Cellulitis 

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

Background

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

Cellulitis was classically considered to be an infection without formation of abscess and without purulent drainage or ulceration. In clinical practice, the division between cellulitis and abscess is not distinct. Frequently, the macular erythema of cellulitis coexists with nodules, areas of ulceration, and frank abscess formation (see Clinical Presentation). The following images illustrate some of these presentations.

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

Cellulitis usually follows a break in the skin, such as a fissure, cut, laceration, insect bite, or puncture wound. 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. However, cellulitis frequently occurs in areas where no apparent injury exists. This is common in dry and irritated skin where microscopic breaks allow penetration of bacteria. Patients with toe web intertrigo and/or tinea pedis and those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity are particularly vulnerable to recurrent episodes of cellulitis.[1, 2, 3, 4]

The vast majority of cases are caused by Streptococcus pyogenes or Staphylococcus aureus. Occasionally, cellulitis may be caused by the emergence of subjacent osteomyelitis. Cellulitis may rarely result from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. This is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine vibrios. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread.[5]

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Etiology

Host factors

Certain host factors predispose to severe infection. The elderly and individuals with diabetes mellitus or hypertension are at risk for more severe disease.[6] Patients with diabetes, immunodeficiency, cancer, venous stasis, chronic liver disease, peripheral arterial disease, and chronic kidney disease appear to be at a higher risk for recurrent infection, owing to an altered host immune response. Other factors that affect host immunity and predispose to cellulitis include concurrent intravenous (IV) or subcutaneous (SC) “skin popping” drug use; infections in this setting may be polymicrobial, but methicillin-resistant S aureus (CA-MRSA) is the most common pathogen in these patients.

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, as their immune responses are not fully developed. The cellulitis may present as sepsis[7] ; underlying osteomyelitis or septic arthritis must be excluded in these infants. (See the image below.)

A case of cellulitis without associated purulence 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).

In children, facial cellulitis is frequently associated with H influenzae type B and S pneumoniae; prophylactic pneumococcal vaccine may be effective in the latter cases. A study of one-half million 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.[8] However, another study noted that 96% of the serotypes that cause facial cellulitis are included in the heptavalent-conjugated pneumococcal vaccine that is licensed in the United States.

Immunocompromised hosts typically become infected from opportunistic organisms, including gram-negative rods (eg, Pseudomonas, Proteus, Serratia, Enterobacter, Citrobacter), anaerobes, and others (eg, Helicobacter cinaedi, Fusarium species). Although fungi (eg, Cryptococcus) may also cause cellulitis, this is 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.[9]

Mycobacterial infections may present as cellulitis. Typically, the lack of response to antibiotics prompts further investigation. The diagnosis is made based on the presence of granulomas, multinucleated giant cells, and acid-fast bacilli (AFB) from biopsy specimens.[10, 11, 12]

S aureus is the leading cause of soft-tissue infections in injection drug users,[13] followed by Streptococcus species.[14]

Gram-negative bacteria may cause bullous cellulitis in patients with cirrhosis.[15] Early recognition is vital, as 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 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, such as those around surgical wounds less than 24 hours postoperatively (group A beta-hemolytic Streptococcus [GABHS] or Clostridium perfringens, which produces gas that may be appreciated as crepitus on examination) or from gunshot wounds or invasive devices (Acinetobacter baumannii is an emerging multidrug-resistant pathogen in these scenarios.)[16]

Cellulitis due to lymphatic obstruction or venectomy is generally caused by non–group A streptococci (ie, groups B, C, and G).[17, 18] Postvenectomy status following saphenous vein stripping can also result in cellulitis[17] and is associated with tinea pedis; culture of toe web spaces may assist in identifying a bacterial pathogen.[19] Lymphadenectomy following tumor excision, such as mastectomy, is also a predisposing factor for cellulitis.

Varicella

Cellulitis can complicate varicella and may be identified by a margin of erythema surrounding the vesicles. In one study, patients with invasive GAS cellulitis complicating varicella were identified.[20] The median onset of GAS infection was day 4 of varicella, with fever, vomiting, and localized swelling reported.[20] 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.[21]

MRSA

Cellulitis can be complicated by abscess formation. A maxim in microbiology states, "The hallmark of staph infection is abscess formation." This has become a significant concern due to changing patterns of antibiotic resistance in S aureus, particularly MRSA.[22]

MRSA was first reported in 1968[23] ; 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.[24] These isolates have been termed CA-MRSA to distinguish them from the previously identified hospital or healthcare-associated MRSA (HA-MRSA). (See the images below.)

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.[25] 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 are infrequently done. Therefore, 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.

Patient with cellulitis of the left ankle. Note thPatient 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 communAbscess 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 methiHand cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

Bite wounds, lacerations, and puncture wounds

Mammalian bite wounds represent a specific subset of cellulitis with unique pathogens. The infections are usually polymicrobial.[26] Human, dog, cat, and wild-animal bites all predispose to cellulitis with unique pathogens, but dogs are the most commonly encountered bite wound in both the primary care and emergency setting.[27] Several organisms are of particular interest in animal bites, including the following[26] :

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

Puncture wounds, especially through the bottom of athletic shoes, may cause Pseudomonas osteomyelitis and/or cellulitis. However, lacerations and puncture wounds sustained in an aquatic environment (eg, oceans, lakes, streams) may be contaminated with bacteria not typically found in land-based injuries, including Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, Mycobacterium marinum, and others.[28] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections (see the image below).[29]

Cellulitis due to documented Vibrio vulnificus infCellulitis due to documented Vibrio vulnificus infection. Image courtesy of Kepler Davis.
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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,[30] and no age predilection is usually described. However, studies have found a higher incidence of cellulitis in general among individuals older than 45 years.[2, 31, 32] Cellulitis was found to be more common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network.[33]

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

  • Historically, buccal cellulitis caused by H influenzae type B was more common in children younger than age 3 years. Vaccination against this organism may have decreased the incidence of buccal cellulitis, but recent data suggest that this source remains a consideration, even in vaccinated cohorts.[8]
  • Facial cellulitis is more common in adults older than 50 years. However, pneumococcal facial cellulitis occurs primarily in young children who are at risk for pneumococcal bacteremia.[9, 34]
  • Perianal cellulitis, usually with GABHS, occurs in children younger than 3 years.[35]
  • Elderly patients with cellulitis are predisposed to thrombophlebitis.

A 2006 study of an insurance database in Utah found an incidence rate of 24.6 cases per 1000 person-years. The incidence was noted to be higher in males and in those individuals aged 45-64 years.[31] In a large epidemiologic hospital-based study on skin, soft-tissue, bone, and joint infections, 37.3% patients were identified as having cellulitis.[36]

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. The study provided data regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States.[37]

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

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Prognosis

The vast majority of 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 standard oral antibiotics. When outpatient therapy is unsuccessful and for patients who require admission initially, IV antibiotics are usually effective.

Because cellulitis may progress to serious illness by uncontrolled contiguous spread or via the lymphatic or circulatory systems, complications include lymphangitis, abscess formation, gangrenous cellulitis, and necrotizing fasciitis.[38] Certain strains of bacteria, 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.[39, 40]

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Patient Education

Depending on the location of the affected area, the patient may want to 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 immediately if they have any of the following features:

  • Fever (>100.5°F), especially when associated with chills
  • Cellulitis with soft, fluctuant areas suggestive of abscess formation
  • A red streak from an area of cellulitis or a fast-spreading area of redness, which indicates that the infection may need a different antibiotic or an IV antibiotic
  • Significant pain not relieved by acetaminophen or ibuprofen
  • Inability to move an extremity or joint because of pain

Patients with diabetes, cancer, or immunosuppression should be made aware that localized cellulitis may become serious.

For additional patient education resources, visit eMedicine's Diabetes Center. Also, see eMedicine's patient education article Cellulitis

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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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