Cutaneous Bacterial Infections C a us ed by S t a p h y l o c o c c u s au r e u s and S t r e p t o c o c c u s p y o g e n e s i n I n f a n t s a n d C h i l d re n Beatriz Larru,
MD, PhD,
Jeffrey S. Gerber,
MD, PhD*
KEYWORDS Skin and soft tissue infection Staphylococcus aureus Streptococcus pyogenes MRSA Cellulitis Abscess KEY POINTS Purulent lesions (eg, abscesses) are generally caused by Staphylococcus aureus; nonpurulent infections (eg, cellulitis, erysipelas) are usually caused by Streptococcus pyogenes. The increase in skin and skin structure infection (SSSI) rates is largely attributed to the emergence of methicillin-resistant S aureus. Careful history and examination and close clinical monitoring are needed to identify severe infections or uncommon causes. Antibiotics are often unnecessary for management of uncomplicated skin abscesses if incision and drainage are performed. Blood cultures are rarely helpful for uncomplicated infections. Their yield is higher in severe disease and can help with antibiotic selection. Management of SSSI should target the most likely organism(s) and minimize both the spectrum and duration of antibiotic therapy.
INTRODUCTION
Acute skin and skin structure infections (SSSIs) are among the most common bacterial infections in children. SSSIs account for nearly 25% of pediatric clinical encounters, most occurring in the outpatient office or emergency department (ED).1–4 SSSIs represent a wide spectrum of disease severity, from impetigo to necrotizing fasciitis. Prompt recognition coupled with timely and judicious antimicrobial use
Disclosure of Funding: None. Division of Infectious Diseases, The Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA * Corresponding author. Center for Pediatric Clinical Effectiveness, The Children’s Hospital of Philadelphia, 3535 Market Street, Philadelphia, PA 19104. E-mail address: [email protected] Pediatr Clin N Am 61 (2014) 457–478 http://dx.doi.org/10.1016/j.pcl.2013.12.004 pediatric.theclinics.com 0031-3955/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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optimizes patient outcomes and minimizes the occurrence of adverse drug effects and the emergence of antimicrobial resistance.5,6 Because specimens for culture are not obtained for many SSSIs, treatment is often empiric and chosen based on the clinical presentation (eg, erysipelas vs abscess) and local microbial epidemiology.7–10 Staphylococcus aureus and Streptococcus pyogenes are the most common causes of community-onset SSSI.11–16 This article describes the epidemiology, clinical presentation, and management of common cutaneous bacterial infections most often caused by S aureus and S pyogenes in children. CURRENT EPIDEMIOLOGY OF S AUREUS AND S PYOGENES S aureus
S aureus is the most common culture-confirmed pathogen from SSSIs in the United States.17–20 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.21–24 The medical burden of SSSIs, particularly abscesses, has increased nationwide since the emergence of community-acquired (CA) methicillin-resistant S aureus (MRSA).25–30 This seems to be driven by additional MRSA cases as opposed to replacement of methicillin-sensitive S aureus (MSSA) with MRSA.31,32 In the United States, the predominant clone is USA300, which has now spread from the community into hospitals.33,34 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 2009.35,36 ED visits for SSSIs have also increased, from 1.2 million visits in 1993 to 3.4 million in 2005.4,37,38 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.37,39 According to the SENTRY antimicrobial surveillance program (covering both the United States and Canada), betahemolytic 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).1,26 However, since the 1980s, severe S pyogenes necrotizing fasciitis has been increasingly reported in the United States and worldwide.5,27 PATHOGENESIS OF SSSI
The main determinant of cutaneous infection is the balance between the virulence of the organism and the host defense. For example, compromised cutaneous barrier function, such as in patients with chronic dermatitis or in premature infants, or immune compromising states, such as children undergoing cancer chemotherapy, can heighten the risk and severity of SSSI.7,9,40 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
Cutaneous Bacterial Infections in Children
conferring resistance to methicillin and antistaphylococcal b-lactams.11,41 CA-MRSA also commonly contains the lukS-PV and lukF-PV genes encoding the PantonValentine 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.21,23,24,42 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).25,42,43 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.5,25,41 CLINICAL AND DIAGNOSTIC APPROACH
Infections of the skin and soft tissues can be broadly classified based on the extent of tissue involvement and the specific anatomic site of infection. Superficial infections involve the epidermis, the dermis, or both. Deep infections involve the hypodermis, fascia, and muscle. Superficial infections usually evolve from local spread of organisms, typically without systemic symptoms; less commonly, small, superficial infections can elicit a robust systemic response caused by elaboration of toxins. Deeper infections tend to arise by the hematogenous spread of organisms from a distant site.6,35,44 SSSIs can also be classified as uncomplicated or complicated, based on the severity of illness and the vulnerability of the host. However, this division is artificial and subjective because of the spectrum of SSSI presentations and patient comorbidities.37,38,43 Although the cause of SSSI is often elusive, this article focuses on SSSIs typically caused by S aureus or S pyogenes (Table 1). Obtaining a detailed history, including the epidemiologic setting and immune status of the child, is key to refining the differential diagnosis and appropriate index of suspicion for specific causal agents (Fig. 1).25,37,45 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.26,44,46 S aureus, especially CA-MRSA, is now the most common cause of cutaneous abscesses in the United States.27,47 Folliculitis, Furuncles, and Carbuncles
Folliculitis results from inflammation of hair follicles, manifesting as clusters of small erythematous papules or pustules.39,40,48 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.41,49 Sycosis barbae is a severe, painful, deep, recurrent form of facial folliculitis caused by S aureus
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Table 1 Causes of SSSI Most Common Causes
Less Common Causesa/Other Considerations
Discrete collection of pus surrounded by a fibrinoid wall within the dermis and subcutaneous tissues
MRSA, MSSA, S pyogenes less common
Enterobacteriaceae, anaerobes, Pseudomonas spp, Mycobacterium spp
Folliculitis
Papular/pustular inflammation of the hair follicle within the epidermis
MRSA, MSSA
Pseudomonas spp (hot-tub folliculitis), Malassezia spp, Klebsiella spp, Enterobacter spp, Escherichia coli, Proteus spp
Furuncle
Painful, firm/fluctuant lesion originating from a hair follicle extending through the dermis Organized collection of adjacent furuncles connected by sinus tract with multiple drainage points
MRSA, MSSA
Consider underlying immunodeficiency (eg, chronic granulomatous diseases, hyper-IgE syndrome) if poorly responsive to appropriate therapy or persistent recurrence
Impetigo
Large vesicles and/or honey-crusted lesions
Nonbullous: MRSA, MSSA, S pyogenes Bullous: MRSA, MSSA
Clinical appearance overlaps with Herpes simplex virus, Varicella-Zoster virus reactivation
Ecthyma
Crusted ulcer penetrating into the dermis with black eschar and elevated margins
MRSA, MSSA, S pyogenes
Ecthyma gangrenosum associated with Pseudomonas aeruginosa bacteremia
Staphylococcal scalded skin syndrome
Local or generalized skin blistering and exfoliation
MSSA, MRSA
Important to differentiate from Stevens-Johnson syndrome and toxic epidermal necrolysis (more serious conditions involving mucous membranes)
Cellulitis
Painful, erythematous infection of deep skin with poorly demarcated borders
S pyogenes, MRSA, MSSA
Pasteurella spp, Capnocytophaga canimorsus (animal bites), Aeromonas hydrophila (freshwater immersion), Erysipelothrix rhusiopathiae (fisherman), Haemophilus influenzae, Streptococcus pneumoniae (periorbital, facial), Pseudomonas aeruginosa, Cryptococcus neoformans (immunosuppression)
Disease
Key Features
Abscess
Carbuncle
MRSA, MSSA
(continued on next page)
Cutaneous Bacterial Infections in Children
Table 1 (continued) Most Common Causes
Less Common Causesa/ Other Considerations
Superficial inflammation of the dermis with sharply demarcated borders and lymphatic involvement
S pyogenes
Group B, C, and G Streptococcus
Intertrigo
Erosion of skin in deep skin folds
S pyogenes
Candida albicans
Paronychia
Inflammation of the soft tissue surrounding the nail bed
MRSA, MSSA, S pyogenes
Mixed aerobic and anaerobic flora (Eikenella corrodens, Bacteroides spp, Fusobacterium spp)
Dactylitis
Inflammation of the distal volar pad of the phalanges
MRSA, MSSA, S pyogenes
Group B Streptococcus (rarely)
Necrotizing fasciitis
Infection of the deeper layer of the superficial fascia with major destruction of tissue
Type II necrotizing fasciitis: S pyogenes MRSA, MSSA
Type I necrotizing fasciitis: mixed flora (anaerobes, GNB, Enterococcus spp) Gas gangrene: Clostridium spp Anaerobic cellulitis: Clostridium spp Meleney synergistic gangrene: MRSA, MSSA, microaerophilic streptococci
Pyomyositis
Acute infection of muscle with abscess formation
MRSA, MSSA
S pyogenes (necrotizing myositis), Clostridium spp (clostridial myonecrosis)
Disease
Key Features
Erysipelas
Abbreviations: GNB, gram-negative bacilli; IgE, immunoglobulin E. a Children and adolescents with immunodeficiency are at higher risk for uncommon causes of SSSI that can have a fulminant course. Data from Shah S. Pediatric practice infectious diseases. New York: McGraw Hill Professional; 2009.
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.35,43,50,51 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. 2A).25,33,43 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.42–44
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History: specific exposures, skin trauma, healthcare contact, presence of comorbidies (including immune status)
Physical examinaon • Extent and locaon of erythema, edema, warmth or tenderness • Presence of fluctuance, purpura, bullae, crepitus, necrosis, systemic signs, lymphangic spread and depth of infecon
Surgical consultaon if severe and deep ssue infecon is suspected
Laboratory studies • Uncomplicated, purulent SSSI/abscesses • culture pus if available and if eology/resistance paern uncertain • Complicated SSSI, consider: • complete blood count with differenal • basic metabolic panel • C-reacve protein • creane phosphokinase • blood culture: yield 12.5% in complicated STTI (
MD, PhD,
Jeffrey S. Gerber,
MD, PhD*
KEYWORDS Skin and soft tissue infection Staphylococcus aureus Streptococcus pyogenes MRSA Cellulitis Abscess KEY POINTS Purulent lesions (eg, abscesses) are generally caused by Staphylococcus aureus; nonpurulent infections (eg, cellulitis, erysipelas) are usually caused by Streptococcus pyogenes. The increase in skin and skin structure infection (SSSI) rates is largely attributed to the emergence of methicillin-resistant S aureus. Careful history and examination and close clinical monitoring are needed to identify severe infections or uncommon causes. Antibiotics are often unnecessary for management of uncomplicated skin abscesses if incision and drainage are performed. Blood cultures are rarely helpful for uncomplicated infections. Their yield is higher in severe disease and can help with antibiotic selection. Management of SSSI should target the most likely organism(s) and minimize both the spectrum and duration of antibiotic therapy.
INTRODUCTION
Acute skin and skin structure infections (SSSIs) are among the most common bacterial infections in children. SSSIs account for nearly 25% of pediatric clinical encounters, most occurring in the outpatient office or emergency department (ED).1–4 SSSIs represent a wide spectrum of disease severity, from impetigo to necrotizing fasciitis. Prompt recognition coupled with timely and judicious antimicrobial use
Disclosure of Funding: None. Division of Infectious Diseases, The Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318, USA * Corresponding author. Center for Pediatric Clinical Effectiveness, The Children’s Hospital of Philadelphia, 3535 Market Street, Philadelphia, PA 19104. E-mail address: [email protected] Pediatr Clin N Am 61 (2014) 457–478 http://dx.doi.org/10.1016/j.pcl.2013.12.004 pediatric.theclinics.com 0031-3955/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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optimizes patient outcomes and minimizes the occurrence of adverse drug effects and the emergence of antimicrobial resistance.5,6 Because specimens for culture are not obtained for many SSSIs, treatment is often empiric and chosen based on the clinical presentation (eg, erysipelas vs abscess) and local microbial epidemiology.7–10 Staphylococcus aureus and Streptococcus pyogenes are the most common causes of community-onset SSSI.11–16 This article describes the epidemiology, clinical presentation, and management of common cutaneous bacterial infections most often caused by S aureus and S pyogenes in children. CURRENT EPIDEMIOLOGY OF S AUREUS AND S PYOGENES S aureus
S aureus is the most common culture-confirmed pathogen from SSSIs in the United States.17–20 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.21–24 The medical burden of SSSIs, particularly abscesses, has increased nationwide since the emergence of community-acquired (CA) methicillin-resistant S aureus (MRSA).25–30 This seems to be driven by additional MRSA cases as opposed to replacement of methicillin-sensitive S aureus (MSSA) with MRSA.31,32 In the United States, the predominant clone is USA300, which has now spread from the community into hospitals.33,34 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 2009.35,36 ED visits for SSSIs have also increased, from 1.2 million visits in 1993 to 3.4 million in 2005.4,37,38 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.37,39 According to the SENTRY antimicrobial surveillance program (covering both the United States and Canada), betahemolytic 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).1,26 However, since the 1980s, severe S pyogenes necrotizing fasciitis has been increasingly reported in the United States and worldwide.5,27 PATHOGENESIS OF SSSI
The main determinant of cutaneous infection is the balance between the virulence of the organism and the host defense. For example, compromised cutaneous barrier function, such as in patients with chronic dermatitis or in premature infants, or immune compromising states, such as children undergoing cancer chemotherapy, can heighten the risk and severity of SSSI.7,9,40 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
Cutaneous Bacterial Infections in Children
conferring resistance to methicillin and antistaphylococcal b-lactams.11,41 CA-MRSA also commonly contains the lukS-PV and lukF-PV genes encoding the PantonValentine 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.21,23,24,42 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).25,42,43 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.5,25,41 CLINICAL AND DIAGNOSTIC APPROACH
Infections of the skin and soft tissues can be broadly classified based on the extent of tissue involvement and the specific anatomic site of infection. Superficial infections involve the epidermis, the dermis, or both. Deep infections involve the hypodermis, fascia, and muscle. Superficial infections usually evolve from local spread of organisms, typically without systemic symptoms; less commonly, small, superficial infections can elicit a robust systemic response caused by elaboration of toxins. Deeper infections tend to arise by the hematogenous spread of organisms from a distant site.6,35,44 SSSIs can also be classified as uncomplicated or complicated, based on the severity of illness and the vulnerability of the host. However, this division is artificial and subjective because of the spectrum of SSSI presentations and patient comorbidities.37,38,43 Although the cause of SSSI is often elusive, this article focuses on SSSIs typically caused by S aureus or S pyogenes (Table 1). Obtaining a detailed history, including the epidemiologic setting and immune status of the child, is key to refining the differential diagnosis and appropriate index of suspicion for specific causal agents (Fig. 1).25,37,45 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.26,44,46 S aureus, especially CA-MRSA, is now the most common cause of cutaneous abscesses in the United States.27,47 Folliculitis, Furuncles, and Carbuncles
Folliculitis results from inflammation of hair follicles, manifesting as clusters of small erythematous papules or pustules.39,40,48 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.41,49 Sycosis barbae is a severe, painful, deep, recurrent form of facial folliculitis caused by S aureus
459
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Table 1 Causes of SSSI Most Common Causes
Less Common Causesa/Other Considerations
Discrete collection of pus surrounded by a fibrinoid wall within the dermis and subcutaneous tissues
MRSA, MSSA, S pyogenes less common
Enterobacteriaceae, anaerobes, Pseudomonas spp, Mycobacterium spp
Folliculitis
Papular/pustular inflammation of the hair follicle within the epidermis
MRSA, MSSA
Pseudomonas spp (hot-tub folliculitis), Malassezia spp, Klebsiella spp, Enterobacter spp, Escherichia coli, Proteus spp
Furuncle
Painful, firm/fluctuant lesion originating from a hair follicle extending through the dermis Organized collection of adjacent furuncles connected by sinus tract with multiple drainage points
MRSA, MSSA
Consider underlying immunodeficiency (eg, chronic granulomatous diseases, hyper-IgE syndrome) if poorly responsive to appropriate therapy or persistent recurrence
Impetigo
Large vesicles and/or honey-crusted lesions
Nonbullous: MRSA, MSSA, S pyogenes Bullous: MRSA, MSSA
Clinical appearance overlaps with Herpes simplex virus, Varicella-Zoster virus reactivation
Ecthyma
Crusted ulcer penetrating into the dermis with black eschar and elevated margins
MRSA, MSSA, S pyogenes
Ecthyma gangrenosum associated with Pseudomonas aeruginosa bacteremia
Staphylococcal scalded skin syndrome
Local or generalized skin blistering and exfoliation
MSSA, MRSA
Important to differentiate from Stevens-Johnson syndrome and toxic epidermal necrolysis (more serious conditions involving mucous membranes)
Cellulitis
Painful, erythematous infection of deep skin with poorly demarcated borders
S pyogenes, MRSA, MSSA
Pasteurella spp, Capnocytophaga canimorsus (animal bites), Aeromonas hydrophila (freshwater immersion), Erysipelothrix rhusiopathiae (fisherman), Haemophilus influenzae, Streptococcus pneumoniae (periorbital, facial), Pseudomonas aeruginosa, Cryptococcus neoformans (immunosuppression)
Disease
Key Features
Abscess
Carbuncle
MRSA, MSSA
(continued on next page)
Cutaneous Bacterial Infections in Children
Table 1 (continued) Most Common Causes
Less Common Causesa/ Other Considerations
Superficial inflammation of the dermis with sharply demarcated borders and lymphatic involvement
S pyogenes
Group B, C, and G Streptococcus
Intertrigo
Erosion of skin in deep skin folds
S pyogenes
Candida albicans
Paronychia
Inflammation of the soft tissue surrounding the nail bed
MRSA, MSSA, S pyogenes
Mixed aerobic and anaerobic flora (Eikenella corrodens, Bacteroides spp, Fusobacterium spp)
Dactylitis
Inflammation of the distal volar pad of the phalanges
MRSA, MSSA, S pyogenes
Group B Streptococcus (rarely)
Necrotizing fasciitis
Infection of the deeper layer of the superficial fascia with major destruction of tissue
Type II necrotizing fasciitis: S pyogenes MRSA, MSSA
Type I necrotizing fasciitis: mixed flora (anaerobes, GNB, Enterococcus spp) Gas gangrene: Clostridium spp Anaerobic cellulitis: Clostridium spp Meleney synergistic gangrene: MRSA, MSSA, microaerophilic streptococci
Pyomyositis
Acute infection of muscle with abscess formation
MRSA, MSSA
S pyogenes (necrotizing myositis), Clostridium spp (clostridial myonecrosis)
Disease
Key Features
Erysipelas
Abbreviations: GNB, gram-negative bacilli; IgE, immunoglobulin E. a Children and adolescents with immunodeficiency are at higher risk for uncommon causes of SSSI that can have a fulminant course. Data from Shah S. Pediatric practice infectious diseases. New York: McGraw Hill Professional; 2009.
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.35,43,50,51 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. 2A).25,33,43 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.42–44
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History: specific exposures, skin trauma, healthcare contact, presence of comorbidies (including immune status)
Physical examinaon • Extent and locaon of erythema, edema, warmth or tenderness • Presence of fluctuance, purpura, bullae, crepitus, necrosis, systemic signs, lymphangic spread and depth of infecon
Surgical consultaon if severe and deep ssue infecon is suspected
Laboratory studies • Uncomplicated, purulent SSSI/abscesses • culture pus if available and if eology/resistance paern uncertain • Complicated SSSI, consider: • complete blood count with differenal • basic metabolic panel • C-reacve protein • creane phosphokinase • blood culture: yield 12.5% in complicated STTI (
