Which symptom indicates the presence of a systemic infection

Practice Essentials

The term cellulitis commonly is used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, usually from acute infection. 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. [1, 2]

Signs and symptoms

Nonpurulent cellulitis is associated with the four cardinal signs of infection, as follows [1] :

• 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, 3]

• 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 [4, 5] :

• 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 [1] :

• 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 skin or soft tissue infection (SSTI) who have signs and symptoms of systemic toxicity [4] :

• 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 [4] :

• Moderate to severe disease [4] (eg, cellulitis complicating lymphedema [6] )

• Cellulitis of specific anatomic sites (eg, facial and especially ocular areas)

• Patients with a history of contact with potentially contaminated water [7]

• Patients with malignancy who are receiving chemotherapy

• Neutropenia or severe cell-mediated immunodeficiency

• Animal bites

Other tests to consider are as follows [1] :

• 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 [8]

• Ultrasonographic-guided aspiration of pus can shorten hospital stay and fever duration in children with cellulitis [9]

• If necrotizing fasciitis is a concern, CT imaging typically is used in stable patients; MRI can be performed, [10] 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 [11, 12, 13]

• 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 [14]

• 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 after incision and drainage of an abscess yields positive results in more than 90% of cases [4]

• Dissection of the underlying fascia to assess for necrotizing fasciitis may be determined by surgical consultation or indicated following initial evaluation and imaging studies [15]

• 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 [4] :

• 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 [1] :

• 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, [4] and beta-lactam antibiotics are appropriate therapy, as noted in the following [1] :

• 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 [1] :

• The cellulitis is most often due to Streptococcus species; daily amoxicillin or a macrolide may be effective for prevention of recurrences. [16]

• If tinea pedis is suspected to be the predisposing cause, treat with topical or systemic antifungals.

• Compressive therapy has been shown to decrease risk for recurrence in patients with chronic edema and recurrent cellulitis. [17]

Patients with severe cellulitis require parenteral therapy, such as the following [1] :

• Cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin for presumed staphylococcal or streptococcal infection

• Clindamycin or vancomycin for penicillin-allergic patients [18]

• Broad gram-positive, gram-negative, and anaerobic coverage for cases associated with diabetic ulcers [19]

• 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 [3] :

• 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.

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). [1]  

Streptococcal species are the most common causes of erysipelas and diffuse cellulitis or nonpurulent cellulitis that is not associated with a defined portal. [4] S aureus is the usual causative organism in purulent cellulitis associated with furuncles, carbuncles, or abscesses.

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. [11, 20, 21, 22]

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 Vibriospecies. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread. [1, 23]

Etiology

Host factors

Certain host factors predispose to severe infection. The elderly and individuals with diabetes mellitus are at risk for more severe disease. [24] 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. [1, 25]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G). [26, 27] Postvenectomy status following saphenous vein stripping can also result in cellulitis. [26] 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. [1]

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. [1, 28]

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. [29] 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. [30]

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. [1, 31, 32, 33]

S aureus is the leading cause of SSTIs in injection drug users, [34] followed by Streptococcus species. [35]

Gram-negative bacteria may cause bullous cellulitis in patients with cirrhosis. [36] 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 fewer 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) usually is the cause. Acinetobacter baumannii is an emerging multidrug-resistant pathogen in these scenarios. [1, 37]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G). [26, 27] Postvenectomy status following saphenous vein stripping can also result in cellulitis. [26] Cellulitis may also be associated with tinea pedis, and in such cases, culture of toe-web spaces may help identify a bacterial pathogen. [38] Lymphadenectomy following tumor excision, such as mastectomy, is also a predisposing factor for cellulitis. [1]

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. [39] 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 SSTIs requiring surgical intervention. [40, 5, 1]

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. [41]

MRSA was first reported in 1968 [42] ; 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 the 1990s, isolates of S aureus were found in patients without risk factors for nosocomial disease. [43] 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 healthcare-associated MRSA (HA-MRSA).

Although reports have indicated that MRSA causes the majority of SSTIs, these studies are plagued by variability in case-finding methodologies. [44] 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 SSTI 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 resistant strains, microbiologic investigations are strongly recommended. [1]

Bite wounds, lacerations, and puncture wounds

Mammalian bite wounds represent a specific subset of cellulitis with unique pathogens, and the infections are usually polymicrobial. [45] 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. [46] Several organisms are of particular interest in animal bites, including the following [45] :

• 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. [47] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections. [48]

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, [49] and usually no age predilection is described. Nonetheless, studies have found a higher incidence of cellulitis in individuals older than 45 years. [21, 50, 51] Cellulitis was more common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network. [52]

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 [29]

• 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 [30, 53]

• Perianal cellulitis, usually with group A beta-hemolytic Streptococcus (GABHS), occurs in children younger than 3 years [54]

• 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. [50] The incidence was higher in males and in those individuals aged 45-64 years. [50] In a large epidemiologic hospital-based study on skin, soft tissue, bone, and joint infections, 37.3% patients were identified as having cellulitis. [55]

Overall rates of visits increased for 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. [56] The study provided data regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States. [56]

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

Prognosis

Many cases of cellulitis and SSTI 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. [1]

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. [57] 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. [1, 58, 59]

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. [1]

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Author

Coauthor(s)

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.

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, 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.

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; Fellow of the Royal College of Physicians, London

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

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

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