Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — Cellulitis, abscess, or both are among the most common skin and soft tissue infections [1-3]. Cellulitis (which includes erysipelas) manifests as an area of skin erythema, edema, and warmth; it develops as a result of bacterial entry via breaches in the skin barrier . A skin abscess is a collection of pus within the dermis or subcutaneous space. Misdiagnosis of these entities is common , and possible alternative diagnoses should be considered carefully. (See 'Differential diagnosis' below.)
The epidemiology, microbiology, clinical manifestations, and diagnosis of cellulitis and skin abscess will be reviewed here. Issues related to treatment of cellulitis and abscess are discussed separately. (See "Cellulitis and skin abscess in adults: Treatment".)
Issues related to skin and soft tissue infections associated with specific epidemiologic factors (such as diabetes, animal bites, and water exposure) are discussed separately. (See "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities" and "Soft tissue infections due to dog and cat bites" and "Soft tissue infections following water exposure".)
Issues related to infection involving the gluteal area and perineum are discussed separately. (See "Intergluteal pilonidal disease: Clinical manifestations and diagnosis" and "Perianal and perirectal abscess".)
EPIDEMIOLOGY — Cellulitis is observed most frequently among middle-aged individuals and older adults. Erysipelas occurs in young children and older adults [6,7]. The incidence of cellulitis is about 200 cases per 100,000 patient-years . Skin abscess may occur in healthy individuals with no predisposing conditions.
Predisposing factors for development of cellulitis and/or skin abscess include [9-18]:
●Skin barrier disruption due to trauma (such as abrasion, penetrating wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use)
●Skin inflammation (such as eczema, radiation therapy)
●Edema due to impaired lymphatic drainage
●Edema due to venous insufficiency
●Immunosuppression (such as diabetes or HIV infection)
●Breaks in the skin between the toes ("toe web intertrigo"); these may be clinically inapparent
●Preexisting skin infection (such as tinea pedis, impetigo, varicella)
Lymphatic compromise may occur following surgical procedures (such as saphenous venectomy or lymph node dissection) or in the setting of congenital abnormalities. (See "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Post-venectomy cellulitis' and "Cellulitis following pelvic lymph node dissection".)
An additional risk factor for development of purulent infection is close contact with others with methicillin-resistant Staphylococcus aureus infection or carriage. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" and "Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum", section on 'Epidemiology and risk factors'.)
Cellulitis and erysipelas — The most common cause of cellulitis is beta-hemolytic streptococci (groups A, B, C, G, and F), most commonly group A Streptococcus or Streptococcus pyogenes; S. aureus (including methicillin-resistant strains) is a notable but less common cause [4,14,19-25]. Gram-negative aerobic bacilli are identified in a minority of cases.
The vast majority of erysipelas cases are caused by beta-hemolytic streptococci [7,19,26,27]. One study of nonpurulent cellulitis including 179 patients found that beta-hemolytic streptococci accounted for 73 percent of cases (diagnosed by positive blood culture results or serologic testing for anti-streptolysin-O and anti-DNase-B antibodies) . No etiology was identified in 27 percent of cases, but the overall clinical response rate to beta-lactam therapy was 96 percent.
Less common causes of cellulitis include Haemophilus influenzae (buccal cellulitis), clostridia and non-spore-forming anaerobes (crepitant cellulitis), Streptococcus pneumoniae, and Neisseria meningitidis [28-34]. In immunocompromised patients, the spectrum of potential pathogens is much broader, and infectious disease consultation is warranted.
Pathogens implicated in special clinical circumstances discussed in detail separately include:
●Pasteurella multocida and Capnocytophaga canimorsus (see "Soft tissue infections due to dog and cat bites" and "Clinical manifestations and initial management of animal and human bites")
●Aeromonas hydrophila and Vibrio vulnificus (see "Soft tissue infections following water exposure")
●Pseudomonas aeruginosa (see "Fever and rash in immunocompromised patients without HIV infection" and "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities" and "Pseudomonas aeruginosa skin and soft tissue infections")
●Group B Streptococcus (see "Group B streptococcal infection in neonates and young infants", section on 'Other focal infection' and "Cellulitis following pelvic lymph node dissection", section on 'Streptococcal sex syndrome')
●Clostridium species (see "Clostridial myonecrosis")
●Erysipelothrix rhusiopathiae (see "Erysipelothrix infection")
●S. pneumoniae (see "Orbital cellulitis")
●Cryptococcus neoformans (see "Fever and rash in immunocompromised patients without HIV infection")
●Streptococcus iniae (see "Fever and rash in the immunocompetent patient")
●Helicobacter cinaedi (see "Fever and rash in HIV-infected patients")
Skin abscess — The most common cause of skin abscess is S. aureus (either methicillin-susceptible or methicillin-resistant S. aureus), which occurs in up to 75 percent of cases. Risk factors are summarized in the table (table 1); many patients with MRSA infection have no risk factors [3,35-40].
A skin abscess can be caused by more than one pathogen [36,41-43]; isolation of multiple organisms (including S. aureus together with S. pyogenes and gram-negative bacilli with anaerobes) is more common in patients with skin abscess involving the perioral, perirectal, or vulvovaginal areas . Organisms of oral origin, including anaerobes, are seen most frequently among intravenous drug users .
Unusual causes of skin abscess include nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis (see related topics).
Most abscesses are due to infection. However, sterile abscesses can occur in the setting of injected irritants. Examples include injected drugs (particularly oil-based ones) that may not be fully absorbed and so remain at the site of injection, causing local irritation. Sterile abscesses can turn into hard, solid lesions as they scar.
CLINICAL MANIFESTATIONS — Patients with skin and soft tissue infection may present with cellulitis, abscess, or both [1-3,35].
Cellulitis and erysipelas — Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth; they develop as a result of bacterial entry via breaches in the skin barrier . Fever may be present. Cellulitis and erysipelas are nearly always unilateral, and the lower extremities are the most common site of involvement (picture 1A-B); bilateral involvement should prompt consideration of alternative causes [4,6,44] (see 'Differential diagnosis' below). The interdigital toe spaces should be examined for fissuring or maceration; minimizing these conditions may reduce the likelihood of recurrent infection. (See "Basic principles of wound management".)
Cellulitis involves the deeper dermis and subcutaneous fat; erysipelas involves the upper dermis and superficial lymphatics (figure 1). Cellulitis may present with or without purulence; erysipelas is nonpurulent [1-3].
Patients with erysipelas tend to have acute onset of symptoms with systemic manifestations including fever and chills, whereas patients with cellulitis tend to have a more indolent course with development of localized symptoms over a few days. In addition, in erysipelas there is clear demarcation between involved and uninvolved tissue . Classic descriptions of erysipelas note "butterfly" involvement of the face. Involvement of the ear (Milian's ear sign) is a distinguishing feature for erysipelas, since this region does not contain deeper dermis tissue.
Additional manifestations of cellulitis and erysipelas include lymphangitis and inflammation of regional lymph nodes. Edema surrounding the hair follicles may lead to dimpling in the skin, creating an appearance reminiscent of an orange peel texture ("peau d'orange"). Vesicles, bullae, and ecchymoses or petechiae may be observed. Crepitant and gangrenous cellulitis are unusual manifestations of cellulitis due to clostridia and other anaerobes. Severe manifestations with systemic toxicity should prompt investigation for additional underlying sources of infection. (See "Epidemiology, clinical manifestations, and diagnosis of streptococcal toxic shock syndrome" and "Staphylococcal toxic shock syndrome".)
Other forms of cellulitis include orbital cellulitis, abdominal wall cellulitis (in morbidly obese individuals), buccal cellulitis (due to S. pneumoniae and, prior to the conjugate vaccine era, H. influenzae type b) and perianal cellulitis (due to group A beta-hemolytic Streptococcus) [46,47]. Rarely, infections involving the medial third of the face (ie, the areas around the eyes and nose) can be complicated by septic cavernous thrombosis, since the veins in this region are valveless (figure 2). (See "Orbital cellulitis" and "Septic dural sinus thrombosis".)
Laboratory findings are nonspecific and may include leukocytosis and elevated inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) [4,48].
Skin abscess — A skin abscess is a collection of pus within the dermis or subcutaneous space (picture 2 and figure 1). It manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis . Spontaneous drainage of purulent material may occur. Regional adenopathy may be observed. Fever, chills, and systemic toxicity are unusual.
A skin abscess may develop via deep infection of a hair follicle (known as a furuncle or boil), which reflects extension of purulent material through the dermis into the subcutaneous tissue. Multiple furuncles can coalesce to form carbuncles (picture 3), which may be associated with systemic symptoms. Common areas of involvement include the back of the neck, face, axillae, and buttocks.
Complications — Complications of cellulitis and abscess include bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome .
DIAGNOSIS — The diagnosis of cellulitis, erysipelas, and skin abscess is usually based upon clinical manifestations. Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth. Erysipelas lesions are raised above the level of surrounding skin with clear demarcation between involved and uninvolved tissue. A skin abscess manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis (picture 2).
Laboratory testing is not required for patients with uncomplicated infection in the absence of comorbidities or complications.
Patients with drainable abscess should undergo incision and drainage, with culture and susceptibility testing of debrided material [49,50]. (See "Cellulitis and skin abscess in adults: Treatment", section on 'Drainable abscess present'.)
Blood cultures are warranted for patients in the following circumstances and should be obtained prior to the initiation of antibiotic therapy [51,52]:
●Extensive skin or soft tissue involvement
●Underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes)
●Special exposures (animal bite, water-associated injury)
Blood cultures are positive in less than 10 percent of cases [53-55]. A skin biopsy may be warranted if the diagnosis is uncertain; cultures of skin biopsy specimens yield a pathogen in 20 to 30 percent of cases [56-59]. Cultures of swabs from intact skin are not helpful and should not be performed [2,3].
Radiographic examination can be useful to determine whether a skin abscess is present (via ultrasonography) and for distinguishing cellulitis from osteomyelitis (via magnetic resonance imaging) [60-63]. Radiographic evaluation may be warranted in patients with underlying conditions such as diabetes, venous insufficiency, or lymphedema and in patients with persistent systemic symptoms. Radiographic examination cannot reliably distinguish cellulitis from necrotizing fasciitis or gas gangrene; if there is clinical suspicion for these entities, radiographic imaging should not delay surgical intervention [64,65]. (See "Necrotizing soft tissue infections" and "Clostridial myonecrosis".)
In patients with recurrent cellulitis, serologic testing for beta-hemolytic streptococci may be a useful diagnostic tool. Assays include the anti-streptolysin-O (ASO) reaction, the anti-deoxyribonuclease B test (anti-DNAse B), the anti-hyaluronidase test (AHT), or the Streptozyme antibody assay . Anti-DNase B and AHT responses are more reliable than the ASO response following group A streptococcal skin infections. (See "Cellulitis and skin abscess in adults: Treatment", section on 'Recurrent infection'.)
DIFFERENTIAL DIAGNOSIS — Rapidly progressive erythema with signs of systemic toxicity should prompt consideration of severe infection, including:
●Necrotizing fasciitis – Necrotizing fasciitis is a deep infection that results in progressive destruction of the muscle fascia. The affected area may be erythematous, swollen, warm, and exquisitely tender. Pain out of proportion to exam findings may be observed. The diagnosis is established surgically with visualization of fascial planes. (See "Necrotizing soft tissue infections".)
●Toxic shock syndrome – Toxic shock syndrome typically presents with pain that precedes physical findings. Clinical signs of soft tissue infection consist of local swelling and erythema followed by ecchymoses and sloughing of skin. Fever is common. Patients may be normotensive on presentation but subsequently become hypotensive. (See "Epidemiology, clinical manifestations, and diagnosis of streptococcal toxic shock syndrome".)
●Gas gangrene – Gas gangrene should be suspected in the setting of fever and severe pain in an extremity, particularly in the setting of recent surgery or trauma. The presence of tissue crepitus favors clostridial infection. Gas gangrene can also be detected radiographically. (See "Clostridial myonecrosis".)
Cellulitis must be distinguished from other infections including:
●Erythema migrans – Erythema migrans is an early manifestation of Lyme disease; it consists of a region of erythema at the site of a tick bite, often with central clearing and a necrotic center (picture 4). The diagnosis is established based on serologic testing, although sensitivity in early disease is low. A similar lesion may occur in patients with Southern tick–associated rash illness. (See "Clinical manifestations of Lyme disease in adults" and "Southern tick-associated rash illness (STARI)".)
●Herpes zoster – The rash of herpes zoster begins as erythematous papules that evolve into grouped vesicles (picture 5). The rash is generally limited to one dermatome but can affect two or three neighboring dermatome. The diagnosis is established by polymerase chain reaction. (See "Clinical manifestations of varicella-zoster virus infection: Herpes zoster".)
●Septic arthritis – Cellulitis may overlie a septic joint. Clinical manifestations include joint pain, swelling, warmth, and limited range of motion. The diagnosis of septic arthritis is established based on synovial fluid examination. (See "Septic arthritis in adults".)
●Septic bursitis – Cellulitis may precede or accompany septic bursitis. Distinguishing cellulitis with and without bursitis depends on skilled palpation. Radiographic imaging is warranted if septic bursitis is suspected. (See "Septic bursitis".)
●Osteomyelitis – Osteomyelitis may underlie an area of cellulitis. It is prudent to pursue imaging for assessment of bone involvement in the setting of chronic soft tissue infection that fails to improve with appropriate antibiotic therapy. (See "Overview of osteomyelitis in adults".)
●Mycotic aneurysm – Mycotic aneurysm should be suspected in the setting of erythema, swelling, and tenderness at an intravenous drug injection site such as antecubital fossa . The diagnosis is established via ultrasonography. (See "Overview of infected (mycotic) arterial aneurysm".)
Noninfectious masqueraders of cellulitis (unilateral) include:
●Contact dermatitis – Contact dermatitis may be distinguished from cellulitis in that the contact dermatitis lesions are pruritic. Clinical features include erythema, edema, vesicles, bullae, and oozing. The reaction is generally limited to the site of contact and is associated with burning, stinging, or pain. (See "Irritant contact dermatitis in adults".)
●Acute gout – Acute gouty arthritis consists of severe pain, warmth, erythema, and swelling overlying a single joint. The diagnosis can be established by synovial fluid analysis, which should demonstrate the characteristic urate crystals of gout or the calcium pyrophosphate crystals of pseudogout. Additional clues suggestive of gout include involvement of the first metatarsophalangeal joint, prior self-limited attacks of arthritis, and presence of tophi. (See "Clinical manifestations and diagnosis of gout".)
●Drug reaction – A drug reaction presents with an erythematous maculopapular rash that involves the trunk and proximal extremities. It may be accompanied by pruritus, low-grade fever, and mild eosinophilia. The diagnosis is suspected in a patient receiving drug treatment who presents with a rash of recent onset. The clinical suspicion can be substantiated by histopathologic examination of a skin biopsy. (See "Exanthematous (morbilliform) drug eruption".)
●Vasculitis – The morphology of cutaneous lesions of vasculitis is variable. Macular and papular lesions are characteristically nonblanchable due to the presence of extravasated erythrocytes in the dermis, which occurs as a result of damaged vessel walls. The diagnosis is established by skin biopsy. (See "Evaluation of adults with cutaneous lesions of vasculitis".)
●Insect bite – An insect bite triggers an inflammatory reaction at the site of the punctured skin, which appears within minutes and consists of pruritic local erythema and edema. In some cases, a local reaction is followed by a delayed skin reaction consisting of local swelling, itching, and erythema. (See "Insect bites".)
●Deep venous thrombosis – Findings suggestive of cellulitis involving the lower extremity should prompt consideration of deep venous thrombosis; the evaluation consists of ultrasound evaluation. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)
●Panniculitis – Panniculitis refers to inflammation of subcutaneous fat and may have many causes, both infectious and noninfectious (table 2). The diagnosis is confirmed via biopsy. (See "Panniculitis: Recognition and diagnosis".)
●Vaccination site reaction – A local reaction to vaccination manifests with erythema, swelling, and tenderness at the injection site; these are typically self-limited. (See "Allergic reactions to vaccines", section on 'Delayed vaccine reactions'.)
●Erythema ab igne - Erythema ab igne is an erythematous pigmented dermatosis resulting from repeated exposures to moderate heat or infrared radiation. The diagnosis is established clinically and may be confirmed by biopsy. (See "Approach to the patient with macular skin lesions", section on 'Erythema ab igne'.)
Noninfectious masqueraders of cellulitis (bilateral) include:
●Stasis dermatitis – Stasis dermatitis is an inflammatory dermatosis of the lower extremities that occurs in patients with chronic venous insufficiency. It is usually bilateral but can be unilateral in the setting of anatomic asymmetry. The diagnosis is usually established clinically. (See "Stasis dermatitis" and "Clinical manifestations of lower extremity chronic venous disease".)
●Lymphedema – Lymphedema is abnormal accumulation of interstitial fluid resulting from injury or anatomic abnormality of the lymphatic system. The diagnosis is usually established clinically. (See "Clinical features and diagnosis of peripheral lymphedema".)
Skin lesions that should be distinguished from skin abscess include:
●Epidermoid cyst – An epidermoid cyst is a skin-colored cutaneous nodule. The diagnosis is usually clinical, based on the clinical appearance of a discrete cyst or nodule, often with a central punctum, that is freely movable on palpation. Epidermoid cysts may become secondarily infected. (See "Overview of benign lesions of the skin", section on 'Epidermoid cyst'.)
●Folliculitis – Folliculitis refers to inflammation of one or more hair follicles. The diagnosis is often established clinically; rarely, Gram stain and culture or skin biopsy may be warranted to differentiate folliculitis from other conditions. (See "Infectious folliculitis".)
●Hidradenitis suppurativa – Hidradenitis suppurativa is a chronic suppurative process involving the skin and subcutaneous tissue of intertriginous skin. The diagnosis is usually established clinically. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)
●Nodular lymphangitis – Nodular lymphangitis presents as nodular subcutaneous swellings along the course of the lymphatic channels. The differential diagnosis is broad and is summarized separately. (See "Lymphangitis", section on 'Nodular lymphangitis'.)
●Botryomycosis – Botryomycosis is a chronic, suppurative infection characterized by a granulomatous inflammatory response to S. aureus and other bacteria; it occurs most commonly in immunocompromised patients. The diagnosis is established via Gram stain, culture, or examination of pus for granules. (See "Botryomycosis".)
●Myiasis – Myiasis presents as an enlarging nodular associated with an insect bite; it is caused by penetration of fly larvae into subdermal tissue. The diagnosis is established via clinical manifestations in the setting of epidemiologic exposure to tropical and subtropical areas. (See "Skin lesions in the returning traveler", section on 'Myiasis'.)
The differential diagnosis for skin and soft tissue infections in immunocompromised patients is summarized separately. (See "Clinical manifestations, diagnosis, and grading of acute graft-versus-host disease", section on 'Differential diagnosis'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Skin and soft tissue infections".)
●Patients with skin and soft tissue infection may present with cellulitis, abscess, or both. Misdiagnosis of these entities is common, and possible alternative diagnoses should be considered carefully. (See 'Introduction' above and 'Differential diagnosis' above.)
●Risk factors for development of cellulitis and/or skin abscess include skin barrier disruption, edema, venous insufficiency, and immunosuppression. However, healthy individuals with no risk factors may also develop these infections. (See 'Epidemiology' above.)
●The most common microbiologic cause of cellulitis is beta-hemolytic streptococci (groups A, B, C, G, and F), most commonly group A Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. The vast majority of erysipelas cases are caused by beta-hemolytic streptococci. The most common microbiologic cause of skin abscess is S. aureus; a skin abscess can be caused by more than one pathogen. (See 'Microbiology' above.)
●Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth. Erysipelas lesions are raised above the level of surrounding skin with clear demarcation between involved and uninvolved tissue. Cellulitis and erysipelas are nearly always unilateral, and the lower extremities are the most common site of involvement. Cellulitis may present with or without purulence; erysipelas is nonpurulent. A skin abscess manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis. (See 'Clinical manifestations' above.)
●The diagnosis of cellulitis, erysipelas, and skin abscess is usually based upon clinical manifestations. Patients with drainable abscess should undergo incision and drainage, with culture and susceptibility testing of debrided material. Blood cultures are warranted for patients in the circumstances described above. (See 'Diagnosis' above.)
●Radiographic examination can be useful to determine whether skin abscess is present (via ultrasonography) and for distinguishing cellulitis from osteomyelitis (via magnetic resonance imaging). Radiographic evaluation may be warranted in patients with underlying conditions such as diabetes, venous insufficiency, or lymphedema and in patients with persistent systemic symptoms. (See 'Diagnosis' above.)
- Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis 2011; 52:e18.
- Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis 2014; 59:e10.
- Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clin Infect Dis 2014; 59:147.
- Raff AB, Kroshinsky D. Cellulitis: A Review. JAMA 2016; 316:325.
- Weng QY, Raff AB, Cohen JM, et al. Costs and Consequences Associated With Misdiagnosed Lower Extremity Cellulitis. JAMA Dermatol 2016.
- Ellis Simonsen SM, van Orman ER, Hatch BE, et al. Cellulitis incidence in a defined population. Epidemiol Infect 2006; 134:293.
- Eriksson B, Jorup-Rönström C, Karkkonen K, et al. Erysipelas: clinical and bacteriologic spectrum and serological aspects. Clin Infect Dis 1996; 23:1091.
- McNamara DR, Tleyjeh IM, Berbari EF, et al. Incidence of lower-extremity cellulitis: a population-based study in Olmsted county, Minnesota. Mayo Clin Proc 2007; 82:817.
- McNamara DR, Tleyjeh IM, Berbari EF, et al. A predictive model of recurrent lower extremity cellulitis in a population-based cohort. Arch Intern Med 2007; 167:709.
- Dan M, Heller K, Shapira I, et al. Incidence of erysipelas following venectomy for coronary artery bypass surgery. Infection 1987; 15:107.
- Baddour LM, Bisno AL. Recurrent cellulitis after saphenous venectomy for coronary bypass surgery. Ann Intern Med 1982; 97:493.
- Baddour LM. Breast cellulitis complicating breast conservation therapy. J Intern Med 1999; 245:5.
- Dankert J, Bouma J. Recurrent acute leg cellulitis after hysterectomy with pelvic lymphadenectomy. Br J Obstet Gynaecol 1987; 94:788.
- Semel JD, Goldin H. Association of athlete's foot with cellulitis of the lower extremities: diagnostic value of bacterial cultures of ipsilateral interdigital space samples. Clin Infect Dis 1996; 23:1162.
- Gordon RJ, Lowy FD. Bacterial infections in drug users. N Engl J Med 2005; 353:1945.
- Begier EM, Frenette K, Barrett NL, et al. A high-morbidity outbreak of methicillin-resistant Staphylococcus aureus among players on a college football team, facilitated by cosmetic body shaving and turf burns. Clin Infect Dis 2004; 39:1446.
- Hilmarsdóttir I, Valsdóttir F. Molecular typing of Beta-hemolytic streptococci from two patients with lower-limb cellulitis: identical isolates from toe web and blood specimens. J Clin Microbiol 2007; 45:3131.
- Quirke M, Ayoub F, McCabe A, et al. Risk factors for nonpurulent leg cellulitis: a systematic review and meta-analysis. Br J Dermatol 2017; 177:382.
- Bernard P, Bedane C, Mounier M, et al. Streptococcal cause of erysipelas and cellulitis in adults. A microbiologic study using a direct immunofluorescence technique. Arch Dermatol 1989; 125:779.
- Leppard BJ, Seal DV, Colman G, Hallas G. The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. Br J Dermatol 1985; 112:559.
- Björnsdóttir S, Gottfredsson M, Thórisdóttir AS, et al. Risk factors for acute cellulitis of the lower limb: a prospective case-control study. Clin Infect Dis 2005; 41:1416.
- Carratalà J, Rosón B, Fernández-Sabé N, et al. Factors associated with complications and mortality in adult patients hospitalized for infectious cellulitis. Eur J Clin Microbiol Infect Dis 2003; 22:151.
- Siljander T, Karppelin M, Vähäkuopus S, et al. Acute bacterial, nonnecrotizing cellulitis in Finland: microbiological findings. Clin Infect Dis 2008; 46:855.
- Jeng A, Beheshti M, Li J, Nathan R. The role of beta-hemolytic streptococci in causing diffuse, nonculturable cellulitis: a prospective investigation. Medicine (Baltimore) 2010; 89:217.
- Bruun T, Oppegaard O, Kittang BR, et al. Etiology of Cellulitis and Clinical Prediction of Streptococcal Disease: A Prospective Study. Open Forum Infect Dis 2016; 3:ofv181.
- Bernard P, Toty L, Mounier M, et al. Early detection of streptococcal group antigens in skin samples by latex particle agglutination. Arch Dermatol 1987; 123:468.
- Chartier C, Grosshans E. Erysipelas. Int J Dermatol 1990; 29:459.
- Swartz MN. Clinical practice. Cellulitis. N Engl J Med 2004; 350:904.
- Parada JP, Maslow JN. Clinical syndromes associated with adult pneumococcal cellulitis. Scand J Infect Dis 2000; 32:133.
- Porras MC, Martínez VC, Ruiz IM, et al. Acute cellulitis: an unusual manifestation of meningococcal disease. Scand J Infect Dis 2001; 33:56.
- Patel M, Ahrens JC, Moyer DV, DiNubile MJ. Pneumococcal soft-tissue infections: a problem deserving more recognition. Clin Infect Dis 1994; 19:149.
- Capdevila O, Grau I, Vadillo M, et al. Bacteremic pneumococcal cellulitis compared with bacteremic cellulitis caused by Staphylococcus aureus and Streptococcus pyogenes. Eur J Clin Microbiol Infect Dis 2003; 22:337.
- Page KR, Karakousis PC, Maslow JN. Postoperative pneumococcal cellulitis in systemic lupus erythematosus. Scand J Infect Dis 2003; 35:141.
- Givner LB, Mason EO Jr, Barson WJ, et al. Pneumococcal facial cellulitis in children. Pediatrics 2000; 106:E61.
- Singer AJ, Talan DA. Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus. N Engl J Med 2014; 370:1039.
- Summanen PH, Talan DA, Strong C, et al. Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use. Clin Infect Dis 1995; 20 Suppl 2:S279.
- Rajendran PM, Young D, Maurer T, et al. Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection. Antimicrob Agents Chemother 2007; 51:4044.
- Ruhe JJ, Smith N, Bradsher RW, Menon A. Community-onset methicillin-resistant Staphylococcus aureus skin and soft-tissue infections: impact of antimicrobial therapy on outcome. Clin Infect Dis 2007; 44:777.
- Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med 2006; 355:666.
- Demos M, McLeod MP, Nouri K. Recurrent furunculosis: a review of the literature. Br J Dermatol 2012; 167:725.
- Meislin HW, Lerner SA, Graves MH, et al. Cutaneous abscesses. Anaerobic and aerobic bacteriology and outpatient management. Ann Intern Med 1977; 87:145.
- Ghoneim AT, McGoldrick J, Blick PW, et al. Aerobic and anaerobic bacteriology of subcutaneous abscesses. Br J Surg 1981; 68:498.
- Brook I, Frazier EH. Aerobic and anaerobic bacteriology of wounds and cutaneous abscesses. Arch Surg 1990; 125:1445.
- Chartier C, Grosshans E. Erysipelas: an update. Int J Dermatol 1996; 35:779.
- Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996; 334:240.
- Barzilai A, Choen HA. Isolation of group A streptococci from children with perianal cellulitis and from their siblings. Pediatr Infect Dis J 1998; 17:358.
- Thorsteinsdottir B, Tleyjeh IM, Baddour LM. Abdominal wall cellulitis in the morbidly obese. Scand J Infect Dis 2005; 37:605.
- Bruun T, Oppegaard O, Hufthammer KO, et al. Early Response in Cellulitis: A Prospective Study of Dynamics and Predictors. Clin Infect Dis 2016; 63:1034.
- Fitch MT, Manthey DE, McGinnis HD, et al. Videos in clinical medicine. Abscess incision and drainage. N Engl J Med 2007; 357:e20.
- Miller LG, Quan C, Shay A, et al. A prospective investigation of outcomes after hospital discharge for endemic, community-acquired methicillin-resistant and -susceptible Staphylococcus aureus skin infection. Clin Infect Dis 2007; 44:483.
- Woo PC, Lum PN, Wong SS, et al. Cellulitis complicating lymphoedema. Eur J Clin Microbiol Infect Dis 2000; 19:294.
- Peralta G, Padrón E, Roiz MP, et al. Risk factors for bacteremia in patients with limb cellulitis. Eur J Clin Microbiol Infect Dis 2006; 25:619.
- Perl B, Gottehrer NP, Raveh D, et al. Cost-effectiveness of blood cultures for adult patients with cellulitis. Clin Infect Dis 1999; 29:1483.
- Gunderson CG, Martinello RA. A systematic review of bacteremias in cellulitis and erysipelas. J Infect 2012; 64:148.
- Torres J, Avalos N, Echols L, et al. Low yield of blood and wound cultures in patients with skin and soft-tissue infections. Am J Emerg Med 2017; 35:1159.
- Hook EW 3rd, Hooton TM, Horton CA, et al. Microbiologic evaluation of cutaneous cellulitis in adults. Arch Intern Med 1986; 146:295.
- Duvanel T, Auckenthaler R, Rohner P, et al. Quantitative cultures of biopsy specimens from cutaneous cellulitis. Arch Intern Med 1989; 149:293.
- Hook EW 3rd, Hooton TM, Horton CA, et al. Microbiologic evaluation of cutaneous cellulitis in adults. Arch Intern Med 1986; 146:295.
- Crisp JG, Takhar SS, Moran GJ, et al. Inability of polymerase chain reaction, pyrosequencing, and culture of infected and uninfected site skin biopsy specimens to identify the cause of cellulitis. Clin Infect Dis 2015; 61:1679.
- Barbic D, Chenkin J, Cho DD, et al. In patients presenting to the emergency department with skin and soft tissue infections what is the diagnostic accuracy of point-of-care ultrasonography for the diagnosis of abscess compared to the current standard of care? A systematic review and meta-analysis. BMJ Open 2017; 7:e013688.
- Tayal VS, Hasan N, Norton HJ, Tomaszewski CA. The effect of soft-tissue ultrasound on the management of cellulitis in the emergency department. Acad Emerg Med 2006; 13:384.
- Alsaawi A, Alrajhi K, Alshehri A, et al. Ultrasonography for the diagnosis of patients with clinically suspected skin and soft tissue infections: a systematic review of the literature. Eur J Emerg Med 2017; 24:162.
- Beltran J. MR imaging of soft-tissue infection. Magn Reson Imaging Clin N Am 1995; 3:743.
- Stamenkovic I, Lew PD. Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy. N Engl J Med 1984; 310:1689.
- Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol 1998; 170:615.
- Jaff MR, Sandager G, Panel A, Panel B. Images in vascular medicine. Mycotic aneurysm. Vasc Med 2000; 5:259.