S aureus

S aureus is the most common culture-confirmed pathogen from SSSIs in the United States. S aureus has a propensity to cause abscesses in any tissue/organ, most commonly the skin. Approximately 25% to 40% of the US children and adults are permanently colonized or are transient carriers of S aureus . Children presenting with purulent SSSIs have a high rate of S aureus nasal colonization. The medical burden of SSSIs, particularly abscesses, has increased nationwide since the emergence of community-acquired (CA) methicillin-resistant S aureus (MRSA). This seems to be driven by additional MRSA cases as opposed to replacement of methicillin-sensitive S aureus (MSSA) with MRSA. In the United States, the predominant clone is USA300, which has now spread from the community into hospitals. US pediatric hospital admissions for SSSIs doubled (0.46% vs 1.01%) from 1997 to 2009, elevating SSSIs from the 21st most common pediatric discharge in 1997 to ninth most common in 2009. ED visits for SSSIs have also increased, from 1.2 million visits in 1993 to 3.4 million in 2005.

S pyogenes

Just as S aureus represents the dominant cause of cutaneous abscesses, S pyogenes causes most nonpurulent SSSIs, such as cellulitis or erysipelas. Infections with S pyogenes are frequent in daily practice but often underrepresented in epidemiologic studies because mild or superficial streptococcal cellulitis is often managed in the outpatient setting without culture confirmation. According to the SENTRY antimicrobial surveillance program (covering both the United States and Canada), beta-hemolytic Streptococcus represents the seventh most common cause (4.1% of isolates) of SSSI in the United States ( S aureus accounted for 44.6% of isolates, 35.9% of which were MRSA). However, since the 1980s, severe S pyogenes necrotizing fasciitis has been increasingly reported in the United States and worldwide.

S aureus

CA-MRSA is not a single microbiological entity but the term for a collection of S aureus clones containing the mobile genetic element, staphylococcal chromosome cassette (SSC) carrying the gene ( mecA ) encoding an altered penicillin binding protein conferring resistance to methicillin and antistaphylococcal β-lactams. CA-MRSA also commonly contains the lukS-PV and lukF-PV genes encoding the Panton-Valentine leukocidin (PVL), a pore-forming toxin associated with deep-seated tissue infection and necrotizing pneumonia. PVL is found less commonly among HA-MRSA or MSSA strains, and might contribute to disease pathogenesis.

S pyogenes

S pyogenes (group A Streptococcus ) is distinguished from other beta-hemolytic streptococci by its carbohydrate cell wall antigens. Subtypes of S pyogenes can be distinguished by the M protein antigens (encoded by the emm gene) in its cell wall, which serve as virulence factors. Most cases of S pyogenes SSSI are caused by strains producing at least one streptococcal pyrogenic exotoxin (A, B, or C). Despite these known virulence factors, the wide spectrum of disease severity associated with S pyogenes suggests that differences in host defense mechanisms likely play a major role in the development of invasive disease.

Cutaneous Abscess

Cutaneous abscesses are localized collections of pus in cavities formed by necrosis or disintegration of tissue within the dermis and subcutaneous fat. They are painful, tender nodules progressing to fluctuant protruding pustules, often surrounded by a rim of erythematous swelling. Buttock abscesses are most frequently encountered in preschool children, whereas extremity abscesses are most frequently found in older children. S aureus , especially CA-MRSA, is now the most common cause of cutaneous abscesses in the United States.

Folliculitis, Furuncles, and Carbuncles

Folliculitis results from inflammation of hair follicles, manifesting as clusters of small erythematous papules or pustules. Inflammation is superficial and pus is only present in the epidermis. The sites most commonly affected include the scalp, extremities, and perioral and paranasal regions, as well as areas of the skin that are occluded or prone to moisture and friction, such as the axillae or medial thighs. Sycosis barbae is a severe, painful, deep, recurrent form of facial folliculitis caused by S aureus that occurs mainly in young African American men. Inflammation involves the entire depth of the hair follicle. Painful papules and pustules can coalesce into plaques that recur after healing with scarring.

Furuncles (or boils) result from folliculitis that extends through the dermis into the subcutaneous tissue. Furunculosis is uncommon in early childhood but the incidence increases in adolescents, particularly those living in crowed conditions with poor hygiene. These painful abscesses can occur anywhere on hairy skin, and are most often located on the scalp, buttocks, or extremities. Severe lesions may heal with scarring ( Fig. 2 A ).

Common SSSI. ( A ) Furuncle, ( B ) Non-bullous impetigo, ( C ) Impetiginized herpetic lesions, ( D ) Cellulitis, ( E ) Ecthyma, ( F ) Staphylococcal Scalded Skin Syndrome, ( G ) Acute paronychia.

Carbuncles consist of groups of furuncles characterized by multiple drainage points and inflammatory changes in the surrounding connective tissue. Carbuncles are commonly found on areas of thickening skin such as the nape of the neck, the back, or the thighs. Fever and systemic symptoms are often present and lesions usually heal with scarring.

Impetigo

Impetigo is a common and highly contagious bacterial infection of the superficial layers of the epidermis. Peak incidence is in children aged 2 to 5 years, although older children may also be affected. It occurs most frequently among economically disadvantaged children in hot and humid regions but is also prevalent in northern climates, particularly in the summer and late fall. Colonization of skin ( S pyogenes ) or nares ( S aureus ) typically precedes the development of impetigo. It usually occurs on exposed areas of the body, such as the face and extremities. Although regional lymphadenitis might occur, systemic symptoms are usually absent. Impetigo is most often caused by S aureus and S pyogenes ; there are no discerning features distinguishing these organisms. Diagnosis can be confirmed by culture of the base of the lesion after removal of the crust or from the intact bullae (see Fig. 2 B, C).

Suppurative complications of streptococcal impetigo are uncommon (2%–5% of cases). Cutaneous infections with nephritogenic strains of S pyogenes are the major antecedent of poststreptococcal glomerulonephritis; however, there are no conclusive data that treatment of streptococcal pyoderma prevents nephritis. Acute rheumatic fever is not a sequela of impetigo.

Nonbullous impetigo accounts for almost 70% of cases, most commonly on the face and limbs. The predominant overall cause is S aureus , and S pyogenes is particularly unusual in children younger than 2 years of age. Lesions begin as papules that rapidly evolve into vesicles surrounded by an area of erythema progressing to the characteristic honey-crusted exudate. Lesions are usually painless and gradually enlarge and break down over a period of 4 to 6 days to form thick crusts. If left untreated the lesions heal slowly, resolving in approximately 2 weeks without scaring.

Bullous impetigo can appear as clusters of bullae or as a solitary, exudative lesion. Bullous impetigo is caused by toxin-producing strains of S aureus , usually from a strain producing exfoliative exotoxin A and B, which can be isolated from bullous lesions. At first, superficial vesicles rapidly enlarge to form flaccid bullae filled with clear yellow fluid, which can darken to become turbid and sometimes purulent. Lesions often coalesce to form large, reddish plaques, particularly around the oronasal orifices. Bullae may rupture, often leaving a thin brown crust resembling lacquer. Constitutional symptoms are more likely to occur than with nonbullous impetigo.

Cellulitis

Cellulitis is an acute infection involving primarily the dermis and subcutaneous tissues. S pyogenes was classically reported as the main cause but over the past decade numerous reports have noted the increasing prevalence of MRSA, particularly when associated with furuncles, carbuncles, or abscess (ie, purulent cellulitis). Streptococci cause diffusely spreading infections, whereas S aureus cellulitis tends to be more localized, often surrounding a purulent lesion (see Fig. 2 D).

Lesions are characterized by edema, pain, tenderness, warmth, erythema, and spreading with irregular margins. Cellulitis may be accompanied by lymphangitis and lymphadenopathy. Most commonly, cellulitis occurs in the lower extremities preceded by clinically unapparent local skin trauma. In children, approximately 25% of cellulitis cases are associated with abscess and roughly 1% with osteomyelitis. Vesicles, bullae, and cutaneous hemorrhagic manifestations such as petechiae or ecchymoses may develop on the inflamed skin. If widespread and associated with systemic toxicity, a deeper infection such as necrotizing fasciitis should be considered ( Box 1 ).

Although cellulitis can occur at virtually any cutaneous surface, there are specific anatomic locations that result in characteristic infections with shared epidemiology, pathophysiology, and clinical presentation:

• •
  

  Perianal cellulitis is associated with rectal pain, pruritus, and sharply circumscribed perianal erythema. It is most often caused by S pyogenes and has a peak incidence between the ages of 3 and 5 years. Perianal cellulitis can be complicated by abscess formation and development of anal fissures. Perianal streptococcal dermatitis has been reported to be an infectious trigger for guttate psoriasis; patients presenting with guttate psoriasis should be examined for asymptomatic S pyogenes infection.

  
  
• •
  

  Periorbital (preseptal) cellulitis is an infection of tissues anterior to the orbital septum characterized by periorbital edema, erythema, warmth, and tenderness. Periorbital cellulitis is typically caused by S pyogenes or S aureus . This condition is to be differentiated from orbital cellulitis, which is an extension of bacterial sinusitis involving postseptal tissues, typically caused in vaccinated children by Streptococcus pneumoniae , Haemophilus influenzae , Moraxella catarrhalis , or anaerobic cocci, and characterized by chemosis, painful limited extraocular movements, proptosis, and reduced visual acuity. Complications of orbital cellulitis include loss of vision, retrobulbar abscess, subperiosteal abscess, osteomyelitis, meningitis, and cavernous sinus thrombosis.

Cellulitis remains a clinical diagnosis and its pathophysiology is still largely unknown. Microbiological diagnosis of cellulitis is elusive. If blood culture is considered the gold standard for microbiological diagnosis, S pyogenes accounts for most cases. However, blood cultures are reported positive in less than 1% of uncomplicated SSSI and in only 12.5% of complicated SSSI, which might bias these distinctions. However, if lesions are subjected to needle aspiration or punch biopsy, then S aureus is recovered most frequently (although at most one-third of such samples recover any pathogen). Given these data coupled with clinical response to various antimicrobial treatment regimens (discussed later), beta-hemolytic streptococci remain the most likely pathogen for nonpurulent cellulitis.

Erysipelas

Erysipelas is a painful, well-demarcated, superficial infection of the dermis that involves the cutaneous lymphatics. Erysipelas occurs most often in young children and older adults. In neonates, erysipelas can originate from the umbilical stump and spread into the abdominal wall. Although mainly caused by S pyogenes , similar lesions can be caused by group C or G streptococci, Streptococcus agalactiae , or S aureus . Erysipelas manifests as an abrupt, intensely erythematous lesion raised above the level of the surrounding skin with characteristic sharply demarcated borders. It most commonly involves the legs or face. Patients are typically febrile; adenopathy and lymphangitis may also be present. Severe pain and/or systemic symptoms may suggest deeper infection or toxic shock syndrome (TSS).

Ecthyma

Ecthyma is a deep, ulcerative infection of the skin. Ecthyma can initially resemble impetigo but progresses to deeper penetration into the dermis, evolving into a crusted ulcer up to 4 cm in diameter with a black eschar and elevated margins. Lesions are usually located in the legs in association with minor trauma or pruritic conditions such as insect bites or scabies. Lymphangitis, cellulitis, and poststreptococcal glomerulonephritis are potential complications of ecthyma. In contrast with the isolated, outside-to-inside progression of typical ecthyma, ecthyma gangrenosum refers to the systemic spread of bacteria with multiple similar-appearing lesions resulting from necrotizing bacterial vasculitis. This condition is often associated with Pseudomonas aeruginosa bacteremia, especially in immunocompromised patients, but can also involve other pathogens, including S aureus (see Fig. 2 E).

Staphylococcal Scalded Skin Syndrome

Staphylococcal scalded skin syndrome (SSSS) is a toxin-mediated epidermolytic disease resulting in severe skin blistering and exfoliation caused by circulation of staphylococcal exfoliative toxins A and B. This condition predominantly occurs in children less than 6 years of age, most commonly in young infants (who have decreased renal excretion of toxin because of immature renal function).

The inciting infection usually occurs in the eye or nasopharynx. SSSS can be limited to a few localized blisters that burst and leave a tender erythematous base (manifesting as localized bullous impetigo in older children), but exfoliation may involve the entire body surface (Ritter disease in neonates).

The hallmark of SSSS is the presence of midepidermal separation at the zona granulosa (Nikolsky sign); with friction, the epidermis peels off easily, often in large sheets. Healing typically occurs without scarring (see Fig. 2 F).

Intertrigo

Intertrigo is created by friction of opposing skin surfaces exacerbated by moisture trapped in deep skin folds. Young infants are especially susceptible because of their abundant deep skin folds. Secondary infections with S pyogenes , S aureus , Candida spp, or other pathogens can occur and can be difficult to differentiate. Intertrigo manifests as intensely erythematous, well-demarcated patches. Associated foul smell; presence of thick, red, macerated, or scaly plaque-type lesions; or presence of low-grade fever or fussiness are typical of S pyogenes intertrigo, whereas satellite lesions favor Candida spp. Recurrence requiring retreatment is common. If the eruption persists, more invasive diagnostic procedures such as skin biopsy should be considered to rule out less common causes, including atopic or seborrheic dermatitis, scabies, erythrasma, contact dermatitis, inverse psoriasis, Langerhans cell histiocytosis, or acrodermatitis enteropathica.

Acute Paronychia

Acute paronychia is an infection of the soft tissue fold surrounding a fingernail or toenail resulting from minor trauma facilitating bacterial entry into the cuticle or nail fold. Acute paronychia is most often caused by S aureus , whereas chronic paronychia is most often caused by Candida spp. Risk factors for paronychia include dermatitis, nail biting, and chronic thumb or finger sucking. Paronychia presents with erythema, edema, and tenderness of the proximal and lateral nail fold or may extend beneath the nail and suppurate (see Fig. 2 G).

Blistering Distal Dactylitis

Blistering distal dactylitis is typically seen in children aged 2 to 16 years and is most often caused by S pyogenes (less commonly by S aureus ). It manifests as a tense, nontender bulla with an erythematous base involving the distal volar fat pad of the phalanges. One or more digits can be affected (particularly in S aureus infections) and systemic symptoms are generally absent.

Necrotizing Fasciitis

Necrotizing fasciitis is an uncommon, severe SSSI characterized by rapidly evolving soft tissue necrosis and pain out of proportion to the physical findings involving the deeper layer of the superficial fascia but largely sparing the adjacent skin, deep fascia, and muscle. S pyogenes is often implicated, although S aureus , including CA-MRSA, is increasingly recognized as a cause of necrotizing fasciitis in the United States. Between roughly 30% and 55% of necrotizing fasciitis cases are polymicrobial. Necrotizing fasciitis may follow minor trauma or surgery, but in approximately half of cases no visible skin lesion is present. Early in the infection, distinguishing between simple cellulitis and necrotizing fasciitis can be difficult (see Box 1 ). Thus, a high clinical suspicion is paramount; most patients with necrotizing fasciitis are not diagnosed at hospital admission. Necrotizing fasciitis is a medical emergency requiring prompt surgical debridement; if necrotizing fasciitis is suspected on clinical grounds, surgical intervention should not be delayed while awaiting confirmation by laboratory testing or imaging studies.

TSS

TSS is a severe, life-threatening, systemic infection resulting from toxin elaboration by S aureus or S pyogenes , often associated with minor or occult cutaneous infection. Staphylococcal TSS is caused by a staphylococcal superantigen (usually TSS-1) that stimulates overproduction of inflammatory mediators leading to capillary leak, hypotension, and multiorgan failure. CA-MRSA rarely produce TSS toxin. Streptococcal TSS is caused by toxin-producing S pyogenes strains with multisystem clinical manifestations that are similar to those of staphylococcal TSS. The initial clinical presentation of streptococcal TSS is often localized to the primary infection site; however, S pyogenes TSS can occur without an identifiable focus of infection. Diagnosis of TSS is mainly clinical ( Fig. 3 ); blood cultures are positive in less than 5% of cases.

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