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Reviewed
August 4, 2004
Department
of
Dermatology
Kenneth
J.
Tomecki, MD
Department
of
Dermatology
Copyright
2003
The Cleveland Clinic Foundation
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BACTERIAL
INFECTIONS
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BACTERIAL
INFECTIONS
Impetigo
FUNGAL
AND
YEAST INFECTIONS
Dermatophyte
(fungal
infections)
Candidiasis
Tinea
(Pityriasis) Versicolor
VIRAL
INFECTIONS
Herpes
Simplex
Herpes
Zoster
Warts
Molluscum Contagiosum
References
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Humans
are natural hosts for many bacterial species that colonize the skin as
normal flora. Staphylococcus aureus and Streptococcus pyogenes
are infrequent resident flora, but they account for a wide variety
of bacterial pyodermas. Predisposing factors to infection include minor
trauma, preexisting skin disease, poor hygiene, and, rarely, impaired
host immunity.
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DEFINITION
AND PREVALENCE
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| Impetigo
is a superficial skin infection usually caused by S aureus and occasionally
by S pyogenes. Impetigo affects approximately 1% of children. |
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PATHOPHYSIOLOGY
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| S
aureus produces a number of cellular and extracellular products, including
exotoxins and coagulase, which contribute to the pathogenicity of impetigo,
especially when coupled with preexisting tissue injury. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Two
clinical types of impetigo exist: nonbullous and bullous impetigo. The nonbullous
type is more common and typically occurs on the face and extremities, initially
with vesicles or pustules on reddened skin that eventually rupture to leave
the characteristic "honey-colored" (yellow-brown) crust (Figure
1). Bullous impetigo, almost exclusively caused by S aureus,
exhibits flaccid bullae with clear yellow fluid that rupture and leave a
golden-yellow crust. Diagnosis depends on clinical presentation and confirmation
by culture.1 |
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MANAGEMENT
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| For
most patients with impetigo, topical treatment is adequate, either with
Polysporin bacitracin or mupirocin (Bactroban), applied three times a day
for 7 to 10 days. Systemic therapy may be necessary for patients with extensive
disease (Table 1).2
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FOLLICULITIS,
FURUNCULOSIS
(furuncles), and CARBUNCULOSIS
(carbuncles)
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DEFINITION
AND PREVALENCE
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| Folliculitis
is a superficial infection of the hair follicles characterized by erythematous,
follicular-based papules and pustules. Furuncles are deeper infections of
the hair follicle characterized by inflammatory nodules with pustular drainage,
which may coalesce to form larger draining nodules. The prevalence of folliculitis
is unknown. |
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PATHOPHYSIOLOGY
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| S
aureus is the usual pathogen, although exposure to Pseudomonas aeruginosa
in hot tubs or swimming pools may lead to folliculitis. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Folliculitis
is generally asymptomatic, but may be pruritic or even painful. Commonly
affected areas are the beard, posterior neck, occipital scalp, and axillae
(Figure 2). Often a continuum
of folliculitis, furunculosis (furuncles) arises in hair-bearing areas as
tender, erythematous, fluctuant nodules that rupture with purulent discharge
(Figure 3). Carbuncles are
larger and deeper inflammatory nodules, often with purulent drainage
(Figure 4), and commonly occur
on the nape of the neck, back, or thighs. Carbuncles are often tender and
painful and occasionally accompanied by fever and malaise.1,2,3
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MANAGEMENT
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Topical treatment
with clindamycin 1% or erythromycin 2%, applied two to three times a day
to affected areas, coupled with an antibacterial wash or soap, is adequate
for most patients with folliculitis. Systemic antistaphylococcal antibiotics
(Table 1)
are usually necessary for furuncles and carbuncles, especially when cellulitis
or constitutional symptoms are present.2
Additionally, small furuncles can be treated with warm compresses three
to four times a day for 15-20 minutes, whereas larger furuncles and carbuncles
often warrant incision and drainage.
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DEFINITION
AND PREVALENCE
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Ecthyma
is a deep infection of the skin that resembles impetigo. Ecthyma is somewhat
common in patients with poor hygiene and/or malnutrition.
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PATHOPHYSIOLOGY
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S
aureus or S pyogenes is the usual pathogen of ecthyma.
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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Infection
begins with vesicles and bullae that progress to punched-out ulcerations
with an adherent crust, which heals with scarring. The most common site
of infection is the legs. Diagnosis depends on clinical presentation with
confirmation by culture.3,4
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MANAGEMENT
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Ecthyma requires treatment
with an oral antistaphylococcal antibiotic (Table
1), coupled with warm compresses three to four times a day for
15-20 minutes.2
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ERYSIPELAS
AND CELLULITIS
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DEFINITION
AND PREVALENCE
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Erysipelas
is a superficial streptococcal infection of the skin. Cellulitis is a
deeper process that extends to the subcutis. Erysipelas has a predilection
for young children and the elderly.
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PATHOPHYSIOLOGY
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S
aureus and S pyogenes are the most common pathogens responsible
for erysipelas and cellulitis. S pyogenes produces enzymes that
promote infection with systemic manifestations, such as fever/chills,
tachycardia, and hypotension. Predisposing factors for erysipelas include
venous stasis/insufficiency, diabetes mellitus, trauma, and alcoholism.3,4
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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Classically,
erysipelas is a tender, well-defined, erythematous, indurated plaque on
the face or legs (Figure 5).
Cellulitis is a warm, tender, erythematous, and edematous plaque with
ill-defined borders that expands rapidly. Cellulitis is often accompanied
by constitutional symptoms, regional lymphadenopathy, and, occasionally,
bacteremia (Figure 6).3,4
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MANAGEMENT
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Penicillin
(250 to 500 mg, four times daily for 7-10 days) is the treatment of choice
for erysipelas; parenteral therapy may be necessary for extensive or facial
disease. An oral antistaphylococcal antibiotic (Table
1) is the treatment of choice for cellulitis; parenteral therapy
is warranted for patients with extensive disease or with systemic symptoms
as well as for immunocompromised patients. Good hygiene, warm compresses
three to four times a day for 15-20 minutes, and elevation of the affected
limb help to expedite healing.
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DEFINITION
AND PREVALENCE
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Necrotizing
fasciitis is a rare infection of the subcutaneous tissues and fascia that
eventually leads to necrosis.
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PATHOPHYSIOLOGY
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S
pyogenes may be the sole pathogen responsible for necrotizing fasciitis,
but most patients have a mixed infection with other aerobes (group B and
C streptococci) and anaerobes (Clostridium). Common predisposing
factors are injury to soft tissues, eg, abdominal surgery, abrasions,
surgical incisions, diabetes, and intravenous drug abuse.5,6
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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Infection
begins with warm, tender, reddened skin, and inflammation that rapidly extends
horizontally and vertically. The most common site for infection is the legs,
followed by the perineum (Figure 7).
Within 48 to 72 hours, affected skin becomes dusky and bullae form, followed
by necrosis and gangrene, often with crepitus. Without prompt treatment,
fever, systemic toxicity, organ failure, and shock may occur, often followed
by death.
Computed tomography or magnetic resonance imaging may help to delineate
the extent of infection. Biopsy for histology, Gram stain, and tissue culture
help to identify the causative organism(s).5,6
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MANAGEMENT
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Necrotizing
fasciitis is a surgical emergency requiring prompt surgical debridement,
fasciotomy, and, occasionally, amputation of the affected extremity to
prevent progression to myonecrosis. Treatment with parenteral antibiotics
(usually gentamicin and clindamycin) is mandatory. Even with treatment,
mortality can approach 70%.
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FUNGAL
AND YEAST INFECTIONS
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DERMATOPHYTE
(Fungal Infections)
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DEFINITION
AND PREVALENCE
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Dermatophytosis
implies infection with fungi, organisms with high affinity for keratinized
tissue, such as the skin, nails, and hair. Trichophyton rubrum is the
most common dermatophyte worldwide.
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PATHOPHYSIOLOGY
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| Three
fungal genera—Trichophyton, Microsporum, and Epidermophyton—account
for the vast majority of infections. Fungal reservoirs for these organisms
include soil, animals, and infected humans. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Tinea
pedis (athlete's foot) is the most common fungal infection in humans in
North America and Europe.4 Affected skin
is usually pruritic, with scaling plaques on the soles, extending to the
lateral aspect of the feet and interdigital spaces (Figure
8), often with maceration. Tinea cruris (jock itch) occurs in the
groin and on the upper, inner thighs and buttocks as scaling annular plaques
(Figure 9); disease is more
common in men and typically spares the scrotum. Tinea capitis, or fungal
infection of the scalp, is most common in children, characterized by scaly,
erythematous skin, often with hair loss. Tinea capitis may resemble seborrheic
dermatitis. Kerion etc is an inflammatory form of tinea capitis, characterized
by boggy nodules, usually with hair loss and regional lymphadenopathy. Tinea
corporis (body), faciei (face), and manuum (hands) represent infections
of different sites, each invariably with annular scaly plaques. Tinea unguium
(onychomycosis) is fungal nail disease, characterized by thickened yellow
nails and subungual debris (Figure
10). Potassium hydroxide preparation and/or culture help to establish
the diagnosis for all forms of fungal infection.2 |
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MANAGEMENT
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| For
most patients, topical treatment with terbinafine (Lamisil), clotrimazole
(Lotrimin, Mycelex), or econazole (Spectazole) cream is adequate when applied
twice daily for 6 to 8 weeks. For onychomycosis, tinea capitis, and extensive
dermatophyte disease, systemic treatment is often necessary—itraconazole
(Sporanox) or terbinafine (Lamisil) for nail disease, and griseofulvin for
scalp or extensive dermatophyte disease.7,8,9
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DEFINITION
AND PREVALENCE
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| Cutaneous
candidiasis is a yeast infection caused primarily by Candida albicans.
Infection is common in immunocompromised patients, diabetics, the elderly,
and patients receiving antibiotics. |
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PATHOPHYSIOLOGY
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| C
albicans commonly resides on skin and mucosal surfaces. Alterations
in the host environment may lead to its proliferation and subsequent skin
disease. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Candidal
intertrigo is a specific infection of the skin folds (axillae, groin), characterized
by reddened plaques, often with "satellite" pustules (Figure
11). Thrush is oropharyngeal candidiasis, characterized by white
nonadherent plaques on the tongue and buccal mucosa. Paronychia is an acute
or chronic infection of the nail characterized by tender, edematous, and
erythematous nail folds, often with purulent discharge (Figure
12); disease is common in diabetics. Angular cheilitis is the presence
of fissures and reddened scaly skin at the corner of the mouth, which often
occurs in diabetics and in those who drool or chronically lick their lips
(Figure 13). Candidal vulvovaginitis
is an acute inflammation of the perineum characterized by itchy, reddish,
scaly skin and mucosa; creamy discharge; and peripheral pustules. The counterpart
in men is balanitis, characterized by shiny reddish plaques on the glans
penis, which may affect the scrotum. Balanitis occurs almost exclusively
in uncircumcised men.2 |
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MANAGEMENT
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| For
candidal intertrigo and balanitis, topical antifungal agents such as clotrimazole,
terbinafine, or econazole cream, applied twice daily for 6 to 8 weeks is
usually curative when coupled with aeration and compresses. For thrush,
the treatment is nystatin suspension or clotrimazole troches four to six
times daily until symptoms resolve. Systemic antifungal drugs such as fluconazole,
100 mg/day to 200 mg/day, or itraconazole, 100 mg/day to 200 mg/day, for
5 to 10 days may be necessary for severe or extensive disease. For paronychia,
treatment consists of aeration and a topical antifungal agent such as terbinafine,
clotrimazole, or clotrimazole for 2 to 3 months; occasionally, oral antistaphylococcal
antibiotics (Table 1)
are needed, coupled with incision and drainage for secondary bacterial
infection. Cheilitis resolves with aeration, application of a topical antifungal
agent, and discontinuation of any aggravating factors. A single 150-mg dose
of fluconazole, coupled with aeration, is usually effective for vulvovaginitis.9
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TINEA
(Pityriasis) VERSICOLOR
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DEFINITION
AND PREVALENCE
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| Tinea
versicolor is a common superficial infection of the skin caused by the ubiquitous
yeast Pityrosporum ovale. Prevalence is high in hot, humid climates.
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PATHOPHYSIOLOGY
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| P
ovale produces phenolic compounds that inhibit tyrosinase, which may
produce hypopigmentation in many patients. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Infection
produces discrete and confluent, finely scaly, well-demarcated, hypopigmented
and/or hyperpigmented plaques on the chest, back, arms, and neck (Figure
14). Disease usually occurs in warmer months or in hot, humid climates.
Potassium hydroxide (KoH) preparation exhibits short hyphae and spores with
a spaghetti-and-meatball appearance. |
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MANAGEMENT
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| Selenium
sulfide shampoo (2.5%) or ketoconazole shampoo is the mainstay of treatment,
applied to the affected areas and the scalp daily for 3 to 5 days, then
once a month thereafter. Alternatively, a variety of topical antifungal
agents, including terbinafine, clotrimazole, or econazole cream, applied
twice daily for 6 to 8 weeks, constitute adequate treatment, especially
for limited disease.10 |
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VIRAL
INFECTIONS
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DEFINITION
AND PREVALENCE
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| Herpes
simplex virus (HSV) infection is a painful, self-limited, often recurrent
dermatitis, characterized by small grouped vesicles on an erythematous base.
Eighty-five percent of the population has antibody evidence of HSV type
1 infection. Twenty to fifty percent of genital ulcerations are the result
of HSV type 2 infection. |
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PATHOPHYSIOLOGY
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| Disease
follows implantation of the virus via direct contact at mucosal surfaces
or on sites of abraded skin. After primary infection, the virus travels
to the adjacent dorsal ganglia where it remains dormant unless reactivated
by psychological or physical stress, menses, or sunlight. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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Primary infection
occurs most often in children, exhibiting vesicles and erosions on reddened
buccal mucosa, palate, tongue and/or lips (acute herpetic gingivostomatitis)
(Figure 15). Herpes labialis,
(fever blisters or cold sores) appears as grouped vesicles on red denuded
skin, usually the vermilion border of the lip; infection represents reactivated
HSV. Primary genital infection is an erosive dermatitis on the external
genitalia that occurs about 7 to 10 days after exposure; intact vesicles
are rare. Recurrent genital disease is common (approximately 40% of affected
patients).
Viral culture helps to confirm the diagnosis; direct fluorescent antibody
(DFA) is a helpful but less specific test. Serology is helpful only for
primary infection.
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MANAGEMENT
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| Acyclovir
remains the treatment of choice for HSV infection; newer antivirals, eg
famciclovir and valacyclovir, are also effective (Table
2). For recurrent infection (more than six episodes per year), suppressive
treatment (Table 2) is warranted. Primary
infection in immunosuppressed patients requires treatment with acyclovir,
10 mg/kg, every 8 hours for 7 days. |
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DEFINITION
AND PREVALENCE
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Herpes zoster (shingles)
is an acute, painful dermatomal dermatitis that affects approximately
10 to 20% of adults, often in the presence of immunosuppression.
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PATHOPHYSIOLOGY
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| Zoster
represents reactivation of latent varicella-zoster virus within a single
dermatome. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Herpes
zoster is primarily a disease of adults. It typically begins with pain in
a dermatomal or band-like pattern followed by grouped vesicles within the
dermatome (Figure 16), and
occasionally accompanied by fever and malaise. Most patients with zoster
do well with only symptomatic treatment, but postherpetic neuralgia (continued
dysthesias and pain after resolution of skin disease) is common in the elderly.
Disseminated zoster is uncommon and occurs primarily in immunocompromised
patients. Diagnostic tests are the same as for HSV.2
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MANAGEMENT
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| Zoster
deserves treatment, if possible, with rest, analgesics, compresses applied
to affected areas, and antiviral therapy, if possible, within 24-72 hours
of disease onset. (Table
2). Disseminated and ophthalmic zoster warrants Rx with acyclovir
10 mg/kg intravenously every 8 hours for 7 days. |
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DEFINITION
AND PREVALENCE
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| Warts
are common and benign epithelial growths caused by human papillomavirus
(HPV). Warts affect approximately 5% of the population. |
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PATHOPHYSIOLOGY
|
| HPV
infection follows inoculation of the virus into the epidermis through direct
contact, usually facilitated by a break in the skin. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| The
common wart is the most common type-a, hyperkeratotic, flesh-colored papule
and/or plaque studded with small black dots (thrombosed capillaries) (Figure
17). Other types of warts include flat warts (verruca plana), plantar
warts, and condyloma acuminatum (venereal warts). Clinical appearance and
location usually suggest the diagnosis. |
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MANAGEMENT
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| Therapy
is variable and often challenging. Most modalities are destructive in nature,
(eg, cryosurgery, electrodesiccation, curettage, and application of various
topical products such as trichloroacetic acid, salicylic acid, podophyllin,
and canthacur). For stubborn warts, laser therapy is often necessary. The
immunomodulator, imiquimod cream (Aldara), is a novel topical agent recently
approved for the treatment of condyloma acuminatum. Sexual partners of patients
with condyloma warrant examination, and women require gynecologic examination.
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DEFINITION
AND PREVALENCE
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| Molluscum
contagiosum is an infectious viral disease caused by the poxvirus. Infection
is common in children, sexually active adults, and in patients with HIV
infection. |
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PATHOPHYSIOLOGY
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| The
disease follows direct contact with the virus, which replicates in the cytoplasm
of the cells and induces hyperplasia. |
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SIGNS,
SYMPTOMS, AND DIAGNOSIS
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| Molluscum
are smooth flesh-colored, dome-shaped, umbilicated papules with a central
keratotic plug (Figure 18),
which usually resolve spontaneously, but often persist in immunocompromised
patients. |
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MANAGEMENT
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| Treatment
may not be necessary. If indicated, treatment is similar to the modalities
outlined for warts. |
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|
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JA. Common bacterial pyodermas. Taking aim against the most likely pathogens.
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- Brook
I, Frazier EH. Clinical and microbiological features of necrotizing
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- Bisno
AL, Stevens DL. Streptococcal infections of skin and soft tissues. N
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LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial
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LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial
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LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial
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- Hay
RJ. The management of superficial candidiasis. J Am Acad Dermatol.
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- Drake
LA, Dinehart SM, Farmer ER, et al. Guidelines of care for superficial
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