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Skin and skin structure infections are diverse in their presentation and severity, and consists of two principal categories-complicated and uncomplicated SSSI. While complicated SSSI frequently require initial hospitalization for intravenous antibiotics with potential incision and drainage, uncomplicated SSSI can often be successfully treated with oral antibiotics or local care in the outpatient setting. Similarities in clinical presentation with inflammatory diseases, coupled to limitations in laboratory findings, pose challenges in definitively diagnosing uncomplicated SSSI in the clinic setting. As such, assessment of risk factors and severity of infection, along with obtaining a detailed medical history and physical exam, are essential in making a diagnosis and formulating a prudent treatment strategy. Pharmacologic treatment is often empirical, requiring a general knowledge of common etiologic agents and local antimicrobial resistance trends.
This chapter provides recent information on the epidemiology, pathophysiology, clinical features, diagnosis, and therapeutic management of SSSI encountered in the outpatient setting. Both bacterial and viral, specifically varicella, etiologies are presented.
Epidemiology (A) (Max)
Pathophysiology (A) (Max)
Predisposing Factors (A)
There are a multitude of factors that predispose patients to developing acute bacterial SSSI. Poor hygiene and crowding can easily facilitate dissemination of contagious infections including impetigo, furuncles and carbuncles. Close contacts with infected individuals (e.g., family members, prisoners and contact sport players) can also spread these infections. Certain medical conditions, including edema from venous insufficiency, pre-existing skin diseases that disrupt the skin barrier (e.g., eczema, impetigo, tinea pedis, and inflammatory dermatoses), impaired lymphatic drainage, and immunosuppression can increase the risk of developing cellulitis and erysipelas. In addition, traumatic injuries that rupture the skin (e.g., injection drug users and insect bites) can predispose to the development of skin abscesses, furuncles, or carbuncles.
While Staphylococcus aureus and Group A streptococci (GAS) are the most common causes of acute bacterial SSSI, patients presenting with certain underlying conditions, exposure, or trauma are at risk for infections caused by other pathogenic bacteria (Tables 1 and 2). For example, skin infections that result from bites are predominantly caused by Eikenella corrodens or Pasteurella multocida depending on offending source.
Bacterial colonization, specifically GAS on the skin and S. aureus in the anterior nares, is also a risk factor for SSSI. Some cases of impetigo are preceded by streptococcal colonization, and nearly all of these GAS strains exhibit D or E patterns of the emm genes that encode a virulence factor. Other than nasal or skin staphylococcal carriage, cutaneous abscesses, furuncles, and carbuncles can develop in healthy individuals with no predisposing conditions. In addition, nasal carriers are at increased risk for recurrent infections.
The prevalence of nasal colonization by S. aureus is 20% to 40% in the general population. Antibiotic use in the previous 3 months, hospitalization in the previous 12 months, or contact with a household member employed at a hospital, have been associated with a 2.5 to 10 times greater risk for methicillin-resistant S. aureus (MRSA) nasal carriage. Furthermore, high rates of community-associated MRSA (CA-MRSA) colonization and infection have been reported among certain populations, including Native Americans, Alaskan Natives, and Pacific Islanders. Compared to other bacterial pathogens, CA-MRSA has emerged as a significant source for cutaneous abscess and suppurative cellulitis, even as spontaneous infections. In one pediatric study, rectal colonization of CA-MRSA has been associated with skin abscesses.
Bacterial Infections (A)
Acute bacterial SSSI are diverse in their presentation and severity. In the sections that follow, clinical presentation, diagnosis, and therapeutic management of uncomplicated SSSI caused by bacteria are presented.
Typical Causative Organisms (B)
S. aureus and GAS are the leading cause of SSSI in both adults and children. The prevalence of these Gram-positive bacteria depends on the type of SSSI, with S. aureus as the most common cause of furuncles and carbuncles and GAS for erysipelas (Table 1). Group A streptococcus is the most likely causative pathogen for nonsuppurative cellulitis, especially if penetrating trauma or underlying abscess is absent. Otherwise, S. aureus is more likely than GAS to be the culprit in causing the SSSI. In patients with diabetes, methicillin-resistant Staphylococcus aureus (MRSA) XXXX
To a lesser extent, Gram-negative bacteria such as Pseudomonas aeruginosa may cause SSSI especially in patients with certain risk factors, including immunocompromised status, chronic ulcers, and injection drug use (Table 2). "Hot tub" folliculitis is contracted through exposure to P. aeruginosa from a contaminated hot tub or whirlpool. In patients who are immunocompromised, other pathogens should be considered, like Nocardia and Cryptococcus for cellulitis and carbuncles.
ADD HERE - few sentences from Max's section on bite wound, diabetic foot etc here.
Antibiotic Resistance (C)
Antibiotic resistance among GAS to erythromycin and S. aureus to methicillin has increased in the recent decades and this inevitably influences the selection of empiric antibiotic treatment for SSSI. With the significant prevalence of GAS resistance, macrolides should be avoided as empiric therapy unless local and up-to-date resistance trends indicate otherwise. Infections caused by MRSA were usually confined to hospitals and long term care facilities; however, MRSA has emerged as a significant pathogen within the community typically presenting as a skin infection and even affecting individuals without risk factors. Rates of these CA-MRSA causing SSSI, mostly as furuncles, carbuncles, and abscesses, have increased steeply during the past two decades. In fact, CA-MRSA now accounts for 3% to 25% of folliculitis. Despites these CA-MRSA isolates being often susceptible to multiple non-ï¢-lactam antimicrobials, efforts to prevent MRSA in communities have escalated to the state and national levels through the Centers for Disease Control and Prevention (CDC).
While SSSI caused by CA-MRSA may occur in any patient (even one without any risk factor), it is still nevertheless important to recognize risk factors for MRSA infections to ensure appropriate empiric therapy (Table 3). In addition to these risk factors, patients with MRSA SSSI, usually as abscesses, incorrectly report spider or insect bites. Over half of these MRSA abscesses contain eschars at the midpoints.
Molecular Features (C)
The mobile segment containing the mecA gene that encodes a penicillin-binding protein 2a to effectively inactivate ï¢-lactam is the staphylococcal cassette chromosome mec (SCCmec). Most CA-MRSA strains in the United States possess SCCmec type IV and V. In addition, the clonal lineages determined by pulsed-field gel electrophoresis that predominate among CA-MRSA isolates in the United States are USA300 and USA400. In large epidemiologic studies, most nasal staphylococcal colonizers exhibit SCCmec type II (USA100). Rectal colonization of CA-MRSA from the USA300 clone has been associated with skin abscesses. Even with its distinct molecular features, it is becoming increasingly challenging to distinguish CA-MRSA from healthcare-associated MRSA (HA-MRSA) as community isolates are emerging pathogens causing serious infections in acute care settings.
Panton-Valentine leukocodin (PVL), a cytotoxin that destroys white blood cells and mediates tissue necrosis, can be detected in CA-MRSA by the polymerase chain reaction. This gene contains two synergistic proteins (lukS-PVL and lukF-PVL), and has been associated with severe necrotizing pneumonia and skin lesions in adults and children. Especially during epidemic disease, 42% of furuncles are caused by PVL-positive S. aureus. Since up to 25% of HA-MRSA exhibit PVL, the role of PVL in serving as a marker for CA-MRSA infections remain uncertain.
In some communities, most isolates of CA-MRSA remain susceptible to clindamycin, and clindamycin is used widely for empiric therapy of common staphylococcal cellulitis, especially in children. However, MRSA that are clindamycin-susceptible but erythromycin-resistant may exhibit inducible resistance to clindamycin (i.e., such isolates may develop resistance to clindamycin upon exposure to the drug). This inducible resistance is mediated through expression of the erythromycin resistance methylase (erm) gene. Standard susceptibility testing does not detect this inducible resistance. As such, the disk diffusion induction test (D-test) should be performed on clindamycin-susceptible, erythromycin-resistant S. aureus isolates should be performed especially for serious infections and those unresponsive to initial therapy. Rapid development of inducible resistance to clindamycin in vitro has been demonstrated among clinical isolates of S. aureus, and clinical failures have been reported in patients with MRSA isolates expressing the erm gene. The prevalence of inducible clindamycin-resistance varies by geographical region and can change over time.
General Treatment Considerations (B)
Antibiotic therapy for uncomplicated SSSI is most often initiated empirically and involves the use of oral agents, including semi-synthetic penicillins, first-generation cephalosporins, macrolides, or clindamycin. Local resistance patterns should be considered since high rates of antibiotic resistance may preclude the use of clindamycin for MRSA with inducible resistance and erythromycin for GAS. Clinical re-evaluation for symptomatic improvement within 24 to 48 hours after initiation of antibiotic therapy is prudent. Lack of clinical improvement despite antibiotic therapy suggests infection by a resistant pathogen, or a deep, serious infection that may require management in the hospital setting.
Non-Pharmacologic Strategies (B)
Non-pharmacologic therapies are generally adequate for SSSI that are not extensive and absent in systemic symptoms. It can also be used concurrently with antimicrobial therapy to optimize resolution of infection. Warm compresses (for folliculitis and small furuncles), and incision and drainage (for large furuncles and minor cutaneous abscess < 5 cm in healthy individuals without any risk factor) promote drainage from these SSSI that are accompanied by abscesses. For impetigo, crusted lesions should be washed gently. Since poor hygiene is a risk factor for impetigo and other SSSI, handwashing is important for reducing spread. Other measures of good hygiene, including those for wound care, are described in Table 4. Patient education is a crucial for infection control especially in the community setting,
Goals of Therapy (B)
The therapeutic goals in patients with SSSI are cessation of the spread of, or reduction in the redness, edema, and/or induration of the lesion(s) within 48 to 72 hours after initiation of therapy, which can either be non-pharmacologic, pharmacologic, or both. Any increase in erythema, edema, and/or induration of the lesion constitutes as clinical failure. Notably, erythema may escalate initially in patients with erysipelas.
In addition to clinical resolution, recovery of symptoms (if present at baseline), eradication of bacterial colonization, and prevention of transmission (particularly for impetigo, furuncles and carbuncles) are other therapeutic goals. Restoration of cosmetic appearance is imperative especially if the face was involved. Ensuring patient adherence and preventing adverse drug reactions are important considerations in the pediatric population. Other goals are prevention of complications and recurrent infection in patients with underlying conditions that predisposes them to SSSI (e.g., recent surgery, immunocompromised status, diabetes)
Triaging Based on Type and Severity of Infection (B)
Treatment in the community is more attractive than hospitalization for SSSI; patient satisfaction is improved, the use of acute medical care resources is minimized, and healthcare-associated infections are prevented. An evaluation of the type and severity of SSSI, along with risk factors and co-morbidities, is important in determining the appropriateness of outpatient management, which may require both oral antibiotics and surgical drainage performed on an outpatient basis.
While mild, superficial SSSI may be treated on an outpatient basis, more serious SSSI, particularly those involving soft tissues, require hospitalization for appropriate management with surgery and parenteral antibiotics. Serious SSSI are generally accompanied by systemic signs and symptoms that consist of fever (oral or tympanic temperature â‰¥ 380C) or hypothermia, tachycardia (heart rate > 100 beats/min), hypotension (systolic blood pressure < 90 mm Hg), confusion, and shortness of breath. Other signs of serious, deep SSSI are: severe pain disproportionate to the physical findings, rapid increase in lesion size, emergence of bullous lesion, and reddish-purple skin coloring. Certain underlying conditions, such as neutropenia or chronic use of steroids, may camouflage the severity of SSSI with subtle clinical signs and symptoms. To ensure proper management, patients with moderate to severe SSSI, including those with underlying conditions that may mask severity of disease, require hospitalization for blood cultures and other diagnostic work-up. Hospitalization facilitates completion of these procedures as well as the need for close observation of disease progression and parenteral antibiotic therapy. In addition, patients with limb-threatening infection, uncontrolled diabetes, nonadherence, and significant nausea, vomiting or diarrhea need hospitalization for appropriate management.
Outpatient parenteral antibiotic therapy may be an alternative to hospitalization, and can be administered at home, or in an infusion clinic. However, this is generally reserved for treatment continuation after a short hospital stay when oral antibiotics are unavailable, or for other infections that require prolonged courses of antibiotic therapy (e.g., osteomyelitis). Information pertaining to outpatient parenteral antibiotic therapy is beyond the scope of this chapter, but is presented in other chapters like osteomyelitis.
The U.S. Food and Drug Administration (FDA) defines cellulitis, erysipelas, wound infection, and major cutaneous abscess as those with a minimum of 75 cm2 in affected surface area that present as redness, edema, and/or induration. In addition, lymph node enlargement or systemic symptoms such as fever must be present. Impetigo does not have a defined surface area, and minor cutaneous abscess are < 5 cm for adolescents and adults.
These definitions provide the foundation for initiating antibacterial drug therapy, and an objective monitoring parameter to document clinical improvement or deterioration. In addition, these designations can be employed in future clinical studies to demonstrate efficacy and assess toxicities of new antimicrobials, specifically superiority trials for mild infections like impetigo and minor cutaneous abscess in which systematic symptoms are not required. However, the translation into current clinical practice, particularly in the outpatient setting, is unclear. The definitions of cellulitis and erysipelas incorporate systemic manifestations, which imply increased severity and hospitalization for therapeutic management. The management strategy still remains uncertain for SSSI that are 75 cm2 or greater but in the absence of systemic symptoms. In these scenarios with lack of systemic symptoms, initiating antimicrobial therapy, perhaps in the outpatient setting, is rational and justifiable to ensure optimal patient outcomes and potentially minimize progression to deep infections. The decision to initiation antibiotic treatment for SSSI that are below 75 cm2, except for impetigo and minor cutaneous abscess, and without systemic manifestations should incorporate assessment for underlying conditions and predisposing factors for infection.
Two types of impetigo exist-the non-bullous form that is caused by GAS, and the bullous form, which has become more prevalent, by S. aureus alone or as a mixed infection with GAS. In bullous impetigo, S. aureus produces an exfoliative toxin A that ruptures the superficial skin layer. Since CA-MRSA strains rarely harbor exfoliative genes, they are not a common cause of impetigo.
Infection can occur from direct bacterial invasion on normal skin, or after minor skin trauma (e.g., abrasions, insect bites, eczema). Colonization of GAS on intact skin generally precedes infection, which may take up to 10 days for lesions to develop after disrupting the skin integrity. While GAS colonizes the skin, staphylococcal colonization occurs in the nose but precedes infection as well. This progression from carriage to infection highlights the importance of proper hygiene for disease prevention. Without proper hygiene, impetigo can easily spread, particularly among close contacts (e.g., preschool children in daycare), and people living in crowded or impoverished conditions. Impetigo rarely leads to invasive complications including pneumonia, osteomyelitis, and septicemia.
Clinical Presentation and Diagnosis (C)
Impetigo occurs mostly in young children aged 2 to 5 years, with epidemics during summer and fall months. It is a contagious superficial bacterial infection caused by S. aureus and beta-hemolytic Streptococcous (primarily group A, but occasionally serogroups C and G). Impetigo usually presents as multiple erythematous, vesicular, and pruritic lesions on exposed body surfaces, primarily the face and extremities. These lesions erupt and form crusts. Symptoms are localized and non-systemic. Although uncommon, two invasive sequelaes of streptococcal impetigo are glomerulonephritis and perhaps acute rheumatic fever, as reported in Australian aboriginal communities. Antibiotic therapy may not prevent these complications.
The diagnosis of impetigo is largely based on clinical findings. Swabs of intact skin offer no value and therefore should not be performed. Serologic tests are also not useful since the anti-streptolysin O (ASO) titer for streptococcal antibodies peak 4 to 6 weeks after infection, and anti-deoxyribonulease B (anti-Dnase B) and antihyaluronidase (AHT) responses are reserved for patients who develop post-streptococcal glomerulonephritis. In patients unresponsive to empiric therapy, cultures of bullae fluid may be useful in tailoring therapy.
Pharmacologic Therapy (C)
Topical and oral therapies are available for treating impetigo. Topical antibiotics are recommended for non-bullous lesions that are limited in number; oral antibiotics for bullous impetigo and infections that are extensive enough to preclude the use of topical products. With the increasing prevalence of bullous impetigo, empiric therapy should provide adequate coverage for S. aureus. Topical mupirocin is as efficacious as fusidic acid (not available in the United States), and both of these topical antibiotics are more effective than oral erythromycin for mild disease. While still infrequent (<5%), mupirocin resistance among MRSA nasal colonizers has been reported worldwide, including the United States. Other topical products, including retapamulin ointment, are described in Table 5.
Anti-staphylococcal oral antibiotics, such as dicloxacillin and cephalexin, are appropriate first-line agents for treating bullous or extensive impetigo (Table 5). Clindamycin, doxycycline, minocycline and trimethoprim-sulfamethoxazole (TMP-SMX) are reasonable alternatives for use in patients with serious allergies to beta-lactams, or for suspected MRSA infection. Antibiotic therapy usually continues for 7 days, but depends on clinical resolution. With the increasing prevalence of GAS and S. aureus resistance, macrolides should be avoided. Similarly, resistance to fluoroquinolones among MRSA limit the use of this class of antibiotics. In one large epidemiologic study of patients admitted to U.S. hospitals between 2009 and 2010, over 80% of MRSA nasal colonizers were resistant to either ciprofloxacin or levofloxacin.
Folliculitis, Furuncles Carbuncles, and Minor Cutaneous Abscesses (B)
Folliculitis, furuncles and carbuncles are SSSI that involve formation of small abscesses surrounding hair follicles and as such occur on hairy surfaces of the skin (e.g., back of the neck, face). Folliculitis is a superficial purulent infection of the epidermis. In contrast, furuncles (single inflamed follicle, or "boils") and carbuncles (amalgamation of multiple inflamed follicles) are abscesses that form below the epidermis, extending into the subcutaneous tissue. These SSSI affect people of all ages, especially those in close contact (e.g., family members, contact sport players, and prisoners) as clusters of infection. Other risk factors include hyperhidrosis, obesity, diabetes, seborrhea, anemia, malnutrition, and immunodeficiency.
Clinical Presentation and Diagnosis (C)
Folliculitis, furuncles and other minor cutaneous abscesses appear as localized painful and swollen erythematous nodules, unlike carbuncles where systemic illness (e.g., fever) may occur. Diagnosis of these SSSI is based on clinical presentation, particularly if involves the hair follicle. Other skin lesions should be excluded during differential diagnosis, including leishmaniasis and myiasis observed in returning travelers. While not routinely performed but if available, drainage fluid should be sent for culture and susceptibility testing.
Pharmacologic Therapy (C)
Mild cases of folliculitis and minor cutaneous abscesses or furuncles are self-limiting and can resolve without antibiotic therapy. Non-pharmacologic therapies, including warm, moist compresses to encourage drainage, and and incision and drainage for minor abscesses, are generally adequate since these SSSI are not extensive and lack systemic symptoms. In fact, minor cutaneous abscesses â‰¤ 5 cm, including some caused by MRSA, may be treated with incision and drainage alone, especially in patients without co-morbidities. Antibiotic therapy should be considered, along with incision and drainage, when lesions are > 5 cm or multiple in number. Furthermore, antibiotic treatment should be initiated in patients with major cutaneous abscess, defined by the FDA as abscesses that are â‰¥ 75 cm2. Patients with concurrent co-morbidities (e.g., diabetes and immunocompromised state), and have very extensive infection or present with systemic symptoms (as evident in carbuncles) should be hospitalized for appropriate management.
Since S. aureus (including CA-MRSA) is the primary pathogen causing large furuncles and carbuncles, anti-staphylococcal therapy for 5 to 7 days should be initiated promptly to prevent dissemination into deeper tissues or other organs. Antibiotics targeting CA-MRSA are preferred in regions with a prevalence exceeding 10% (Table 5). In patients at risk for endocarditis, a single dose of anti-MRSA antibiotic should be administered before incision and drainage. While other bacterial pathogens, including the skin flora, can cause cutaneous abscesses outside the hair follicles, antibiotic therapy is unnecessary if the infection is small and purulent fluid is removed completely.
Some children and immunocompromised patients may have recurrent infections. Based on two randomized, control studies in children and adults, TMP-SMX may prevent recurrent infections.
For recurrent furunculosis, clindamycin, due to its nasal penetration, appears to decrease future episodes by 80% (Table 5). Eradication of nasal colonization using mupirocin ointment should also be considered in these scenarios. Lastly, outbreaks of furunculosis have been reported and additional measures to prevent transmission should be implemented. These measures include bathing with antibacterial soaps, meticulous washing of clothes, towels and beddings, and minimize sharing of towels.
Cellulitis and Erysipelas (B)
As skin infections marked by diffused, swollen erythemas, cellulitis and erysipelas occur in all ages and are challenging to distinguish clinically from each other. However, erysipelas is more common in infants, young children and elderly patients. Since erysipelas affects the upper dermis (of primarily our lower extremities), it is characterized by intense erythema and sharply demarcated, palpable borders. In contrast, cellulitis involves the deeper dermis and subcutaneous fat, and thus it is less pronounced in swelling without any distinct margins.
Clinical Presentation and Diagnosis (C)
Spreading erythema, edema, tenderness and warmth are observed or felt for both cellulitis and erysipelas. Regional inflammation of lymphatic channels and lymph nodes, and systemic effects, including fever and leukocytosis, may accompany these SSSI. Cellulitis may be purulent or nonpurulent. Compared to other erythematous skin lesions, cellulitis occurs unilaterally and unlikely to have a disseminated distribution (except in an immunocompromised host).
Cellulitis and erysipelas can be acquired secondary to conditions such as a compromised cutaneous barrier (e.g., impetigo, tinea pedis), penetrating traumas (e.g., injection drug use, insect or animal bites), impaired lymphatic drainage (usually from surgical procedures), or immunosuppression. Cellulitis may also develop following specific exposures (e.g., Aeromonas hydrophila or Vibrio vulnificus with water exposure and Pasteurella multocida with dog or cat bites).
Similar to other SSSI, the diagnosis of cellulitis or erysipelas is largely based on clinical appearance. Assessment of recent exposure or trauma and risk factors can help identify probable pathogens causing infection. Cultures of punch biopsy or aspirate of the leading edge of redness, purulent material (if present) from biopsy or needle aspiration, and blood are not useful for mild infections. However, they may be informative in tailoring therapy for patients with serious infections, have co-morbidities, or recurrent cellulitis. Serologic tests for ASO and streptococcal anti-Dnase B may also be useful for recurrent cellulitis. Radiologic tests can support exclusion of deep invasive infections (e.g., necrotizing fasciitis, gas gangrene, and osteomyelitis), particularly when rapid progression of local symptoms and systemic effects are present.
Pharmacologic Therapy (C)
While GAS is the main culprit for erysipelas, S. aureus, followed by GAS, are the most common causes of uncomplicated, non-suppurative cellulitis. Infections that are â‰¥ 75 cm2 in surface area should prompt initiation of antibiotic therapy. Initial antibiotic therapy should target these likely causative pathogens, including oral penicillin or amoxicillin for erysipelas and dicloxacillin or cephalexin for cellulitis (Table 5). The Infectious Diseases Society of America (IDSA) guidelines recommend dicloxicillin as the preferred oral agent for patients with suspected MSSA. Cephalexin is as efficacious as dicloxacillin for children with SSSI caused by MSSA. However, treatment failures with dicloxacillin have been reported in adult patients with uncomplicated cellulitis, potentially from poor absorption due to hypoclorhydria. Clindamycin is an alternative for patients with serious penicillin allergy, and a fluoroquinolone (moxifloxacin, gatifloxacin, and levofloxacin) for those intolerant to these antibiotics. Compared to levofloxacin, moxifloxacin has lower minimum inhibitory concentrations for many organisms. Gatifloxacin is contraindicated in diabetic patients due to the increased risk of glycemic imbalance. While clinical data remains non-existent, QT prolongation associated with the fluoroquinolone class may increase the risk of torsades de pointes. Notably, overuse of fluoroquinolones may facilitate further development of resistance. Currently 80% of MRSA nasal colonizers possess resistance to either ciprofloxacin or levofloxacin.
Tetracyclines and TMP-SMX do not adequately cover GAS and hence not recommended as monotherapy for erysipelas nor cellulitis. However, these antibiotics may be combined with amoxicillin for treating cellulitis. Medication adherence should be certain for these two-antibiotic combinations, compared to other one- antibiotic alternatives.
Most cases of suppurative cellulitis (i.e., cellulitis complicated by abscess formation) are caused by CA-MRSA, followed by MSSA. As such, oral antibiotics active against CA-MRSA should be used initially, including clindamycin (if local resistance rates are < 10 - 15%, or D-test negative), TMP-SMX, or a tetracycline (if allergic to sulfa) (Table 5). While oral linezolid is comparable to dicloxacillin in efficacy, with the additional CA-MRSA and HA-MRSA coverage, it should be reserved for serious complicated infections, or those unresponsive to other antibiotics. The infected area should be elevated to stimulate drainage of edema and inflammatory substances.
A 5- to 10-day treatment course is typically recommended for erysipelas and uncomplicated cellulitis, but longer courses of up to 14 days may be necessary depending on clinical resolution. Five days of antibiotic treatment is as effective as 10 days for uncomplicated cellulitis. Symptomatic and clinical improvements are generally observed within 24 to 72 hours of antibiotic initiation; however, erythema may intensify initially in some patients, particularly those with erysipelas. This waning erythema is caused by the increased release of inflammatory mediators from bacterial destruction. Concurrent administration of corticosteroids with antibiotics may reduce healing time and antibiotic duration, but not relapse nor recurrence. Longer duration of therapy may be necessary for complicated cellulitis and should be individualized based on patient response. Patients with deeper infections or underlying conditions (e.g., diabetes, chronic venous insufficiency, or lymphedema) may respond slowly, but should be monitored closely for expanding erythema or worsening systemic symptoms. Overall prognosis is excellent with early diagnosis and proper treatment.
Recurrent infection can occur from lymphedema caused by repeated episodes of cellulitis or erysipelas. Recurrences can be minimized by treating the underlying conditions (including edema by elevation of affected area, compressive stockings or diuretic therapy), skin hydration with emollients, and preventive measures to reduce staphylococcal dissemination. Antibiotic prophylaxis may be warranted if these measures are not effective, particularly in patients with lymphatic obstruction from surgical procedures such as saphenous venectomy, axillary breast node dissection, and pelvic lymph node dissection. Serologic testing with ASO, anti-DNAse B, and AHT (the latter two more reliable than the ASO following GAS skin infections) may guide prophylactic antibiotic selection.
Prophylactic options for beta-hemolytic streptococci include intramuscular benzathine penicillin injections 0.6 to 1.2 million units monthly or bimonthly, or oral penicillin V 250 to 500 mg twice daily; and clindamycin 150 mg orally once daily for S. aureus. Prophylaxis usually lasts several months. An alternative that may be suitable for reliable patients is self-initiation of antibiotic therapy with onset of symptoms; this shortens exposure to antibiotics. Oral selenium for 3 weeks may reduce recurrent erysipelas due to lymphedema in patients with cancer.
Wound Infection (B)