Cellulitis

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Practice Essentials

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

Essential update: Overuse of antibiotics found in many cases of uncomplicated cellulitis

In a retrospective cohort study of 364 children and adults treated for uncomplicated cellulitis, wound infection, or cutaneous abscess, Hurley and colleagues found that avoidable antibiotic exposure occurred in 46% of the 292 cases with complete prescribing data available, including use of antibiotics with broad gram-negative activity in 4% of cases, use of combination therapy in 12%, and treatment for ≥10 days in 42%. In 61% of cases of cellulitis, antibiotics active against methicillin-resistant Staphylococcus aureus were prescribed.[1]

Signs and symptoms

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

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

The following findings suggest severe infection:

Indications for emergent surgical evaluation are as follows[3] :

See Clinical Presentation for more detail.

Diagnosis

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

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[3] :

Blood cultures should also be done in the following circumstances[3] :

Other tests to consider are as follows:

Imaging studies

Aspiration, Dissection, and Biopsy

Hospital admission

The IDSA recommends considering inpatient admission in patients with hypotension and/or the following laboratory findings[3] :

See Workup for more detail.

Management

Treatment of cellulitis is as follows:

In cases of cellulitis without draining wounds or abscess, streptococci continue to be the likely etiology,[3] and beta-lactam antibiotics are appropriate therapy, as noted in the following:

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

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

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

See Treatment and Medication for more detail.

Image library


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Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....

Background

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

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


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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....


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Swelling seen in cellulitis involving the hand. In a situation with hand cellulitis, always rule out deep infection by imaging studies or by obtaining....


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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....


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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.[3] S aureus is the usual causative organism in purulent cellulitis associated with furuncles, carbuncles, or abscesses.

Pathophysiology

Cellulitis usually follows a breach in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. In some cases, there is no obvious portal of entry and the breach may be due to microscopic changes in the skin or invasive qualities of certain bacteria. Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis. Facial cellulitis of odontogenic origin may also occur. Patients with toe-web intertrigo and/or tinea pedis —as well as those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity—are particularly vulnerable to recurrent episodes of cellulitis.[17, 18, 19, 9]

The vast majority of cases of cellulitis are likely caused by Streptococcus pyogenes and, to a lesser degree, by Staphylococcus aureus. In rare cases, cellulitis results from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. Distant seeding is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.[20]

Etiology

Host factors

Certain host factors predispose to severe infection. The elderly and individuals with diabetes mellitus are at risk for more severe disease.[21] 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.[22]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G).[23, 24] Postvenectomy status following saphenous vein stripping can also result in cellulitis.[23] 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).


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Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....


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Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. o....


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Hand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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.[25]

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.[26] 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.[27]

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.[28, 29, 30]

S aureus is the leading cause of soft-tissue infections in injection drug users,[31] followed by Streptococcus species.[32]

Gram-negative bacteria may cause bullous cellulitis in patients with cirrhosis.[33] 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.[34]

Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G).[23, 24] Postvenectomy status following saphenous vein stripping can also result in cellulitis.[23] Cellulitis may also be associated with tinea pedis, and in such cases, culture of toe-web spaces may help identify a bacterial pathogen.[35] 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.[36] 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.[37]

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.[38]

MRSA was first reported in 1968[39] ; for years, MRSA infections were identified only in patients with recent hospitalization, surgery, renal dialysis, residence in long-term-care facilities, or IV drug use. However, in recent years, isolates of S aureus have been found in patients without risk factors for nosocomial disease.[40] 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.)


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Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Ph....


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Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. o....


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Hand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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.[41] 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.[42] 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.[43] Several organisms are of particular interest in animal bites, including the following[42] :

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.[44] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections (see the image below).[45]


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

Epidemiology

Because cellulitis is not a reportable disease, the exact prevalence is uncertain; however, it is a relatively common infection, affecting all racial and ethnic groups. There is no statistically significant difference in the incidence of cellulitis in men and women,[46] and no age predilection is usually described. Nonetheless, studies have found a higher incidence of cellulitis in individuals older than 45 years.[18, 47, 48] Cellulitis was found to be more common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network.[49]

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

A study of an insurance database in Utah found an incidence rate of 24.6 cases per 1000 person-years.[47] The incidence was noted to be higher in males and in those individuals aged 45-64 years.[47] In a large epidemiologic hospital-based study on skin, soft-tissue, bone, and joint infections, 37.3% patients were identified as having cellulitis.[52]

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.[53] The study provided data regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States.[53]

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

Prognosis

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

Cellulitis may progress to serious illness by uncontrolled contiguous spread, including via the lymphatic or circulatory systems. Associated conditions or complications include lymphangitis, abscess formation, and, rarely, gangrenous cellulitis or necrotizing fasciitis.[54] 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.[55, 56]

Patient Education

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

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

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.

History

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.[18]

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[57] 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.[58, 59, 60, 61] Impaired lymphatic drainage and edema are also considered predisposing factors to leg cellulitis following saphenous vein resection for coronary artery bypass.[23] In addition, the presence of foreign bodies, including indwelling IV catheters, external orthopedic pins, and other surgical devices, may predispose to infection.

Physical Examination

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 Infectious Diseases Society of America (ISDA) 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[3] :

Approach Considerations

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

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.[3] 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 Infectious Disease Society of America (ISDA) 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).[3]

Considerations for hospitalization

The ISDA 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.[3]

If a complicated or deep infection is suspected, imaging studies and/or surgical consultations should be done promptly.[3]

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.[66]


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Guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess. AFB = acid-fast bacilli; BID = twice daily;....

Moderate to Severe Cases and Systemic Symptoms

The following laboratory tests may be considered in patients who present with moderate to severe cellulitis and/or systemic symptoms:

Ultrasonography, CT Scanning, and MRI

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.[6] Ultrasonographic-guided aspiration of pus has been shown to shorten hospital stay and fever duration in children with cellulitis.[7]

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,[8] but MRI typically takes much longer than CT scanning. However, 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 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.[9, 10, 11]

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.[12] By contrast, Gram stain and culture following incision and drainage of an abscess yields positive results in more than 90% of cases.[3]

Dissection of the underlying fascia to assess for necrotizing fasciitis may be determined by surgical consultation or indicated following initial evaluation and imaging studies.[13]

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.

Histologic Findings

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).


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Gross photograph of complicated cellulitis. Instead of the presence of yellow fat, the tissue is hemorrhagic and necrotic.


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Hematoxylin and eosin (H&E) stain, high power. This image shows deeper subcutaneous tissue involved in a case of cellulitis, with acute inflammatory c....


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Hematoxylin and eosin (H&E) stain, high power. This image shows cellulitis caused by herpes simplex virus, with the multinucleated organism in the cen....

Approach Considerations

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.[3] 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.[3] Of the strains of S pyogenes resistant to macrolides, 99.5% seem to remain susceptible to clindamycin and 100% to penicillin.[3] Most community-acquired MRSA infections (CA-MRSA) are apparently susceptible to trimethoprim-sulfamethoxazole and tetracycline.

In 2011, the Infectious Diseases Society of American (ISDA) published updated guidelines regarding management of MRSA in adults and children, and in 2012, the updated ISDA guidelines for the Diagnosis and Treatment of Diabetic Foot Infections were published. Readers are encouraged to check the ISDA guidelines Web site for the 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections, which is expected to be published in the spring of 2013.[68, 69]

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

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.[14] 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.[70, 71]

Severe cellulitis

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

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:

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:

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:

MRSA

In many communities, CA-MRSA is the most common isolate obtained from abscesses.[72] Antibiotics used to treat cellulitis associated with abscess or purulent drainage should target CA-MRSA until proven otherwise with culture data. In contrast, for outpatients with nonpurulent cellulitis, the Infectious Diseases Society of America (ISDA) recommends empiric therapy for infection due to beta-hemolytic streptococci, as it is believed that CA-MRSA plays an uncommon role in these scenarios.[68]

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).[73] It is important to note that TMP-SMX or tetracyclines may not have adequate streptococcal coverage and should not be the first choice unless purulence is present.[74] Clindamycin may also be a reasonable choice, depending on local sensitivities of CA-MRSA, but the IDSA estimates that up to 50% of MRSA isolates have intrinsic or constitutive resistance to clindamycin in some regions.[3]

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.[75] Daptomycin has been associated with more rapid resolution of signs and symptoms of cellulitis in some trials.[76, 77] However, vancomycin continues to be the drug of choice because of its overall excellent tolerability profile, efficacy, and cost.[75]

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


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See Table

Outpatient Care

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.[78] In general, consider the following:

IV Antibiotic Therapy

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.[3]

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.[3] 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[9] :

Surgical Examination and Drainage

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.[79] 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.

Impetigo

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.[3] The Infectious Diseases Society of America (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.[3]

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.[3] 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.[3]

The ISDA recommends use of the following antibiotics for managing impetigo in adults, with treatment duration of about 7 days (based on the clinical response)[3] :

In children (excluding neonates), the ISDA recommends the following antibiotic regimens, with treatment duration of about 7 days (based on the clinical response)[3] :

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.

MSSA and MSRA SSTIs

MSSA SSTIs

The ISDA indicates the following adult antibiotic regimens may be used to treat methicillin-sensitive Staphylococcus aureus (MSSA) skin and soft-tissue infections (SSTIs)[3] :

The ISDA indicates that the following pediatric (except neonates) antibiotic regimens may be used to treat MSSA SSTI[3] :

Doxycycline and minocycline are not recommended in children younger than 8 years.

MRSA SSTIs

The ISDA indicates that the following adult antibiotic regimens may be used to treat MRSA SSTIs[3] :

The ISDA indicates that the following pediatric (except neonates) antibiotic regimens may be used to treat MRSA SSTIs[3] :

In 2011, the Infectious Diseases Society of American (ISDA) published updated guidelines regarding management of MRSA in adults and children, and in 2012, the updated ISDA guidelines for the Diagnosis and Treatment of Diabetic Foot Infections were published. Readers are encouraged to check the ISDA guidelines Web site for the 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections, which is expected to be published in the spring of 2013.[68, 69]

Erysipelas and Cellulitis

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.[3]

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.[3]

In refractory cases, causes may include the following:

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.[3]

Necrotizing Infections

Common causes of monomicrobial necrotizing fasciitis include Streptococcus pyogenes, Vibrio vulnificus, and Aeromonas hydrophila.[3] 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.[3] 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.[3]

Emergent surgical evaluation and management is the first-line treatment in necrotizing fasciitis and gas gangrene in the presence of the following[3] :

The ISDA recommends IV clindamycin and penicillin therapy for severe group A streptococcal and clostridial necrotizing infections.[3] 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 ISDA recommends the following as first-line antibiotic treatments in managing adult mixed necrotizing infections[3] :

The following are first-line treatments in managing adult S aureus (MSSA) infections[3] :

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.[3] 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 ISDA guidelines Website for the 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections, which is expected to be published in the spring of 2013.

See also the Medscape Reference articles Necrotizing fasciitis and Clostridial Gas Gangrene.

Animal- or Human-Bite Infections

Animal bites

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).[3]

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.[3] 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.[3]

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).[3]

The ISDA 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.[3]

See also the Medscape Reference articles Animal Bites and Human Bites.

Surgical Site Infections

In general, infections at surgical sites occur 48 hours after surgery, with rare exceptions occurring earlier because of group A streptococci or clostridial species.[3] The Infectious Diseases Society of America (ISDA) 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.[3]

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.[3] 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.[3]

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.[3] The ISDA guidelines provides an algorithm, as well as a table of antibiotic selections, based on the operative site.[3]

The ISDA is expected to publish 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections in the spring of 2013.

Infections in the Immunocompromised Host

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.[3] 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.[3]

Ceftaroline is a new, 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.[3]

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.[3] These patients require biopsy and early, aggressive management.

The ISDA guidelines provides a table of antibiotic selections based on the predisposing factor (eg, neutropenia, cellular immune deficiency) and pathogen (eg, bacteria, viruses, fungi).[3] Empiric treatment must be determined on the basis of local susceptibilities.

Readers are encouraged to check the ISDA Web site for the 2013 updated recommendations for the diagnosis and management of skin and soft-tissue infections, which are expected to be published in the spring of 2013.

Medication Summary

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,[80] 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.[81] In patients whose condition is not responding to therapy, consultation with an infectious disease specialist may be helpful.[82]

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).[83, 84]

Penicillin G aqueous (Pfizerpen)

Clinical Context:  Penicillin G interferes with the synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.

Class Summary

The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide.

Amoxicillin (Moxatag)

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.

Amoxicillin and clavulanate (Augmentin)

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.

Ampicillin and sulbactam (Unasyn)

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.

Class Summary

The aminopenicillins, or third-generation penicillins, are semisynthetic modifications of natural penicillin that have a broader spectrum of activity.

Oxacillin

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.

Dicloxacillin

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.

Nafcillin

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).

Class Summary

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.

Piperacillin and tazobactam (Zosyn)

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.

Class Summary

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.

Cephalexin (Keflex)

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.

Cefazolin

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.

Ceftriaxone (Rocephin)

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.

Cefuroxime (Ceftin, Zinacef)

Clinical Context:  Cefuroxime is a second-generation oral cephalosporin antibiotic that inhibits cell wall synthesis and is bactericidal.

Cefadroxil

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.

Cefepime (Maxipime)

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.

Ceftazidime (Fortaz, Tazicef)

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.

Ceftaroline (Teflaro)

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.

Class Summary

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.

Azithromycin (Zithromax, Zmax)

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.

Erythromycin (Erythrocin, E.E.S., Ery-Tab, EryPed)

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.

Clarithromycin (Biaxin, Biaxin XL)

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.

Class Summary

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.

Imipenem and cilastatin (Primaxin)

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.

Ertapenem (Invanz)

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.

Class Summary

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.

Levofloxacin (Levaquin)

Clinical Context:  Levofloxacin is used to treat pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Ciprofloxacin (Cipro)

Clinical Context:  Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material.

Class Summary

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.

Clindamycin (Cleocin)

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.

Linezolid (Zyvox)

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.[85]

Tigecycline (Tygacil)

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.

Vancomycin

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.

Daptomycin (Cubicin)

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.

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

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.

Metronidazole (Flagyl)

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.

Class Summary

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.

Doxycycline (Doryx, Adoxa)

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.

Minocycline (Dynacin, Minocin Kit, Minocin, Myrac, Solodyn, Vectrin)

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.

Class Summary

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.

Itraconazole (Sporanox)

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.

Terbinafine (Lamisil, Terbinex)

Clinical Context:  Terbinafine inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use medication until symptoms significantly improve.

Class Summary

Antifungal agents such as itraconazole and terbinafine work by inhibiting the biosynthesis of ergosterol, which is an essential component of the fungal cell membrane.

Author

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

Disclosure: Nothing to disclose.

Coauthor(s)

Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Department of Internal Medicine, Director of Infectious Disease Fellowship, Harper Hospital, 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

Disclosure: Nothing to disclose.

Additional Contributors

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Pfizer Inc Honoraria Speaking and teaching

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Elsevier Royalty Other

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Baxter International and Johnson & Johnson Royalty Other

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

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

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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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.)

Hand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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.)

Hand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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.)

Hand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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 cellulitisGroup A streptococci much more likely than Staphylococcus aureusCephalexin or dicloxacillin

or clindamycin

Cefazolin or oxacillin

or nafcillin

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

or

Clindamycin

Vancomycin

Daptomycin

Ceftaroline

Dog bitePasteurella species (50% of wounds)

S aureus

Streptococcus pyogenes

Staphylococci, streptococci

Aerobes --Moraxella and Neisseria

Anaerobes --Fusobacterium, Bacteroides, Porphyromonas, and Prevotella

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

Avoid first-generation cephalosporins/ erythromycin/ dicloxacillin.

High likelihood of infection –

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

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

Amoxicillin/ clavulanate

Penicillin allergic:

Moxifloxacin

Deep wounds or severe wounds;

infections not responding to oral antibiotics

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

or

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

fluoroquinolone plus metronidazole

or

carbapenem (ertapenem)

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

Aerobic gram-positive cocci, anaerobes

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

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

Amoxicillin/ clavulanate

Penicillin allergic:

Moxifloxacin

or

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

Third-generation cephalosporin (Rocephin) plus metronidazole

or

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

or

fluoroquinolone plus metronidazole

or

carbapenem (ertapenem)

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

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

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

Amoxicillin/ clavulanate

Penicillin allergic --

Moxifloxacin

or

(Clindamycin or metronidazole) plus

(doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)

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

or

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

fluoroquinolone plus metronidazole

or

carbapenem (ertapenem)

Preseptal (periorbital) cellulitisHaemophilus influenzae type b, Streptococcus pneumoniae, S aureus, other streptococcal species, and anaerobesNocardia brasiliensis, Bacillus anthracis, Pseudomonas aeruginosa, Neisseria gonorrhoeae, Proteus species, Pasteurella multocida, Mycobacterium tuberculosisLargest study indicates that H influenzae type b and S pneumoniae not diminished in facial cellulitis as a result of immunizations[26] Amoxicillin-clavulanate, cefpodoxime, cefdinirAge < 1 y/ more severe disease require intravenous antibioticThird-generation cephalosporin (Rocephin)
Lower extremity --

Complicating saphenous venectomy site after coronary bypass grafting

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

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

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

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

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

Complicating breast cancer surgery/lymph node dissection

No pathogen identifiable in most infections

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

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

or

ciprofloxacin plus beta-lactam

or

monotherapy with piperacillin/tazobactam or cefepime

Aquatic environment --

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

Puncture/ laceration

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

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

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

Lacerations of extensor tendon

Amoxicillin/ clavulanate; penicillin allergic:

Moxifloxacin

or

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

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

Anaerobes: Prevotella and Peptostreptococcus species

Require extraction or root canalAmoxicillin-clavulanate

or

clindamycin

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

clindamycin