Nonbullous Impetigo

Nonbullous impetigo accounts for > 70% of cases. Lesions typically begin on the skin of the face or on extremities that have been traumatized. The most common lesions that precede nonbullous impetigo are insect bites, abrasions, lacerations, chickenpox, scabies pediculosis, and burns. A tiny vesicle or pustule forms initially and rapidly develops into a honey-colored crusted plaque that is generally <2 cm in diameter (Fig. 657-1). The infection may be spread to other parts of the body by the fingers, clothing, and towels. Lesions are associated with little to no pain or surrounding erythema, and constitutional symptoms are generally absent. Pruritus occurs occasionally, regional adenopathy is found in up to 90% of cases, and leukocytosis is present in about 50%.

Figure 657-1 Multiple crusted and oozing lesions of impetigo.

Bullous Impetigo

Bullous impetigo is mainly an infection of infants and young children. Flaccid, transparent bullae develop most commonly on skin of the face, buttocks, trunk, perineum, and extremities. Neonatal bullous impetigo can begin in the diaper area. Rupture of a bulla occurs easily, leaving a narrow rim of scale at the edge of shallow, moist erosion. Surrounding erythema and regional adenopathy are generally absent. Unlike those of nonbullous impetigo, lesions of bullous impetigo are a manifestation of localized staphylococcal scalded skin syndrome and develop on intact skin.

Differential Diagnosis

The differential diagnosis of nonbullous impetigo includes viruses (herpes simplex, varicella-zoster), fungi (tinea corporis, kerion), arthropod bites, and parasitic infestations (scabies, pediculosis capitis), all of which may become impetiginized.

The differential diagnosis of bullous impetigo in neonates includes epidermolysis bullosa, bullous mastocytosis, herpetic infection, and early scalded skin syndrome. In older children, allergic contact dermatitis, burns, erythema multiforme, linear immunoglobulin (Ig) A dermatosis, pemphigus, and bullous pemphigoid must be considered, particularly if the lesions do not respond to therapy.

Etiology

Cellulitis is characterized by infection and inflammation of loose connective tissue, with limited involvement of the dermis and relative sparing of the epidermis. A break in the skin due to previous trauma, surgery, or an underlying skin lesion predisposes to cellulitis. Cellulitis is also more common in individuals with lymphatic stasis, diabetes mellitus, or immunosuppression.

Streptococcus pyogenes and S. aureus are the most common etiologic agents. In patients who are immunocompromised or have diabetes mellitus, a number of other bacterial or fungal agents may be involved, notably Pseudomonas aeruginosa; Aeromonas hydrophila and, occasionally, other Enterobacteriaceae; Legionella spp.; the Mucorales, particularly Rhizopus spp., Mucor spp., and Absidia spp.; and Cryptococcus neoformans. Children with relapsed nephrotic syndrome may experience cellulitis due to Escherichia coli. In children age 3 mo to 3-5 yr, Haemophilus influenzae type b was once an important cause of facial cellulitis, but its incidence has declined significantly since the institution of immunization against this organism.

Clinical Manifestations

Cellulitis manifests clinically as an area of edema, warmth, erythema, and tenderness. The lateral margins tend to be indistinct because the process is deep in the skin, primarily involving the subcutaneous tissues in addition to the dermis. Application of pressure may produce pitting. Although distinction cannot be made with certainty in any particular patient, cellulitis due to S. aureus tends to be more localized and may suppurate, whereas infections due to S. pyogenes (group A streptococci) tend to spread more rapidly and may be associated with lymphangitis. Regional adenopathy and constitutional signs and symptoms such as fever, chills, and malaise are uncommon. Complications of cellulitis are common but include subcutaneous abscess, bacteremia, osteomyelitis, septic arthritis, thrombophlebitis, endocarditis, and necrotizing fasciitis. Lymphangitis or glomerulonephritis can also follow infection with S. pyogenes.

Diagnosis

Aspirates from the site of inflammation, skin biopsy, and blood cultures allow identification of the causal organism in about 25% of cases of cellulitis. Yield of the causative organism is approximately 30% when the site of origin of the cellulitis is apparent, such as an abrasion or ulcer. An aspirate taken from the point of maximum inflammation yields the causal organism more often than a leading-edge aspirate. Lack of success in isolating an organism stems primarily from the low number of organisms present within the lesion.

Treatment

Empirical therapy for cellulitis should be directed by the history of the illness, the location and character of the cellulitis, and the age and immune status of the patient. Cellulitis in a neonate should prompt a full sepsis evaluation, followed by initiation of empirical intravenous therapy with a β-lactamase–stable antistaphylococcal antibiotic such as methicillin or vancomycin and an aminoglycoside such as gentamicin or a cephalosporin such as cefotaxime. Treatment of cellulitis in an infant or child younger than about 5 yr should provide coverage for S. pyogenes and S. aureus as well as H. influenzae type b and S. pneumoniae. The evaluation should include a blood culture, and if the infant is younger than 1 yr, if signs of systemic toxicity are present, or if an adequate examination cannot be carried out, a lumbar puncture should also be performed. In most cases of cellulitis on an extremity, regardless of age, S. aureus and S. pyogenes are the cause and bacteremia is highly unlikely in an otherwise well-appearing child. Blood cultures should be performed if sepsis is suspected.

If fever, lymphadenopathy, and other constitutional signs are absent (white blood cell count < 15,000), treatment of cellulitis on an extremity may be initiated orally on an outpatient basis with a penicillinase-resistant penicillin such as dicloxacillin or cloxacillin or a first-generation cephalosporin such as cephalexin or, if MRSA is suspected, with clindamycin. If improvement is not noted or the disease progresses significantly in the first 24-48 hr of therapy, parenteral therapy is necessary. If fever, lymphadenopathy, or constitutional signs are present, parenteral therapy should be initiated. Oxacillin or nafcillin is effective in most cases, although if systemic toxicity is significant, consideration should be given to the addition of clindamycin or vancomycin. Once the erythema, warmth, edema, and fever have decreased significantly, a 10-day course of treatment may be completed on an outpatient basis. Immobilization and elevation of an affected limb, particularly early in the course of therapy, may help reduce swelling and pain.

Etiology

Necrotizing fasciitis is a subcutaneous tissue infection that involves the deep layer of superficial fascia but largely spares adjacent epidermis, deep fascia, and muscle.

Relatively few organisms possess sufficient virulence to cause necrotizing fasciitis when acting alone. The majority (55-75%) of cases of necrotizing fasciitis are polymicrobial in nature, with an average of 4 different organisms isolated. The organisms most commonly isolated in polymicrobial necrotizing fasciitis are S. aureus, streptococcal species, Klebsiella species, E. coli, and anaerobic bacteria.

The rest of the cases and the most fulminant infections, associated with toxic shock syndrome and a high case fatality rate, are usually caused by S. pyogenes (Chapter 176). Streptococcal necrotizing fasciitis may occur in the absence of toxic shock–like syndrome and is potentially fatal and associated with substantial morbidity. Necrotizing fasciitis can occasionally be caused by S. aureus; Clostridium perfringens; Clostridium septicum; P. aeruginosa; Vibrio spp., particularly Vibrio vulnificus; and fungi of the order Mucorales, particularly Rhizopus spp., Mucor spp., and Absidia spp. Necrotizing fasciitis has also been reported on rare occasions to result from non–group A streptococci such as group B, C, F, or G streptococci, S. pneumoniae, or H. influenzae type b.

Infections due to any one organism or combination of organisms cannot be distinguished clinically from one another, although development of crepitance signals the presence of Clostridium spp. or gram-negative bacilli such as E. coli, Klebsiella, Proteus, or Aeromonas.

Clinical Manifestations

Necrotizing fasciitis may occur anywhere on the body. Polymicrobial infections tend to occur on perineal and trunk areas. The incidence of necrotizing fasciitis is highest in hosts with systemic or local tissue immunocompromise, such as those with diabetes mellitus, neoplasia, or peripheral vascular disease as well as those who have recently undergone surgery, who abuse intravenous drugs, or who are undergoing immunosuppressive treatment, particularly with corticosteroids. The infection can also occur in healthy individuals after minor puncture wounds, abrasions, or lacerations; blunt trauma; surgical procedures, particularly of the abdomen, gastrointestinal or genitourinary tracts, or the perineum; or hypodermic needle injection.

Since the mid-1980s, there has been a resurgence of fulminant necrotizing soft tissue infections due to S. pyogenes, which may occur in previously healthy individuals. Streptococcal necrotizing cellulitis is classically located on an extremity. There may be a history of recent trauma to or operation in the area. Necrotizing fasciitis due to S. pyogenes may also occur after superinfection of varicella lesions. Children with this disease have tended to display onset, recrudescence, or persistence of high fever and signs of toxicity after the 3rd or 4th day of varicella. Common predisposing conditions in neonates are omphalitis and balanitis after circumcision.

Necrotizing fasciitis begins with acute onset of local swelling, erythema, tenderness, and heat. Fever is usually present, and pain, tenderness, and constitutional signs are out of proportion to cutaneous signs, especially with involvement of fascia and muscle. Lymphangitis and lymphadenitis may be absent. The infection advances along the superficial fascial plane, and initially there are few cutaneous signs to herald the serious nature and extent of the subcutaneous tissue necrosis that is occurring. Skin changes may appear over 24-48 hr as nutrient vessels are thrombosed and cutaneous ischemia develops. Early clinical findings include ill-defined cutaneous erythema and edema that extends beyond the area of erythema. Additional signs include formation of bullae filled initially with straw-colored and later bluish to hemorrhagic fluid, and darkening of affected tissues from red to purple to blue. Skin anesthesia and, finally, frank tissue gangrene and slough develop owing to the ischemia and necrosis. Vesiculation or bulla formation, ecchymoses, crepitus, anesthesia, and necrosis are ominous signs indicative of advanced disease. Children with varicella lesions may initially show no cutaneous signs of superinfection with invasive S. pyogenes, such as erythema or swelling. Significant systemic toxicity may accompany necrotizing fasciitis, including shock, organ failure, and death. Advance of the infection in this setting can be rapid, progressing to death within hours. Patients with involvement of the superficial or deep fascia and muscle tend to be more acutely and systemically ill and have more rapidly advancing disease than those with infection confined solely to subcutaneous tissues above the fascia. In an extremity, a compartment syndrome may develop, manifesting as tight edema, pain on motion, and loss of distal sensation and pulses; this is a surgical emergency.

Diagnosis

Definitive diagnosis of necrotizing fasciitis is made by surgical exploration, which should be undertaken as soon as the diagnosis is suspected. Necrotic fascia and subcutaneous tissue are gray and offer little resistance to blunt probing. Although MRI aids in delineating the extent and tissue planes of involvement, this procedure should not delay surgical intervention. Frozen-section incisional biopsy specimens obtained early in the course of the infection can aid management by decreasing the time to diagnosis and helping establish margins of involvement. Gram staining of tissue can be particularly useful if chains of gram-positive cocci, indicative of infection with S. pyogenes, are seen.

Treatment

Early supportive care, surgical debridement, and parenteral antibiotic administration are mandatory for necrotizing fasciitis. All devitalized tissue should be removed to freely bleeding edges, and repeat exploration is generally indicated within 24-36 hr to confirm that no necrotic tissue remains. This procedure may need to be repeated on several occasions until devitalized tissue has ceased to form. Meticulous daily wound care is also paramount.

Parenteral antibiotic therapy should be initiated as soon as possible with broad-spectrum agents against all potential pathogens. Initial empirical therapy should be instituted with vancomycin, linezolid, daptomycin, or quinupristin to cover gram-positive and quinolones to cover gram-negative organisms. Therapy should then be based on sensitivity of isolated organisms.

Prognosis

The combined case fatality rate among children and adults with necrotizing fasciitis and toxic shock–like syndrome due to S. pyogenes has been as high as 60%. Death is less common in children, however, and in cases not complicated by toxic shock–like syndrome.