dosage of 50 to 200 mg daily for 1 to 4 weeks
(18,21). It also has been used for treatment of onychomycoses caused by
dermatophytes but has not been approved for this indication.

 

Fluconazole has been noted to have significant drug interactions with
terbinafine, astemizole, oral hypoglycemic agents, coumarin derivatives,
phenytoin sodium (Dilantin), cyclosporine (Neoral, Sandimmune, SangCya),
theophylline, and cisapride (Propulsid) (21). Side effects to its use are more
common among HIV-positive patients and include nausea, headache, rash,
vomiting, diarrhea, and toxic effects on the liver (21).

 

Summary

Superficial fungal infections of the skin are a common presentation in
clinical practice. Any skin surface, the mucous membranes, nail plates, and
nail beds can be affected. Tinea pedis is the most common fungal infection and
may affect up to 70% of the adult population worldwide. Ubiquitous candidal
organisms are found in the oral flora of many healthy persons and result in
infection in the presence of certain host factors or immunodeficiency
disorders. Onychomycosis has had an increasing incidence worldwide, and it now
accounts for almost half of all nail disorders. These and many other infections
can have varying presentations as well as features that resemble nonfungal
disorders. Therefore, it is important that primary care physicians are familiar
with the many cutaneous fungal infections and their differential diagnosis to
ensure that appropriate therapy is selected.

 

References

Swiggum SM, Adam JE. Cutaneous fungal diseases in the elderly. Geriatr
Consultant 1993;10:22-9

Drake LA, Dinehart SM, Farmer ER, et al. Guidelines of care for
superficial mycotic infections of the skin: tinea corporis, tinea cruris, tinea
faciei, tinea manuum, and tinea pedis. J Am Acad Dermatol 1996;34(2 pt 1):282-6

Masri-Fridling GD. Dermatophytosis of the feet. Dermatol Clin 1996;14(1):33-40

Brooks KE, Bender JF. Tinea pedis: diagnosis and treatment. Clin Podiatr
Med Surg 1996;13(1):31-46

Rosen T. Dermatophytosis: diagnostic pointers and therapeutic pitfalls.
Consultant 1997 June:1545-7

Webster SB. How I manage jock itch. Phys Sportsmed 1984;12(5):109-13

Savin R. Diagnosis and treatment of tinea versicolor. J Fam Pract
1996;43(2):127-32

Silva-Lizama E. Tinea versicolor. Int J Dermatol 1995;34(9):611-7

Assaf RR, Weil ML. The superficial mycoses. Dermatol Clin
1996;14(1):57-67

Faergemann J. Pityrosporum infections. J Am Acad Dermatol 1994;31(3 Pt
2):S18-20

Schwartz RA, Janniger CK. Tinea capitis. Cutis 1995;55(1):29-33

Howard R, Frieden IJ. Tinea capitis: new perspectives on an old disease.
Semin Dermatol 1995;14(1):2-8

Elewski B. Tinea capitis. Dermatol Clin 1996;14(1):23-31

Elewski BE, Hay RJ. International summit on cutaneous antifungal
therapy, focus on tinea capitis, Boston, Massachusetts, November 11-13, 1994.
Pediatr Dermatol 1996;13(1):69-77

Emanuel D, McNeely MC. Tinea faciei. Hosp Med 1996 Aug:12

Cirillo-Hyland V, Humphreys T, Elenitsas R. Tinea faciei. J Am Acad
Dermatol 1993;29(1):119-20

Bergus GR, Johnson JS. Superficial tinea infections. Am Fam Physician
1993;48(2):259-68

Hay RJ. Yeast infections. Dermatol Clin 1996;14(1):113-24

Andre J, Berger T, De Doncker P, et al. The second international
symposium on onychomycosis: an update on the issues. Med Monitor 1996;2(1):1-8

Smith EB. Topical antifungal drugs in the treatment of tinea pedis,
tinea cruris, and tinea corporis. J Am Acad Dermatol 1993;28(5 Pt 1):S24-8

Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea
infections. Am Fam Physician 1998;58(1):163-78

Dr Zuber is program director, department of family practice, Saginaw
Cooperative Hospitals, and director of the dermatology clinic, Aleda E. Lutz
Veterans Affairs Medical Center, Saginaw, Michigan, and associate professor,
Michigan State University, East Lansing. Dr Baddam is a member of the
department of family practice, Saginaw Cooperative Hospitals, and clinical
instructor, Michigan State University. Correspondence: Thomas J. Zuber, MD,
Department of Family Practice, Saginaw Cooperative Hospitals, 1000 Houghton
Ave, Saginaw, MI 48602. E-mail: zuber@pilot.msu.edu.

 

 

 

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http://zgrdxw.peopledaily.com.cn/big5/paper68/3/class006800008/hwz93737.htm

紅癬

 

臨床表現

 

本病致病菌為微細棒狀杆菌（Corynebacterium
minutissimum),臨床特點為境界清楚、紅褐色的斑疹，其上有細碎脫屑。好發於成人的股內側、腋窩及女性乳房下等易摩擦部位，一般無自覺癥狀。皮損累及肛門者，可引起瘙癢，此外，還有一種泛發性紅癬，廣泛分布於軀干及四肢。

 

診斷及鋻別診斷

 

根據皮損特點，好發部位及皮損外處皮膚在Woood燈光下顯珊瑚紅色熒光可診斷，但需要與花斑癬、股癬、擦爛紅斑、脂溢性皮炎等相鋻別。

 

治療

 

紅霉素250mg口服，第日4次，共用10-21天；或四環素，每日1-2g，服2周；氯霉素也療效。

 

局部可使用發癬退液、癬藥膏、硫磺水楊酸軟膏等。本病治愈後容易復發，治療務求徹底。經常使用抗菌肥皂有預防作用。