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.
View Image
Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....
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; daily amoxicillin or a macrolide may be effective for prevention of recurrences.[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
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.
View Image
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....
View Image
Swelling seen in cellulitis involving the hand. In a situation with hand cellulitis, always rule out deep infection by imaging studies or by obtaining....
View Image
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 eryt....
View Image
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....
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.
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 Vibriospecies. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.[19]
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).
View Image
Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....
View Image
Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. o....
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 the 1990s, isolates of S aureus were 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.)
View Image
Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....
View Image
Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. o....
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]
View Image
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
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.
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]
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.
A directed history is vital to the proper care of a patient with cellulitis. The patient may or may not relate an episode of trauma that preceded symptoms; when cellulitis develops, it is usually several days after the inciting trauma. Rapid progression or significant pain is a concerning sign that may indicate a severe problem, such as necrotizing fasciitis, which should be managed promptly.
If the patient recalls an episode of trauma, the clinician should ask about circumstances surrounding the incident that may elicit clues to a particular etiology. For example, exposure to standing or brackish water could mean that Aeromonas or Vibrio is the cause of infection; or a cut that occurred while butchering may be an important clue to consider Erysipelothrix rhusiopathiae. Identifying the specific inciting cause helps the clinician identify the most likely pathogen, choose appropriate antibiotic therapy, and offer appropriate immunization, such as tetanus toxoid (Td or Tdap), if indicated.
The patient should also be questioned about the presence of other skin disorders, including various types of dermatitis and especially any preceding fungal infection, which may serve as a portal of entry for bacterial pathogens.[17]
The past medical history should focus on the presence of comorbid conditions that may increase the risk for cellulitis, with the most common ones being diabetes mellitus, human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS), chronic kidney disease, and chronic liver disease.
The surgical history may include a recent procedure that resulted in wound infection. For example, severe bacterial cellulitis may occur as a postsurgical complication following hip replacement[56] or liposuction. Alternatively, a remote surgical history involving lymph node dissection (eg, following either radical mastectomy or conservative breast surgery) may predispose to cellulitis, even years after the surgery, because of lymphatic occlusion.[57, 58, 59, 60] Impaired lymphatic drainage and edema are also considered predisposing factors to leg cellulitis following saphenous vein resection for coronary artery bypass.[22] In addition, the presence of foreign bodies, including indwelling IV catheters, external orthopedic pins, and other surgical devices, may predispose to infection.
The physical examination should first focus on the area of concern. Nonpurulent cellulitis is associated with 4 cardinal signs of infection: erythema, pain, swelling, and warmth. Several physical examination findings may help the clinician identify the most likely pathogen and assess the severity of the infection, thereby facilitating appropriate treatment. Those findings include the following:
The involved site(s)is/are red, hot, swollen, and tender
Unlike erysipelas, the borders are not elevated or sharply demarcated
The involved site is the leg, which is the most common site[46, 61]
Regional lymphadenopathy is present
Malaise, chills, fever, and toxicity are present
Skin infection without underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by streptococci; on the other hand, S aureus, often community-acquired methicillin-resistant S aureus (CA-MRSA), is the most likely pathogen when these factors are present[1]
Perianal cellulitis is usually observed in children with perianal fissures; it is characterized by perianal erythema and pruritus, purulent secretions, painful defecation, and blood in the stools[62]
Cellulitis characterized by violaceous color and bullae suggests more serious or systemic infection with organisms such as V vulnificus (see the image below) or S pneumoniae
View Image
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
Lymphangitic spread (red lines streaking away from the area of infection), crepitus, and hemodynamic instability are indications of severe infection, requiring more aggressive treatment
Circumferential cellulitis or pain that is disproportional to examination findings should prompt consideration of severe soft-tissue infection
The IDSA indicates that the following are also signs/symptoms of potentially severe deep soft-tissue infection (Note: these frequently appear later in the course of necrotizing infections), which necessitate emergent surgical evaluation[2] :
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, chills, dehydration, altered mental status, tachypnea, tachycardia, hypotension)
No risk factors for serious illness (eg, extremes of age, general debility, immunocompromised status)
Because the bacterial etiology of cellulitis in typical cases is expected to represent streptococcal and, less commonly, staphylococcal infection, additional procedures are also usually unnecessary. However, in more severe disease or unique clinical scenarios, additional procedures may be indicated.
For serious infections, perform a blood culture, Gram stain, and culture of needle aspiration or punch biopsy specimens to pinpoint the etiology.[2] Blood cultures are only positive in 5-15% of patients with cellulitis. Aspiration of the leading edge of cellulitis margins rarely yields positive results but may be performed if clinicians are facing difficult situations.
The IDSA recommends bloodwork for patients with soft-tissue infection who have signs and symptoms of systemic toxicity; such tests include blood cultures, complete blood cell (CBC) with differential, and levels of creatinine, bicarbonate, creatine phosphokinase, and C-reactive protein (CRP).[2]
Considerations for hospitalization
The IDSA also recommends considering inpatient admission in the presence of hypotension and/or the following laboratory findings: an elevated creatinine level; an elevated creatine phosphokinase level (2-3 times the upper limit of normal [ULN]); a CRP level >13 mg/L (123.8 mmol/L); a low serum bicarbonate level; or a marked left shift on the CBC with differential.[2]
If a complicated or deep infection is suspected, imaging studies and/or surgical consultations should be done promptly.[2]
Jenkins et al also developed guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess (see the following image). The guidelines were shown to decrease the use of resources without an adverse effect on clinical outcomes.[65]
View Image
Guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess. AFB = acid-fast bacilli; BID = twice daily;....
The following laboratory tests may be considered in patients who present with moderate to severe cellulitis and/or systemic symptoms.
A complete blood cell (CBC) count often shows leukocytosis in the setting of severe disease; leukopenia may also be present in severe disease, especially in cases of toxin-mediated cellulitis.
The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) level are also frequently elevated, especially in patients with severe disease requiring prolonged hospitalization.[61]
In most cases of cellulitis, blood cultures are neither necessary nor cost-effective,[9, 66] but they should be performed in patients with moderate to severe disease,[2] such as patients with cellulitis complicating lymphedema,[3] because the prevalence of bacteremia is higher in these individuals. Blood cultures are also recommended for cellulitis of specific anatomic sites, such as facial and especially ocular areas; in patients with a history of contact with potentially contaminated water;[4] , in patients with malignancy on chemotherapy, neutropenia, or severe cell-mediated immunodeficiency; and in patients with animal bites.
Gram stain, whether obtained via biopsy or aspiration of the infected area, has a low yield and is unnecessary in most cases, unless purulent material is draining or bullae or abscess is present.
If recurrent episodes of cellulitis are suspected to be secondary to tinea pedis or onychomycosis, mycologic investigations are advisable .
Creatinine levels may be helpful to assess baseline renal function in order to correctly prescribe antimicrobial agents.
Current data suggest that ultrasonography may play a role in the detection of occult abscess and direction of care, especially in an emergency department setting.[5] Ultrasonographic-guided aspiration of pus has been shown to shorten hospital stay and fever duration in children with cellulitis.[6]
If necrotizing fasciitis is a concern, computed tomographic (CT) imaging is typically used to help rule out this condition in stable patients; magnetic resonance imaging (MRI) can be performed,[7] but MRI typically takes much longer than CT scanning. However, strong clinical suspicion of necrotizing fasciitis should prompt surgical consultation without delay for imaging.
Needle aspiration should be performed only in selected patients and/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] By contrast, 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. Tissue stains and microscopy reveal findings of soft-tissue inflammation. Leukocyte infiltration, capillary dilatation, and bacterial invasion of tissue are observed.
In cases in which cellulitis is extensive and tissue is no longer viable, debridement may be performed. In such cases, the normally bright-yellow fat becomes hemorrhagic and necrotic (see the first image below). Microscopic evaluation shows clusters of neutrophils (acute inflammation) invading adipose tissue, which can produce fat necrosis if it is extensive enough (see the second image below). An abscess forms when neutrophils aggregate into large clusters. Rarely, organisms can be seen on routine histologic stains (see the third image below).
View Image
Gross photograph of complicated cellulitis. Instead of the presence of yellow fat, the tissue is hemorrhagic and necrotic.
View Image
Hematoxylin and eosin (H&E) stain, high power. This image shows deeper subcutaneous tissue involved in a case of cellulitis, with acute inflammatory c....
View Image
Hematoxylin and eosin (H&E) stain, high power. This image shows cellulitis caused by herpes simplex virus, with the multinucleated organism in the cen....
Antibiotic regimens are effective in more than 90% of patients. However, all but the smallest of abscesses require drainage for resolution, regardless of the microbiology of the infection. In many instances, if the abscess is relatively isolated, with little surrounding tissue involvement, drainage may suffice without the need for antibiotics.
Note that management of cellulitis may be complicated because of the emergence of methicillin-resistant Staphylococcus aureus (MRSA) and macrolide- or erythromycin-resistant Streptococcus pyogenes.[2] Nonsevere cases of cellulitis may be treated empirically with semisynthetic penicillins, first- or second-generation oral cephalosporins, macrolides, or clindamycin.
Unfortunately, for patients with cellulitis surrounding abscess formation, 50% of MRSA strains also have inducible or constitutive clindamycin resistance.[2] Of the strains of S pyogenes resistant to macrolides, 99.5% seem to remain susceptible to clindamycin and 100% to penicillin.[2] Most community-acquired MRSA infections (CA-MRSA) are apparently susceptible to trimethoprim-sulfamethoxazole and tetracycline.
In 2011, the IDSA published updated guidelines regarding management of MRSA in adults and children, and in 2012, the updated IDSA guidelines for the Diagnosis and Treatment of Diabetic Foot Infections were published.[67, 68] Readers are encouraged to check the IDSA guidelines Web site for the 2014 updated recommendations for the diagnosis and management of skin and soft-tissue infections.[2]
Consider consulting an infectious disease specialist if the patient is not improving with standard treatment or if an unusual organism is identified; a critical care specialist for patients who are systemically ill and require admission to a critical care unit; or an ophthalmologist in cases of orbital cellulitis.
Cellulitis without draining or abscess
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, and cephalexin are all reasonable choices.
Clindamycin or a macrolide (clarithromycin or azithromycin) are reasonable alternatives in patients who are allergic to penicillin.
Levofloxacin may also represent an alternative, but the prevalence of resistant strains has increased, and additional toxicity associated with fluoroquinolones has been recognized. Therefore, fluoroquinolones are best reserved for situations with limited alternatives, such as gram-negative organisms with sensitivity demonstrated by culture.[8, 2]
Some clinicians prefer an initial dose of parenteral antibiotic with a long half-life (eg, ceftriaxone followed by an oral agent).
Recurrent cellulitis
In the occasional patient with recurrent disease usually related to venous or lymphatic obstruction, 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.
In a randomized, controlled trial in 274 patients who had experienced 2 or more episodes of cellulitis of the leg, a 12-month course of low-dose penicillin helped prevent recurrent cellulitis. The median time to first cellulitis recurrence was 626 days in the patients receiving penicillin (250 mg twice daily), versus 532 days in the placebo group. During the prophylaxis phase, 22% of the penicillin group (30 of 136 participants) had a recurrence, as compared to 37% of the placebo group (51 of 138 participants). However, the protective effect progressively diminished once the drug therapy ceased.[69, 70]
Severe cellulitis
Patients with severe cellulitis require parenteral therapy, such as the following:
Usually, cellulitis is presumed to be due to staphylococci or streptococci infection and may be treated with cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin.
Antimicrobial options in patients who are allergic to penicillin include clindamycin or vancomycin.[14]
Infections associated with diabetic ulcers are often polymicrobial; empiric coverage in this setting should include broad coverage of gram-positive, gram-negative, and anaerobic organisms.[15]
If the cellulitis appears to be related to a furuncle or an abscess or if it is a postsurgical infection, include coverage for MRSA for severe cases until culture and sensitivity information is available.
Mammalian bites
CA-MRSA is not commonly associated with bite wounds. Cellulitis associated with mammalian bite wounds is often polymicrobial and should be treated empirically with antimicrobials that target anaerobic bacteria in addition to the common cellulitis pathogens, as described below:
Mild cases can be treated on an outpatient basis with amoxicillin-clavulanate; in patients with penicillin allergy, combination therapy is usually required; fluoroquinolone plus clindamycin or trimethoprim-sulfamethoxazole (TMP-SMX) plus metronidazole would be reasonable alternatives
Inpatients can be treated with ampicillin-sulbactam or piperacillin-tazobactam; alternative agents in patients with penicillin allergy would be the same as the above but in parenteral form
Odontogenic cellulitis
Cellulitis of odontogenic origin is typically polymicrobial. Identified organisms include viridans streptococci, Neisseria and Eikenella species, and the anaerobes Prevotella and Peptostreptococcus. Treatment includes the following:
IV regimens that have demonstrated therapeutic response include clindamycin or ampicillin-sulbactam
Oral regimens that have demonstrated therapeutic response include clindamycin or amoxicillin-clavulanate
Aquatic lacerations and punctures
Lacerations and puncture wounds sustained in an aquatic environment may be contaminated with bacteria such as Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, and others. Treatment in such cases includes the following:
Antibiotic treatment should address common gram-positive and gram-negative aquatic organisms
Appropriate antibiotic regimens for saltwater or brackish water include doxycycline and ceftazidime, or a fluoroquinolone
Appropriate regimens for injuries sustained in freshwater include a third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or a fluoroquinolone (eg, ciprofloxacin or levofloxacin)
Apparent infection that is not responsive to initial courses of antibiotics as above should raise suspicion for Mycobacterium marinum infection; in such situations, wound biopsy for mycobacterial stains and culture should be considered
MRSA
In many communities, MRSA is the most common isolate obtained from abscesses.[71] Antibiotics used to treat cellulitis associated with abscess or purulent drainage should target MRSA until proven otherwise with culture data. In contrast, for outpatients with nonpurulent cellulitis, the IDSA recommends empiric therapy for infection due to beta-hemolytic streptococci, as it is believed that MRSA plays an uncommon role in these scenarios.[67]
Mild cases that require only outpatient therapy may be treated with TMP-SMX or a tetracycline agent such as doxycycline or minocycline. Available data suggest that doxycycline and TMP-SMX are equivalent for the treatment of mild skin and soft-tissue infections (SSTIs).[72] It is important to note that TMP-SMX and tetracyclines may not have adequate streptococcal coverage and should not be the first choice unless purulence is present.[73] Clindamycin may also be a reasonable choice, depending on local sensitivities of MRSA, but the IDSA estimates that up to 50% of MRSA isolates have intrinsic or constitutive resistance to clindamycin in some regions.[2]
In more severe cases that require parenteral antibiotics to cover MRSA, vancomycin, daptomycin, tigecycline, ceftaroline, and linezolid are appropriate choices. Data are more limited for the newer agents, but they have been shown to have similar efficacy to vancomycin in some clinical trials.[74] Daptomycin has been associated with more rapid resolution of signs and symptoms of cellulitis in some trials.[75, 76] However, vancomycin continues to be the drug of choice because of its overall excellent tolerability profile, efficacy, and cost.[74]
If tinea pedis is considered a possible cause of recurrent cellulitis episodes, treatment with a topical antifungal is recommended. Oral antifungals, such as itraconazole or terbinafine, may be considered in cases of refractory chronic changes or if onychomycosis is providing a source for repeated infection.
Table 1, below, provides an overview of empiric antibiotic therapy by etiology and anatomic location.
Table 1. Empiric Antibiotic Therapy for Cellulitis by Etiology and Anatomic Location
Patients with cellulitis who have mild local symptoms and no evidence of systemic disease can be treated on an outpatient basis. Facial cellulitis of odontogenic origin requires extraction or root canal as well as antibiotic therapy. Elevating limbs with cellulitis expedites resolution of the swelling. Cool sterile saline dressings may be used to remove purulent discharge from any open lesion.
Treatment duration for cellulitis is controversial; shorter-duration therapy may be as effective as longer-duration therapy.[77] In general, consider the following:
A transient increase in erythema over the first day of treatment is common and represents an inflammatory reaction to cell lysis caused by antibiotics
The patient should be reassessed with short-interval follow-up—ideally within 48-72 hours—to ensure improvement.
In patients who respond slowly to therapy, antibiotics may need to be continued until inflammation resolves. If infection does not regress after outpatient treatment, antibiotic resistance or a more serious infection should be ruled out; an alternative diagnosis should also be considered
Development of systemic symptoms should prompt reevaluation and consideration for admission.
Concomitant hypotension and tachycardia indicate systemic disease and warrant intensive monitoring
Severely ill patients and those whose condition is unresponsive to standard oral antibiotic therapy should be treated with inpatient intravenous (IV) antibiotics. The selection of antibiotic therapy should be based on suspicion for likely organisms as well as results of Gram stain, culture, and drug susceptibility analysis, if available.[2]
In hospitalized patients in which S aureus infection is a concern, it is wise to assume methicillin (oxacillin) resistance because of the high prevalence of community-acquired methicillin-resistant strains (CA-MRSA); administer agents that are usually effective against MRSA, such as vancomycin, linezolid, ceftaroline, or daptomycin.[2] Step-down treatment for S aureus– related soft-tissue infections may focus upon tetracyclines, trimethoprim-sulfamethoxazole, or other agents, depending on the results of susceptibility tests and following an initial clinical response.
Other individuals who may require inpatient IV antibiotic include the following[8] :
Immunosuppressed patients
Patients with facial cellulitis
Any patient with a clinically significant concurrent condition, including lymphedema and cardiac, hepatic, or renal failure
Individuals with newly elevated creatinine, creatine phosphokinase, and/or low serum bicarbonate levels or marked left-shift polymorphonuclear neutrophils
Urgent consultation with a surgeon should be sought in the setting of crepitus, circumferential cellulitis, necrotic-appearing skin (bronzing), evolving bullae, rapidly evolving cellulitis, pain disproportional to physical examination findings, severe pain on passive movement, or other clinical concern for necrotizing fasciitis. Wong et al have developed a scoring tool to assist in the diagnosis of necrotizing fasciitis.[78] Cellulitis associated with an abscess requires surgical drainage of the source of infection for adequate treatment.
Serious concern for necrotizing fasciitis and/or the presence of necrotic skin should prompt examination of the fascial planes by immediate computed tomographic imaging or surgical direct observation, which, in most cases, can be performed at the bedside by an experienced surgeon. Circumferential cellulitis may result in compartment syndrome, which may require surgical decompression. Measurement of compartment pressures may be helpful in diagnosis.
See also the Medscape Reference article Skin and Soft Tissue Infections - Incision, Drainage, and Debridement.
Although both Staphylococcus aureus and Streptococcus pyogenes cause impetigo ,historically, streptococcal infections were the most common, but recent series have indicated S aureus is now the leading cause. Management is based on the number of lesions, the location of the infection (eg, face, eyelid, mouth), and limiting infectivity.[2] The IDSA indicates mupirocin to be the best topical agent, despite some reports of resistance, and older preparations (eg, bacitracin and neomycin) to be much less effective.[2]
Administer oral antibiotic agents effective against both S aureus and S pyogenes in patients with many lesions or in those who do not respond to topical agents.[2] Note that some strains of S pyogenes may cause glomerulonephritis, a rare complication of impetigo, but there is currently no available evidence that treating impetigo will prevent glomerulonephritis. Also note that some strains of S aureus and S pyogenes may be resistant to erythromycin and erythromycin ethylsuccinate.[2]
The IDSA recommends use of the following antibiotics for managing impetigo in adults, with treatment duration of about 7 days (based on the clinical response)[2] :
Mupirocin ointment applied topically tid in patients with a limited number of lesions
Dicloxacillin, cephalexin, or erythromycin 250 mg PO qid, or
Erythromycin ethylsuccinate 400 mg PO qid, or
Clindamycin 300-400 mg PO tid, or
Amoxicillin-clavulanate (875/125 mg) PO bid
In children (excluding neonates), the IDSA recommends the following antibiotic regimens, with treatment duration of about 7 days (based on the clinical response)[2] :
Mupirocin ointment applied topically tid in patients with a limited number of lesions
Dicloxacillin 12 mg/kg/day PO, in 4 divided doses
Cephalexin 25 mg/kg/day PO, in 4 divided doses
Erythromycin 40 mg/kg/day PO, in 4 divided doses
Clindamycin 10-20 mg/kg/day PO in 3 divided doses
Amoxicillin-clavulanate 25 mg/kg/day of the amoxicillin component PO in 2 divided doses
See also the Medscape Reference articles Cellulitis Organism-Specific Therapy, Cellulitis Empiric Therapy, Periorbital Cellulitis Organism-Specific Therapy, Periorbital Cellulitis Empiric Therapy, Orbital Cellulitis Organism-Specific Therapy, and Orbital Cellulitis Empiric Therapy.
The IDSA indicates the following adult antibiotic regimens may be used to treat methicillin-sensitive Staphylococcus aureus (MSSA) skin and soft-tissue infections (SSTIs)[2] :
Nafcillin or oxacillin 1-2 g IV q4h (IV agent of choice; inactive against methicillin-resistant S aureus [MRSA])
Cefazolin 1 g IV q 8h (for penicillin-allergic patients but not those with immediate hypersensitivity reactions)
Clindamycin 600 mg/kg IV q8h or 300-450 mg PO tid (may have cross-resistance and emergence resistance in erythromycin-resistant strains; induces resistance in MRSA)
Dicloxacillin (PO agent of choice for MSSA) or cephalexin (for penicillin-allergic patients but not those with immediate hypersensitivity reactions) 500 mg PO qid
Doxycycline or minocycline 100 mg PO bid
Trimethoprim-sulfamethoxazole (TMP-SMZ) 1-2 double-strength (DS) tablets PO bid
The IDSA indicates that the following pediatric (except neonates) antibiotic regimens may be used to treat MSSA SSTI[2] :
Nafcillin or oxacillin 100-150 mg/kg/day IV, in 4 divided doses (IV agent of choice; inactive against MRSA)
Cefazolin 50 mg/kg/day IV, in 3 divided doses (for penicillin-allergic patients but not those with immediate hypersensitivity reactions)
Clindamycin 25-40 mg/kg/day IV, in 3 divided doses, or 10-20 mg/kg/day PO, in 3 divided doses (may have cross-resistance and emergence resistance in erythromycin-resistant strains; induces resistance in MRSA)
Dicloxacillin (PO agent of choice for MSSA) or cephalexin (for penicillin-allergic patients but not those with immediate hypersensitivity reactions), 25 mg/kg/day PO in 4 divided doses
TMP-SMZ 8-12 mg/kg (based on the TMP component) in 4 divided doses IV or 2 divided doses PO
Doxycycline and minocycline are not recommended in children younger than 8 years.
MRSA SSTIs
The IDSA indicates that the following adult antibiotic regimens may be used to treat MRSA SSTIs[2] :
Vancomycin 30 mg/kg/day IV, in 2 divided doses (IV agent of choice for MRSA; penicillin-allergic patients)
Linezolid 600 mg IV q12h or 600 mg PO bid
Clindamycin 600 mg/kg IV q8h or 300-450 mg PO tid (may have cross-resistance and emergence resistance in erythromycin-resistant strains; induces resistance in MRSA)
Daptomycin 4 mg/kg IV q24h (may cause myopathy)
Doxycycline, minocycline 100 mg PO bid
TMP-SMZ 1-2 double-strength (DS) tablets PO bid
The IDSA indicates that the following pediatric (except neonates) antibiotic regimens may be used to treat MRSA SSTIs[2] :
Vancomycin 40 mg/kg/day IV, in 4 divided doses (IV agent of choice for MRSA; penicillin-allergic patients)
Linezolid 10 mg/kg IV q12h or PO
Clindamycin 25-40 mg/kg/day IV, in 3 divided doses, or 10-20 mg/kg/day PO, in 3 divided doses (may have cross-resistance and emergence resistance in erythromycin-resistant strains; induces resistance in MRSA)
TMP-SMZ 8-12 mg/kg (based on the TMP component) in 4 divided doses IV or 2 divided doses PO
In 2011, the IDSA published updated guidelines regarding management of MRSA in adults and children, and in 2012, the updated IDSA guidelines for the Diagnosis and Treatment of Diabetic Foot Infections were published.[67, 68] Readers are encouraged to check the IDSA guidelines Web site for the 2014 updated recommendations for the diagnosis and management of skin and soft-tissue infections.[2]
As noted, streptococcal species are the most common causes of erysipelas and diffuse cellulitis or cellulitis that is not associated with a defined portal, and Staphylococcus aureus is the usual causative organism in cellulitis that is associated with furuncles, carbuncles, or abscesses.[2]
First-line treatment of erysipelas is either IV or PO penicillin, depending on the severity of the condition. In cases of cellulitis (except in areas with streptococcal/staphylococcal resistance), select a penicillinase-resistant semisynthetic penicillin or a first-generation cephalosporin. Clindamycin or vancomycin is an alternative in patients who are allergic to penicillin.[2]
In refractory cases, causes may include the following:
Unusual organisms
Streptococcal or staphylococcal resistance to the selected antimicrobial therapy
More severe conditions (eg, necrotizing fasciitis, myonecrosis)
Patients who exhibit clinical deterioration or increasing toxicity require an aggressive evaluation and management strategy with antimicrobial therapy dependent on the results of Gram stain, culture, and drug-susceptibility analysis, if these are available.[2]
Common causes of monomicrobial necrotizing fasciitis include Streptococcus pyogenes, Vibrio vulnificus, and Aeromonas hydrophila.[2] Polymicrobial necrotizing fasciitis is more common, especially in postoperative patients or in those with comorbid conditions, such as peripheral vascular disease, diabetes, and decubitus ulcers.
Clostridium species such as C perfringens, C septicum, C histolyticum, and C novyi are toxic causes of life-threatening gas gangrene, usually as a result of significant penetrating trauma or crush injuries that interrupt the blood supply.[2] Other predisposing factors include intracutaneous injection of black tar heroin (C perfringens, C novyi) or spontaneous gas gangrene (C septicum) in individuals with colonic lesions, adenocarcinoma, or neutropenia.[2]
Emergent surgical evaluation and management is the first-line treatment in necrotizing fasciitis and gas gangrene in the presence of the following[2] :
Violaceous bullae
Skin sloughing
Rapid progression
Gas in the tissue (crepitus or seen radiographically)
The IDSA recommends IV clindamycin and penicillin therapy for severe group A streptococcal and clostridial necrotizing infections.[2] For mixed necrotizing infections, in which gas in deep tissues is a frequent finding, select antimicrobials with efficacy against aerobic gram-positive/gram-negative organisms and anaerobes.
The IDSA recommends the following as first-line antibiotic treatments in managing adult mixed necrotizing infections[2] :
Ampicillin-sulbactam 1.5-3.0 g IV q6-8h (for patients with severe penicillin hypersensitivity: clindamycin or metronidazole plus an aminoglycoside or fluoroquinolone; add an appropriate agent in the presence of [or if there is a suspicion of] staphylococcal infection) or piperacillin-tazobactam 3.37 g IV q6-8h plus clindamycin 600-900 mg/kg IV q8h plus ciprofloxacin 400 mg IV q12h
Imipenem-cilastatin 1 g IV q6-8h
Meropenem 1 g IV q8h
Ertapenem 1 g IV qd
Cefotaxime 2 g IV q6h plus metronidazole 500 mg IV q6h or clindamycin 600-900 mg/kg IV q8h
The following are first-line treatments in managing adult S aureus (MSSA) infections[2] :
Nafcillin (for patients with severe penicillin hypersensitivity: vancomycin, linezolid, quinupristin-dalfopristin, or daptomycin; add an appropriate agent in the presence of [or if there is a suspicion of] staphylococcal infection) or oxacillin 1-2 IV q4h
Cefazolin 1 g IV q8h
Clindamycin 600-900 mg/kg IV q8h (may have cross-resistance and emergence resistance in erythromycin-resistant strains; induces resistance in MRSA)
First-line agents in managing severe adult streptococcal infection are penicillin 2-4 MU IV every 4-6 hours plus clindamycin 600-900 mg/kg IV every 8 hours.[2] For patients with severe penicillin hypersensitivity, use vancomycin, linezolid, quinupristin-dalfopristin, or daptomycin. Add an appropriate agent if a staphylococcal infection is present or suspected.
For clostridial infections, first-line agents are clindamycin 600-900 mg/kg IV every 8 hours, as well as penicillin 2-4 MU IV every 4-6 hours.
Readers are encouraged to check the IDSA guidelines Website for the 2014 updated recommendations for the diagnosis and management of skin and soft-tissue infections.
See also the Medscape Reference articles Necrotizing fasciitis and Clostridial Gas Gangrene.
Pasteurella species are the most commonly found organisms in cat- and dog-bite wounds; however, on average, 5 different aerobic and anaerobic bacteria are isolated from such wounds (eg, S aureus, Bacteroides tectum, Fusobacterium, Capnocytophaga, or Porphyromonas).[2]
The severity and depth of the wound, as well as the time since the bite occurred, help clinicians determine antimicrobial management, such as route of administration (eg, IV, PO). In non–penicillin-allergic patients, administer amoxicillin-clavulanate PO or ampicillin-sulbactam IV or ertapenem IV.[2] Other agents are not recommended because of either poor activity against P multocida (eg, dicloxacillin, cephalexin, erythromycin, clindamycin) or inadequate anaerobic coverage (eg, cefuroxime, cefotaxime, ceftriaxone).
Patients with mild penicillin allergies may receive cefoxitin IV or carbapenem agents IV. Individuals with severe penicillin hypersensitivity may receive doxycycline, TMP-SMZ, or a fluoroquinolone plus clindamycin, either PO or IV.[2]
Human bites
As in animals, the human mouth is contaminated with multiple organisms; therefore, any human-bite wound necessitates early recognition and management to avoid complications and infection. Common culprits include aerobic organisms (eg, streptococci, S aureus, Eikenella corrodens), as well as anaerobic organisms (eg, Fusobacterium, Peptostreptococcus, Prevotella, Porphyromonas).[2]
The IDSA recommends parenteral ampicillin-sulbactam or cefoxitin therapy in patients with human-bite wounds, because E corrodens is resistant to first-generation cephalosporins, macrolides, clindamycin, and aminoglycosides.[2]
See also the Medscape Reference articles Animal Bites and Human Bites.
In general, infections at surgical sites rarely occur in the first 48 hours after surgery, with the exceptions of group A streptococci or clostridial species.[2] The IDSA indicates that, usually, management with observation, dressing changes, or opening the incision is sufficient in patients with a temperature below 101.3°F (38.5° C) without tachycardia.[2]
Antibiotics and opening the incision are usually required in febrile patients with temperatures above 101.3°F (38.5° C) or tachycardia of 100 beats/min or greater.[2] Empiric therapy with agents active against the most likely organisms (eg, mixed gram-positive/gram-negative organisms for procedures involving the intestinal or genital tract; S aureus, MRSA, and streptococcal organisms for procedures involving nonintestinal sites) can be initiated until results from Gram stain and wound cultures are received.[2]
Procedures that involve nonsterile tissue (eg, intestinal/genital tract, respiratory mucosa) are frequently necessary because of mixed aerobic and anaerobic organism and can involve deeper soft tissues such as fascia and muscle.[2] The IDSA guidelines provide an algorithm, as well as a table of antibiotic selections, based on the operative site.[2]
Skin and soft-tissue infections (SSTIs) in immunocompromised patients can be caused by a variety of organisms, including those that don’t usually produce illness in healthy individuals, or may be the result of an underlying systemic infection.[2] The clinical findings of such SSTIs can be obscured by the degree and type of the patient’s immune deficiency.
Hospital-acquired SSTIs
Immunocompromised patients may acquire infections in the hospital, which can present a therapeutic challenge because of the emergence of resistant gram-positive and gram-negative bacteria. In general, severely ill or toxic patients require very broad-spectrum empiric agents that are effective against resistant gram-positive bacteria, including methicillin-resistant Staphylococcus aureus (MRSA); these antimicrobials include vancomycin, linezolid, daptomycin, and quinupristin-dalfopristin.[2] Ceftaroline is a newer, advanced-generation cephalosporin that includes coverage for MRSA and that has received FDA approval for treatment of SSTIs.
Gram-negative bacterial coverage includes monotherapy with a cephalosporin effective against strains of Pseudomonas (if such concerns exist with a patient), carbapenems, or a combination of either a fluoroquinolone or an aminoglycoside (monitor renal function), plus either an extended-spectrum penicillin or a cephalosporin.[2]
SSTIs in patients with cell-mediated immunodeficiency
Common or unusual bacteria (eg, Mycobacterium, Nocardia), viruses, protozoa, helminths, or fungi can cause SSTIs in patients with conditions such as Hodgkin disease, lymphoma, and human immunodeficiency virus (HIV) infection, as well as in patients who have had a bone marrow transplantation or have received long-term high-dose immunosuppressant therapy.[2] These patients require biopsy and early, aggressive management.
The IDSA guidelines provides a table of antibiotic selections based on the predisposing factor (eg, neutropenia, cellular immune deficiency) and pathogen (eg, bacteria, viruses, fungi).[2] Empiric treatment must be determined on the basis of local susceptibilities.
Readers are encouraged to check the IDSA Web site for the 2014 updated recommendations for the diagnosis and management of skin and soft-tissue infections.
In 2014, the Infectious Diseases Society of America (IDSA) published updated guidelines for the management of various skin and soft tissue infections (SSTIs), with emphasis on the clinical skills needed to properly treat the likely pathogens before and after culture results are available.[2]
The guidelines include a treatment algorithm that begins by determining whether the cellulitis is nonpurulent or purulent, as follows:[2]
Nonpurulent cellulitis includes rapidly spreading superficial cellulitis and erysipelas; typically involves groups A, B, C, and G beta-hemolytic streptococci and, occasionally, methicillin-susceptible Staphylococcus aureus (MSSA); these infections are diagnosed clinically, and cultures are not mandatory since there is usually no reliable and easily accessible source of specimen to culture
Purulent cellulitis includes cutaneous abscesses, carbuncles, furuncles, and sebaceous cyst infection typically involving S aureus, both MSSA and methicillin-resistant S aureus (MRSA); culture should be performed when possible to determine the pathogen’s presence and resistance pattern
Outpatient therapy with oral antibiotics is indicated for healthy individuals who have no evidence of systemic inflammatory response syndrome (SIRS).[2]
Inpatient therapy with parenteral antibiotics is recommended in patients with associated SIRS, hemodynamic instability, and/or mental status changes. Poor compliance, failure to respond to oral antibiotics, facial involvement, and immune suppression are additional indications for inpatient parenteral therapy until the patient is stable and improving. The initial antibiotic selection should cover MRSA in patients with coexisting penetrating and/or surgical trauma, evidence of MRSA infection elsewhere, known nasal MRSA colonization, and/or intravenous drug abuse. Coverage should also take into consideration the prevalence of MRSA in the patient’s hospital and community.[2]
According to the IDSA treatment algorithm, incision and drainage of abscess is indicated for all purulent infections and is sufficient for mild infections. For moderate infections, options for oral antibiotics include the following:
Doxycycline or minocycline
Trimethoprim-sulfamethoxazole
For severe infection or patients in whom incision and drainage plus oral antibiotics have failed, inpatient intravenous treatments include the following:
Staphylococcal and Streptococcal Skin and Soft Tissue Infections
Once microorganisms are identified based on cultures, treatment is tailored to the patient’s needs. The most common organisms are staphylococcal and streptococcal strains.[2]
Impetigo (Staphylococcus and Streptococcus)
IDSA treatment recommendations include any of the following oral antibiotics[2] :
Dicloxacillin
Cephalexin
Erythromycin (some strains of S aureus and S pyogenes are resistant)
Clindamycin
Amoxicillin-clavulanate
In patients with a limited number of lesions, retapamulin or mupirocin ointment may be applied topically.
Methicillin-susceptible S aureus (MSSA)
IDSA guidelines recommend oral dicloxacillin or IV nafcillin or oxacillin as the drugs of choice, but note that nafcillin and oxacillin are inactive against MRSA. For patients allergic to penicillin, cefazolin is indicated.[2]
Methicillin-resistant S aureus (MRSA)
IDSA recommends the following outpatient oral antibiotics:[2]
Doxycycline
Clindamycin
Trimethoprim-sulfamethoxazole
Linezolid
Some MRSA strains have inducible resistance, and this may result in treatment failure; a D-test can be performed by microbiology for evaluation.
Inpatient IV antibiotic treatment options include the following:[2]
The goals of antimicrobial therapy are to eradicate the infection, reduce morbidity, and prevent complications. Knowledge of local organisms and resistance patterns plays an integral role in appropriate antimicrobial selection.
Beta-lactam agents have long been the mainstay of therapy for cellulitis. However, the recent increase in the prevalence of community-acquired MRSA (CA-MRSA) in the general population,[79] especially in cases of cellulitis associated with abscess or purulent drainage, has changed this treatment paradigm to some degree. Common beta-lactam agents that are traditionally used to treat cellulitis do not cover CA-MRSA, so alternative agents or combination therapies are increasingly being used.
In general, the clinician should choose empiric antimicrobial coverage for common pathogens in each given clinical scenario and narrow coverage if culture data become available. Inappropriate antimicrobial selection and dosing have been found to be independent risk factors for clinical failure in patients admitted to the hospital for cellulitis with or without abscess.[80] In patients whose condition is not responding to therapy, consultation with an infectious disease specialist may be helpful.[81]
Treatment of cellulitis caused by uncommon organisms, such as Vibrio species or gram-negative bacteria, should be individualized (eg, tetracyclines, fluoroquinolones or aminoglycosides for Vibrio infection).[82, 83]
Clinical Context:
Penicillin G interferes with the synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.
The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.
Clinical Context:
Amoxicillin is a derivative of ampicillin and has a similar antibacterial spectrum—namely, certain gram-positive and gram-negative organisms. It has superior bioavailability and stability to gastric acid and has a broader spectrum of activity than penicillin. Amoxicillin is somewhat less active than penicillin against Streptococcus pneumococcus. Penicillin-resistant strains also are resistant to amoxicillin, but higher doses may be effective. It interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Clinical Context:
Amoxicillin inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins. The addition of clavulanate inhibits beta-lactamase–producing bacteria. Resistance is caused by a change in penicillin-binding proteins. It is recommended for bites from cats, dogs, and humans.
Clinical Context:
This is a drug combination of a beta-lactamase inhibitor and ampicillin. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. It is an alternative to amoxicillin-clavulanate if the patient is unable to take medication orally. It covers skin, enteric flora, and anaerobes. It is ideal for mammalian bite wounds, but it is not ideal for nosocomial pathogens because of increasing rates of resistance of gram-negative organisms.
Clinical Context:
Oxacillin is a bactericidal antibiotic that inhibits cell wall synthesis. It is used in the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when a methicillin-sensitive staphylococcal infection (MSSA) is suspected.
Clinical Context:
Dicloxacillin binds to one or more penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. It is used for the treatment of infections caused by streptococci and penicillinase-producing staphylococci. It may be used to initiate therapy when staphylococcal or streptococcal infection is suspected. Resistance to this drug results from alterations in penicillin-binding proteins. This drug does not cover MRSA.
Clinical Context:
Nafcillin binds to penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. Resistance occurs by alterations in penicillin-binding proteins. It is used as initial therapy for suspected streptococcal and penicillin-resistant staphylococcal infections (not MRSA).
The penicillinase-resistant, or second-generation, penicillins are semisynthetic modifications of natural penicillins that are resistant to bacterial enzyme beta-lactamase, which accounts for typical penicillin resistance.
Clinical Context:
Piperacillin-tazobactam is a semisynthetic penicillin with an increased spectrum against gram-negative bacilli. The addition of tazobactam inhibits beta-lactamases produced by bacteria. It is a broad-spectrum drug for gram-positive, gram-negative, and anaerobic bacteria; it covers most gram-positive organisms except MRSA.
Extended-spectrum, or fourth-generation, penicillins are semisynthetic modifications of natural penicillin that have an extended spectrum of activity, particularly against gram-negative bacteria such as Pseudomonas, Enterobacter, Proteus, and Klebsiella species.
Clinical Context:
Cephalexin binds to penicillin-binding proteins, which, in turn, inhibits synthesis of bacterial cell walls. Resistance occurs by alteration of penicillin-binding proteins. It is used for the treatment of infections caused by streptococci or penicillinase-producing staphylococci. It may be used to initiate therapy when streptococcal or staphylococcal (non-MRSA) infection is suspected. Because of the drug's short half-life, q8h or q12h dosing is not optimal.
Clinical Context:
Cefazolin is a first-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Resistance occurs by alterations in penicillin-binding proteins. It is primarily active against skin flora, including Staphylococcus aureus. Cefazolin is typically used alone for skin and skin-structure coverage but does not cover MRSA.
Clinical Context:
Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity; it has lower efficacy against gram-positive organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. It exerts its antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of the bacterial cell wall. Bacteria eventually lyse because of the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested. It is highly stable in the presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Ceftriaxone does not cover MRSA.
Clinical Context:
Cefadroxil is a first-generation semisynthetic cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms, including S aureus (not MRSA), S pneumoniae, S pyogenes, Moraxella catarrhalis, E coli, Klebsiella species, and Proteus mirabilis.
Clinical Context:
Cefepime is a fourth-generation cephalosporin. Its gram-negative coverage is comparable to ceftazidime, but it has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitterion; it rapidly penetrates gram-negative cells. Cefepime is the best beta-lactam for intramuscular administration. Its poor capacity to cross the blood-brain barrier precludes its use for meningitis.
Clinical Context:
Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity, including pseudomonal activity; it has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis.
Clinical Context:
Beta-lactam cephalosporin with activity against aerobic and anaerobic gram-positive and aerobic gram-negative bacteria. Demonstrates activity in vivo against methicillin-resistant Staphylococcus aureus (MRSA) strains and in vitro against vancomycin-resistant and linezolid-resistant S aureus. It is indicated for community-acquired bacterial pneumonia and for acute bacterial skin and skin structure infections, including MRSA.
Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into first, second, third, and fourth generation. First-generation cephalosporins have greater activity against gram-positive bacteria, and succeeding generations have increased activity against gram-negative bacteria and decreased activity against gram-positive bacteria.
Clinical Context:
Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms and blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. It is used to treat mild to moderate microbial infections.
Clinical Context:
Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used for the treatment of staphylococcal (not MRSA) and streptococcal infections.
Clinical Context:
Clarithromycin is a semisynthetic macrolide antibiotic that reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition. It has a similar susceptibility profile to erythromycin but has fewer adverse effects.
Macrolides are agents that bind to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of protein synthesis. Examples such as azithromycin, erythromycin, and clarithromycin are all reasonable alternatives in patients who are allergic to penicillins.
Clinical Context:
Imipenem-cilastatin is used for severe disease and to treat multiple-organism infections for which other agents do not have broad-spectrum coverage or are contraindicated because of their potential for toxicity.
Clinical Context:
Ertapenem has bactericidal activity resulting from the inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin-binding proteins. It is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, cephalosporinases, and extended-spectrum beta-lactamases.
Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to cell death. They are active against gram-negative, gram-positive, and anaerobic organisms.
Clinical Context:
Ciprofloxacin inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material.
Clinical Context:
Delafloxacin inhibits bacterial DNA synthesis and growth by inhibiting bacterial topoisomerase IV and DNA gyrase. Delafloxacin exhibits concentration-dependent bactericidal activity against gram-positive and gram-negative bacteria in vitro.
Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material.
Clinical Context:
Clindamycin is a lincosamide used for the treatment of serious skin and soft-tissue staphylococcal infections, including some community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clinical Context:
Linezolid prevents the formation of functional 70S initiation complex, which is essential for the bacterial translation process. It is bacteriostatic against enterococci and staphylococci, including MRSA and CA-MRSA. Linezolid is bactericidal against most strains of streptococci.
The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[84]
Clinical Context:
Tigecycline is a glycylcycline antibiotic that is structurally similar to tetracycline antibiotics. It inhibits bacterial protein translation by binding to the 30S ribosomal subunit and blocks entry of amino-acyl tRNA molecules in the ribosome A site. It is indicated for complicated skin and skin-structure infections caused by E coli, E faecalis (vancomycin-susceptible isolates only), S aureus (methicillin-susceptible and methicillin-resistant isolates), S agalactiae, S anginosus group (includes S anginosus, S intermedius, and S constellatus), S pyogenes, and B fragilis.
Clinical Context:
Vancomycin is indicated for patients who cannot receive or who have not responded to penicillins and cephalosporins or have infections with resistant staphylococci, including CA-MRSA and MRSA. To avoid toxicity, the current recommendation is to assay vancomycin trough levels after the fourth dose, drawn a half hour before the next dosing. Use creatinine clearance to adjust the dose in patients with renal impairment.
Clinical Context:
Daptomycin binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis and ultimately causing cell death. It is indicated to treat complicated skin and skin-structure infections caused by Staphylococcus aureus (including methicillin-resistant strains), S pyogenes, S agalactiae, S dysgalactiae, and E faecalis (vancomycin-susceptible strains only). Monitoring for muscle inflammation by monitoring creatinine phosphokinase levels is recommended.
Clinical Context:
Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. It may be considered an alternative to vancomycin in some cases of MRSA infection, especially CA-MRSA.
Clinical Context:
Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents.
Anti-infectives such as metronidazole, clindamycin, aztreonam, and trimethoprim- sulfamethoxazole are effective against some types of bacteria that have become resistant to other antibiotics. Vancomycin, daptomycin, tigecycline, and linezolid are appropriate choices In more severe cases that require parenteral antibiotics in areas where MRSA is thought to be a possible pathogen.
Clinical Context:
Doxycycline inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. It provides good coverage against spirochetes, many gram-negative organisms, anaerobic organisms, atypical bacteria, and many gram-positive organisms, including most CA-MRSA.
Clinical Context:
Minocycline inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. This drug covers gram-positive and gram-negative organisms, as well as CA-MRSA. Minocycline is a first-line agent against organisms such as Afipia felis, Borrelia recurrentis, Chlamydia species, Coxiella burnetii, Mycoplasma hominis, Mycobacterium marinum, Mycobacterium smegmatis, and V cholerae.
Clinical Context:
Aminomethylcycline antibacterial within the tetracycline drug class that binds to the 30S ribosomal subunit and blocks protein synthesis. It is active in vitro against gram-positive bacteria expressing tetracycline resistance active efflux pumps (tetK and tet L) and ribosomal protection proteins (tet M). It is indicated for treatment of acute bacterial skin and skin structure infections (ABSSSIs) caused by susceptible microorganisms including Staphylococcus aureus (methicillin-susceptible and methicillin-resistant isolates), Staphylococcus lugdunensis, Streptococcus pyogenes, Streptococcus anginosus group (includes Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus), Enterococcus faecalis, Enterobacter cloacae, and Klebsiella pneumoniae. Available for IV or PO administration.
The tetracyclines reversibly bind to the 30S subunit of the bacterial ribosome. They prevent the binding of aminoacyl transfer RNA and inhibit protein synthesis and cell growth. Tetracyclines are effective against both gram-positive and gram-negative organisms.
Clinical Context:
Itraconazole is a synthetic triazole that has fungistatic activity. It slows fungal cell growth by inhibiting cytochrome P-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.
Antifungal agents such as itraconazole and terbinafine work by inhibiting the biosynthesis of ergosterol, which is an essential component of the fungal cell membrane.
Which imaging studies are suggested for cellulitis?How is cellulitis treated?What is cellulitis?What are the signs and symptoms of cellulitis?What workup or tests should be completed in cellulitis diagnosis?When are aspiration, dissection, and biopsy suggested for cellulitis?When is hospital admission suggested for cellulitis?What is the pathophysiology of cellulitis?What causes cellulitis?What does the term cellulitis indicate?How do streptococcal species relate to cellulitis?What are the most common etiologies of cellulitis in injection drug users?Which host factors predispose to cellulitis?What are the most common causative organisms of cellulitis in infants and children?What causes impetigo?Which nontraditional organisms can cause cellulitis in immunocompromised patients?How is malignant cellulitis caused by pneumococci recognized?How do mycobacterial infections differ from cellulitis?What causes bullous cellulitis in patients with cirrhosis?What causes recurrent staphylococcal cellulitis?Which hospital-acquired infections lead to cellulitis?How does cellulitis affect varicella?How common is MRSA as a cause of cellulitis?Which pathogens cause cellulitis due to puncture wounds, lacerations, and bite wounds?What is the prevalence of cellulitis?What types of cellulitis are commonly found in specific age groups?How often do patients with skin and soft-tissue infections (SSTIs), including cellulitis and abscess, seek medical care?What is the prognosis of cellulitis?What information should be provided to patients with cellulitis?What is the role of the patient’s medical history in determining cellulitis treatment?During the medical history review, which findings might offer a clue to cellulitis etiology?Which skin disorders should be asked about in a patient presenting with cellulitis?Which comorbid conditions increase the risk of cellulitis?Why is surgical history important when cellulitis is present?Which physical findings suggest cellulitis and which indicate severe infection?What are the differential diagnoses for Cellulitis?What conditions should be considered in the differential diagnosis of cellulitis or in cases of treatment failure?When is a workup for cellulitis unnecessary?When is a blood culture or bloodwork necessary in the workup of cellulitis?What are the IDSA guidelines for the workup for cellulitis?When should hospitalization of a patient with cellulitis be considered?Which lab tests should be considered in patients presenting with moderate to severe cellulitis and/or systemic symptoms?What role does ultrasonography play in the workup of cellulitis?What role does CT imaging and MRI play in the workup of cellulitis?What are the roles of aspiration, dissection, and biopsy in the workup of cellulitis?What is the role of debridement in the workup and treatment of cellulitis, and what are the histologic findings?How is severe cellulitis treated?How is cellulitis treated?How effective are antibiotics in the treatment of MRSA cellulitis?When should cellulitis prompt consultation with a specialist?How is cellulitis without draining wounds or abscess treated?How is recurrent cellulitis treated?How is cellulitis associated with bite wounds treated?How is odontogenic cellulitis treated?How is cellulitis resulting from lacerations and puncture wounds sustained in an aquatic environment treated?How is MRSA cellulitis treated?When can cellulitis be treated on an outpatient basis?What is the treatment duration of cellulitis for outpatients?When should IV antibiotic therapy be considered for cellulitis and how is the antibiotic selected?When should surgical consultation and exam be considered for cases of cellulitis?What are the causes and treatments for impetigo in adults?What are the IDSA guidelines on the treatment of impetigo in children?Which antibiotics are recommended to treat methicillin-sensitive Staphylococcus aureus (MSSA) skin and soft-tissue infections (SSTIs) in children?Which antibiotics are recommended to treat MRSA skin and soft-tissue infections (SSTIs)?Which antibiotics are recommended to treat MRSA skin and soft-tissue infections (SSTIs) in children?Which antibiotics are recommended to treat methicillin-sensitive Staphylococcus aureus (MSSA) skin and soft-tissue infections (SSTIs)?How is erysipelas treated?What are the causes of refractory erysipelas?When is an aggressive evaluation and management strategy needed in patients with erysipelas?Which antibiotics are recommended in the treatment of adult Staphylococcus aureus (MSSA) infections?Which antibiotics are recommended in the treatment of severe streptococcal necrotizing infections in adults?What are the common causes of monomicrobial necrotizing fasciitis?When is surgical evaluation and management necessary in treating necrotizing fasciitis and gas gangrene?Which antibiotics are recommended in the treatment of mixed necrotizing infections?Which antibiotics are recommended in the treatment of clostridial necrotizing infections?How should animal bites be treated to prevent infection?How should human bites be treated to prevent infection?How should surgical site infections be treated?Which organisms cause skin and soft-tissue infections (SSTIs) in immunocompromised patients?How are hospital-acquired skin and soft-tissue infections (SSTIs) treated in immunocompromised patients?How are skin and soft-tissue infections (SSTIs) treated in patients with cell-mediated immunodeficiency?What are the IDSA treatment guidelines for skin and soft tissue infections (SSTIs), including cellulitis?Which oral antibiotics are indicated in the treatment of mild nonpurulent cellulitis?Which IV antibiotics are indicated in the treatment of moderate nonpurulent cellulitis?Which antibiotics are indicated in the treatment of severe nonpurulent cellulitis?What are the treatment guidelines for mild purulent cellulitis?Which oral antibiotics are recommended in the treatment of moderate purulent cellulitis?Which IV antibiotics are recommended in the treatment of severe purulent cellulitis?Which antibiotics do the guidelines recommend for the treatment of staphylococcal and streptococcal impetigo?What antibiotics do the IDSA guidelines recommend for the treatment of methicillin-susceptible S aureus (MSSA)?Which antibiotics do the IDSA guidelines recommend for the treatment of MRSA skin and soft tissue infections (STTIs)?What are the goals of antimicrobial therapy for cellulitis?What is the role of beta-lactam agents in the treatment of cellulitis?How should antimicrobials be chosen for common pathogens in patients with cellulitis?How are uncommon organisms treated in cellulitis?Which medications in the drug class Penicillins, Natural are used in the treatment of Cellulitis?Which medications in the drug class Penicillins, Amino are used in the treatment of Cellulitis?Which medications in the drug class Penicillins, Penicillinase Resistant are used in the treatment of Cellulitis?Which medications in the drug class Penicillins, Extended-Spectrum are used in the treatment of Cellulitis?Which medications in the drug class Cephalosporins, Other are used in the treatment of Cellulitis?Which medications in the drug class Macrolides are used in the treatment of Cellulitis?Which medications in the drug class Carbapenems are used in the treatment of Cellulitis?Which medications in the drug class Fluoroquinolones are used in the treatment of Cellulitis?Which medications in the drug class Antibiotics, Other are used in the treatment of Cellulitis?Which medications in the drug class Tetracyclines are used in the treatment of Cellulitis?Which medications in the drug class Antifungal Agents are used in the treatment of Cellulitis?
Thomas E Herchline, MD, Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Consultant, Public Health, Dayton and Montgomery County (Ohio) Tuberculosis Clinic
Disclosure: Nothing to disclose.
Coauthor(s)
Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University School of Medicine
Disclosure: Nothing to disclose.
Subramanian Swaminathan, DNB, MD, Fellow, Department of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine
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
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
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.
Swartz MN. Clinical practice. Cellulitis. N Engl J Med. Feb 26 2004. 350(9):904-12.
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.
Chao HC, Lin SJ, Huang YC, Lin TY. Sonographic evaluation of cellulitis in children. J Ultrasound Med. Nov 2000. 19(11):743-9.
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.
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.
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.
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.
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.
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.
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.
Lipsky BA. New developments in diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev. May-Jun 2008. 24 Suppl 1:S66-71.
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.
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.
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.
Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg. Sep 2007. 26(3):168-78.
Baddour LM, Bisno AL. Recurrent cellulitis after saphenous venectomy for coronary bypass surgery. Ann Intern Med. Oct 1982. 97(4):493-6.
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.
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.
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.
Chin PW, Koh CK, Wong KT. Cutaneous tuberculosis mimicking cellulitis in an immunosuppressed patient. Singapore Med J. Jan 1999. 40(1):44-5.
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.
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.
Bassetti S, Battegay M. Staphylococcus aureus infections in injection drug users: risk factors and prevention strategies. Infection. Jun 2004. 32(3):163-9.
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.
Horowitz Y, Sperber AD, Almog Y. Gram-negative cellulitis complicating cirrhosis. Mayo Clin Proc. Feb 2004. 79(2):247-50.
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.
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.
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.
Waldhausen JH, Holterman MJ, Sawin RS. Surgical implications of necrotizing fasciitis in children with chickenpox. J Pediatr Surg. Aug 1996. 31(8):1138-41.
Lowy FD. Staphylococcus aureus infections. N Engl J Med. Aug 20 1998. 339(8):520-32.
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.
Four Pediatric Deaths from Community-Acquired Methicillin-Resistant Staphylococcus aureus -- Minnesota and North Dakota, 1997-1999. CDC. August 20, 1999. 707-10.
Brook I. Microbiology and management of human and animal bite wound infections. Prim Care. Mar 2003. 30(1):25-39.
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.
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.
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.
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.
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.
Givner LB, Mason EO Jr, Barson WJ, et al. Pneumococcal facial cellulitis in children. Pediatrics. Nov 2000. 106(5):E61.
Kokx NP, Comstock JA, Facklam RR. Streptococcal perianal disease in children. Pediatrics. Nov 1987. 80(5):659-63.
Durupt F, Dalle S, Ronger S, Thomas L. Does erysipelas-like rash after hip replacement exist?. Dermatology. 2006. 212(3):216-20.
Simon MS, Cody RL. Cellulitis after axillary lymph node dissection for carcinoma of the breast. Am J Med. Nov 1992. 93(5):543-8.
Masmoudi A, Maaloul I, Turki H, et al. Erysipelas after breast cancer treatment (26 cases). Dermatol Online J. Dec 1 2005. 11(3):12.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Baxdela (delafloxacin) [package insert]. 300 Tri-State International Lincolnshire, Illinois, USA: Melinta Therapeutics, Inc. 6/2017. Available at
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.)
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.
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.)
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.)
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
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.
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.
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.
Location
Likely Organisms
Other Organisms
Complication/ Discussion
Antibiotic Regimen -- Oral/ Outpatient
Indication for Hospitalization
Antibiotic Regimen -- Parenteral/ Hospitalized
Uncomplicated cellulitis
Group 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 concern
Group A streptococci and S aureus
[(Cephalexin or dicloxacillin or clindamycin) plus trimethoprim/ sulfamethoxazole]
or
Clindamycin
Vancomycin
Daptomycin
Ceftaroline
Dog bite
Pasteurella 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.
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 bite
Eikenella 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
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 antibiotics
Third-generation cephalosporin (Rocephin) plus metronidazole
or
beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or
fluoroquinolone plus metronidazole
or
carbapenem (ertapenem)
Preseptal (periorbital) cellulitis
Haemophilus influenzae type b, Streptococcus pneumoniae, S aureus, other streptococcal species, and anaerobes
Largest study indicates that H influenzae type b and S pneumoniae not diminished in facial cellulitis as a result of immunizations[25]
Amoxicillin-clavulanate, cefpodoxime, cefdinir
Age < 1 y/ more severe disease require intravenous antibiotic
Third-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
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}
){kind=link}