Chapter 367. Skin Infections and Exanthems

Topical therapies for some common pediatric bacterial skin infections are outlined in Table 367-1.

Impetigo

Impetigo is a highly contagious infection of the superficial epidermis noted predominantly in preschool-age children. Although group A β-hemolytic streptococci (GABHS) were traditionally most frequently isolated in the United States, Staphylococcus aureus now appears to predominate. Community-acquired methicillin-resistant S aureus (MRSA) has been present for more than a decade, but has more recently become more widespread, now representing approximately 90% of MRSA infections in cutaneous and subcutaneous tissue in children.1,2 Children in daycare and athletes are some of the persons at higher risk, but most patients are young, healthy, and immunocompetent.1 When diagnosing and treating infections caused by S aureus, the possibility of MRSA must be considered, particularly when standard treatment is not efficacious. See Chapter 284 for more information regarding MRSA and treatment considerations. Anaerobic bacteria are a less common cause of impetigo. In general, intact skin is resistant to impetiginization, and some form of compromise of the epidermal surface is necessary to permit infection. Predisposing factors include minor abrasions and lacerations, arthropod bites, burns, varicella, and several types of dermatitis, especially atopic dermatitis. Exposed areas such as the face, arms, and legs are most commonly affected, and impetigo is most common during the summer months.

Impetigo usually presents in one of two clinical forms. Nonbullous (crusted) impetigo, which accounts for more than 70% of cases, begins with small vesicles or vesiculopustules that rupture rapidly, leaving behind a honey-colored crust superimposed on a moist red base. Lesions are minimally symptomatic, although mild pain or pruritus may be present. Autoinoculation of the infection from scratching or digital manipulation may result in the spread of lesions. Associated findings include lymphadenopathy in 90% of patients, and leukocytosis, in up to 50% of cases.

Bullous impetigo is caused by infection with a toxin-producing strain of S aureus, primarily by phage group 2 or type 71, and less commonly types 3A, 3B, 3C, and 55. The initial lesions consist of flaccid bullae that rupture easily given the superficial, subcorneal location of lysis caused by the action of the toxin on the epidermis. Patients usually present with shallow, moist, erythematous erosions with a surrounding collarette of residual blister roof (Fig. 367-1). Even in the absence of intact bullae, the clinical lesions are usually quite diagnostic. Lesions of bullous impetigo may have a propensity for moist, intertriginous areas such as the diaper region, axillae, and neck folds. The S aureus toxin of bullous impetigo also causes staphylococcal scalded skin syndrome (SSSS).3-5

Folliculitis

Folliculitis is a superficial infection of the pilosebaceous unit, most typically caused by S aureus. Patients present with erythematous papules and papulopustules centered around hair follicles (Fig. 367-2) that are most often distributed over the scalp, thighs, and/or buttocks. Warmth, moisture, and maceration predispose to folliculitis, and many cases therefore occur during the warmer summer months. Treatment is with both topical antibacterial therapy and systemic antibiotics when more severe.

There are a variety of other types of folliculitis. Gram-negative folliculitis, most often caused by Klebsiella, Enterobacter, or Proteus, may be seen in patients with acne vulgaris on oral antibiotic therapy. In these patients, lesions are most common in the facial “T zone.” Another form of gram-negative folliculitis, Pseudomonas (hot tub) folliculitis, occurs within a few days of exposure to a poorly chlorinated whirlpool or hot tub. These lesions are most common over the buttocks, legs, and arms and may be accompanied by mild constitutional symptoms such as fever and malaise. Immunocompromised patients may develop folliculitis from normally nonpathogenic organisms such as Pityrosporum or the hair follicle mite, Demodex. Noninfectious forms of folliculitis may also occasionally occur. Sterile folliculitis may occur as a result of the frequent application of exogenous agents such as hair gels, which obstruct the orifice of the pilosebaceous unit. Eosinophilic pustular folliculitis occurs as recurrent pruritic follicular papules and pustules, especially on the scalp and forehead of infants. These pustules are sterile and reveal clusters of eosinophils. A similar entity has been described in adult patients with HIV infection. In pediatric patients, this is not the case, and the diagnosis as a distinct entity has more recently been questioned.6,7

Other Superficial Infections

Furuncles and Carbuncles

More deeply seated infections of the pilosebaceous unit are termed furuncles and carbuncles and are usually caused by S aureus. Patients with furuncles present with erythematous, painful, fluctuant nodules (abscesses). A carbuncle is a collection of furuncles that is multiloculated and composed of interconnecting sinuses. Incision and drainage of these lesions is necessary in addition to antibiotic therapy, particularly for MRSA abscesses.1

Noninfectious causes of abscesses include those associated with acne vulgaris (as a result of follicular rupture and a brisk inflammatory reaction), those in response to a foreign body in the skin, or those that follow spontaneous rupture of an epidermal cyst. “Cold” abscesses, which are only mildly erythematous and tender, may be seen in individuals with the hyperimmunoglobulin-E (hyper IgE) syndrome.

Perianal Streptococcal Cellulitis

This infection occurs predominantly in children ages 6 months to 10 years and is caused most often by GABHS, and occasionally by S aureus. It is characterized by sharply circumscribed, bright red perianal erythema, which may be accompanied by pruritus, anal fissures, constipation, and pain on defecation. Blood-streaked stools and purulent anal discharge may be present, although systemic symptoms are rare. Because similar signs and symptoms are seen with other more common dermatologic conditions, diagnosis is frequently delayed. Flares of guttate psoriasis may be associated with perianal streptococcal cellulitis; hence, perianal examination is recommended in all patients with this presentation. Perianal streptococcal cellulitis may be confirmed with a bacterial culture.8,9

Blistering Dactylitis

Patients present with bullae on an erythematous base, usually distributed over the volar fat pad of distal phalanges (Fig. 367-3), occasionally with dorsal finger or palmar involvement. More than one digit is usually involved. Gram stain and bacterial culture of blister fluid often reveals GABHS, but S aureus has more recently been found to be more common,10 and group B streptococci can sometimes be found. The intact blisters in blistering dactylitis, an unusual feature of streptococcal-mediated skin infections, are likely related to the thickness of the stratum corneum in the volar sites to which this condition is usually localized.11

Acute Paronychia

This common infection of the skin surrounding the nail, presents with erythema, edema, and tenderness of both the proximal and lateral nail folds. Small pustules or abscesses may also be present around the base of the nail. Predisposing conditions include trauma, dermatitis, frequent hand washing, and onychophagia (nail biting). S aureus is most commonly isolated, although mixed infection, including anaerobic organisms, may be present. In addition to antimicrobial therapy directed against S aureus, incision and drainage may be necessary.

Corynebacteria Skin Infection

Erythrasma is a superficial skin infection, primarily occurring in intertriginous zones, caused by Corynebacteria minutissimum. The clinical presentation is characterized by slightly red to tan patches with mild scaling, in the toe webs, axillae, inframammary creases, groin, or gluteal crease. Lesions are asymptomatic to mildly pruritic and may be confused with cutaneous fungal infections. Wood’s lamp examination is helpful in confirming the diagnosis and reveals coral red fluorescence, related to the production of porphyrin compounds by the corynebacteria.

Pitted keratolysis is also caused by corynebacteria and presents with plantar hyperhidrosis, burning, foul odor, and small punctate pits. It is seen most commonly in males with a history of prolonged use of occlusive footwear (ie, military personnel, athletes), especially in warm, damp environments.

Ecthyma Contagiosum

This disorder is caused primarily by the combination of group A β-hemolytic streptococci (GABHS) and S aureus, is a deep cutaneous infection that extends through the epidermis into the dermis. An impetiginous crust enlarges and on removal reveals an underlying punched-out ulcer, which may be filled with purulent material. The most common sites of involvement are the lower legs; if left untreated, ecthyma may progress to cellulitis or lymphangitis. Healing takes place with scar formation. Ecthyma gangrenosum is a cutaneous manifestation of sepsis with Pseudomonas aeruginosa. Patients are usually systemically ill and have an underlying illness such as hematologic malignancy or immunodeficiency, but a number of healthy children have also been described.12 They present with 0.5- to 2-cm hemorrhagic papules, nodules, bullae, or ulcers, usually distributed in the genital region. These lesions rapidly progress to necrosis and eschar formation. The organism can be cultured from swabs of the lesions or biopsy tissue, and blood cultures are positive. Therapy with intravenous antibiotics must be rapidly initiated. Occasionally, other organisms (ie, other gram-negative bacteria, Candida, Aspergillus, Fusarium) may cause ecthyma gangrenosum–like lesions, and treatment should be directed accordingly.13

Cellulitis

Cellulitis is an acute infection of the subcutaneous tissues that may be caused by many different bacterial organisms. GABHS and S aureus are again the most common etiologic agents, and the lower extremities and feet are the locations most often affected. There is frequently a history of a predisposing break in the skin barrier, such as that caused by atopic dermatitis, contact dermatitis, inflammatory tinea pedis, or trauma. Associated fever, malaise, and chills may be present. In the absence of preexisting skin lesions or in the presence of fever or systemic symptoms, bacteremia should be considered, especially in very young children.

Erysipelas is a superficial form of cellulitis that presents with marked redness and pain in the affected area and often demonstrates well-demarcated, elevated borders. There may be a history of a fissured dermatitis, ulcer, or puncture wound, and GABHS is the most common etiologic agent. Although the diagnosis of both cellulitis and erysipelas is usually suggested on clinical grounds, fine-needle aspiration with Gram stain and culture may be useful in patients with immunocompromise or a suboptimal response to therapy.

Preseptal (periorbital) cellulitis is a form of cellulitis that involves the periorbital skin and soft tissues. It must be differentiated from orbital cellulitis, a potentially sight-threatening emergency that can occur from direct extension of preseptal cellulitis through the orbital septum, hematogenous seeding, or direct extension from infected paranasal sinuses. Preseptal cellulitis presents with erythema and edema, which tends to be fairly well demarcated. If decreased ocular movement or proptosis is present, orbital cellulitis must be considered and should be evaluated with radiologic imaging, along with consultation by ophthalmologic colleagues. Although Haemophilus influenzae type B (HiB) has traditionally been the most frequently implicated etiologic agent, the advent of the HiB vaccine has greatly decreased the incidence, of many HiB-associated childhood diseases, including preseptal and orbital cellulitis. Other organisms, especially Streptococcus spp, are now a more frequent cause of preseptal and orbital cellulitis. Prompt institution of intravenous antibacterial therapy is critical for a favorable outcome.14

Necrotizing Fasciitis

This is a rare, rapidly progressive, and potentially fatal soft tissue infection that develops at the level of the superficial fascia and often involves the overlying dermis, which may result in the incorrect initial diagnosis of cellulitis. Deep fascia and muscle are spared in most cases, although circumferential involvement may lead to compartment syndrome. A penetrating or blunt traumatic skin injury can be the source of the bacterial infection. Polymicrobial infection with a mix of aerobic and anaerobic organisms, including group A streptococcus, S aureus, Escherichia coli, Bacteroides (spp), Peptostreptococcus (spp), Clostridium (spp), and Pseudomonas aeruginosa,15 are the usual etiologic agents. Patients usually present with erythema, swelling, along with exquisite tenderness and pain, usually in an extremity. Anesthesia of the overlying skin may aid in the differentiation from cellulitis. Bullae may develop that become hemorrhagic with eventual necrosis and frank cutaneous gangrene with crepitance. Fever is present in most patients. Patients with invasive GABHS infection may develop associated toxic shock syndrome. Soft tissue gas on plain radiography may be present. Although MR or CT imaging, fine-needle aspiration, and tissue biopsy may be helpful in making the diagnosis, direct surgical inspection of fascia is the fastest and most sensitive technique. Aggressive surgical debridement, parenteral antimicrobial therapy, fluid replacement, and blood pressure support are crucial in the treatment of patients with necrotizing fasciitis. Mortality is high, ranging from 30% to 70%.16

Warts

An extremely common condition in children, verrucae (warts) are caused by infection of the squamous epithelium of skin or mucous membranes with the human papillomavirus (HPV). More than 80 subtypes of HPV have now been described; different types may reveal specific tropisms for distinct cell types. For example, HPV types 1, 2, 4, and 7 are associated with plantar, palmar, and common warts; types 3, 10, and 28 with flat warts; and types 6, 11, 16, 18, 31, and 33 with anogenital and genital tract warts and tumors. Treatments for warts and molluscum contagiosum are outlined in Table 367-2.

Common warts (verruca vulgaris) can be found on all body surfaces. Frequent locations are the fingers, periungual regions, palms, and soles (see discussion on plantar warts that follows). They present as flesh-colored, hyperkeratotic papules, which may be solitary or multiple. Filiform lesions may occur and are characterized by a slender stalk with numerous projections distally. Tiny black dots representing thrombosed capillaries may be visualized centrally, especially after manual debridement of devitalized tissue, and may be a useful diagnostic clue. Autoinoculation, presenting as lesions in a linear array, may be related to scratching and manual dissemination of the virus. Spontaneous wart regression occurs in up to 85% of lesions within 2 years and is believed to be related to cell-mediated immune processes. Specific anti-HPV therapies are lacking, and most effective treatments rely on mechanical destruction of infected tissues and the resultant inflammatory response. Excessively traumatic procedures (especially in the pediatric patient) or those that result in scarring are unwarranted in the treatment of warts.

Plantar warts occur most often on weight-bearing portions of the soles and may induce significant hyperkeratosis (or epidermal thickening) with resultant pain on ambulation. Manual debridement of the hyperkeratotic surface by paring with a scalpel blade again reveals thrombosed capillaries, which may help differentiate them from corns and calluses and relieve discomfort. Therapy of plantar warts is difficult given their location and endophytic nature, which is a result of weight bearing.

Flat warts present as small (1- to 10-mm), flat, flesh-colored to pink papules and are most commonly distributed on the face (Fig. 367-4), dorsal hands, and arms. No hyperkeratosis or scale is present. Treatment is usually unnecessary.17

Condylomata acuminata (anogenital warts) are more common in sexually active adolescents, but may occur in infants and prepubertal children as well. The importance of identifying anogenital warts in the pediatric patient lies in the possible association with a sexual mode of transmission and sexual abuse. However, it is well recognized that benign modes of transmission can result in pediatric anogenital warts, and their presence is not pathognomonic of sexual abuse. Nonsexual modes of transmission may occur, especially in children younger than 3 years and may include innocent heteroinoculation, autoinoculation, or vertical transmission from passage through an infected birth canal. They present as flesh-colored papules in perianal, genital, and perigenital tissues. Anogenital warts may be caused by genital HPV types, such as 6, 11, 16, or 18, or by uncommon HPV types, such as type 2, but HPV type cannot be differentiated on the basis of appearance.18,19 Given the association of certain genital HPV types with anogenital carcinomas and the uncertain prognostic significance in children, periodic follow-up for anogenital dysplasia is suggested. The American Academy of Pediatrics Committee on Child Abuse and Neglect considers condylomata acuminata in infants (if not perinatally acquired) and prepubertal children “suspicious” for sexual abuse and recommends reporting to the appropriate child protective agency.20

Molluscum Contagiosum

The lesions of molluscum contagiosum, a common skin infection caused by a poxvirus, are most common in children, particularly those with a history of atopic dermatitis,21 although they may also occur in adults as a sexually transmitted disease or in association with immunosuppression. They are transmitted via skin-to-skin contact or autoinoculation and occasionally by fomites. Molluscum may occur at any site, but are most often seen on the inner thighs, popliteal or antecubital fossae, axillae, and abdomen. Individual lesions are flesh-colored, pearly, dome-shaped papules that may have a central umbilication and usually range in size between 1 and 5 mm (Fig. 367-5). Associated inflammation and scaling, so-called molluscum dermatitis, can be severely pruritic and improves with topical corticosteroids. The natural course of molluscum contagiosum is one of spontaneous involution, although the timing is unpredictable, and lesions may become numerous or symptomatic, necessitating therapy.

Herpes Virus Infections

Infections with herpes simplex virus (HSV), a member of the Herpesviridae family, range from a mild illness (common cold sores or gingivostomatitis) to severe or life-threatening involvement (encephalitis). There are two serologic subtypes of HSV: type 1 (HSV-1) and type 2 (HSV-2). Infections of the oral cavity are most commonly due to HSV-1 and may be spread to the face, conjunctivae, or cornea. Beyond the neonatal period, encephalitis is virtually always caused by HSV-1. Infection with HSV-2 in childhood may be indicative of, but is not pathognomonic for, sexual abuse. HSV infections in the neonate are usually acquired via passage through an infected birth canal and may be limited to skin, eyes, and mucosa (SEM disease) or may be more severe and involve the central nervous system or have multiple organ dissemination. HSV-2 causes approximately 75% of these illnesses. Neonatal HSV is discussed in more detail in Chapter 309.

The treatment of choice for cutaneous HSV infection is acyclovir, which is available in a suspension containing 200 mg/tsp (5 ml). Although information regarding pediatric dosing is limited, 200 mg five times a day seems effective for children older than 2 years. The decision regarding therapy of HSV is based on several factors, including severity, symptomatology, frequency of recurrences, and immune status of the patient.

Gingivostomatitis is the most common clinical manifestation of primary HSV infection in young children.22 It is most commonly seen between the ages of 9 months and 3 years and, although self-limited over 10 to 14 days, may be associated with extreme discomfort, fever, refusal to drink, and dehydration. Malaise, irritability, and lymphadenopathy may also be present. Small vesicles or erosions on an erythematous base over the gingiva, palate, lips, and tongue is the usual presentation. Grouped vesicles or erosions on an erythematous base may be present in the perioral area. Treatment is primarily symptomatic, with analgesics, antipyretics, and fluids. Oral acyclovir, if initiated within the first 3 days of illness, can help decrease the symptomatology.23

Orolabial herpes or herpes labialis (fever blisters or cold sores) most often involves the lips or perioral areas, sometimes in association with gingival lesions. These outbreaks usually represent reactivation of latent HSV and are often precipitated by sunlight or fever. Grouped vesicles or crusted erosions on an erythematous base aretingling or burning sensation, or “aura,” 1 to 2 days prior to the onset of actual lesions.

Herpetic whitlow occurs after inoculation of HSV into the skin of the fingers and presents with erythema, pain, and, often, vesicles, pustules, or bullae. Whitlow can occur as a primary infection related to autoinoculation from another site, heteroinoculation, or as reactivation of a latent infection. Acyclovir is often indicated because of extreme pain, to accelerate healing.

Eczema herpeticum, also known as Kaposi varicelliform eruption, refers to HSV infection occurring in areas of skin with preexisting damage to the epidermal barrier, most commonly in patients with atopic dermatitis. Vesicles and erosions occur in a widespread fashion over areas involved with the dermatitis (Fig. 367-6), and may be associated with fever and malaise. Secondary bacterial impetiginization may be the initial clinical impression, although grouping of the blisters or erosions may offer a subtle clue to the correct diagnosis. Mild to moderate cases can usually be adequately managed with cool compresses and oral acyclovir; toxic or immunosuppressed patients with severe involvement require hospitalization and intravenous acyclovir. Concomitant bacterial infection needs to be considered, and appropriate skin cultures and sensitivity testing performed.

Varicella (chickenpox), caused by the varicella-zoster virus (VZV), is a highly contagious disease of childhood transmitted by respiratory droplets. Although most cases are mild, severe complications such as bacterial superinfection can ensue. The epidemiology of varicella is evolving as a result of a live-attenuated vaccine licensed in the United States in 1995 and has led to attenuated cases of varicella.

Wild-type varicella presents as a generalized rash, which initially appears on the trunk, face, and scalp and spreads in a centrifugal fashion; low-grade fever and malaise may be present. Crops of erythematous macules develop a clear vesicle, giving the classic “dew drop on a rose petal” appearance. The lesions form crusts within a few days, and lesions in all stages of evolution are characteristic. Bullous lesions are occasionally present, usually in association with superinfection with a toxin-producing strain of S aureus. Group A β-hemolytic streptococci (GABHS) superinfection is one of the most common, and potentially life-threatening, complications of acute varicella and should be suspected in any child with prolonged fever (beyond 4 or 5 days) or unusually aggressive skin lesions (including induration, ulceration, or necrosis). Patients with varicella are considered contagious until all skin lesions are in the crusted stage, and treatment is primarily supportive. Systemic antiviral therapy may be useful in shortening the time to healing and reducing symptoms, and is indicated in all patients at high risk for associated complications. Secondary bacterial superinfection should be promptly treated with appropriate antimicrobial therapy.

Infection with varicella during pregnancy may lead to congenital varicella. Fetal varicella syndrome is acquired early in gestation and is characterized by a variety of anomalies, including scarring and hypoplasia of skin in a dermatomal distribution, low birth weight, mental retardation, seizures, and a range of ophthalmologic, skeletal, gastrointestinal, and genitourinary defects. Neonatal varicella results from transmission shortly before (or, in some cases, shortly after) birth. Infants at highest risk for severe disease are those who acquire the infection from a mother who develops acute varicella during the last 5 days of pregnancy or within 2 days after delivery because protection from maternally derived antibodies is lacking. These newborns may appear normal at birth, but present within the first few days of life with vesicular lesions that erupt in crops and eventually crust over. In these patients, dissemination to multiple organs may occur, and prompt recognition, diagnosis, and initiation of antiviral therapy is essential.

Herpes zoster, or shingles, represents reactivation of VZV, which has remained dormant in the sensory root ganglia following acute infection. The incidence is low in immunocompetent children, although the risk seems to be greater in those who had either intrauterine exposure to VZV or acute varicella early in life. Herpes zoster presents with grouped vesicles on an erythematous base that are distributed within one to three sensory dermatomes (Fig. 367-7); this may be preceded by pain or paresthesias in the affected areas. The most common dermatomes to be affected are the ophthalmic (V1) branch of the trigeminal nerve and the thoracic dermatomes. Ophthalmologic examination should be performed in all patients with involvement of the V1 dermatome given the possibility of associated eye involvement. Lesions of herpes zoster may be more generalized in immunosuppressed patients, and visceral involvement may be present. Postherpetic neuralgia, a persistent pain syndrome involving the affected dermatomes, is more common in the elderly, and is very rare in children. Antiviral therapy of pediatric herpes zoster is indicated in immunosuppressed patients to lower the risk of dissemination and may be beneficial in immunocompetent patients to reduce symptoms, minimize complications, and accelerate healing. A detailed discussion of other manifestations of varicella/zoster is found in Chapter 314.

Lyme Disease

Lyme disease is a systemic illness caused by the spirochete Borrelia burgdorferi discussed in detail in Chapter 267. The skin lesion, which occurs at the site of the tick bite, erythema migrans (EM), occurs in two-thirds of patients and represents early localized disease. It presents as an expanding red patch that often shows central clearing. Epidermal changes such as scaling are absent, and vesicular or necrotic areas in the center of the lesion are present only rarely. The lesion is usually nonpruritic and may be accompanied by systemic symptoms including fever, myalgias, or malaise. A final diameter of 10 to 30 cm may be reached before fading occurs, which may take up to several weeks. As many as one-fourth of patients develop multiple EM lesions, which are generally smaller in size than the original lesion. These secondary lesions herald early disseminated disease, during which time dissemination to multiple organs, including the heart and central nervous system, may occur. Late disease is classically manifest by arthritis, primarily of the large joints.

Neisseria Meningitidis

Neisseria meningitidis is discussed in detail in Chapter 275. Skin lesions are found at presentation in 70% to 90% of patients with meningococcemia. The abrupt onset is characterized by fever, chills, malaise, and a rash that appears either purpuric or petechial in approximately half of patients (Fig. 275-1); other presentations include a nonspecific macular or papular eruption, and purpura fulminans, which has a poor prognosis (eFigs. 275.5 and 275.6). Less common morphologies include pustules or bullae. The purpuric lesions of meningococcemia are discrete, small, gray-purple papules that may be tender. The trunk and lower extremities are most commonly affected, and, left untreated, the rash progresses rapidly to purpura fulminans. Skin biopsy of purpuric lesions reveals leukocytoclastic vasculitis, with emboli containing gram-negative diplococci. Associated findings in patients with meningococcemia may include hypotension, nuchal rigidity, altered levels of consciousness, seizures, disseminated intravascular coagulation, and multiorgan failure.

Scarlet Fever

Scarlet fever, also known as scarlatina, is caused by toxin-producing strains of group A β-hemolytic streptococci as discussed in Chapter 285. The characteristic rash appears initially as tiny punctate red papules, which become confluent and spread to involve the entire body (Fig. 285-1). The rash has been likened to sandpaper or “sunburn with goose pimples.” Helpful diagnostic features include a perioral rim of sparing (circumoral pallor) and linear streaks of more intense erythema or petechiae in folds (Pastia’s lines), including the antecubital fossae and axillae. The enanthem includes an exudative pharyngitis, posterior soft palatal petechiae, and strawberry tongue. Resolution of the disease may be associated with desquamation, especially of distal extremities and digits.

Staphylococcal Scalded Skin Syndrome

Staphylococcal scalded skin syndrome (SSSS) is caused by exfoliative toxin-producing strains of S aureus and occurs mainly in children under 5 years old. The increased susceptibility of infants and young children may be related to immature mechanisms of renal clearance of the toxin. Predisposing factors in adults, in whom SSSS is rare, include renal failure, immunosuppression, and HIV infection. Most S aureus isolates causing SSSS belong to phage group II, types 71 and 55. Patients with SSSS usually have a primary infection at sites other than the skin, such as the nasopharynx, conjunctiva, middle ear, or umbilicus in neonates and the toxin is hematogenously disseminated. The toxin targets desmoglein 1, resulting in cleavage of the epidermis in a superficial location beneath the stratum corneum or stratum granulosum.24

Patients with SSSS usually present with fever, irritability, and tender erythema of the skin, most marked in flexural areas and around the mouth and nose. Perioral and periocular crusting with radial fissures is a characteristic feature (Fig. 367-8). Within 12 to 24 hours, flaccid blisters and superficial erosions form and may be followed by widespread superficial peeling of the skin in sheets, especially in infants (Fig. 367-9). Superficial separation of the skin after rubbing (Nikolsky sign) is present. Subsequent denudation of the skin with a moist, glistening, red surface at sites of prior blistering may lead to significant cutaneous fluid losses and secondary infection with resulting sepsis. Mucosal surfaces are spared. Older children may present with more mild forms of SSSS, with more localization of lesions and less toxicity. The differential diagnosis of SSSS in various stages may include toxic epidermal necrolysis, graft versus host disease, scarlet fever, toxic shock syndrome, and Kawasaki disease. In most cases the history, clinical presentation, and physical examination aid in the differentiation of SSSS from these entities. Although cultures of skin and blister fluid are characteristically negative, recovery of S aureus from the blood, nasopharynx, throat, or conjunctiva confirms the diagnosis of SSSS. Although SSSS can be a severe disease, the majority of affected children do well and recover without sequelae, and the mortality rate in children is low, around 3%. Antistaphylococcal antibiotics are a mainstay of therapy for SSSS. Clindamycin has the ability to inhibit toxin production and may therefore be advantageous over penicillin antibiotics.25 Older children with localized involvement and no toxicity may be managed as outpatients with oral antibiotics, but affected newborns and any patient with severe disease require hospitalization with parenteral antibiotic therapy and aggressive supportive management. Supportive measures include intravenous fluids, electrolyte management, impeccable wound care with minimal handling, and pain control.

Toxic Shock Syndrome

Toxic shock syndrome (TSS) is a toxin-mediated multisystem disease defined by the presence of fever, hypotension, and a diffuse rash with desquamation as well as clinical or laboratory abnormalities in three or more organ systems (see Chapter 284). The cause of TSS can be either toxin-producing strains of S aureus or group A streptococci. An important feature of streptococcal toxic-shock-like syndrome is the frequent association with a preceding skin or soft tissue infection as the portal of entry for the organism. Localized swelling and erythema, usually of an extremity, are the most common findings with this presentation. Cutaneous involvement in TSS presents as diffuse blanchable erythema, which may have a flexural accentuation. A papular “scarlatiniform” eruption may also be seen. Palms and soles are frequently involved and are among the most common sites for desquamation to occur, usually 1 to 2 weeks into the course of the disease.

Kawasaki Disease

Kawasaki disease does not have a proven infectious etiology, but even though speculative any discussion of infectious exanthems must include the disorder, given its protean cutaneous manifestations and potential for serious morbidity and mortality. A detailed discussion of Kawsaki disease is found in Chapter 488. Characteristics of Kawasaki disease include fever for more than 5 days, nonpurulent conjunctival injection, oropharyngeal changes, peripheral extremity changes, cervical lymphadenopathy, and a polymorphous rash. The rash of Kawasaki disease usually consists of polymorphous erythematous macules, patches, and plaques with a diffuse distribution. Desquamation is usually a feature later in the course, and is most notable over the distal extremities, hands, and feet, as well as in periungual locations. Accentuation of the eruption may be noted in the perineum and is often accompanied or soon followed by desquamation as well. Other reported patterns of the rash include morbilliform or scarlatiniform lesions and, occasionally, pustules. Blisters, epidermal changes (such as erosions or crusting), petechiae, and purpura are not characteristic of the rash of Kawasaki disease. The hands and feet often reveal edema, erythema, and induration.

Candida

Candida species may cause infection of mucosal epithelia, skin, and nail plates, and, although not a component of normal skin flora, favors warm, moist regions such as the diaper region, intertriginous zones, web spaces between fingers and toes, and the corners of the mouth. Part of normal oral and intestinal flora, Candida albicans is the most common pathogen. Most candidal infections are noninvasive and limited, although invasive candidal infections are seen with increasing frequency in the settings of immunosuppression, HIV infection, diabetes, and prematurity. Diagnosis of cutaneous candidal infections is made on clinical grounds, in conjunction with fungal culture and potassium hydroxide (KOH) examination, which reveals budding yeasts and pseudohyphae.

Diaper candidiasis may occur as a primary process or, more commonly, as a secondary infection in the setting of a primary irritant contact dermatitis. Predisposing factors include oropharyngeal candidiasis, diarrhea, and antibiotic therapy. Intense perianal and flexural erythema, sometimes with maceration, followed by the development of superficial pustules is the most common presentation. Spread is accomplished via “satellite lesions” of erythematous papules and papulopustules at the periphery of the erythema. The genitalia, inferior abdomen, inner thighs, perineum, and buttocks may all eventually be involved. In male infants, involvement of the glans penis (candidal balanitis) (Fig. 367-10) is common, as is involvement of the scrotum, which helps differentiate candidiasis from tinea cruris. Involvement of the inguinal creases helps distinguish candidiasis from irritant contact dermatitis, in which the fold regions are often spared.

Management of diaper candidiasis includes frequent diaper changes, diaper-free periods where feasible, protective barrier pastes or ointments, and topical antifungal agents, including nystatin or imidazole antifungals (econazole, ketoconazole, clotrimazole, miconazole). Low-potency topical corticosteroids, such as hydrocortisone, may be a useful adjunct to help decrease associated inflammation, but combination steroid-antifungal preparations should be avoided in the diaper area. Secondary bacterial infection may need to be considered, especially in recalcitrant cases or those with a vesiculobullous or erosive component. Although sometimes advocated because Candida species are known to colonize the intestine, the effectiveness of concomitant oral antifungal therapy remains unproven.

Oropharyngeal candidiasis, or thrush, is infection of the oral cavity with C albicans. This is most commonly acquired during passage through an infected birth canal or during nursing from the skin of an infected breast. Left untreated, most cases of oropharyngeal candidiasis will resolve spontaneously, although this may require 4 to 8 weeks. Although frequently asymptomatic in immunocompetent children, occasional infants with thrush may experience pain and impairment of sucking and swallowing, which may ultimately progress to candidal esophagitis and nutritional compromise.

Oropharyngeal candidiasis presents as white to gray patches, which may form “pseudomembranes” composed of epithelial cells, white blood cells, food debris, and yeast forms that cover the buccal mucosae, tongue, and gingivae. Less common sites of involvement include the soft palate, uvula, and tonsils. Removal of the patches by scraping with a tongue depressor reveals an erythematous, eroded base; a KOH examination reveals ovoid yeast forms and pseudohyphae. Treatment consists of topical nonabsorbable antifungal agents such as nystatin, miconazole, or clotrimazole applied four times daily. Oral fluconazole has been found effective in the treatment of oropharyngeal candidiasis in immunocompromised children.26

Congenital candidiasis, a rare entity, is a benign infection in the full-term infant, but life-threatening in the premature newborn. Organisms gain entry to the amniotic fluid from a colonized vagina. Presentation is during the first week, and usually the first few days, of life. The placenta and/or umbilical cord of affected infants may reveal white-yellow plaques.27,28 Invasive candidiasis, including sepsis, pneumonitis, and renal and central nervous system infection, is more likely in premature neonates and is associated with a poor prognosis.

Cutaneous lesions of congenital candidiasis, which are present in up to one half of patients, may be diffuse, intensely erythematous macules and papules involving the trunk and extremities, often with sparing of the diaper area; a papulopustular eruption with erosions and possible involvement of the palms and soles that then resolves with desquamation; or a burnlike dermatitis (mainly in extremely low birth weight premature infants). Oral thrush and nail dystrophy may be present, with isolated nail changes occasionally being the sole mucocutaneous manifestation. Bullae are rarely present. Topical antifungal therapy is usually sufficient for skin-limited disease, but intravenous amphotericin B, sometimes in combination with 5-flucytosine, fluconazole or caspofungin are indicated with evidence of respiratory compromise, other signs of disseminated infection or in the premature infant with systemic infection.27

Chronic paronychia is a long-standing infection of the skin folds surrounding the nails that is usually caused by C albicans, although a mixed infection with Candida species and bacteria may often be present. Periungual erythema, cuticle loss, and transverse ridging of the nail plate are the presenting signs. Other nail changes may include yellow discoloration and thickening. Pain, purulence, and discharge are usually absent. The diagnosis may be confirmed by the finding of budding yeasts and pseudohyphae on KOH examination or via culture. Avoidance of moisture, which favors growth of yeast cells, and application of topical antifungal creams are the mainstays of therapy. A combination steroid-antifungal cream such as triamcinolone-nystatin (Mycolog II) is also effective and oral antifungal treatment may be necessary in severe cases.

Angular cheilitis (perlèche) is characterized by erythema, fissuring, and crusting at the mouth angles. Predisposing conditions include any situation that results in excessive moisture collecting in these areas, such as frequent drooling, lip licking, and use of orthodontic appliances. Differential diagnosis includes contact dermatitis and nutritional deficiency (riboflavin, zinc, or biotin). C albicans is usually present, and concomitant bacterial infection may also occur. Therapy is aimed at correcting predisposing conditions, treating infection with topical antifungal (and antibacterial, if necessary) agents, and applying thick barrier ointments to decrease further exposure to moisture and subsequent maceration. Low-strength topical corticosteroid ointments may be helpful in patients with significant inflammation.

Tinea Versicolor

Tinea versicolor is a superficial skin infection caused by the dimorphic lipophilic fungus Malassezia furfur, also known as Pityrosporum ovale and Pityrosporum orbiculare, depending on the form of the yeast phase. This organism is a lipid-dependent yeast that is part of normal human skin flora in 90% to 100% of individuals. Although most cases occur during the postpubertal period, tinea versicolor may occasionally occur in prepubertal children. Infection localizes to areas of skin that are rich in lipid-producing sebaceous glands, including the chest, back, and face.

Tinea versicolor occurs when the yeast form of the organism converts to the mycelial form, a transition that may be prompted by various predisposing factors, including heat, humidity, sweating, and skin occlusion. Individual host susceptibility and immunosuppression may also play a role. The most common clinical findings are sharply demarcated, hypopigmented macules and patches that may have associated fine scaling (Fig. 367-11). Other presentations include hyperpigmented or erythematous patches, particularly in dark-skinned individuals. Pruritus is occasionally present. The hypopigmented areas become more noticeable after unprotected sun exposure, caused by uneven tanning of the surrounding uninvolved skin. The hypopigmentation seen in tinea versicolor is attributed to a product of the fungus, azelaic acid, which inhibits dopa-tyrosinase, an enzyme involved in the melanin synthetic pathway.

Differential diagnosis of tinea versicolor includes pityriasis alba and vitiligo. Pityriasis alba is most common on the face, and patients often have an associated atopic diathesis. Vitiligo results in complete depigmentation and is most common in periorificial regions (around the eyes, mouth, and genitalia) and over bony prominences. Scaling is usually minimal to absent in these two disorders.29 Other differential diagnoses include psoriasis, seborrheic dermatitis, dermatophyte infection, and confluent and reticulate papillomatosis of Gougerot and Carteaud. In darkly pigmented patients, hypopigmented lesions of cutaneous T-cell lymphoma must be considered, especially in cases with an unusual distribution or a history of recalcitrance to therapy.

Potassium hydroxide (KOH) examination of scrapings from lesions of tinea versicolor reveals numerous clusters of spores and short, stubby hyphae, the so-called pattern of “spaghetti and meatballs.” Culture is not useful because M furfur is a normal skin inhabitant.

There are several treatment options, both topical and oral. Either selenium sulfide 2.5% or ketoconazole 2% shampoo can be applied to the affected areas and left on for 5 to 10 minutes prior to rinsing, for 1 to 2 weeks.30 Topical antifungal agents may be effective, but are often limited by the widespread involvement and hence the need to apply large amounts of the medication. The allylamine antifungal terbinafine in a 1% spray has been approved for treatment of tinea versicolor in patients 12 years of age and older. Oral antifungal agents are also quite effective and may be helpful in severe or recurrent cases of tinea versicolor. Fluconazole, itraconazole, and ketoconazole have all been demonstrated to be effective in a variety of dosage regimens.31-34 One oral regimen is fluconazole in an adult dose of 300 mg once weekly for 2 weeks.31 Drug delivery to the skin may be augmented by exercise following oral ingestion, and showering should be avoided for 12 hours to maximize the effect.

The treatment of dermatophyte infections is outlined in Table 367-3.

Tinea Capitis

Tinea capitis is the most common of the cutaneous mycoses in children. It occurs worldwide and in all age groups, although prepubertal children older than 6 months are most commonly affected, with a higher incidence in African Americans and Hispanics.

Tinea capitis is caused by dermatophytes in the genera Microsporum and Trichophyton. In the United States, the most common etiologic agent is the anthropophilic (human-to-human) organism Trichophyton tonsurans, with occasional infections caused by the zoophilic (animal-to-human) organism Microsporum canis, usually acquired from infected puppies or kittens. Microsporum audounii, another anthropophilic organism that was once one of the main causes of tinea capitis in this country, is now rarely implicated. The disease is spread easily from child to child as well as via infected fomites, including hair brushes, combs, furniture, and clothing. The asymptomatic carrier state is a significant problem, especially among family members of infected children, and is an important consideration in terms of reinfection of the patient and spread to other individuals.

The clinical presentation of tinea capitis is variable. Erythematous papules, plaques, and patches are common, and pustules and crusting may also be present. Subtle scaling of the scalp without inflammation or alopecia may be confused with seborrheic dermatitis, resulting in a delay in diagnosis. A significant pustular eruption may mimic an acute bacterial pyoderma. Alopecia is frequently present; one distinct form, so-called black dot tinea, is marked by multiple tiny black dots at the skin surface, representing broken hair shafts (Fig. 367-12). A marked host inflammatory reaction to the infectious agent, which is often one of the zoophilic organisms, is called a kerion, which presents as a boggy, tender, edematous plaque with crusting and alopecia. Secondary bacterial infection may complicate healing. Cervical or suboccipital lymphadenopathy may be present in any of the forms of tinea capitis.

Fungal culture and direct microscopic examination are most useful in diagnosing tinea capitis. Because the majority of cases are caused by the nonfluorescing endothrix (arthroconidia inside the hair shaft only) organism T tonsurans, Wood’s lamp examination is rarely helpful. In the occasional case caused by an ectothrix (arthroconidia inside and outside the hair shaft) organism, Wood’s lamp examination reveals bright green fluorescence of the hair. KOH examination of scale or hairs reveals characteristic branching, septate hyphae, and the presence of arthroconidia within or on the outside of infected hairs. Specimens for KOH examination may be obtained by gentle scraping with a no. 15 scalpel blade, gentle hair removal (preferably from an area of broken hairs) with a forceps, or the use of a moistened gauze pad to rub the scalp, with the ultimate transfer of broken hairs and scale from the gauze to the slide with a forceps. The KOH examination may be difficult (with a fairly high percentage of false negatives) in tinea capitis and is often negative in extremely inflammatory presentations, such as kerions.

Fungal culture is the gold standard for diagnosis of tinea capitis, and specimens may be obtained by vigorously rubbing a cotton swab, sterile disposable toothbrush, or cytobrush over both affected and apparently unaffected areas. These swabs are then plated on fungal culture media, such as Dermatophyte Test Medium (DTM), which has a color indicator with positive cultures, or Mycosel agar. The cotton swab technique has been shown to be very reliable, even with a delay in transport and/or plating of the culture.35 The cytobrush method has also been shown to yield very accurate results.36 After plating, the caps are loosely placed on the culture bottles to allow for gas exchange, and the bottles incubated for 3 to 4 weeks before deemed negative for growth.

The specifics of therapy for tinea capitis are outlined in Table 367-3. Topical therapy is ineffective due to involvement of hair follicles, and systemic therapy is the treatment of choice. Patients may have a clinical cure without a true mycologic cure, and therefore, treatment should be continued until a repeat fungal culture is negative. Premature discontinuation of therapy is likely to lead to a relapse of infection. Because of the high contagiousness of tinea capitis, therapy should be instituted in a timely fashion and, in some cases, empirically if the clinical presentation is highly suggestive and other diagnoses seem unlikely. A diffuse, pruritic, papular eruption referred to as a dermatophytid (id) reaction may be seen in patients with tinea capitis. This represents immune hyperreactivity to fungal antigen and may show widespread skin involvement concomitant with the beginning of therapy. It is treated symptomatically with topical corticosteroids and oral antihistamines and should not be confused with a drug hypersensitivity reaction.37

Tinea Corporis

Tinea corporis, or “ringworm,” may occur on any part of the body. T tonsurans (most common), Trichophyton rubrum, and Trichophyton mentagrophytes are causative agents. An erythematous papule that expands to form a larger, scaly, erythematous plaque is the usual presentation. Central clearing often occurs, resulting in annular lesions. Less common findings include vesicles, pustules, bullae, or crusting. Pruritus is variable. Lesions vary from a few millimeters to several centimeters in size and may range in number from one to several. Numerous lesions are uncommon, except for in the immunocompromised population. Involvement of hair follicles leads to a granulomatous inflammatory response with papules called Majocchi granuloma. Tinea faciei, a dermatophyte infection of the face, may present with prominent erythema and less scaling than typical of tinea corporis. When located over hairy areas, vesicles, pustules, and crusting may develop. Diagnosis is often delayed, and oral therapy is often necessary to adequately eradicate tinea faciei.

The differential diagnosis of tinea corporis includes nummular dermatitis, psoriasis, and erythema annulare centrifugum. Erythema chronicum migrans (Lyme disease) and granuloma annulare, although they may present with annular lesions, usually lack the epidermal changes present in tinea. The herald patch of pityriasis rosea is frequently confused with tinea corporis. The subsequent appearance of the Christmas tree pattern of secondary lesions establishes the diagnosis of pityriasis rosea; alternatively, the “trailing scale” on the inner side of the lesion may distinguish pityriasis rosea from tinea, in which case the scale is usually around the periphery and pointing outward.

Diagnosis of tinea corporis is accomplished via the demonstration of hyphae on KOH examination or by fungal culture. In obtaining the material for these examinations, the ideal site for sampling is the scale found at the advancing border of the plaques, which generally contains the highest concentration of fungal organisms.

Tinea Pedis and Tinea Manuum

Dermatophyte infection of the feet (tinea pedis) and hands (tinea manuum) is more common in adults, but does occur in pediatric patients. The most common organism implicated is T rubrum. Tinea pedis is related to the wearing of shoes, which contributes to an environment (warmth, moisture) that favors growth of dermatophyte fungi. Clinical findings vary from mild asymptomatic peeling to pruritic erythema and scaling in a “moccasin” distribution. Deep-seated vesicles may be present, and erythema and maceration of the toe web spaces are common. Bullae rarely occur and are most common in response to infection with a zoophilic organism. Tinea manuum, with palmar scaling and mild erythema, is often accompanied by tinea pedis in the “one hand, two feet” distribution. Finger web spaces are usually spared, and vesicles or pustules are occasionally present. When involvement of the dorsal hand occurs, the presentation is more similar to tinea corporis with well-demarcated, scaly, red plaques. The diagnosis of tinea pedis or manuum is established by a positive KOH preparation or fungal culture.

Onychomyocosis

Onychomycosis is a dermatophyte infection of the nail plate. It is uncommon in young children and has an increasing incidence with increasing age. Predisposing factors include nail trauma, immunosuppression, long-term therapy with corticosteroids, concomitant presence of tinea pedis, and family history of onychomycosis. The most commonly isolated organisms are T rubrum and T mentagrophytes, and diagnosis is confirmed either by direct microscopy with KOH examination or fungal culture. The differential diagnosis of onychomycosis includes psoriasis, lichen planus, contact dermatitis, trauma, and pachyonychia congenita.

There are several presentations of onychomycosis. The distal subungual form is the most common and presents with onycholysis (separation of the nail plate from the nail bed) and subungual thickening with debris at the distal (free) end of the nail. In the proximal subungual form, subungual thickening and leukonychia (white nail discoloration) occur in the proximal (near the cuticle) portion of the nail. White superficial onychomycosis presents as occurs when the fungus invades the superficial layers of the nail and results in white islands on the nail plate, which coalesce and spread with progression of the disease. Candida spp may cause a chronic paronychia (see the discussion on Candida). Successful treatment of dermatophyte infections of the nail generally requires the administration of systemic antifungal agents, as outlined in Table 367-3.