Executive Summary Soft-tissue infections are common, generally of mild to modest severity, and are easily treated with a variety of agents. An etiologic diagnosis of simple cellulitis is frequently difficult and generally unnecessary for patients with mild signs and symptoms of illness. Clinical assessment of the severity of infection is crucial, and several classification schemes and algorithms have been proposed to guide the clinician. However, most clinical assessments have been developed from either retrospective studies or from an author's own “clinical experience,” illustrating the need for prospective studies with defined measurements of severity coupled to management issues and outcomes.
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Until then, it is the recommendation of this committee that patients with soft-tissue infection accompanied by signs and symptoms of systemic toxicity (e.g., fever or hypothermia, tachycardia heart rate, 100 beats/min, and hypotension systolic blood pressure, 13 mg/L, hospitalization should be considered and a definitive etiologic diagnosis pursued aggressively by means of procedures such as Gram stain and culture of needle aspiration or punch biopsy specimens, as well as requests for a surgical consultation for inspection, exploration, and/or drainage. Other clues to potentially severe deep soft-tissue infection include the following: (1) pain disproportionate to the physical findings, (2) violaceous bullae, (3) cutaneous hemorrhage, (4) skin sloughing, (5) skin anesthesia, (6) rapid progression, and (7) gas in the tissue. Unfortunately, these signs and symptoms often appear later in the course of necrotizing infections. In these cases, emergent surgical evaluation is of paramount importance for both diagnostic and therapeutic reasons. Emerging antibiotic resistance among Staphylococcus aureus (methicillin resistance) and Streptococcus pyogenes (erythromycin resistance) are problematic, because both of these organisms are common causes of a variety of skin and soft-tissue infections and because empirical choices of antimicrobials must include agents with activity against resistant strains. Minor skin and soft-tissue infections may be empirically treated with semisynthetic penicillin, first-generation or second-generation oral cephalosporins, macrolides, or clindamycin (A-I); however, 50% of methicillin-resistant S.
Aureus (MRSA) strains have inducible or constitutive clindamycin resistance. Most community-acquired MRSA strains remain susceptible to trimethoprim-sulfamethoxazole and tetracycline, though treatment failure rates of 21% have been reported in some series with doxycycline or minocycline. Therefore, if patients are sent home receiving these regimens, it is prudent to reevaluate them in 24–48 h to verify a clinical response.
Progression despite receipt of antibiotics could be due to infection with resistant microbes or because a deeper, more serious infection exists than was previously realized. Infectious Diseases Society of America—US Public Health Service Grading System for ranking recommendations in clinical guidelines. Patients who present to the hospital with severe infection or whose infection is progressing despite empirical antibiotic therapy should be treated more aggressively, and the treatment strategy should be based upon results of appropriate Gram stain, culture, and drug susceptibility analysis. In the case of S. Aureus, the clinician should assume that the organism is resistant, because of the high prevalence of community-associated MRSA strains, and agents effective against MRSA (i.e., vancomycin, linezolid, or daptomycin) should be used (A-I).
Step-down to treatment with other agents, such as tetracycline or trimethoprim-sulfamethoxazole, for MRSA infection may be possible, based on results of susceptibility tests and after an initial clinical response. In the United States, not all laboratories perform susceptibility testing on S. However, the Centers for Disease Control and Prevention has provided national surveillance data that suggest a gradual trend of increasing macrolide resistance of S. Pyogenes from 4%–5% in 1996–1998 to 8%–9% in 1999–2001. Of interest, 99.5% of strains remain susceptible to clindamycin, and 100% are susceptible to penicillin. Impetigo, erysipelas, and cellulitis.
Impetigo may be caused by infection with S. Aureus and/or S. The decision of how to treat impetigo depends on the number of lesions, their location (face, eyelid, or mouth), and the need to limit spread of infection to others. The best topical agent is mupirocin (A-I), although resistance has been described ; other agents, such as bacitracin and neomycin, are considerably less effective treatments. Patients who have numerous lesions or who are not responding to topical agents should receive oral antimicrobials effective against both S.
Aureus and S. Pyogenes (A-I). Although rare in developed countries (. Antimicrobial therapy for impetigo and for skin and soft-tissue infections. Classically, erysipelas, is a fiery red, tender, painful plaque with well-demarcated edges and is commonly caused by streptococcal species, usually S.
Cellulitis may be caused by numerous organisms that are indigenous to the skin or to particular environmental niches. Cellulitis associated with furuncles, carbuncles, or abscesses is usually caused by S.
In contrast, cellulitis that is diffuse or unassociated with a defined portal is most commonly caused by streptococcal species. Important clinical clues to other causes include physical activities, trauma, water contact, and animal, insect, or human bites.
In these circumstances appropriate culture material should be obtained, as they should be in patients who do not respond to initial empirical therapy directed against S. Aureus and S. Pyogenes and in immunocompromised hosts. Unfortunately, aspiration of skin is not helpful in 75%–80% of cases of cellulitis, and results of blood cultures are rarely positive (8 years of age, pending identification of the offending agent (B-III). Adults and children who receive a diagnosis of tularemia should receive an aminoglycoside, preferably streptomycin or gentamicin, for 7–10 days. In mild cases, doxycycline or tetracycline for 14 days is recommended (B-III) (comments regarding treatment of children.
Antibiotic therapy for community-acquired and bioterrorism-related cutaneous anthrax. Data regarding antibiotic efficacy for treatment of cat-scratch disease are inconclusive, although 1 small study demonstrated more-rapid lymph node regression in patients receiving azithromycin, compared with patients receiving no treatment. Cutaneous bacillary angiomatosis has not been systematically studied, but treatment with erythromycin or doxycycline in standard doses for 4 weeks has been effective in very small series (B-III). On the basis of very incomplete data, erysipeloid is best treated with oral penicillin or amoxicillin for 10 days (B-III). Rhusiopathiae is resistant in vitro to vancomycin, teicoplanin, and daptomycin (E-III). Surgical site infections. Surgical soft-tissue infections include those occurring postoperatively and those severe enough to require surgical intervention for diagnosis and treatment.
The algorithm presented clearly indicates that surgical site infection rarely occurs during the first 48 h after surgery, and fever during that period usually arises from noninfectious or unknown causes. In contrast, after 48 h, surgical site infection is a more common source of fever, and careful inspection of the wound is indicated. For patients with a temperature 38.5°C or a heart rate 110 beats/min generally require antibiotics as well as opening of the suture line.
Infections developing after surgical procedures involving nonsterile tissue, such as colonic, vaginal, biliary or respiratory mucosa, may be caused by a combination of aerobic and anaerobic bacteria. These infections can rapidly progress and involve deeper structures than just the skin, such as fascia, fat, or muscle (see ). Antibiotic choices for incisional surgical site infections (SSIs). Infections in the immunocompromised host. Skin and soft tissues are common sites of infection in compromised hosts and usually pose major diagnostic challenges for the following 3 reasons: (1) infections are caused by diverse organisms, including organisms not ordinarily considered to be pathogens in otherwise healthy hosts; (2) infection of the soft tissues may occur as part of a broader systemic infection; and (3) the degree and type of immune deficiency attenuate the clinical findings.
The importance of establishing a diagnosis and performing susceptibility testing is crucial, because many infections are hospital acquired, and mounting resistance among both gram-positive and gram-negative bacteria make dogmatic empirical treatment regimens difficult, if not dangerous. In addition, fungal infections may present with cutaneous findings. Immunocompromised patients who are very ill or experiencing toxicity typically require very broad-spectrum empirical agents that include specific coverage for resistant gram-positive bacteria, such as MRSA (e.g., vancomycin, linezolid, daptomycin, or quinupristin/dalfopristin). Coverage for gram-negative bacteria may include monotherapy with a cephalosporin possessing activity against Pseudomonas species, with carbapenems, or with a combination of either a fluoroquinolone or an aminoglycoside plus either an extended-spectrum penicillin or cephalosporin. Infections in patients with cell-mediated immunodeficiency (such as that due to Hodgkin disease, lymphoma, HIV infection, bone marrow transplantation, and receipt of long-term high-dose immunosuppressive therapy) can be caused by either common or unusual bacteria, viruses, protozoa, helminths, or fungi. Although infection may begin in the skin, cutaneous lesions can also be the result of hematogenous seeding. A well-planned strategy for prompt diagnosis, including biopsy and aggressive treatment protocols, is essential.
Diagnostic strategies require laboratory support capable of rapid processing and early detection of bacteria (including Mycobacteria and Nocardia species), viruses, and fungi. The algorithm presented provides an approach to diagnosis and treatment. The empirical antibiotic guidelines are based on results of clinical trials, national surveillance antibiograms, and consensus meetings.
Because antimicrobial susceptibilities vary considerably across the nation, clinicians must base empirical treatment on the antibiograms in their own location. Microbiologic cultures are important in establishing a specific diagnosis, and testing the drug susceptibility of organisms is critical for optimal antimicrobial treatment. This guideline offers recommendations for empirical treatment of specific community-acquired and hospital-acquired infections.
Nonetheless, therapy may fail for several reasons: (1) the initial diagnosis and/or treatment chosen is incorrect, (2) the etiologic agent from a given locale is resistant to antibiotics, (3) antimicrobial resistance develops during treatment, and (4) the infection is deeper and more complex than originally estimated. Introduction This practice guideline provides recommendations for diagnosis and management of skin and soft-tissue infections in otherwise healthy hosts and compromised hosts of all age groups. These infections have diverse etiologies that depend, in part, on the epidemiological setting. Thus, obtaining a careful history, including information about the patient's immune status, the geographical locale, travel history, recent trauma or surgery, previous antimicrobial therapy, lifestyle, hobbies, and animal exposure or bites is key to developing an adequate differential diagnosis and an appropriate index of suspicion for specific etiological agents. Recognizing the physical examination findings and understanding the anatomical relationships of skin and soft tissue are also crucial for establishing the correct diagnosis.
In some cases, this information is insufficient, and biopsy or aspiration of tissue may be necessary. In addition, radiographic procedures may be useful to determine the level of infection and the presence of gas or abscess. Finally, surgical exploration or debridement is an important diagnostic, as well as therapeutic, procedure in immunocompromised hosts or in patients with necrotizing infections or myonecrosis. Three contemporary problems confounding the clinical evaluation of patients with skin and soft-tissue infection are diagnosis, severity of infection, and pathogen-specific antibiotic resistance patterns. Dozens of microbes may cause soft-tissue infections, and although specific bacteria may cause a particular type of infection, considerable overlaps in clinical presentations exist.
Clues to the diagnosis or algorithmic approaches to diagnosis are covered in detail in the text to follow. Specific recommendations for therapy are given, each with a rating that indicates the strength of and evidence for recommendations, expressed using the Infectious Diseases Society of America—US Public Health Service grading system for ranking recommendations in clinical guidelines. Impetigo Impetigo, a skin infection that is common throughout the world, consists of discrete purulent lesions that are nearly always caused by β-hemolytic streptococci and/or S. Impetigo occurs most frequently among economically disadvantaged children in tropical or subtropical regions, but it is also prevalent in northern climates during the summer months. Its peak incidence is among children aged 2–5 years, although older children and adults may also be afflicted ,. There is no sex predilection, and all races are susceptible.
Prospective studies of streptococcal impetigo have demonstrated that the responsible microorganisms initially colonize the unbroken skin , an observation that probably explains the influence of personal hygiene on disease incidence. Skin colonization with a given streptococcal strain precedes the development of impetiginous lesions by a mean duration of 10 days. Inoculation of surface organisms into the skin by abrasions, minor trauma, or insect bites then ensues. During the course of 2– 3 weeks, streptococcal strains may be transferred from the skin and/or impetigo lesions to the upper respiratory tract.
In contrast, in patients with staphylococcal impetigo, the pathogens are usually present in the nose before causing cutaneous disease. Impetigo usually occurs on exposed areas of the body, most frequently the face and extremities. The lesions remain well-localized but are frequently multiple and may be either bullous or nonbullous in appearance. Bullous lesions appear initially as superficial vesicles that rapidly enlarge to form flaccid bullae filled with clear yellow fluid, which later becomes darker, more turbid, and sometimes purulent.
The bullae may rupture, often leaving a thin brown crust resembling lacquer. The lesions of nonbullous impetigo begin as papules that rapidly evolve into vesicles surrounded by an area of erythema and then become pustules that gradually enlarge and break down over a period of 4–6 days to form characteristic thick crusts. The lesions heal slowly and leave depigmented areas.
A deeply ulcerated form of impetigo is known as ecthyma. Although regional lymphadenitis may occur, systemic symptoms are usually absent.
Bullous impetigo is caused by strains of S. Aureus that produce a toxin causing cleavage in the superficial skin layer. In the past, nonbullous lesions were usually caused by streptococci. Now, most cases are caused by staphylococci alone or in combination with streptococci ,.
Streptococci isolated from lesions are primarily group A organisms, but occasionally, other serogroups (such as C and G) are responsible. Assays of streptococcal antibodies are of no value in the diagnosis and treatment of impetigo, but they provide helpful supporting evidence of recent streptococcal infection in patients suspected of having poststreptococcal glomerulonephritis. The anti—streptolysin O response is weak in patients with streptococcal impetigo , , presumably because skin lipids suppress streptolysin O response , but anti—DNAse B levels are consistently elevated ,. In the past, therapy directed primarily at group A streptococci (e.g., penicillin) was successful, both in healing the lesions and decreasing recurrences of nonbullous impetigo for at least several weeks ,. Aureus currently accounts for most cases of bullous impetigo, as well as for a substantial portion of nonbullous infections , , penicillinase-resistant penicillins or first- generation cephalosporins are preferred (A-I), although impetigo caused by MRSA is increasing in frequency. Erythromycin has been a mainstay of pyoderma therapy, but its utility may be lessened in areas where erythromycin-resistant strains of S.
Aureus, or more recently, S. Pyogenes, are prevalent. Topical therapy with mupirocin is equivalent to oral systemic antimicrobials (A-I) and may be used when lesions are limited in number. It is expensive, however, and some strains of staphylococci are resistant. Suppurative complications of streptococcal impetigo are uncommon, and for as yet unexplained reasons, rheumatic fever has never occurred after streptococcal impetigo. On the other hand, cutaneous infections with nephritogenic strains of group A streptococci are the major antecedent of poststreptococcal glomerulonephritis in many areas of the world.
No conclusive data indicate that treatment of streptococcal pyoderma prevents nephritis , but such therapy is important as an epidemiologic measure in eradicating nephritogenic strains from the community. Abscesses, Cellulitis, and Erysipelas Cutaneous abscesses. Cutaneous abscesses are collections of pus within the dermis and deeper skin tissues.
They are usually painful, tender, and fluctuant red nodules, often surmounted by a pustule and surrounded by a rim of erythematous swelling. Cutaneous abscesses are typically polymicrobial, containing bacteria that constitute the normal regional skin flora, often combined with organisms from adjacent mucous membranes. Aureus is present, usually as a single pathogen, in only ∼25% of cutaneous abscesses overall.
Epidermoid cysts, often erroneously labeled “sebaceous cysts,” ordinarily contain skin flora in the cheesy keratinous material, even when uninflamed. Cultures of inflamed cysts also yield the same organisms, suggesting that the inflammation and purulence occur as a reaction to rupture of the cyst wall and extrusion of its contents into the dermis, rather than as an infectious complication. Effective treatment of abscesses and inflamed epidermoid cysts entails incision, thorough evacuation of the pus, and probing the cavity to break up loculations (A-I).
Simply covering the surgical site with a dry dressing is usually the easiest and most effective treatment of the wound , , although some clinicians pack it with gauze or suture it closed. Gram stain, culture, and systemic antibiotics are rarely necessary (E-III). Unusual exceptions include the presence of multiple lesions, cutaneous gangrene, severely impaired host defenses, extensive surrounding cellulitis, or severe systemic manifestations of infection, such as high fever. Furuncles and carbuncles. Furuncles (or “boils”) are infections of the hair follicle, usually caused by S. Aureus, in which suppuration extends through the dermis into the subcutaneous tissue, where a small abscess forms. They differ, therefore, from folliculitis, in which inflammation is more superficial and pus is present in the epidermis.
Furuncles can occur anywhere on hairy skin. Each lesion consists of an inflammatory nodule and an overlying pustule through which hair emerges. When infection extends to involve several adjacent follicles, producing a coalescent inflammatory mass with pus draining from multiple follicular orifices, the lesion is called a carbuncle. Carbuncles tend to develop on the back of the neck and are especially likely to occur in diabetic persons.
For small furuncles, moist heat, which seems to promote drainage, is satisfactory. Larger furuncles and all carbuncles require incision and drainage. Systemic antibiotics are usually unnecessary, unless extensive surrounding cellulitis or fever occurs (E-III). Outbreaks of furunculosis caused by MSSA, as well as by MRSA, may occur in families and other settings involving close personal contact (e.g., prisons), especially when skin injury is common, such as sports teams or outdoor recreation groups. Inadequate personal hygiene and exposure to others with furuncles are important predisposing factors in these settings. In some cases, fomites may harbor the organism and facilitate transmission of the infection. Depending on the individual circumstances, control of outbreaks may require bathing with antibacterial soaps, such as chlorhexidine; thorough laundering of clothing, towels, and bed wear; separate use of towels and washcloths; and attempted eradication of staphylococcal carriage among colonized persons (B-III).
Some individuals have repeated attacks of furunculosis. A few of these persons, particularly children, have abnormal systemic host responses, but for most, the only identifiable predisposing factor is the presence of S. Aureus in the anterior nares or, occasionally, elsewhere, such as the perineum. The prevalence of nasal staphylococcal colonization in the general population is 20%–40%, but why some carriers develop recurrent skin infections and others do not is usually unclear. The major method of controlling recurrent furunculosis is the use of antibacterial agents to eradicate staphylococcal carriage.
For persons with nasal colonization, one approach is the application of mupirocin ointment twice daily in the anterior nares for the first 5 days each month (A-I). This regimen reduces recurrences by ∼50%. Few systemic antibiotics attain adequate levels in the nasal secretions to achieve protracted elimination of staphylococci. Clindamycin is an exception, and probably the best program for recurrent furunculosis caused by susceptible S. Aureus is a single oral daily dose of 150 mg of this agent for 3 months, which decreases subsequent infections by ∼80% (A-I).
Cellulitis and erysipelas. These terms refer to diffuse, spreading skin infections, excluding infections associated with underlying suppurative foci, such as cutaneous abscesses, necrotizing fasciitis, septic arthritis, and osteomyelitis. Unfortunately, physicians use the words “cellulitis” and “erysipelas” inconsistently. For some, the distinction between the 2 terms relates to the depth of inflammation: erysipelas affects the upper dermis, including the superficial lymphatics, whereas cellulitis involves the deeper dermis, as well as subcutaneous fat. In practice, however, distinguishing between cellulitis and erysipelas clinically may be difficult, and some physicians, especially in northern Europe, use the term “erysipelas” to describe both infections. Erysipelas is distinguished clinically from other forms of cutaneous infection by the following 2 features: the lesions are raised above the level of the surrounding skin, and there is a clear line of demarcation between involved and uninvolved tissue.
This disorder is more common among infants, young children, and older adults. It is almost always caused by β-hemolytic streptococci (usually group A), but similar lesions can be caused by streptococci from serogroups C or G. Rarely, group B streptococci or S. Aureus may be involved. In older reports, erysipelas characteristically involved the butterfly area of the face, but at present, the lower extremities are more frequently affected ,.
With early diagnosis and proper treatment, the prognosis is excellent. Rarely, however, the infection may extend to deeper levels of the skin and soft tissues. Penicillin, given either parenterally or orally depending on clinical severity, is the treatment of choice (A-III). If staphylococcal infection is suspected, a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin should be selected (A-III). In a randomized, prospective multicenter trial , the efficacy of roxithromycin, a macrolide antimicrobial, was equivalent to that for penicillin.
Macrolide resistance among group A streptococci, however, is increasing in the United States ,. Cellulitis is an acute spreading infection of the skin, extending more deeply than erysipelas to involve the subcutaneous tissues. It therefore lacks the distinctive anatomical features described above for erysipelas. Although most cellulitis is caused by β-hemolytic streptococci, a number of other microorganisms may give rise to this disorder (see below). Both erysipelas and cellulitis are manifested clinically by rapidly spreading areas of edema, redness, and heat, sometimes accompanied by lymphangitis and inflammation of the regional lymph nodes. The skin surface may resemble an orange peel (i.e., peau d'orange) because superficial cutaneous edema surrounds the hair follicles, which causes dimpling in the skin because they remain tethered to the underlying dermis. Vesicles, bullae, and cutaneous hemorrhage in the form of petechiae or ecchymoses may develop on the inflamed skin.
Systemic manifestations are usually mild, but fever, tachycardia, confusion, hypotension, and leukocytosis are sometimes present and may even occur hours before the skin abnormalities appear. Vesicles and bullae filled with clear fluid are common. Petechiae and ecchymoses may develop in inflamed skin; if these are widespread and associated with systemic toxicity, a deeper infection such as necrotizing fasciitis should be considered. These infections arise when organisms enter through breaches in the skin.
Predisposing factors for these infections include conditions that make the skin more fragile or local host defenses less effective, such as obesity, previous cutaneous damage, and edema from venous insufficiency or lymphatic obstruction or other causes. The origin of the disrupted cutaneous barrier may be trauma, preexisting skin infections such as impetigo or ecthyma, ulceration, fissured toe webs from maceration or fungal infection, and inflammatory dermatoses, such as eczema. Often, however, the breaks in the skin are small and clinically inapparent. These infections can occur at any location but are most common on the lower legs. Surgical procedures that increase the risk for cellulitis, presumably due to disruption of lymphatic drainage, include saphenous venectomy , , axillary node dissection for breast cancer , , and operations for gynecologic malignancies that involve lymph node dissection, especially when followed by radiation therapy, such as radical vulvectomy and radical hysterectomy ,.
Blood culture results are positive in ⩽5% of cases. Results of culture of needle aspirations of the inflamed skin are bewilderingly variable, varying from ⩽5% to ∼40% in reported series , and probably depending on the patient population, the definition of cellulitis, the inclusion or exclusion of cases with associated abscesses, and the determination of whether isolates are pathogens or contaminants. Culture of punch biopsy specimens yields an organism in 20%–30% of cases , , but the concentration of bacteria is usually quite low. Culture of these specimens, as well as other available evidence, including serologic studies and techniques employing immunofluorescent antibodies to detect antigens in skin biopsy specimens , , indicate that most of the infections arise from streptococci, often group A, but also from other groups, such as B, C, or G. The source of the pathogens is frequently unclear, but in many infections of the lower extremities, the responsible streptococci are present in the macerated or fissured interdigital toe spaces , , emphasizing the importance of detecting and treating tinea pedis and other causes of toe web abnormalities in these patients.
Occasionally, the reservoir of streptococci is the anal canal or the vagina, especially for group B streptococci causing cellulitis in patients with previous gynecologic cancer treated with surgery and radiation therapy. Aureus less frequently causes cellulitis, often associated with previous penetrating trauma, including injection sites of illicit drug use. Many other infectious agents can produce cellulitis, but usually only in special circumstances. With cat or dog bites, for example, the organism responsible is typically Pasteurella species, especially P. Multocida, or Capnocytophaga canimorsus.
Hydrophila may cause cellulitis following immersion in fresh water, whereas infection after saltwater exposure can arise from Vibrio species, particularly V. Vulnificus in warm climates. In rare cases, Streptococcus iniae or E.
Rhusiopathiae may cause infection in persons employed in aquaculture or meatpacking, respectively. Periorbital cellulitis due to Haemophilus influenzae can occur in children. Diagnostic and therapeutic considerations of this infection have been reported by the Committee on Infectious Diseases, American Academy of Pediatrics. In neutropenic hosts, infection may be due to Pseudomonas aeruginosa or other gram-negative bacilli, and in patients infected with HIV, the responsible organism may be Helicobacter cinaedi. Occasionally, Cryptococcus neoformans causes cellulitis in patients with deficient cell-mediated immunity.
Because of their very low yield, blood cultures are not fruitful for the typical case of erysipelas or cellulitis, unless it is particularly severe. Needle aspirations and skin biopsies are also unnecessary in typical cases, which should respond to antibiotic therapy directed against streptococci and staphylococci.
These procedures may be more rewarding for patients with diabetes mellitus, malignancy, and unusual predisposing factors, such as immersion injury, animal bites, neutropenia, and immunodeficiency. Diseases sometimes confused with cellulitis include acute dermatitis, such as that due to contact with an allergen; gout, with marked cutaneous inflammation extending beyond the joint involved; and herpes zoster. Acute lipodermatosclerosis, a panniculitis that occurs predominantly in obese women with lower extremity venous insufficiency, causes painful, erythematous, tender, warm, indurated, and sometimes scaly areas in the medial leg that resemble cellulitis. Therapy for the typical case of erysipelas or cellulitis should include an antibiotic active against streptococci. Many clinicians choose an agent that is also effective against S. Aureus, although this organism rarely causes cellulitis unless associated with an underlying abscess or penetrating trauma. A large percentage of patients can receive oral medications from the start.
Suitable agents include dicloxacillin, cephalexin, clindamycin, or erythromycin, unless streptococci or staphylococci resistant to these agents are common in the community (A-I). Macrolide resistance among group A streptococci has increased regionally in the United States. For parenteral therapy, which is indicated for severely ill patients or for those unable to tolerate oral medications, reasonable choices include a penicillinase-resistant penicillin such as nafcillin, a first-generation cephalosporin such as cefazolin, or, for patients with life-threatening penicillin allergies, clindamycin or vancomycin (A-I). In cases of uncomplicated cellulitis, 5 days of antibiotic treatment is as effective as a 10-day course.
Antibiotic treatment alone is effective in most patients with cellulitis. However, patients who are slow to respond may have a deeper infection or underlying conditions, such as diabetes, chronic venous insufficiency, or lymphedema. In some patients, cutaneous inflammation sometimes worsens after initiating therapy, probably because the sudden destruction of pathogens releases potent enzymes that increase local inflammation. In a single randomized, double-blind, placebo-controlled trial, systemic corticosteroids attenuated this reaction and hastened resolution. Specifically, 108 patients with a diagnosis of uncomplicated erysipelas were randomized to receive antibiotics (90% received benzyl penicillin) plus either an 8-day tapering oral course of corticosteroid therapy beginning with 30 mg of prednisolone or a placebo.
Treatment of necrotizing infections of the skin, fascia, and muscle. Necrotizing fasciitis and/or streptococcal toxic shock syndrome caused by group A streptococci should be treated with clindamycin and penicillin (A-II). The rationale for clindamycin is based on in vitro studies demonstrating both toxin suppression and modulation of cytokine (i.e., TNF) production, on animal studies demonstrating superior efficacy versus that of penicillin, and on 2 observational studies demonstrating greater efficacy for clindamycin than for β-lactam antibiotics ,.
Penicillin should be added because of the increasing resistance of group A streptococci to macrolides, although in the United States, only 0.5% of macrolide-resistant group A streptococci are also clindamycin resistant. A recommendation to use intravenous γ-globulin (IVIG) to treat streptococcal toxic shock syndrome cannot be made with certainty (B-II). Although there is ample evidence for the role of extracellular streptococcal toxins in shock, organ failure, and tissue destruction, different batches of IVIG contain variable quantities of neutralizing antibodies to some of these toxins, and definitive clinical data are lacking. One observational study demonstrated better outcomes in patients receiving IVIG, but these patients were more likely to have had surgery and to have received clindamycin than were historical control subjects.
A second study, which was a double-blind, placebo-controlled trial from northern Europe, showed no statistically significant improvement in survival, and, specific to this section, no reduction in the time to no further progression of necrotizing fasciitis (69 h for the IVIG group, compared with 36 h for the placebo group). Results of these studies provide some promise.
However, this committee believes that additional studies of the efficacy of IVIG are necessary before a recommendation can be made regarding use of IVIG for treatment of streptococcal toxic shock syndrome. Anaerobic Streptococcal Myositis Anaerobic streptococci cause a more indolent infection than other streptococci. Unlike other necrotizing infections, infection of the muscle and fascial planes by anaerobic streptococci usually is associated with trauma or a surgical procedure. Incision and drainage are critical. Necrotic tissue and debris are resected but the inflamed, viable muscle should not be removed, because it can heal and regain function.
The incision should be packed with moist dressings. Antibiotic treatment is highly effective. These organisms are all susceptible to penicillin or ampicillin, which should be administered in high doses. Pyomyositis Pyomyositis, which is caused mainly by S. Aureus, is the presence of pus within individual muscle groups. Occasionally, S.
Pneumoniae or a gram-negative enteric bacillus is responsible. Blood culture results are positive in 5%–30% of cases. Because of its geographical distribution, this condition is often called “tropical pyomyositis,” but cases are increasingly recognized in temperate climates, especially in patients with HIV infection or diabetes. Presenting findings are localized pain in a single muscle group, muscle spasm, and fever. The disease occurs most often in an extremity, but any muscle group can be involved, including the psoas or trunk muscles. Initially, it may not be possible to palpate a discrete abscess because the infection is localized deep within the muscle, but the area has a firm, wooden feel associated with pain and tenderness.
In the early stages, ultrasonography or CT scan may be performed to differentiate this entity from a deep venous thrombosis. In more advanced cases, a bulging abscess is usually clinically apparent.
Appropriate antibiotics plus extensive surgical incision and drainage are required for appropriate management. Synergistic Necrotizing Cellulitis This is simply a necrotizing soft-tissue infection that involves muscle groups in addition to superficial tissues and fascia. The level of involvement depends on the depth and the tissue planes affected by the original operation or pathological process that precedes the infection.
Major predisposing causes are perirectal and ischiorectal abscesses. Recognition and treatment are similar to necrotizing fasciitis, but operative exploration reveals its deeper location. Fournier Gangrene This variant of necrotizing soft-tissue infection involves the scrotum and penis or vulva and can have an insidious or explosive onset ,. The mean age of onset is 50 years. Most patients have significant underlying disease, particularly diabetes, but 20% will have no discernible cause. Most patients initially have a perianal or retroperitoneal infection that has spread along fascial planes to the genitalia; a urinary tract infection, most commonly secondary to a urethral stricture, that involves the periurethral glands and extends into the penis and scrotum; or previous trauma to the genital area, providing access of organisms to the subcutaneous tissues.
The infection can begin insidiously with a discrete area of necrosis in the perineum that progresses rapidly over 1–2 days with advancing skin necrosis. At the outset, it tends to cause superficial gangrene, limited to skin and subcutaneous tissue, and extending to the base of the scrotum. The testes, glans penis, and spermatic cord usually are spared, because they have a separate blood supply. The infection may extend to the perineum and the anterior abdominal wall through the fascial planes. Most cases are caused by mixed aerobic and anaerobic flora. Staphylococci and Pseudomonas species are frequently present, usually in mixed culture, but occasionally, S. Aureus is the only pathogen.
Pseudomonas is another common organism in the mixed culture. As with other necrotizing infections, prompt and aggressive surgical exploration and appropriate debridement is necessary to remove all necrotic tissue, sparing the deeper structures when possible (A-III). Clostridial Myonecrosis Clostridial gas gangrene (i.e., myonecrosis) is most commonly caused by C. Perfringens, C. Histolyticum, and C. Perfringens is the most frequent cause of trauma-associated gas gangrene. Increasingly severe pain beginning at the injury site ⩽24 h after infection is the first reliable symptom.
Skin may initially be pale, but it quickly changes to bronze and then to a purplish red. The infected region becomes tense and tender, and bullae filled with reddish-blue fluid appear. Gas in the tissue, detected as crepitus or on the basis of imaging studies, is universally present by this late stage. Signs of systemic toxicity, including tachycardia, fever, and diaphoresis, develop rapidly, followed by shock and multiple organ failure. In contrast to traumatic gas gangrene, spontaneous gangrene is principally associated with the more aerotolerant C. Septicum and occurs predominantly in patients with neutropenia and gastrointestinal malignancy. It develops in normal skin in the absence of trauma as a result of hematogenous spread from a colonic lesion, usually cancer.
A rather innocuous early lesion may evolve to all of the above signs over the course of 24 h. Frequently, the diagnosis is unsuspected until gas is detected in tissue or systemic signs of toxicity appear. Early surgical inspection and debridement are necessary, and Gram stain of removed tissue shows large, spore-forming gram-positive bacilli.
Both traumatic and spontaneous clostridial gas gangrene are fulminant infections requiring meticulous intensive care, supportive measures, aggressive surgical debridement, and appropriate antibiotics. The role of hyperbaric oxygen treatment remains unclear. Altemeier and Fullen reported a significant reduction in mortality among patients with gas gangrene using penicillin and tetracycline plus aggressive surgery in the absence of hyperbaric oxygen.
Treatment of experimental gas gangrene has demonstrated that tetracycline, clindamycin, and chloramphenicol were more effective than penicillin or hyperbaric oxygen treatment. Because 5% of strains of C. Perfringens are clindamycin resistant, the recommended antibiotic treatment is penicillin plus clindamycin (B-III). Animal Bites One-half of all Americans are bitten during their lifetime, usually by a dog. Fortunately, 80% of the wounds are minor, but the remaining 20% that require medical care will account for 1% of all emergency department visits and for 10,000 inpatient admissions yearly. Most bites are due to dogs or cats, but bites from exotic pets and from feral animals also occur. The predominant pathogens in these wounds are the normal oral flora of the biting animal, along with human skin organisms and occasional secondary invaders (e.g., S.
Aureus and S. Pyogenes) ,. There are no published large case series on the therapy of bite wounds, but there are many smaller series and anecdotal reports especially focusing on complications.
Bacteriologic characteristics. Patients who present. Recommended therapy for infections following animal or human bites.
Intravenous options include the β-lactam/β-lactamase combinations (such as ampicillin sulbactam), piperacillin/tazobactam, second-generation cephalosporins (such as cefoxitin), and carbapenems (such as ertapenem, imipenem, and meropenem) (B-II). Second-generation and third-generation cephalosporins, such as cefuroxime, ceftriaxone, and cefotaxime, may be used but may require the addition of an antianaerobic agent. Penicillin-allergic pregnant women constitute a special population, because tetracyclines, sulfa compounds (during late pregnancy), and metronidazole are contraindicated. Similarly, the selection of an antimicrobial for penicillin-allergic children is problematic when tetracyclines and fluoroquinolones are contraindicated. In these situations, macrolides (e.g., azithromycin 250–500 mg every day or telithromycin 400 mg, 2 tablets by mouth every day) are occasionally used. However, these patients should be observed closely and the potential increased risk of failure noted. The duration of therapy varies by the severity of the injury/infection.
Cellulitis and abscess often respond to 5–10 days of therapy. The therapy for early presenting, noninfected wounds remains controversial. Wounds that are moderate to severe, have associated crush injury, have associated edema (either preexisting or subsequent), that are on the hands or in proximity to a bone or a joint, or that are in compromised hosts should receive 3–5 days of “prophylactic” antimicrobial therapy. These wounds are often colonized with potential pathogens (85% of cases), and it is difficult to determine whether the wound will become infected. Infectious complications of bite wounds include septic arthritis, osteomyelitis, subcutaneous abscess formation, tendonitis, and, rarely, bacteremia.
Pain disproportionate to the severity of injury but located near a bone or joint should suggest periosteal penetration. Hand wounds are often more serious than wounds to fleshy parts of the body. These wound complications will necessitate prolonged therapy, such as 4–6-week courses for osteomyelitis and 3–4 -week courses for synovitis. Noninfectious complications include nerve or tendon injury or severance, compartment syndromes, postinfectious and traumatic arthritis, fracture, and bleeding. Adjunctive therapeutic measures are often as important as antimicrobial therapy. Wounds should be cleansed with sterile normal saline (no need for iodine- or antibiotic-containing solutions) and superficial debris removed. Deeper debridement is usually unnecessary, but, if performed, should be done very cautiously to avoid enlarging the wound and impairing skin closure.
Infected wounds should not be closed. Suturing wounds early (.