Bacterial Skin Infections
- Duha Al-Zubeidi
- Mary Anne Jackson
Normal Skin
Anatomy
The epidermal skin layer provides the primary barrier to invasion by microorganisms and an interface between the body and the environment. Hair follicles, sebaceous glands, nails, and sweat glands are considered epidermal appendages and as such may be involved in skin infection. A dermal layer composed of collagen and elastic fibers gives skin its elasticity; however, other cell elements that are present, including mast cells, blood and lymph vessels, and cutaneous nerves, may be involved in the inflammatory process in response to infection. The subcutaneous fat layer is just beneath the dermis and contributes primarily to thermal stability, but it also may be involved when infection extends beyond the epidermal-dermal layer.
Flora
Colonization is defined as the presence of a microorganism on the skin without either clinical signs or symptoms of infection at the time of isolation. Normal bacterial skin colonization is divided into resident and transient flora. Resident flora predominates and includes typical nonpathogens, such as Staphylococcus epidermidis and Propionibacterium acnes, in addition to other anaerobic diphtheroids (Corynbacteriaceae) and micrococci. Transient flora include pathogenic organisms, such as Staphylococcus aureus, streptococci, gram-negative enteric organisms, and Candida albicans; these pathogens usually are present in smaller numbers than the resident flora and may be removed by skin cleansing. Fungal species such as Malassezia spp. can be found as part of the normal skin flora. Acutely or chronically damaged skin, contact with animate and inanimate environmental sources, and exposure to antimicrobial agents or indwelling devices can modify the skin flora and predispose to infection by resident or acquired transient flora.
Cutaneous Infection and Dermatologic Manifestations of Systemic Disease
Dermatologic manifestations of infection can occur when the skin is infected primarily or as a secondary phenomenon. Prompt diagnosis and treatment of certain systemic or disseminated diseases may be accomplished when the secondary dermatologic manifestations are recognized. Empiric treatment of systemic diseases such as endocarditis (septic emboli) or septicemia caused by bacterial pathogens, such as Neisseria meningitidis or Pseudomonas aeruginosa , is possible when the dermatologic manifestations (i.e., purpura fulminans, ecthyma gangrenosum) are noted. Generalized viral infections may be heralded by pathognomonic skin findings, such as occur in varicella or measles. Alternatively skin manifestations may be mediated by toxin (staphylococcal scalded skin syndrome or toxic shock syndrome) or by immunologic mechanisms (gonococcemia).
The list of bacterial infectious agents associated with skin infections is extensive ( Table 60A.1 ). This section focuses on the bacterial skin infections most frequently encountered by practicing clinicians. Viral, bacterial, and fungal systemic or disseminated diseases are categorized in Chapter 58 and are also presented in the specific chapters in Part III of this book.
| Anthrax | Bacillus anthracis |
| Blistering dactylitis | Streptococcus pyogenes |
| Streptococcus agalactiae | |
| Staphylococcus aureus | |
| Cellulitis | S. pyogenes |
| S. aureus | |
| Haemophilus influenzae type b | |
| Streptococcus pneumoniae | |
| Chancroid | Haemophilus ducreyi |
| Diphtheria | Corynebacterium diphtheriae |
| Ecthyma gangrenosum | Pseudomonas aeruginosa |
| Erysipelas | S. pyogenes |
| S. agalactiae; groups C, G streptococci | |
| S. pneumoniae | |
| Erysipeloid | Erysipelothrix rhusiopathiae |
| Folliculitis | S. aureus |
| Coagulase-negative staphylococci | |
| Klebsiella spp. | |
| Enterobacter spp. | |
| Escherichia coli | |
| P. aeruginosa | |
| Proteus spp. | |
| Erythrasma | Corynebacterium minutissimum |
| Furunculosis | S. aureus |
| Hidradenitis suppurativa | S. aureus |
| Streptococcus milleri | |
| E. coli | |
| Anaerobic streptococci | |
| Granuloma inguinale | Calymmatobacterium granulomatis |
| Impetigo | |
| Simple superficial | S. aureus |
| S. pyogenes | |
| Bullous | S. aureus |
| Lymphogranuloma venereum | Chlamydia trachomatis |
| Melioidosis | Burkholderia pseudomallei |
| Necrotizing fasciitis | S. pyogenes |
| Polymicrobial | |
| Nocardiosis | Nocardia brasiliensis |
| Nocardia asteroides | |
| Paronychia | Polymicrobial |
| Perianal dermatitis | S. pyogenes |
| Pitted keratolysis | Coryneform bacteria |
| Syphilis | Treponema pallidum |
Impetigo
Nonbullous or Simple Superficial Impetigo
The bacterial skin infection most commonly encountered in children is nonbullous impetigo, which accounts for more than 70% of impetigo cases in children. This superficial infection is seen predominantly in summer, with insect bites, cutaneous injuries, and primary dermatitis serving as the portal of entry.
Nonbullous impetigo, sometimes called thick crusted impetigo, is characterized by the appearance of erythematous maculopapules that rapidly evolve from a vesicular to a pustular stage. Centrally crusted plaques range in size from a few millimeters to 1 cm and are surrounded by a distinct margin of erythema. The honey-colored crust is a classic feature, and removal of the crust results in the reaccumulation of fresh exudate. Regional lymphadenopathy can occur and often is the reason that the patient seeks medical attention. Spread to exposed areas, usually the face, neck, and limbs, occurs frequently. This form of pyoderma often is associated with a 2- to 3-week delay in establishing the diagnosis because the lesions are slow to progress, only mildly tender at the site of the lesion, and generally not associated with systemic signs or symptoms.
Nonbullous impetigo classically has been associated with infection caused by group A β-hemolytic streptococcus (GAS). More recent data underscore the importance of S. aureus, however, which now accounts for most cases of nonbullous impetigo in the United States.
Primarily a disease of children, nonbullous impetigo is spread within families and by close physical contact. It is prevalent during warm, humid seasons and is seen year-round in tropical regions. Endemic disease occurs in the southeastern United States and Hawaii.
Epidemics of streptococcal impetigo have been associated with postinfectious glomerulonephritis, and streptococcal strains, including types 2, 31, 49, 53, 55, 56, 57, and 60, have been implicated in such outbreaks. Studies published in the 1950s and 1960s from the Red Lake Indian Reservation in Minnesota first confirmed the association of impetigo in school-aged children with a postinfectious nephritis that occurred 18 to 21 days after the onset of impetigo and implicated the so-called Red Lake strain, M-type 49. Further studies in this population performed in the early 1970s found that GAS was isolated from normal skin in 23 of 31 high-risk children a mean of 10 days before the development of impetigo. Local trauma and other environmental factors seemed to explain the predilection of exposed skin to streptococcal infection, especially the skin of the legs, where 62% of the total lesions were noted. Secondary acquisition of streptococcal isolates in other family members occurred a mean of 5 days after the primary case, a time frame that was noted to be significantly shorter than that of secondary respiratory acquisition. Rheumatic fever does not occur as a postinfectious sequela of streptococcal skin infection.
Cutaneous botryomycosis, an indolent infection reminiscent of crusted impetigo, usually is caused by S. aureus . Characterized by plaquelike lesions with superficial pustules and crusts, this entity has a predilection for patients with altered immune function. Histologic examination may suggest the diagnosis of actinomycosis if a granulomatous lesion with granules resembling those seen with Actinomyces is noted. Successful treatment can be accomplished after the bacterial pathogen has been identified.
Bullous Impetigo
Bullous impetigo is diagnosed when the primary lesion begins as small vesicles and later appears as flaccid, painless bullae, generally measuring greater than 1 cm ( Fig. 60A.1 ). Initially filled with clear fluid, the lesions eventually may exhibit a purulent fluid level. Rupture of the thin bullae usually reveals a moist, erythematous base that dries to a shiny lacquer-like appearance, sometimes described as a varnished finish ( Fig. 60A.2 ). Systemic toxicity is not seen except in neonates, in whom disseminated disease may occur.
In contrast to thick, crusted impetigo, in virtually all cases of bullous impetigo, staphylococci are isolated in pure culture from aspirated bulla fluid. Other bullous dermatitides of childhood, such as pemphigus or Stevens-Johnson syndrome, may be excluded by isolation of the organism. Occasionally biopsy is done in cases in which extensive bullae or an atypical clinical appearance is noted. Confirmation of a cleavage plane high in the epidermis with gram-positive organisms and polymorphonuclear leukocytes present is a definitive diagnosis of bullous staphylococcal disease.
Infection generally is caused by phage group II strains, particularly phage type 71, but also 3A, 3C, and 55, which are noted to elaborate epidermolytic toxins A and B. Pathologically these toxins act by disrupting the intercellular attachment of epidermal cells of the stratum granulosum. The toxin is thought to function as a protease in separating the upper layers of the epidermis of adult and infant human skin. Production of antibody to epidermolytic toxin occurs with age; however, it does not protect against the development of new bullous lesions during the localized impetiginous stage of this staphylococcal disease.
Epidemiologically large outbreaks of bullous impetigo have been traced most notably to hospital nurseries, where identification of infected infants always occurs within the first month of life but after the infant has been sent home. A more severe, generalized form of the epidermolytic toxin–mediated disease (Ritter disease) may be seen in a few infants during one of these outbreaks, underscoring the importance of infection control surveillance practices in recognizing such an outbreak ( Fig. 60A.3 ).
Treatment of Impetigo
Topical mupirocin 2% cream (Bactroban) may be used in cases of nonbullous impetigo in which adequate coverage of the affected sites can be ensured. In other cases, systemic treatment with an oral antistaphylococcal antimicrobial agent, such as cephalexin, should be employed. As in other staphylococcal diseases, an increase in community-acquired, methicillin-resistant S. aureus (MRSA) cases has been noted in the past decade. In cases for which traditional antistaphylococcal agents are unsuccessful or in patients with recurrent disease, culture should be done to identify the bacterial strain and susceptibility pattern. Currently the majority of community-acquired MRSA isolates are susceptible to clindamycin, but sensitivity patterns vary throughout the United States.
A recent study comparing clindamycin versus trimethoprim-sulfamethoxazole (TMP-SMX) for skin infections involved 524 patients; S. aureus was isolated from 41.4% of the patients, and 77% of these patients had MRSA. Clindamycin resistance was confirmed in 21% of the MRSA patients and in 9.9% of methicillin-susceptible S. aureus (MSSA) patients. Overall there was no significant difference between clindamycin and TMP-SMX for the treatment of skin infections. However, one should remember that by choosing TMP-SMX, good coverage is lacking for GAS. The Infectious Diseases Society of America (IDSA) cautions the use of TMP-SMX alone as an oral option when GAS is suspected or isolated and suggests adding a β-lactam (e.g., penicillin, cephalexin, or amoxicillin) as a second agent.
Perianal Streptococcal Dermatitis
Formerly called perianal cellulitis , perianal streptococcal dermatitis, a commonly recognized superficial skin infection, is characterized by the presence of marked, well-demarcated, perirectal erythema with associated swelling, pruritus, and tenderness but an absence of systemic symptoms or progressive disease. Approximately half of patients complain of significant rectal pain on defecation, and a third note blood in their stools.
Heavy growth of GAS is seen on perianal culture, and, in one study, isolation of a specific T-type Streptococcus (T 28) raised the question of whether certain streptococcal strains have tropism for the perineal region. Asymptomatic patients were evaluated in two studies, and only sparse growth of GAS was noted in 6% of cases.
Perianal streptococcal dermatitis is treated with oral penicillin agents. Topical mupirocin also has been used successfully. Recurrences are noted commonly, however. In one large series of patients, one-third had recurrent disease. Intrafamilial spread of disease frequently occurs and may provide a vector for recurrence. For patients with recurrent or persistent disease, clindamycin or a β-lactam agent plus rifampin may be used, and identification and treatment of other affected family members may be necessary.
Blistering Distal Dactylitis
Most commonly identified in school-aged children, blistering distal dactylitis is a distinctive superficial skin infection classically associated with GAS. Bullae 2 cm in diameter develop over the anterior fat pad of the distal phalanges, sometimes extending to involve the nail folds. Involvement of the proximal phalanges or the palms occasionally is noted. Frankly pustular lesions may occur, but the lesions themselves usually are asymptomatic or only mildly tender. A thin purulent exudate generally is apparent on incision and drainage.
The diagnosis is confirmed by recovery of the etiologic agent on culture, most commonly GAS, although group B streptococcus and S. aureus also have been noted. Concurrent recovery of GAS in the pharynx has been reported in a few cases. Treatment includes a 10-day course of an oral β-lactam agent, usually penicillin or amoxicillin, in addition to incision and drainage of any tense bullae.
Erysipelas
The superficial cellulitis erysipelas, referred to as St. Anthony’s fire in the Middle Ages, is characterized by the appearance of a bright erythematous plaque with a distinct, elevated border that sharply demarcates affected from unaffected skin. The lesion most often involves the face or lower extremity, although extensive involvement of the trunk has been noted. The involved skin is warm and tender and may have a peau d’orange appearance. Large tension bullae may be seen in the erythematous zone. The patient generally appears toxic and is highly febrile, and rapid extension of the affected skin may occur over the course of hours.
Histopathologic findings include intense edema with vascular dilation of the dermis and uppermost subcutaneous tissue. Involvement of lymphatic channels and tissue spaces with polymorphonuclear leukocytes is a typical finding.
Surgical wounds, the umbilicus of the neonate, or any break in the skin may serve as the portal of entry; however, the initial lesion may be inapparent. Localized edema, such as occurs from a renal or lymphatic source, is a predisposing factor, and antecedent respiratory tract infection often is reported. An increased risk for development of erysipelas has been noted in patients with hypogammaglobulinemia, certain malignancies such as lymphoma, or lymphedema complicating radiation therapy.
The diagnosis generally is recognized on clinical grounds, and GAS traditionally has been isolated by aspiration of the advancing margin of the lesion. A few case reports have identified other streptococci (including groups B, C, and G), Moraxella spp., Haemophilus influenzae, and Streptococcus pneumoniae as etiologic agents. A combination of intravenous penicillin and clindamycin should be used until the results of culture are available. Erysipelas has a classic clinical appearance, and appropriate diagnosis and therapy result in a prompt clinical response in most cases. Penicillin prophylaxis may be considered for patients with recurrent erysipelas, particularly patients with underlying risk factors.
Ecthyma
Ecthyma gangrenosa is a deep-seated infectious process that manifests as a necrotic ulcer covered by a black eschar. Usually the initial lesion, a vesicopustule, sits on an erythematous base; it eventually erodes through the epidermis to the dermis, where it forms a crusted ulcer with heaped-up borders and then becomes frankly necrotic.
This process rarely occurs in an otherwise healthy child, and, if it does, an immunodeficiency workup should ensue. Chromobacterium violaceum has been reported to cause ecthyma and similarly should result in an immunologic evaluation focusing on neutrophil defects, including disorders such as chronic granulomatous disease.
Ecthyma can occur as a primary cutaneous infection in an immunocompetent host, and other etiologic agents that have been confirmed include S. aureus, Aeromonas hydrophila, and GAS. A similar-appearing lesion is seen with cutaneous anthrax; however, extensive nonpitting edema of the surrounding soft tissues is an important clue to this diagnosis. Ecthymatous-like lesions have been seen in patients with herpes simplex infection. Additionally, human orf infections result in ulcerative skin lesions that appear similar to lesions of ecthyma; the clue to establishing the diagnosis is contact with an infected animal, usually sheep or goats, or a contaminated fomite.
When an ecthymatous lesion is noted in a febrile neutropenic host, it generally signals disseminated infection. P. aeruginosa is the etiologic pathogen identified most commonly in such cases, but other gram-negative pathogens and fungi, including Enterobacter, Escherichia coli, Morganella, Pseudomonas cepacia, Serratia marcescens, Stenotrophomonas maltophilia, Aspergillus, Mucor, Fusarium, and C. albicans, have been implicated in ecthyma gangrenosum in compromised hosts. Ecthyma has been seen as the heralding manifestation of acute lymphoblastic leukemia in children. Empiric antimicrobial therapy for ecthyma gangrenosum in a neutropenic host should include intravenous therapy with an anti- Pseudomonas agent plus an aminoglycoside. Biopsy of the lesion may provide more specific etiologic information and allow for confirmation of antimicrobial susceptibility.
Folliculitis, Furunculosis, and Carbuncles
Folliculitis, furunculosis, and carbuncles represent a group of infections characterized by their origin in the hair follicles and the formation of abscesses. Virtually always caused by S. aureus, these infections were seen commonly in the 1950s in disease that often involved multiple family members. Outbreaks among athletes likewise have been reported.
By definition, these infections involve sites where body hair is present, including the axilla, breast area, perineum, neck, and extremities. Lesions of folliculitis represent abscesses of a single hair follicle with limited surrounding tissue involvement. When deeper inflammatory nodules are associated with tissue edema, furunculosis is diagnosed. When several interconnecting furuncles are present, the lesion is referred to as a carbuncle. Generally, older children and adolescents are predisposed to the development of follicular infections, and individuals with diabetes mellitus, abnormal neutrophil chemotaxis, and impaired circulation may have recurrent disease.
Although S. aureus nearly always is the cause of folliculitis as in the past, outbreaks of so-called hot tub folliculitis have been described and almost always are caused by P. aeruginosa; rarely other gram-negative organisms have been reported. Folliculitis in an immunocompromised host often is caused by unusual fungal pathogens. Although typically associated with hot tubs and whirlpools, a large outbreak of Pseudomonas folliculitis reported in 1984 involved 117 individuals after swimming in an indoor pool. An incubation period of 24 to 30 hours could be ascertained, and a typical follicular, pustular eruption was noted. The mean duration of the folliculitis, 15 days, is consistent with other reports, but some patients continued to complain of rash for weeks, and recurrent pustules appearing months later have been reported in other studies.
A more recent report has identified four cases of Mycobacterium fortuitum complex furunculosis that developed after pedicures, suggesting this pathogen may be added to the differential diagnosis in such cases when a patient presents with nonhealing furuncles on the lower legs, especially when bacterial cultures have been negative or the disease is unresponsive to antistaphylococcal therapy (including MRSA). Early recognition and institution of appropriate therapy are essential, and the history of pedicures may be a clue to establishing the diagnosis. Cutaneous myiasis has been reported to manifest as a chronic boil or furuncle, but the diagnosis should be considered only in such cases in which an appropriate travel history is elicited.
Recognition of the typical skin lesion usually is sufficient to establish the diagnosis. Unless the patient has a history of exposure to a hot tub or whirlpool or recently has had a pedicure, a regimen of antistaphylococcal therapy should be sufficient. In the era of MRSA infection, local susceptibility profiles should be used to confirm appropriate therapy. Isolated boils resolve with drainage alone. Systemic therapy may be considered in cases in which lesions are large or multiple. TMP-SMX is a good choice for a nontoxic patient older than 2 months. Clindamycin is a good choice for most locales, although resistance may be increasing. Because MRSA now accounts for 75% of cases in which children present with skin and soft tissue infection, treatment should be individualized based on type of presentation, patient age, and underlying disease. Systemic agents should be used for 7 to 10 days in patients who are toxic, who have extensive disease, or who have associated cellulitis. Large lesions, specifically larger than 5 cm, should be incised and drained, and culture should be done in all cases to confirm susceptibility testing. In some patients, hematogenous metastatic spread may occur, and a search for foci in the heart, bones, joints, deep tissues, or brain should be done in patients with significant systemic toxicity.
For patients in whom recurrent disease develops, chronic dermatoses, such as eczema, should be identified, and in obese adolescents, the diagnosis of diabetes mellitus should be considered. The patient should be cautioned to refrain from sharing washcloths or towels, and skin trauma and use of irritants such as deodorants should be avoided.
The utility of decolonizing regimens with topical agents, such as mupirocin (nares and perianal area) and chlorhexidine or bleach baths (skin), may be considered in certain cases. S. aureus colonization of the nares, rectum, or skin can be detected by culture of these areas, but confirmation of carriage is likely necessary only in specific cases for which decolonization is desirable. The indications for and benefit of decolonization vary depending on host factors, underlying disease, and circumstances related to the health care setting. Outbreaks of MRSA colonization or infection require a multifaceted approach, including attention given to hand washing, cohorting, barrier measures, and decolonization strategies. Implementation of a decolonization regimen should be considered in special circumstances including (1) patients who are immunosuppressed and colonized and at risk for development of systemic infections, (2) patients who are more likely to spread the organisms owing to behavior, (3) patients who have repeated infections caused by the MRSA strain they carry, or (4) patients undergoing certain surgeries (cardiac, implantable devices) in whom colonization is confirmed; in addition, targeted prophylaxis should be used preoperatively. Most children with recurrent furunculosis are otherwise healthy, and no specific immunologic evaluation is necessary; however cases of recurrent furunculosis in patients with hyper-IgE syndrome and common variable immunodeficiency have been reported, and an association with mannose-binding lectin deficiency was confirmed in a family. Rarely children with white blood cell defects may have recurrent staphylococcal skin abscesses, and tests of white blood cell function may be considered in specific patients. Data suggest that vitamin C may be beneficial in cases of recurrent folliculitis.
Hidradenitis Suppurativa
Hidradenitis suppurativa, a chronic, debilitating condition, is a disorder of the apocrine glands that involves primarily skin in the axilla and anogenital region, although scalp, umbilical, and breast involvement has been reported. Seen mainly in adolescents, this androgen-dependent condition is manifested by the development of multiple painful nodules and the formation of deep abscesses in the skin in areas where apocrine glands are present. The formation of fistulas, ulcers, and contracted scars may complicate the course, and recurrent relapses may be noted. Infection usually is polymicrobial, and pathogens to consider include S. aureus, gram-negative enteric organisms, and anaerobes. Drainage of abscesses and institution of systemic antimicrobial therapy may be necessary. When fistulas associated with anogenital disease develop, adjacent structures, including the urethra, bladder, and rectum, may be involved. Surgery usually is required for cure. Carbon dioxide laser treatment in some cases may be beneficial.
Cellulitis
The diagnosis of cellulitis is made when the subcutaneous tissues and dermis are involved in a clinical process manifested as localized edema, erythema, warmth, and tenderness of the tissues. The leading edge of the involved site may be notable, but it is not raised and well demarcated as in erysipelas.
Infection usually is caused by coagulase-positive staphylococci and GAS; however, infection also is caused by group B streptococcus (neonates) and S. pneumoniae, and, in the past, H. influenzae type b cellulitis was described. Streptococcal and staphylococcal cellulitis can involve patients of any age and any site, although the extremity is noted most often. Frequently the patient has a history of antecedent trauma at the site of involvement, but the injury may not have appeared significant. Some researchers advocate culture of the cellulitic site, but in practice, it rarely is performed. Blood cultures are valuable in individuals with disease caused by group B streptococcus, S. pneumoniae, and H. influenzae type b.
Group B streptococcal cellulitis occurs in neonates and generally is seen as part of invasive, late-onset disease. Unilateral involvement of the face or submandibular sites occurs most commonly, but inguinal, scrotal, and prepatellar involvement has been described. When cellulitis occurs in an infant younger than 3 months, group B streptococcal bacteremia should be suspected, even in the absence of other signs of systemic infection.
Pneumococcal soft tissue infections are common findings. Patients with connective tissue disorders, such as systemic lupus erythematosus, seem especially prone, although these infections can occur in healthy infants and children. Sites of involvement include the head, neck, leg, and torso.
H. influenzae type b cellulitis often involves the face of infants ( Fig. 60A.4 ). A violaceous hue of the cellulitic area, which some researchers thought to be pathognomonic, might be observed. This process nearly always was the result of hematogenous seeding by H. influenzae type b, and meningitis occurred in 15% to 20% of such patients. As has been the case with other forms of H. influenzae type b disease, almost complete eradication has been achieved in the past decade with the use of conjugate vaccine.
Treatment of simple cellulitis in patients with a clear-cut area of preceding trauma should include an agent that is active against S. aureus and GAS; in most locales, clindamycin remains a good choice for therapy, although resistance for S. aureus (10% to 15%) and GAS (2% to 3%) is noted. The aforementioned caveats for treating staphylococcal skin infections should be followed. In infants with buccal or periorbital involvement or in infants with soft tissue involvement but without a clear-cut focus of infection, a third-generation cephalosporin, such as cefotaxime or ceftriaxone, should be included with clindamycin. Vancomycin always should be included in cases of a patient who is toxic and when metastatic suppurative disease is suspected.
Antibiotic-resistant gram-negative infections should be considered in the hospitalized patient who develops cellulitis, especially in those who are immunosuppressed, and broad-spectrum therapy should be considered empirically until results of cultures are available.
Necrotizing Fasciitis
Necrotizing fasciitis is a rapidly progressive bacterial infection of the soft tissues associated with a fulminant course and a high mortality rate. This infection spreads rapidly in the plane between the subcutaneous tissue and superficial muscle fascia and causes widespread necrosis. Prompt and aggressive medical and surgical management is necessary to ensure a good outcome.
In children, necrotizing fasciitis usually is caused by GAS; traumatic lesions involving the skin, including varicella, burns, or eczema, may predispose to this aggressive process. An association has been noted among varicella, ibuprofen use, and invasive GAS infection, although no data convincingly link this triad to necrotizing infection. Patients with congenital or acquired immunodeficiencies are at greater risk for the development of necrotizing fasciitis, and in neonates, omphalitis and circumcision are predisposing conditions.
Clinical Manifestations
The child generally has a high fever and is fussy. In infants, the irritability may be profound and may not appear to be localized to an involved site, unless the clinician is meticulous in conducting the examination. An extremity most commonly is involved, and older infants and children often refuse to bear weight or move the affected extremity. Swelling of soft tissue usually is noted, but the erythema may be subtle. The hallmark tip-off on examination is the finding of intense pain on manipulation of the involved site that is out of proportion to the cutaneous signs. Skin changes that occur during the subsequent 24 to 48 hours include blistering with bleb formation, and a dusky appearance of the involved site is noted as vessels are thrombosed and cutaneous ischemia develops. Skin necrosis is a late sign and indicates a poor prognosis ( Fig. 60A.5 ).
Recognition of the manifestations of toxic shock syndrome (see Chapter 64 ) is crucial because mortality rates of 60% have been reported in patients with associated fasciitis. Multisystem complaints, including vomiting, diarrhea, and severe myalgia, are present when GAS fasciitis is associated with streptococcal toxic shock syndrome. Tachycardia out of proportion to fever and altered mental status may be early signs of toxic shock syndrome. Renal and hepatic dysfunctions occur typically, and signs and symptoms of acute respiratory distress syndrome often are identified.
Diagnosis
The diagnosis cannot be based on the appearance of the involved site because none of the early findings of necrotizing fasciitis is pathognomonic. Plain radiographs usually are normal and of no value in establishing the diagnosis. Magnetic resonance imaging (MRI) is the preferred technique to detect soft tissue involvement. MRI permits visualization of the soft tissue edema infiltrating the fascial planes. Although MRI may be helpful, it should not delay performing surgical intervention. Waiting for a radiographic procedure to be performed to confirm the diagnosis may serve only to delay implementing definitive surgical therapy and to increase the risk for development of systemic complications, contributing further to the increased morbidity and mortality rates. In the typical clinical scenario in which the index of suspicion for necrotizing fasciitis is high, surgical exploration is appropriate, even in the presence of “normal” MRI findings.
Laboratory manifestations of streptococcal toxic shock syndrome should be sought in any pediatric patient with fasciitis. Typically, the white blood cell count is normal; however, most patients have a significant increase in band forms (>50%) noted on the peripheral blood smear. Thrombocytopenia and evidence of coagulopathy are found commonly, and marked hypoalbuminemia with hypocalcemia is a typical finding. Laboratory findings associated with renal failure, myocardial dysfunction, and acute respiratory distress syndrome may develop during the first 48 to 72 hours.
A microbiologic diagnosis can be made by isolating bacteria from blood, tissue, or wound culture. In some cases, a polymicrobial etiology has been noted, particularly in patients with so-called Fournier gangrene or necrotizing fasciitis of the perineum. In these cases, S. aureus, GAS, and one or more anaerobes, including Peptostreptococcus, Prevotella, Bacteroides fragilis, and Porphyromonas, have been implicated in infection. Fasciitis caused by P. aeruginosa or Clostridium septicum has been seen in neutropenic patients. In the past decade, GAS has been reported widely as a single pathogen and is the etiologic agent in most cases of pediatric fasciitis. As in other cases of invasive disease caused by GAS, virulence is related to certain structural characteristics of the organism and to its ability to produce biologically active substances, some of which facilitate invasion and spread of the pathogen.
Treatment
Surgical debridement of necrotic tissue is the key to managing necrotizing fasciitis, and increased mortality rates have been observed when debridement is delayed more than 24 hours. Mandatory return to the operating room for examination and repeat debridement should occur during the following 24 to 48 hours. Careful management of fluids, attention to pain control, anticipation and management of multisystem organ failure, and administration of appropriate parenteral antimicrobial therapy should be initiated promptly. The use of intravenous immunoglobulin may be considered in cases of toxic shock syndrome–associated fasciitis.
Appropriate therapy includes intravenous penicillin 150,000 U/kg per day divided into four to six doses, clindamycin 40 mg/kg per day divided into four doses, and vancomycin 40 mg/kg per day divided into three to four doses. The use of additional coverage with agents active against P. aeruginosa and gram-negative enteric organisms should be considered in neutropenic patients.
Response to therapy is assessed by careful serial examination. Control of pain is crucial in such patients, while keeping in mind that persistent, severe pain suggests ongoing tissue necrosis and may signal the need for further surgical intervention. Careful attention to nutritional support should be maintained throughout the child’s hospital stay. Physical therapy is necessary for most patients, especially patients who require amputation, skin grafting, or extensive reconstructive surgery, and providing for the psychosocial needs of the child and the family is imperative.
Contaminated Wounds
Although staphylococci and streptococci are the most likely causes of infection after traumatic skin lesions, the list of causes may be extensive, depending on the nature of the injury. Specific pathogens should be considered when infections develop after human or animal bites, soil or water contamination, or various types of injuries. Management of such infections depends on recognizing infection patterns and obtaining cultures for careful identification of the specific organism or organisms involved ( Table 60A.2 ).
