Cellulitis Medication

  • Author: Thomas E Herchline, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Nov 7, 2011
 

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,[66] especially in cellulitis associated with abscess or purulent drainage, has changed this treatment paradigm to some degree. Common beta-lactam agents traditionally used to treat cellulitis do not cover CA-MRSA, and alternative agents 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. In patients whose condition is not responding to therapy, consultation with an infectious disease specialist may be helpful.[67]

Treatment of cellulitis caused by uncommon organisms, such as Vibrio species or gram-negative bacteria, should be individualized (eg, tetracyclines, chloramphenicol, or aminoglycosides for Vibrio infection).[68, 69]

Cellulitis Without Draining or Abscess

In cases of cellulitis without draining wounds or abscess, streptococci continue to be the likely etiology,[54] and beta-lactam antibiotics are appropriate therapy, as noted in the following:

  • In mild cases of cellulitis treated on an outpatient bases, 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 fluoroquinolones are best reserved for organisms with sensitivity demonstrated by culture.[4, 54]
  • Some clinicians prefer an initial dose of parenteral antibiotic with a long half-life—for example, ceftriaxone, followed by an oral agent.

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.[70]
  • 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.[71]

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 species. 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, Mycobacterium marinum, 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 fresh water include a third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or a fluoroquinolone (eg, ciprofloxacin or levofloxacin).

MRSA

In many communities, CA-MRSA is the most common isolate from abscesses.[72] Antibiotics used to treat cellulitis with abscess or purulent drainage should target CA-MRSA until proven otherwise with culture data.

Mild cases that require only outpatient therapy may be treated with TMP/SMX and doxycycline. Available data suggest that doxycycline and TMP/SMX are equivalent in the treatment of mild SSTIs.[73] It is important to note that TMP/SMX 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 Infectious Disease Society of America (IDSA) estimates that up to 50% of MRSA isolates have intrinsic or constitutive resistance to clindamycin in some regions.[54]

In more severe cases that require parenteral antibiotics in areas where MRSA is thought to be a possible pathogen, vancomycin, daptomycin, tigecycline, and linezolid are appropriate choices. The newer agents have more limited data but have shown 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 mycologic investigations performed to rule out tinea pedis as a possible cause of recurrent episodes of cellulitis detect the presence of fungal infection in toe webs or feet, treatment with topical antifungals is recommended. With severe chronic changes or if onychomycosis is providing a source for repeated infection, oral antifungals such as itraconazole or terbinafine may be considered.

The following table provides an overview of empiric antibiotic therapy by etiology and anatomic location.

Table. Empiric Antibiotic Therapy of Cellulitis by Etiology and Anatomic Location (Open Table in a new window)

LocationLikely



Organisms



Other



Organisms



Complication/ DiscussionAntibiotic Regimen -- Oral/ OutpatientIndication for HospitalizationAntibiotic



Regimen -- Parenteral/ Hospitalized



Uncomplicated cellulitisGroup A streptococci and Staphylococcus aureusCephalexin or dicloxacillin



or clindamycin



Cefazolin or oxacillin



or nafcillin



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



or



Clindamycin



Vancomycin
Dog bitePasteurella canis (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 --



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



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 anaerobe, 29% of wounds)



Aerobic gram-positive cocci, anaerobes



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



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



Amoxicillin/ clavulanate



Penicillin allergic - - (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 -- (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[8] 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 --



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; typically 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 methicillin-resistant S aureus is present.



First-generation cephalosporin (cefazolin); clindamycin; vancomycin
Breast/arm - -



Complicating breast cancer surgery/lymph node dissection



No pathogen identifiable in most infections --



Non-group A beta-hemolytic streptococci most likely organism



Dicloxacillin, cephalexin. Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if methicillin-resistant S aureus is present.Fever, recent chemotherapy, neutropeniaMultiple regimens, none clearly superior --Piperacillin 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)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 - (clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole) Failure to respond to oral therapy marked by increasing pain and swelling or purulent drainageFirst-generation cephalosporin (cefazolin)



or



beta-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



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Penicillins

Class Summary

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

Penicillin G aqueous

 

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

Amoxicillin

 

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.

Oxacillin

 

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 staphylococcal infection is suspected.

Dicloxacillin

 

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.

Nafcillin (Nafcil, Unipen, Nallpen)

 

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.

Amoxicillin and clavulanate (Augmentin)

 

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.

Piperacillin and tazobactam (Zosyn)

 

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.

Ampicillin and sulbactam (Unasyn)

 

This is a drug combination of a beta-lactamase inhibitor with 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 not ideal for nosocomial pathogens.

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Cephalosporins

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.

Cephalexin (Keflex, Biocef, Keftab)

 

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 infection is suspected. Because of drug's short half-life, q8h or q12h dosing is not optimal.

Cefazolin (Ancef, Kefzol, Zolicef)

 

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 S aureus. Cefazolin is typically used alone for skin and skin-structure coverage.

Ceftriaxone (Rocephin)

 

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 bacterial cell wall. Bacteria eventually lyse, owing to 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.

Cefuroxime (Ceftin, Kefurox)

 

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

Cefadroxil (Duricef)

 

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, S pneumoniae, S pyogenes, Moraxella catarrhalis, E coli, Klebsiella species, and Proteus mirabilis.

Cefepime (Maxipime)

 

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 the cross blood-brain barrier precludes its use for meningitis.

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

 

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)

 

Beta-lactam cephalosporin with activity against aerobic and anaerobic gram-positive and aerobic gram-negative bacteria. Demonstrates activity in vivo against resistant methicillin-resistant Staphylococcus aureus (MRSA) strains and in vitro against vancomycin-resistant and linezolid-resistant S aureus.

Indicated for community-acquired bacterial pneumonia. Also indicated for acute bacterial skin and skin structure infections, including MRSA.

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Macrolides

Class Summary

Macrolides are bacteriostatic 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.

Azithromycin (Zithromax)

 

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)

 

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 and streptococcal infections.

Clarithromycin (Biaxin, Biaxin XL)

 

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.

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Carbapenems

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.

Imipenem and cilastatin (Primaxin)

 

This 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)

 

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.

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Fluoroquinolones

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.

Levofloxacin (Levaquin)

 

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

Ciprofloxacin (Cipro)

 

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.

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Anti-infectives

Class Summary

Anti-infectives such as metronidazole, clindamycin, aztreonam, and sulfamethoxazole-trimethoprim are effective against some types of bacteria that have become resistant to other antibiotics. In more severe cases that require parenteral antibiotics in areas where MRSA is thought to be a possible pathogen, vancomycin, daptomycin, tigecycline, and linezolid are appropriate choices

Clindamycin (Cleocin)

 

Clindamycin is a lincosamide used for the treatment of serious skin and soft-tissue staphylococcal infections, including some CA-MRSA. 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)

 

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.[78]

Tigecycline (Tygacil)

 

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 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 (Vancocin)

 

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, current the 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)

 

Daptomycin binds to bacterial membranes and causes rapid membrane potential depolarization, thereby inhibiting protein, DNA, and RNA synthesis, ultimately causing cell death. It is indicated to treat complicated skin and skin-structure infections caused by S aureus (including methicillin-resistant strains), S pyogenes, S agalactiae, S dysgalactiae, and E faecalis (vancomycin-susceptible strains only).

Trimethoprim and sulfamethoxazole (Cotrimoxazole, Bactrim, Septra)

 

Trimethoprim-sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. It may be considered an alternative to vancomycin in selected cases of MRSA infection.

Metronidazole (Flagyl)

 

Metronidazole is an imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents

Chloramphenicol

 

Chloramphenicol binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is effective against gram-negative and gram-positive bacteria. The oral form is not available in the United States.

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Tetracyclines

Class Summary

The tetracyclines are bacteriostatic and 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.

Doxycycline

 

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.

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Antifungal Agents

Class Summary

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

Itraconazole (Sporanox)

 

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)

 

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

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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 of Sciences, and Society for Academic Emergency 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

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.

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.

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.

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.

Specialty Editor Board

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.

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

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, American Geriatrics Society, 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, Infectious Diseases Society of 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

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.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Dennis Cunningham, MD, and Robert Edelman, MD, to the development and writing of the source articles.

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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 presentation of mild cellulitis.
Cellulitis involving the hand.
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. Note the area of drainage. 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. 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 Feb 28.
Table. Empiric Antibiotic Therapy of Cellulitis by Etiology and Anatomic Location
LocationLikely



Organisms



Other



Organisms



Complication/ DiscussionAntibiotic Regimen -- Oral/ OutpatientIndication for HospitalizationAntibiotic



Regimen -- Parenteral/ Hospitalized



Uncomplicated cellulitisGroup A streptococci and Staphylococcus aureusCephalexin or dicloxacillin



or clindamycin



Cefazolin or oxacillin



or nafcillin



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



or



Clindamycin



Vancomycin
Dog bitePasteurella canis (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 --



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



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 anaerobe, 29% of wounds)



Aerobic gram-positive cocci, anaerobes



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



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



Amoxicillin/ clavulanate



Penicillin allergic - - (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 -- (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[8] 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 --



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; typically 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 methicillin-resistant S aureus is present.



First-generation cephalosporin (cefazolin); clindamycin; vancomycin
Breast/arm - -



Complicating breast cancer surgery/lymph node dissection



No pathogen identifiable in most infections --



Non-group A beta-hemolytic streptococci most likely organism



Dicloxacillin, cephalexin. Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if methicillin-resistant S aureus is present.Fever, recent chemotherapy, neutropeniaMultiple regimens, none clearly superior --Piperacillin 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)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 - (clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole) Failure to respond to oral therapy marked by increasing pain and swelling or purulent drainageFirst-generation cephalosporin (cefazolin)



or



beta-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



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