Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Cellulitis

  • Author: Thomas E Herchline, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Aug 15, 2016
 

Practice Essentials

The term cellulitis is commonly used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, usually from acute infection (see the image below). Cellulitis usually follows a breach in the skin, although a portal of entry may not be obvious; the breach may involve microscopic skin changes or invasive qualities of certain bacteria.

Patient with cellulitis of the left ankle. This cePatient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)

Signs and symptoms

Nonpurulent cellulitis is associated with the 4 cardinal signs of infection, as follows:

  • Erythema
  • Pain
  • Swelling
  • Warmth

Physical examination findings that suggest the most likely pathogen include the following:

  • Skin infection without underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by streptococci; Staphylococcus aureus, often community-acquired MRSA, is the most likely pathogen when these factors are present[1]
  • Violaceous color and bullae suggest more serious or systemic infection with organisms such as Vibrio vulnificus or Streptococcus pneumoniae

The following findings suggest severe infection:

  • Malaise, chills, fever, and toxicity
  • Lymphangitic spread (red lines streaking away from the area of infection)
  • Circumferential cellulitis
  • Pain disproportionate to examination findings

Indications for emergent surgical evaluation are as follows[2] :

  • Violaceous bullae
  • Cutaneous hemorrhage
  • Skin sloughing
  • Skin anesthesia
  • Rapid progression
  • Gas in the tissue
  • Hypotension

See Clinical Presentation for more detail.

Diagnosis

Generally, no workup is required in uncomplicated cases of cellulitis that meet the following criteria:

  • Limited area of involvement
  • Minimal pain
  • No systemic signs of illness (eg, fever, altered mental status, tachypnea, tachycardia, hypotension)
  • No risk factors for serious illness (eg, extremes of age, general debility, immunocompromise)

The Infectious Disease Society of America (IDSA) recommends the following blood tests for patients with soft-tissue infection who have signs and symptoms of systemic toxicity[2] :

  • Blood cultures
  • CBC with differential
  • levels of creatinine, bicarbonate, creatine phosphokinase, and C-reactive protein (CRP)

Blood cultures should also be done in the following circumstances[2] :

  • Moderate to severe disease[2] (eg, cellulitis complicating lymphedema[3] )
  • Cellulitis of specific anatomic sites (eg, facial and especially ocular areas)
  • Patients with a history of contact with potentially contaminated water[4]
  • Patients with malignancy who are receiving chemotherapy
  • Neutropenia or severe cell-mediated immunodeficiency
  • Animal bites

Other tests to consider are as follows:

  • Mycologic investigations are advisable if recurrent episodes of cellulitis are suspected to be secondary to tinea pedis or onychomycosis
  • Creatinine levels help assess baseline renal function and guide antimicrobial dosing

Imaging studies

  • Ultrasonography may play a role in the detection of occult abscess and direction of care[5]
  • Ultrasonographic-guided aspiration of pus can shorten hospital stay and fever duration in children with cellulitis[6]
  • If necrotizing fasciitis is a concern, CT imaging is typically used in stable patients; MRI can be performed,[7] but MRI typically takes much longer than CT scanning
  • Strong clinical suspicion of necrotizing fasciitis should prompt surgical consultation without delay for imaging

Aspiration, Dissection, and Biopsy

  • Needle aspiration should be performed only in selected patients or in unusual cases, such as in cases of cellulitis with bullae or in patients who have diabetes, are immunocompromised, are neutropenic, are not responding to empiric therapy, or have a history of animal bites or immersion injury[8, 9, 10]
  • Aspiration or punch biopsy of the inflamed area may have a culture yield of 2-40% and is of limited clinical value in most cases[11]
  • Gram stain of aspiration or biopsy specimens has a low yield and is unnecessary in most cases, unless purulent material is draining or bullae or abscess is present; however, Gram stain and culture following incision and drainage of an abscess yields positive results in more than 90% of cases[2]
  • Dissection of the underlying fascia to assess for necrotizing fasciitis may be determined by surgical consultation or indicated following initial evaluation and imaging studies[12]
  • Skin biopsy is not routine but may be performed in an attempt to rule out a noninfectious entity

Hospital admission

The IDSA recommends considering inpatient admission in patients with hypotension and/or the following laboratory findings[2] :

  • Elevated creatinine level
  • Elevated creatine phosphokinase level (2-3 times the upper limit of normal)
  • CRP level >13 mg/L (123.8 mmol/L)
  • Low serum bicarbonate level
  • Marked left shift on the CBC with differential

See Workup for more detail.

Management

Treatment of cellulitis is as follows:

  • Antibiotic regimens are effective in more than 90% of patients
  • All but the smallest of abscesses require drainage for resolution, regardless of the pathogen
  • Drainage only, without antibiotics, may suffice if the abscess is relatively isolated, with little surrounding tissue involvement

In cases of cellulitis without draining wounds or abscess, streptococci continue to be the likely etiology,[2] and beta-lactam antibiotics are appropriate therapy, as noted in the following:

  • In mild cases of cellulitis treated on an outpatient basis: Dicloxacillin, amoxicillin, or cephalexin
  • In patients who are allergic to penicillin: Clindamycin or a macrolide (clarithromycin or azithromycin)
  • An initial dose of parenteral antibiotic with a long half-life (eg, ceftriaxone) followed by an oral agent

Treatment of recurrent disease (usually related to venous or lymphatic obstruction) is as follows:

  • The cellulitis is most often due to Streptococcus species, and penicillin G or amoxicillin (250 mg bid) or erythromycin (250 mg qd or bid) may be effective[13]
  • If tinea pedis is suspected to be the predisposing cause, treat with topical or systemic antifungals

Patients with severe cellulitis require parenteral therapy, such as the following:

  • Cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin for presumed staphylococcal or streptococcal infection
  • Clindamycin or vancomycin for penicillin-allergic patients[14]
  • Broad gram-positive, gram-negative, and anaerobic coverage for cases associated with diabetic ulcers[15]
  • Coverage for MRSA, until culture and sensitivity information become available, for severe cellulitis apparently related to a furuncle or an abscess

For cellulitis involving wounds sustained in an aquatic environment, recommended antibiotic regimens vary with the type of water involved, as follows:

  • Saltwater or brackish water: Doxycycline and ceftazidime, or a fluoroquinolone
  • Freshwater: A third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or a fluoroquinolone (eg, ciprofloxacin or levofloxacin)
  • Lack of response to an appropriate antibiotic regimen should raise suspicion for Mycobacterium marinum infection and suggest wound biopsy for mycobacterial stains and culture

See Treatment and Medication for more detail.

Next

Background

The term cellulitis is commonly used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, a process usually related to acute infection that does not involve the fascia or muscles. Cellulitis is characterized by localized pain, swelling, tenderness, erythema, and warmth.

Cellulitis has been classically considered to be an infection without formation of abscess (nonpurulent), purulent drainage, or ulceration. At times, cellulitis may overlap with other conditions, so that the macular erythema coexists with nodules, areas of ulceration, and frank abscess formation (purulent cellulitis) (see Presentation). The following images illustrate some of these presentations.

Mild cellulitis with a fine lacelike pattern of erMild cellulitis with a fine lacelike pattern of erythema. This lesion was only slightly warm and caused minimal pain, which is typical for the initial presentation of mild cellulitis.
Swelling seen in cellulitis involving the hand. InSwelling seen in cellulitis involving the hand. In a situation with hand cellulitis, always rule out deep infection by imaging studies or by obtaining surgical consultation.
Severe cellulitis of the leg in a woman aged 80 yeSevere cellulitis of the leg in a woman aged 80 years. The cellulitis developed beneath a cast and was painful and warm to the touch. Significant erythema is evident. The margins are irregular but not raised. An ulcerated area is visible in the center of the photograph.
Burns complicated by cellulitis. The larger lesionBurns complicated by cellulitis. The larger lesion is a second-degree burn (left), and the smaller lesion is a first-degree burn (right), each with an expanding zone of erythema consistent with cellulitis.

Streptococcal species are the most common causes of erysipelas and diffuse cellulitis or nonpurulent cellulitis that is not associated with a defined portal.[2] S aureus is the usual causative organism in purulent cellulitis associated with furuncles, carbuncles, or abscesses.

Previous
Next

Pathophysiology

Cellulitis usually follows a breach in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. In some cases, there is no obvious portal of entry and the breach may be due to microscopic changes in the skin or invasive qualities of certain bacteria. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. Facial cellulitis of odontogenic origin may also occur. Patients with toe-web intertrigo and/or tinea pedis —as well as those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity—are particularly vulnerable to recurrent episodes of cellulitis.[16, 17, 18, 8]

The vast majority of cases of cellulitis are likely caused by Streptococcus pyogenes and, to a lesser degree, by Staphylococcus aureus. In rare cases, cellulitis results from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. Distant seeding is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.[19]

Previous
Next

Etiology

Host factors

Certain host factors predispose to severe infection. The elderly and individuals with diabetes mellitus are at risk for more severe disease.[20] In addition, patients with diabetes, immunodeficiency, cancer, venous stasis, chronic liver disease, peripheral arterial disease, and chronic kidney disease appear to be at higher risk for recurrent infection because of an altered host immune response. Local control of immune function through interleukin-driven neutrophil recruitment, protective action of antimicrobial peptides, and the integrity of the cutaneous barrier have significant effects on the host’s defense against infection.[21]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G).[22, 23] Postvenectomy status following saphenous vein stripping can also result in cellulitis.[22] Lymphadenectomy following tumor excision, such as mastectomy, is also a predisposing factor for cellulitis.

Immunogenetic factors may play a role in some families who have an underlying susceptibility to an infection progressing to cellulitis. Other factors that affect host immunity and predispose to cellulitis include concurrent intravenous or subcutaneous “skin popping” drug use; infections in this setting may be polymicrobial, but community-acquired methicillin-resistant S aureus (CA-MRSA) is the most common pathogen in these patients (see the following images).

Patient with cellulitis of the left ankle. This cePatient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Abscess and associated cellulitis caused by communAbscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)

In individuals with normal host defenses, the most common causative organisms are group A streptococci (GAS) and S aureus. Group B Streptococcus cellulitis occurs in infants younger than 6 months, because their immune responses are not fully developed, and it may also be seen in adults with comorbidities such as diabetes or liver disease. For infantile cellulitis, presentations may include sepsis.[24]

Historically, facial cellulitis in children was frequently associated with H influenzae type B and S pneumoniae, but this is now generally considered a rarity because of routine H influenza e type B and pneumococcal vaccines. However, a study of 500,000 pediatric hospitalizations demonstrated that, although bacterial meningitis and epiglottitis diminished as a result of immunization for H influenzae type B and S pneumoniae, the incidence of facial cellulitis was unaffected.[25] Nonetheless, another study noted that 96% of the serotypes that cause facial cellulitis were included in the heptavalent-conjugated pneumococcal vaccine that was routinely used at the time of the study.

Impetigo is commonly caused by strains of S aureus and/or S pyogenes, and erysipelas (acute infection of the upper dermis, characterized by a sharply demarcated, raised border) is more commonly caused by streptococcal species such as S pyogenes.

Immunocompromised hosts may become infected from nontraditional cellulitis organisms, including gram-negative rods (eg, Pseudomonas, Proteus, Serratia, Enterobacter, Citrobacter), anaerobes, and others (eg, Helicobacter cinaedi, Fusarium species). Although fungi (eg, Cryptococcus) and herpes simplex virus may also cause cellulitis, these causes are rare.

Pneumococci may cause a particularly malignant form of cellulitis that is frequently associated with tissue necrosis, suppuration, and bloodstream invasion. Two distinct syndromes are recognized: the first is marked by involvement of the extremities in patients with diabetes or substance abuse, and the second is marked by involvement of the head, neck, and upper torso in patients with systemic lupus erythematosus, nephrotic syndrome, or hematologic disorders.[26]

Mycobacterial infections may present as cellulitis. In contradistinction to the usual bacterial cellulitis, these presentations often range from subacute to chronic and are typically unresponsive to short courses of antibiotics—which should then prompt further investigation. The diagnosis is made on the basis of the presence of granulomas, multinucleated giant cells, and acid-fast bacilli (AFB) from biopsy specimens or mycobacterial culture.[27, 28, 29]

S aureus is the leading cause of soft-tissue infections in injection drug users,[30] followed by Streptococcus species.[31]

Gram-negative bacteria may cause bullous cellulitis in patients with cirrhosis.[32] Early recognition is vital, because the course of the disease is rapid, typically progressing to septic shock and death. Gram stain and culture of fluid aspirated from the bullae may aid in management.

Recurrent staphylococcal cellulitis may occur in otherwise immunologically normal patients with nasal carriage of staphylococci and those with Job syndrome.

Hospital-acquired infections

Various hospital-acquired infections following soft-tissue trauma may lead to cellulitis. It is unusual to have infection occur in areas around surgical wounds less than 24 hours postoperatively, but if there is such a clinical problem, group A beta-hemolytic Streptococcus [GABHS] or Clostridium perfringens (which produces gas that may be appreciated as crepitus on examination) is the usually cause. Acinetobacter baumannii is an emerging multidrug-resistant pathogen in these scenarios.[33]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G).[22, 23] Postvenectomy status following saphenous vein stripping can also result in cellulitis.[22] Cellulitis may also be associated with tinea pedis, and in such cases, culture of toe-web spaces may help identify a bacterial pathogen.[34] Lymphadenectomy following tumor excision, such as mastectomy, is also a predisposing factor for cellulitis.

Varicella

Cellulitis can complicate varicella and may be identified by larger margins of erythema surrounding the vesicles. One study identified patients with invasive GAS cellulitis complicating varicella.[35] The median onset of GAS infection was day 4 of varicella, with fever, vomiting, and localized swelling reported. This condition mandates antibiotic treatment and careful clinical follow-up. Untreated cellulitis in association with varicella may progress to severe necrotizing soft-tissue infections requiring surgical intervention.[36]

MRSA

Although cellulitis can be complicated by abscess formation, it typically develops from an abscessogenic focus. One maxim in microbiology is the following: "The hallmark of staph infection is abscess formation." This has become a significant concern because of changing patterns of antibiotic resistance of S aureus, particularly MRSA.[37]

MRSA was first reported in 1968[38] ; for years, MRSA infections were identified only in patients with recent hospitalization, surgery, renal dialysis, residence in long-term-care facilities, or IV drug use. However, in recent years, isolates of S aureus have been found in patients without risk factors for nosocomial disease.[39] These isolates, which mostly maintain susceptibility to antibiotics such as trimethoprim-sulfamethoxazole or tetracycline, have been termed CA-MRSA to distinguish them from the previously identified hospital or health-care-associated MRSA (HA-MRSA). (See the images below.)

Patient with cellulitis of the left ankle. This cePatient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Abscess and associated cellulitis caused by communAbscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)

Although reports have indicated that MRSA causes the majority of skin and soft-tissue infections (SSTIs), these studies are plagued by variability in case-finding methodologies.[40] Furthermore, in the context of cellulitis, the finding is misleading in that these reports come from analysis of wound cultures in cases in which abscess formation occurred. Cultures in cellulitis are difficult to perform and frequently do not yield positive results; therefore, these tests are rarely done clinically. Consequently, the results of these studies cannot be generalized to cellulitis without abscess formation. Studies are under way to determine the incidence of S aureus —in particular, CA-MRSA in soft-tissue infection in which there is no identifiable abscess. However, until results of those studies are available, treatment decisions must be made on clinical grounds. Because treatment failures after empiric treatment may often occur, because of the emergence of resistantstrains,microbiologicinvestigations are strongly recommended.

Bite wounds, lacerations, and puncture wounds

Mammalian bite wounds represent a specific subset of cellulitis with unique pathogens. The infections are usually polymicrobial.[41] Human, dog, cat, and wild-animal bites all predispose to cellulitis with unique pathogens, but dog bites are the most commonly encountered bite wound in both the primary care and the emergency setting.[42] Several organisms are of particular interest in animal bites, including the following[41] :

  • Capnocytophaga canimorsus (dog)
  • Eikenella corrodens (human)
  • Pasteurella multocida (dog or cat)
  • Streptobacillus moniliformis (rat)

Puncture wounds, especially through the bottom of athletic shoes, may cause Pseudomonas osteomyelitis and/or cellulitis. However, lacerations and puncture wounds sustained in an aquatic environment (eg, oceans, lakes, streams) may be contaminated with bacteria not typically found in land-based injuries, including Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, and Mycobacterium marinum.[43] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections (see the image below).[44]

Cellulitis due to documented Vibrio vulnificus infCellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
Previous
Next

Epidemiology

Because cellulitis is not a reportable disease, the exact prevalence is uncertain; however, it is a relatively common infection, affecting all racial and ethnic groups. There is no statistically significant difference in the incidence of cellulitis in men and women,[45] and no age predilection is usually described. Nonetheless, studies have found a higher incidence of cellulitis in individuals older than 45 years.[17, 46, 47] Cellulitis was found to be more common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network.[48]

Certain age groups are at higher risk in some unique scenarios, such as the following:

  • Historically, buccal cellulitis caused by H influenzae type B was more common in children younger than 3 years; vaccination against this organism may have decreased the incidence of buccal cellulitis, but recent data suggest that this source remains a consideration, even in vaccinated cohorts[25]
  • Facial cellulitis is more common in adults older than 50 years; however, pneumococcal facial cellulitis occurs primarily in young children who are at risk for pneumococcal bacteremia[26, 49]
  • Perianal cellulitis, usually with group A beta-hemolytic Streptococcus (GABHS), occurs in children younger than 3 years[50]
  • Elderly patients with cellulitis are predisposed to thrombophlebitis

A study of an insurance database in Utah found an incidence rate of 24.6 cases per 1000 person-years.[46] The incidence was noted to be higher in males and in those individuals aged 45-64 years.[46] In a large epidemiologic hospital-based study on skin, soft-tissue, bone, and joint infections, 37.3% patients were identified as having cellulitis.[51]

Overall rates of visits increased for skin and soft-tissue infections (SSTIs) from 32.1 to 48.1 visits per 1000 population and reached 14.2 million by 2005, and visits for abscess and cellulitis increased from 17.3 to 32.5 visits per 1000 population and accounted for more than 95% of the increase, according to the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey.[52] The study provided data regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States.[52]

Cellulitis was found to account for approximately 3% of emergency medical consultations at one United Kingdom district general hospital.

Previous
Next

Prognosis

Many cellulitis and soft-tissue infections can be treated on an outpatient basis with oral antibiotics and do not result in lasting sequelae. Most patients’ conditions respond well to oral antibiotics. When outpatient therapy is unsuccessful, or for patients who require admission initially, IV antibiotics are usually effective.

Cellulitis may progress to serious illness by uncontrolled contiguous spread, including via the lymphatic or circulatory systems. Associated conditions or complications include lymphangitis, abscess formation, and, rarely, gangrenous cellulitis or necrotizing fasciitis.[53] Certain species, most notably group A beta-hemolytic Streptococcus (GABHS) and S aureus, produce toxins that may mediate a more severe systemic infection, leading to septic shock and death.[54, 55]

Previous
Next

Patient Education

Depending on the location of the affected area, the patient should decrease physical activity and elevate the extremity, if possible. They may take over-the-counter (OTC) pain medication such as acetaminophen (Tylenol) or ibuprofen (Advil, Motrin) for pain, if approved by their physician.

Patients should call their doctor's office or seek urgent evaluation if they have any of the following features:

  • Fever (>100.5°F), especially when associated with chills
  • Cellulitis with surrounding soft, fluctuant areas that are suggestive of abscess formation
  • Red streaking from an area of cellulitis or a fast-spreading area of redness, which indicates that the infection may need closer observation, change in antibiotic treatment, or inpatient supportive care
  • Significant pain not relieved by acetaminophen or ibuprofen
  • Inability to move an extremity or joint because of pain

Although any cellulitis infection may be severe, patients with diabetes, cancer, chronic lymphedema, or immunosuppression should be made aware that they are more predisposed to serious infection. Patients with an underlying genetic condition, such as an immunodeficiency disease, are also at especially high risk for minor skin infections to progress to cellulitis.

Previous
 
 
Contributor Information and Disclosures
Author

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Subramanian Swaminathan, DNB, MD Fellow, Department of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine

Subramanian Swaminathan, DNB, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, International AIDS Society, HIV Medicine Association

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy ofSciences,andSociety for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Dennis Cunningham, MD Assistant Professor of Pediatrics, Section of Infectious Diseases, Children's Hospital, Ohio State College of Medicine

Disclosure: Nothing to disclose.

Danny Lee Curtis, MD Clinical Assistant Professor of Medicine, University of South Florida College of Medicine; Consulting Staff, James A Haley Veterans Hospital

Danny Lee Curtis, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Robert Edelman, MD Professor, Associate Director for Clinical Research, Department of Medicine, Division of Geographic Medicine, Center for Vaccine Development, University of Maryland School of Medicine

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Eric S Halsey, MD Head, Virology Department, Naval Medical Research Center Detachment-Peru (NMRCD-Peru); Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Eric S Halsey, MD is a member of the following medical societies: Armed Forces Infectious Diseases Society, HIV Medicine Association of America, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Isaac P Humphrey, MD Assistant Professor of Internal Medicine, Uniformed Services University of the Health Sciences; Clinical Assistant Professor of Internal Medicine, Wright State University Boonshoft School of Medicine

Isaac P Humphrey, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Sungnack Lee, MD Vice President of Medical Affairs, Professor, Department of Dermatology, Ajou University School of Medicine, Korea

Sungnack Lee, MD is a member of the following medical societies: American Dermatological Association

Disclosure: Nothing to disclose.

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Mark Louden, MD, FACEP Assistant Medical Director, Emergency Department, Duke Raleigh Hospital

Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Giuseppe Micali, MD Head, Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Giuseppe Micali, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Christen M Mowad, MD Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Maria R Nasca, MD, PhD Assistant Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Disclosure: Nothing to disclose.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, AmericanGeriatricsSociety, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, InfectiousDiseases Societyof America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Baxter International and Johnson & Johnson Royalty Other

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Busch BA, Ahern MT, Topinka M, Jenkins JJ 2nd, Weiser MA. Eschar with cellulitis as a clinical predictor in community-acquired MRSA skin abscess. J Emerg Med. Jul 8 2008.

  2. [Guideline] Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, 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 Jul 15. 59(2):e10-52. [Medline].

  3. Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY. Cellulitis complicating lymphoedema. Eur J Clin Microbiol Infect Dis. Apr 2000. 19(4):294-7.

  4. Swartz MN. Clinical practice. Cellulitis. N Engl J Med. Feb 26 2004. 350(9):904-12.

  5. 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. Apr 2006. 13(4):384-8.

  6. Chao HC, Lin SJ, Huang YC, Lin TY. Sonographic evaluation of cellulitis in children. J Ultrasound Med. Nov 2000. 19(11):743-9.

  7. Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol. Mar 1998. 170(3):615-20.

  8. Gabillot-Carré M, Roujeau JC. Acute bacterial skin infections and cellulitis. Curr Opin Infect Dis. 2007 Apr. 20(2):118-23. [Medline].

  9. Stevenson A, Hider P, Than M. The utility of blood cultures in the management of non-facial cellulitis appears to be low. N Z Med J. Mar 11 2005. 118(1211):U1351.

  10. Sachs MK. The optimum use of needle aspiration in the bacteriologic diagnosis of cellulitis in adults. Arch Intern Med. Sep 1990. 150(9):1907-12.

  11. Zahar JR, Goveia J, Lesprit P, Brun-Buisson C. Severe soft tissue infections of the extremities in patients admitted to an intensive care unit. Clin Microbiol Infect. Jan 2005. 11(1):79-82.

  12. Edlich RF, Cross CL, Dahlstrom JJ, Long WB 3rd. Modern Concepts of the Diagnosis and Treatment of Necrotizing Fasciitis. J Emerg Med. Dec 10 2008.

  13. Kremer M, Zuckerman R, Avraham Z, Raz R. Long-term antimicrobial therapy in the prevention of recurrent soft-tissue infections. J Infect. Jan 1991. 22(1):37-40.

  14. Seaton RA, Bell E, Gourlay Y, Semple L. Nurse-led management of uncomplicated cellulitis in the community: evaluation of a protocol incorporating intravenous ceftriaxone. J Antimicrob Chemother. May 2005. 55(5):764-7.

  15. Lipsky BA. New developments in diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev. May-Jun 2008. 24 Suppl 1:S66-71.

  16. Roujeau JC, Sigurgeirsson B, Korting HC, Kerl H, Paul C. Chronic dermatomycoses of the foot as risk factors for acute bacterial cellulitis of the leg: a case-control study. Dermatology. 2004. 209(4):301-7.

  17. Björnsdóttir S, Gottfredsson M, Thórisdóttir AS, Gunnarsson GB, Ríkardsdóttir H, Kristjánsson M, et al. Risk factors for acute cellulitis of the lower limb: a prospective case-control study. Clin Infect Dis. Nov 15 2005. 41(10):1416-22.

  18. Roberts S, Chambers S. Diagnosis and management of Staphylococcus aureus infections of the skin and soft tissue. Intern Med J. Dec 2005. 35 Suppl 2:S97-105.

  19. Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg. Sep 2007. 26(3):168-78.

  20. Lin JN, Chang LL, Lai CH, Lin HH, Chen YH. Clinical and molecular characteristics of invasive and noninvasive skin and soft tissue infections caused by group A Streptococcus. J Clin Microbiol. 2011 Oct. 49(10):3632-7. [Medline]. [Full Text].

  21. Miller LS, Cho JS. Immunity against Staphylococcus aureus cutaneous infections. Nat Rev Immunol. 2011. 11:505-18. [Medline].

  22. Baddour LM, Bisno AL. Recurrent cellulitis after saphenous venectomy for coronary bypass surgery. Ann Intern Med. Oct 1982. 97(4):493-6.

  23. Baddour LM, Bisno AL. Non-group A beta-hemolytic streptococcal cellulitis. Association with venous and lymphatic compromise. Am J Med. Aug 1985. 79(2):155-9.

  24. Kalliola S, Vuopio-Varkila J, Takala AK, Eskola J. Neonatal group B streptococcal disease in Finland: a ten-year nationwide study. Pediatr Infect Dis J. Sep 1999. 18(9):806-10.

  25. Cieslak TJ, Rajnik M, Roscelli JD. Immunization against Haemophilus influenzae type B fails to prevent orbital and facial cellulitis: results of a 25-year study among military children. Mil Med. Oct 2008. 173(10):941-4.

  26. Parada JP, Maslow JN. Clinical syndromes associated with adult pneumococcal cellulitis. Scand J Infect Dis. 2000. 32(2):133-6.

  27. Chin PW, Koh CK, Wong KT. Cutaneous tuberculosis mimicking cellulitis in an immunosuppressed patient. Singapore Med J. Jan 1999. 40(1):44-5.

  28. Elkayam O, Gat A, Lidgi M, Segal R, Yaron M, Caspi D. Atypical cutaneous findings in a patient with systemic lupus erythematosus. Lupus. 2003. 12(5):413-7.

  29. Hsu PY, Yang YH, Hsiao CH, Lee PI, Chiang BL. Mycobacterium kansasii infection presenting as cellulitis in a patient with systemic lupus erythematosus. J Formos Med Assoc. Aug 2002. 101(8):581-4.

  30. Bassetti S, Battegay M. Staphylococcus aureus infections in injection drug users: risk factors and prevention strategies. Infection. Jun 2004. 32(3):163-9.

  31. Sierra JM, Sanchez F, Castro P, et al. Group A streptococcal infections in injection drug users in Barcelona, Spain: epidemiologic, clinical, and microbiologic analysis of 3 clusters of cases from 2000 to 2003. Medicine (Baltimore). May 2006. 85(3):139-46.

  32. Horowitz Y, Sperber AD, Almog Y. Gram-negative cellulitis complicating cirrhosis. Mayo Clin Proc. Feb 2004. 79(2):247-50.

  33. Sebeny PJ, Riddle MS, Petersen K. Acinetobacter baumannii skin and soft-tissue infection associated with war trauma. Clin Infect Dis. Aug 15 2008. 47(4):444-9.

  34. 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. Nov 1996. 23(5):1162-4.

  35. Vugia DJ, Peterson CL, Meyers HB, et al. Invasive group A streptococcal infections in children with varicella in Southern California. Pediatr Infect Dis J. Feb 1996. 15(2):146-50.

  36. Waldhausen JH, Holterman MJ, Sawin RS. Surgical implications of necrotizing fasciitis in children with chickenpox. J Pediatr Surg. Aug 1996. 31(8):1138-41.

  37. Lowy FD. Staphylococcus aureus infections. N Engl J Med. Aug 20 1998. 339(8):520-32.

  38. Barrett FF, McGehee RF Jr, Finland M. Methicillin-resistant Staphylococcus aureus at Boston City Hospital. Bacteriologic and epidemiologic observations. N Engl J Med. Aug 29 1968. 279(9):441-8.

  39. Four Pediatric Deaths from Community-Acquired Methicillin-Resistant Staphylococcus aureus -- Minnesota and North Dakota, 1997-1999. CDC. August 20, 1999. 707-10. [Full Text].

  40. Furuya EY, Cook HA, Lee MH, Miller M, Larson E, Hyman S. Community-associated methicillin-resistant Staphylococcus aureus prevalence: how common is it? A methodological comparison of prevalence ascertainment. Am J Infect Control. Aug 2007. 35(6):359-66. [Medline].

  41. Brook I. Microbiology and management of human and animal bite wound infections. Prim Care. Mar 2003. 30(1):25-39.

  42. Dendle C, Looke D. Review article: Animal bites: an update for management with a focus on infections. Emerg Med Australas. Dec 2008. 20(6):458-67.

  43. Noonburg GE. Management of extremity trauma and related infections occurring in the aquatic environment. J Am Acad Orthop Surg. Jul-Aug 2005. 13(4):243-53.

  44. Dechet AM, Yu PA, Koram N, Painter J. Nonfoodborne Vibrio infections: an important cause of morbidity and mortality in the United States, 1997-2006. Clin Infect Dis. Apr 1 2008. 46(7):970-6.

  45. McNamara DR, Tleyjeh IM, Berbari EF, et al. Incidence of lower-extremity cellulitis: a population-based study in Olmsted county, Minnesota. Mayo Clin Proc. Jul 2007. 82(7):817-21.

  46. Ellis Simonsen SM, van Orman ER, Hatch BE, et al. Cellulitis incidence in a defined population. Epidemiol Infect. Apr 2006. 134(2):293-9. [Medline].

  47. Lamagni TL, Darenberg J, Luca-Harari B, et al. Epidemiology of severe Streptococcus pyogenes disease in Europe. J Clin Microbiol. Jul 2008. 46(7):2359-67. [Medline].

  48. Lederman ER, Weld LH, Elyazar IR, et al. Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance Network. Int J Infect Dis. Nov 2008. 12(6):593-602.

  49. Givner LB, Mason EO Jr, Barson WJ, et al. Pneumococcal facial cellulitis in children. Pediatrics. Nov 2000. 106(5):E61.

  50. Kokx NP, Comstock JA, Facklam RR. Streptococcal perianal disease in children. Pediatrics. Nov 1987. 80(5):659-63.

  51. Lipsky BA, Weigelt JA, Gupta V, Killian A, Peng MM. Skin, soft tissue, bone, and joint infections in hospitalized patients: epidemiology and microbiological, clinical, and economic outcomes. Infect Control Hosp Epidemiol. Nov 2007. 28(11):1290-8. [Medline].

  52. Hersh AL, Chambers HF, Maselli JH, Gonzales R. National trends in ambulatory visits and antibiotic prescribing for skin and soft-tissue infections. Arch Intern Med. Jul 28 2008. 168(14):1585-91. [Medline].

  53. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group. N Engl J Med. Aug 22 1996. 335(8):547-54. [Medline].

  54. Bisno AL, Cockerill FR 3rd, Bermudez CT. The initial outpatient-physician encounter in group A streptococcal necrotizing fasciitis. Clin Infect Dis. Aug 2000. 31(2):607-8. [Medline].

  55. Francis JS, Doherty MC, Lopatin U, Johnston CP, Sinha G, Ross T. Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton-Valentine leukocidin genes. Clin Infect Dis. Jan 1 2005. 40(1):100-7. [Medline].

  56. Durupt F, Dalle S, Ronger S, Thomas L. Does erysipelas-like rash after hip replacement exist?. Dermatology. 2006. 212(3):216-20.

  57. Simon MS, Cody RL. Cellulitis after axillary lymph node dissection for carcinoma of the breast. Am J Med. Nov 1992. 93(5):543-8.

  58. Masmoudi A, Maaloul I, Turki H, et al. Erysipelas after breast cancer treatment (26 cases). Dermatol Online J. Dec 1 2005. 11(3):12.

  59. Zippel D, Siegelmann-Danieli N, Ayalon S, Kaufman B, Pfeffer R, Zvi Papa M. Delayed breast cellulitis following breast conserving operation. Eur J Surg Oncol. May 2003. 29(4):327-30.

  60. El Saghir NS, Otrock ZK, Bizri AR, Uwaydah MM, Oghlakian GO. Erysipelas of the upper extremity following locoregional therapy for breast cancer. Breast. Oct 2005. 14(5):347-51.

  61. Lazzarini L, Conti E, Tositti G, de Lalla F. Erysipelas and cellulitis: clinical and microbiological spectrum in an Italian tertiary care hospital. J Infect. Dec 2005. 51(5):383-9.

  62. Spear RM, Rothbaum RJ, Keating JP, Blaufuss MC, Rosenblum JL. Perianal streptococcal cellulitis. J Pediatr. Oct 1985. 107(4):557-9.

  63. Markham RB, Polk BF. Seal finger. Rev Infect Dis. May-Jun 1979. 1(3):567-9.

  64. Crum NF, Higginbottom PA, Fehl FC, Graham BS. Sweet's syndrome masquerading as facial cellulitis. Cutis. Jun 2003. 71(6):469-72.

  65. Jenkins TC, Knepper BC, Sabel AL, Sarcone EE, Long JA, Haukoos JS, et al. Decreased Antibiotic Utilization After Implementation of a Guideline for Inpatient Cellulitis and Cutaneous Abscess. Arch Intern Med. 2011 Jun 27. 171(12):1072-9. [Medline].

  66. Perl B, Gottehrer NP, Raveh D, Schlesinger Y, Rudensky B, Yinnon AM. Cost-effectiveness of blood cultures for adult patients with cellulitis. Clin Infect Dis. Dec 1999. 29(6):1483-8.

  67. 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 Feb. 52:1-38. [Medline].

  68. Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America Clinical Practice Guideline for the Diagnosis and Treatment of Diabetic Foot Infections. Clin Infect Dis. 2012. 54(12):3132-3172. [Full Text].

  69. Brown T. Recurrent Cellulitis: Penicillin Effective for Prevention. Medscape Medical News, May 1, 2013. Available at http://www.medscape.com/viewarticle/803476. Accessed: May 8, 2013.

  70. Thomas KS, Crook AM, Nunn AJ, Foster KA, Mason JM, Chalmers JR, et al. Penicillin to prevent recurrent leg cellulitis. N Engl J Med. 2013 May 2. 368(18):1695-703. [Medline].

  71. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med. Aug 17 2006. 355(7):666-74.

  72. Cenizal MJ, Skiest D, Luber S, Bedimo R, Davis P, Fox P, et al. Prospective randomized trial of empiric therapy with trimethoprim-sulfamethoxazole or doxycycline for outpatient skin and soft tissue infections in an area of high prevalence of methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother. Jul 2007. 51(7):2628-30.

  73. Daum RS. Clinical practice. Skin and soft-tissue infections caused by methicillin-resistant Staphylococcus aureus. N Engl J Med. Jul 26 2007. 357(4):380-90.

  74. Stryjewski ME, Chambers HF. Skin and soft-tissue infections caused by community-acquired methicillin-resistant Staphylococcus aureus. Clin Infect Dis. Jun 1 2008. 46 Suppl 5:S368-77.

  75. Davis SL, McKinnon PS, Hall LM, Delgado G Jr, Rose W, Wilson RF. Daptomycin versus vancomycin for complicated skin and skin structure infections: clinical and economic outcomes. Pharmacotherapy. Dec 2007. 27(12):1611-8.

  76. Krige JE, Lindfield K, Friedrich L, Otradovec C, Martone WJ, Katz DE. Effectiveness and duration of daptomycin therapy in resolving clinical symptoms in the treatment of complicated skin and skin structure infections. Curr Med Res Opin. Sep 2007. 23(9):2147-56.

  77. Hepburn MJ, Dooley DP, Skidmore PJ, Ellis MW, Starnes WF, Hasewinkle WC. Comparison of short-course (5 days) and standard (10 days) treatment for uncomplicated cellulitis. Arch Intern Med. Aug 9-23 2004. 164(15):1669-74.

  78. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004 Jul. 32(7):1535-41. [Medline].

  79. King MD, Humphrey BJ, Wang YF, Kourbatova EV, Ray SM, Blumberg HM. Emergence of community-acquired methicillin-resistant Staphylococcus aureus USA 300 clone as the predominant cause of skin and soft-tissue infections. Ann Intern Med. Mar 7 2006. 144(5):309-17.

  80. Halilovic J, Heintz BH, Brown J. Risk factors for clinical failure in patients hospitalized with cellulitis and cutaneous abscess. J Infect. 2012 Mar 21. [Epub ahead of print]. [Medline].

  81. Byl B, Clevenbergh P, Jacobs F, Struelens MJ, Zech F, Kentos A. Impact of infectious diseases specialists and microbiological data on the appropriateness of antimicrobial therapy for bacteremia. Clin Infect Dis. Jul 1999. 29(1):60-6; discussion 67-8.

  82. Chuang YC, Yuan CY, Liu CY, Lan CK, Huang AH. Vibrio vulnificus infection in Taiwan: report of 28 cases and review of clinical manifestations and treatment. Clin Infect Dis. Aug 1992. 15(2):271-6.

  83. Fernandez JM, Serrano M, De Arriba JJ, Sanchez MV, Escribano E, Ferreras P. Bacteremic cellulitis caused by Non-01, Non-0139 Vibrio cholerae: report of a case in a patient with hemochromatosis. Diagn Microbiol Infect Dis. May 2000. 37(1):77-80.

  84. US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm265305.htm. Accessed: July 27, 2011.

  85. Hurley HJ, Knepper BC, Price CS, Mehler PS, Burman WJ, Jenkins TC. Avoidable antibiotic exposure for uncomplicated skin and soft tissue infections in the ambulatory care setting. Am J Med. 2013 Dec. 126(12):1099-106. [Medline].

Previous
Next
 
Mild cellulitis with a fine lacelike pattern of erythema. This lesion was only slightly warm and caused minimal pain, which is typical for the initial presentation of mild cellulitis.
Swelling seen in cellulitis involving the hand. In a situation with hand cellulitis, always rule out deep infection by imaging studies or by obtaining surgical consultation.
Severe cellulitis of the leg in a woman aged 80 years. The cellulitis developed beneath a cast and was painful and warm to the touch. Significant erythema is evident. The margins are irregular but not raised. An ulcerated area is visible in the center of the photograph.
Burns complicated by cellulitis. The larger lesion is a second-degree burn (left), and the smaller lesion is a first-degree burn (right), each with an expanding zone of erythema consistent with cellulitis.
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
A case of cellulitis without associated purulence in an infant. Note the presence of lymphedema, a risk factor for cellulitis.(Photo courtesy of Amy Williams.)
Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess. AFB = acid-fast bacilli; BID = twice daily; CRP = C reactive protein; CT = computed tomography scanning; DS = double strength; DM = diabetes mellitus; ESR = erythrocyte sedimentation rate; ESRD = end-stage renal disease; HIV = human immunodeficiency virus; ICU = intensive care unit; I&D = incision and drainage; ID = infectious disease; IDU = injection drug user; IV = intravenous; LRINEC = Laboratory Risk Indicator for Necrotizing Fasciitis; MRI = magnetic resonance imaging; MSRA = methicillin-resistant Staphylococcus aureus; NSAIDS = nonsteroidal anti-inflammatory drugs; PO = by mouth; SSTI = skin and soft-tissue infections; TID = 3 times daily. Adapted from Jenkins TC, Knepper BC, Sabel AL, et al. Decreased antibiotic utilization after implementation of a guideline for inpatient cellulitis and cutaneous abscess. Arch Intern Med. 2011;171(12):1072-9.
A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited pain on eye movement, fever, headache, and malaise.
A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.
Gross photograph of complicated cellulitis. Instead of the presence of yellow fat, the tissue is hemorrhagic and necrotic.
Hematoxylin and eosin (H&E) stain, high power. This image shows deeper subcutaneous tissue involved in a case of cellulitis, with acute inflammatory cells and fat necrosis.
Hematoxylin and eosin (H&E) stain, high power. This image shows cellulitis caused by herpes simplex virus, with the multinucleated organism in the center of the picture.
Table 1. Empiric Antibiotic Therapy for Cellulitis by Etiology and Anatomic Location
Location Likely Organisms Other Organisms Complication/ Discussion Antibiotic Regimen -- Oral/ Outpatient Indication for Hospitalization Antibiotic Regimen -- Parenteral/ Hospitalized
Uncomplicated cellulitisGroup A streptococci much more likely than Staphylococcus aureus  Cephalexin or dicloxacillin



or clindamycin



 Cefazolin or oxacillin



or nafcillin



Cellulitis, concern for methicillin-resistant S aureus is a concernGroup A streptococci and S aureus  [(Cephalexin or dicloxacillin or clindamycin) plus trimethoprim/ sulfamethoxazole]



or



Clindamycin



 Vancomycin



Daptomycin



Ceftaroline



Dog bitePasteurella species (50% of wounds)



S aureus



Streptococcus pyogenes



Staphylococci, streptococci



Aerobes --Moraxella and Neisseria



Anaerobes --Fusobacterium, Bacteroides, Porphyromonas, and Prevotella



Capnocytophaga canimorsus may cause sepsis in patients with asplenia/hepatic disease.



Avoid first-generation cephalosporins/ erythromycin/ dicloxacillin.



High likelihood of infection –



Prophylactic antibiotics indicated for the following wounds: deep puncture, hands, requiring surgical repair, immunocompromised host, venous or lymphatic compromise, crush injury.



Requires close follow-up care within 24-48 h.



Amoxicillin/ clavulanate



Penicillin allergic:



Moxifloxacin



Deep wounds or severe wounds;



infections not responding to oral antibiotics



Third-generation cephalosporin (ceftriaxone [Rocephin]) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Human biteEikenella corrodens (gram-negative facultative anaerobe, 29% of wounds)



Aerobic gram-positive cocci, anaerobes



 Clenched fist lacerations over metacarpophalangeal joints should be considered human bites; anesthetize wounds and irrigate; reevaluate within 24-48 h.



Intercanine distance >3 cm is likely bite from adult; if wound to child, consider abuse.



Amoxicillin/ clavulanate



Penicillin allergic:



Moxifloxacin



or



(Clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



 Third-generation cephalosporin (Rocephin) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam)



or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Cat bitePasteurella multocida and P septica (75% of wounds)Staphylococci, streptococci, Bacteroides, Peptostreptococcus, Actinomyces, Fusobacterium, Porphyromonas, and Veillonella parvulaAvoid first-generation cephalosporins/ erythromycin/ dicloxacillin



High likelihood of infection -- Prophylactic antibiotics indicated for the following wounds: deep puncture, hands, requiring surgical repair, immunocompromised host, venous or lymphatic compromise.



Requires close follow-up care within 24-48 h.



Amoxicillin/ clavulanate



Penicillin allergic --



Moxifloxacin



or



(Clindamycin or metronidazole) plus



(doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



Deep wounds or severe wounds; infections not responding to oral antibioticsThird-generation cephalosporin (Rocephin) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Preseptal (periorbital) cellulitisHaemophilus influenzae type b, Streptococcus pneumoniae, S aureus, other streptococcal species, and anaerobesNocardia brasiliensis, Bacillus anthracis, Pseudomonas aeruginosa, Neisseria gonorrhoeae, Proteus species, Pasteurella multocida, Mycobacterium tuberculosisLargest study indicates that H influenzae type b and S pneumoniae not diminished in facial cellulitis as a result of immunizations[25] Amoxicillin-clavulanate, cefpodoxime, cefdinirAge < 1 y/ more severe disease require intravenous antibioticThird-generation cephalosporin (Rocephin)
Lower extremity --



Complicating saphenous venectomy site after coronary bypass grafting



No pathogen identifiable in most infections, but it is likely to be streptococcal (> staphylococcal)



Non-group A beta-hemolytic streptococci most likely organism; S aureus less common



 Recurrent episodes common; may be associated with rigors, extreme fatigue, myalgias, and hypotension; some associated with tinea pedis (toe web cultures may be useful in establishing probable pathogen) Dicloxacillin or cephalexin.



Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if concern for methicillin-resistant S aureus



 First-generation cephalosporin (cefazolin); clindamycin; vancomycin
Breast/arm - - (not mastitis)



Complicating breast cancer surgery/lymph node dissection



No pathogen identifiable in most infections



Group A or Non-group A beta-hemolytic streptococci most likely organisms



  Dicloxacillin, cephalexin. Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if concern for methicillin-resistant S aureusFever, recent chemotherapy, neutropeniaMultiple regimens, none clearly superior –Piperacillin/tazobactam or ceftazidime plus aminoglycoside;



or



ciprofloxacin plus beta-lactam



or



monotherapy with piperacillin/tazobactam or cefepime



Aquatic environment --



Fresh water/ salt water/ brackish water/ swimming pools/ aquarium



Puncture/ laceration



Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, Mycobacterium marinum, and others A hydrophila and Vibrio vulnificus may produce rapidly progressive soft-tissue infection and sepsisFluoroquinolone (eg, ciprofloxacin or levofloxacin)



Note: For M marinum infection, use clarithromycin plus either ethambutol or rifampin



 Third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or fluoroquinolone (eg, ciprofloxacin or levofloxacin)
Clenched-fist injuryE corrodens (gram-negative anaerobe, 29 % of wounds); aerobic gram-positive cocci, anaerobes Lacerations over metacarpophalangeal joints should be considered human bites; anesthetize wounds and irrigate; reevaluate within 24-48 h



Lacerations of extensor tendon



Amoxicillin/ clavulanate; penicillin allergic:



Moxifloxacin



or



(clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



Failure to respond to oral therapy marked by increasing pain and swelling or purulent drainageBeta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam)
Odontogenic facial cellulitisAerobic and facultative organisms: group A beta-hemolytic streptococci, Neisseria and Eikenella species



Anaerobes: Prevotella and Peptostreptococcus species



 Require extraction or root canalAmoxicillin-clavulanate



or



clindamycin



 Beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



clindamycin



Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.