Cellulitis - Practice Essentials, Background, Pathophysiology

5/22/2017 Cellulitis: Practice Essentials, Background, Pathophysiology
This site is intended for healthcare professionals
Cellulitis
Updated: Aug 15, 2016
Author: Thomas E Herchline, MD; Chief Editor: Michael Stuart Bronze, MD more...
OVERVIEW
Practice Essentials
The term cellulitis is commonly used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, usually from acute infection (see
the image below). Cellulitis usually follows a breach in the skin, although a portal of entry may not be obvious; the breach may involve microscopic
skin changes or invasive qualities of certain bacteria.
Patient with cellulitis of the left ankle. This cellulitis was caused by communityacquired methicillinresistant Staphylococcus aureus (CAMRSA). (Photo courtesy of
Texas Dept. of Public Health.)
View Media Gallery
Signs and symptoms
Nonpurulent cellulitis is associated with the 4 cardinal signs of infection, as follows:
Erythema
Pain
Swelling
Warmth
Physical examination findings that suggest the most likely pathogen include the following:
Skin infection without underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by streptococci; Staphylococcus
aureus, often communityacquired MRSA, is the most likely pathogen when these factors are present [1]
Violaceous color and bullae suggest more serious or systemic infection with organisms such as Vibrio vulnificus or Streptococcus pneumoniae
The following findings suggest severe infection:
Malaise, chills, fever, and toxicity
Lymphangitic spread (red lines streaking away from the area of infection)
Circumferential cellulitis
Pain disproportionate to examination findings
Indications for emergent surgical evaluation are as follows [2] :
Violaceous bullae
Cutaneous hemorrhage
Skin sloughing
Skin anesthesia
Rapid progression
Gas in the tissue
Hypotension
See Clinical Presentation for more detail.
Diagnosis
Generally, no workup is required in uncomplicated cases of cellulitis that meet the following criteria:
Limited area of involvement
Minimal pain
No systemic signs of illness (eg, fever, altered mental status, tachypnea, tachycardia, hypotension)
No risk factors for serious illness (eg, extremes of age, general debility, immunocompromise)
The Infectious Disease Society of America (IDSA) recommends the following blood tests for patients with softtissue infection who have signs and
symptoms of systemic toxicity [2] :
Blood cultures
CBC with differential
levels of creatinine, bicarbonate, creatine phosphokinase, and Creactive protein (CRP)
http://emedicine.medscape.com/article/214222overview 1/14
levels of creatinine, bicarbonate, creatine phosphokinase, and Creactive protein (CRP)
Blood cultures should also be done in the following circumstances [2] :
Moderate to severe disease [2] (eg, cellulitis complicating lymphedema [3] )
Cellulitis of specific anatomic sites (eg, facial and especially ocular areas)
Patients with a history of contact with potentially contaminated water [4]
Patients with malignancy who are receiving chemotherapy
Neutropenia or severe cellmediated immunodeficiency
Animal bites
Other tests to consider are as follows:
Mycologic investigations are advisable if recurrent episodes of cellulitis are suspected to be secondary to tinea pedis or onychomycosis
Creatinine levels help assess baseline renal function and guide antimicrobial dosing
Imaging studies
Ultrasonography may play a role in the detection of occult abscess and direction of care [5]
Ultrasonographicguided aspiration of pus can shorten hospital stay and fever duration in children with cellulitis [6]
If necrotizing fasciitis is a concern, CT imaging is typically used in stable patients; MRI can be performed, [7] but MRI typically takes much longer
than CT scanning
Strong clinical suspicion of necrotizing fasciitis should prompt surgical consultation without delay for imaging
Aspiration, Dissection, and Biopsy
Needle aspiration should be performed only in selected patients or in unusual cases, such as in cases of cellulitis with bullae or in patients who
have diabetes, are immunocompromised, are neutropenic, are not responding to empiric therapy, or have a history of animal bites or immersion
injury [8, 9, 10]
Aspiration or punch biopsy of the inflamed area may have a culture yield of 240% and is of limited clinical value in most cases [11]
Gram stain of aspiration or biopsy specimens has a low yield and is unnecessary in most cases, unless purulent material is draining or bullae or
abscess is present; however, Gram stain and culture following incision and drainage of an abscess yields positive results in more than 90% of
cases [2]
Dissection of the underlying fascia to assess for necrotizing fasciitis may be determined by surgical consultation or indicated following initial
evaluation and imaging studies [12]
Skin biopsy is not routine but may be performed in an attempt to rule out a noninfectious entity
Hospital admission
The IDSA recommends considering inpatient admission in patients with hypotension and/or the following laboratory findings [2] :
Elevated creatinine level
Elevated creatine phosphokinase level (23 times the upper limit of normal)
CRP level >13 mg/L (123.8 mmol/L)
Low serum bicarbonate level
Marked left shift on the CBC with differential
See Workup for more detail.
Management
Treatment of cellulitis is as follows:
Antibiotic regimens are effective in more than 90% of patients
All but the smallest of abscesses require drainage for resolution, regardless of the pathogen
Drainage only, without antibiotics, may suffice if the abscess is relatively isolated, with little surrounding tissue involvement
In cases of cellulitis without draining wounds or abscess, streptococci continue to be the likely etiology, [2] and betalactam antibiotics are appropriate
therapy, as noted in the following:
In mild cases of cellulitis treated on an outpatient basis: Dicloxacillin, amoxicillin, or cephalexin
In patients who are allergic to penicillin: Clindamycin or a macrolide (clarithromycin or azithromycin)
An initial dose of parenteral antibiotic with a long halflife (eg, ceftriaxone) followed by an oral agent
Treatment of recurrent disease (usually related to venous or lymphatic obstruction) is as follows:
The cellulitis is most often due to Streptococcus species, and penicillin G or amoxicillin (250 mg bid) or erythromycin (250 mg qd or bid) may be
effective [13]
If tinea pedis is suspected to be the predisposing cause, treat with topical or systemic antifungals
Patients with severe cellulitis require parenteral therapy, such as the following:
Cefazolin, cefuroxime, ceftriaxone, nafcillin, or oxacillin for presumed staphylococcal or streptococcal infection
Clindamycin or vancomycin for penicillinallergic patients [14]
Broad grampositive, gramnegative, and anaerobic coverage for cases associated with diabetic ulcers [15]
Coverage for MRSA, until culture and sensitivity information become available, for severe cellulitis apparently related to a furuncle or an
abscess
For cellulitis involving wounds sustained in an aquatic environment, recommended antibiotic regimens vary with the type of water involved, as follows:
Saltwater or brackish water: Doxycycline and ceftazidime, or a fluoroquinolone
Freshwater: A third or fourthgeneration cephalosporin (eg, ceftazidime or cefepime) or a fluoroquinolone (eg, ciprofloxacin or levofloxacin)
Lack of response to an appropriate antibiotic regimen should raise suspicion for Mycobacterium marinum infection and suggest wound biopsy
for mycobacterial stains and culture
See Treatment and Medication for more detail.
Background
The term cellulitis is commonly used to indicate a nonnecrotizing inflammation of the skin and subcutaneous tissues, a process usually related to
acute infection that does not involve the fascia or muscles. Cellulitis is characterized by localized pain, swelling, tenderness, erythema, and warmth.
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.
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.
View Media Gallery
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.
View Media Gallery
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.
View Media Gallery
Burns complicated by cellulitis. The larger lesion is a seconddegree burn (left), and the smaller lesion is a firstdegree burn (right), each with an expanding zone of
erythema consistent with cellulitis.
View Media Gallery
Streptococcal species are the most common causes of erysipelas and diffuse cellulitis or nonpurulent cellulitis that is not associated with a defined
portal. [2] S aureus is the usual causative organism in purulent cellulitis associated with furuncles, carbuncles, or abscesses.
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 toeweb
intertrigo and/or tinea pedis —as well as those with lymphatic obstruction, venous insufficiency, pressure ulcers, and obesity—are particularly
vulnerable to recurrent episodes of cellulitis. [16, 17, 18, 8]
The vast majority of cases of cellulitis are likely caused by Streptococcus pyogenes and, to a lesser degree, by Staphylococcus aureus. In rare cases,
cellulitis results from the metastatic seeding of an organism from a distant focus of infection, especially in immunocompromised individuals. Distant
seeding is particularly common in cellulitis due to S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas
aeruginosa, Brucella species, and Legionella species have also been reported as rare causes of cellulitis resulting from hematogenous spread. [19]
Etiology
Host factors
Certain host factors predispose to severe infection. The elderly and individuals with diabetes mellitus are at risk for more severe disease. [20] In
addition, patients with diabetes, immunodeficiency, cancer, venous stasis, chronic liver disease, peripheral arterial disease, and chronic kidney
disease appear to be at higher risk for recurrent infection because of an altered host immune response. Local control of immune function through
interleukindriven neutrophil recruitment, protective action of antimicrobial peptides, and the integrity of the cutaneous barrier have significant effects
on the host’s defense against infection. [21]
Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G). [22, 23] Postvenectomy
status following saphenous vein stripping can also result in cellulitis. [22] Lymphadenectomy following tumor excision, such as mastectomy, is also a
predisposing factor for cellulitis.
Immunogenetic factors may play a role in some families who have an underlying susceptibility to an infection progressing to cellulitis. Other factors
that affect host immunity and predispose to cellulitis include concurrent intravenous or subcutaneous “skin popping” drug use; infections in this setting
may be polymicrobial, but communityacquired methicillinresistant S aureus (CAMRSA) is the most common pathogen in these patients (see the
following images).
View Media Gallery
Abscess and associated cellulitis caused by communityacquired methicillinresistant Staphylococcus aureus (CAMRSA). (Photo courtesy of Texas Dept. of Public
Health.)
View Media Gallery
In individuals with normal host defenses, the most common causative organisms are group A streptococci (GAS) and S aureus. Group B
Streptococcus cellulitis occurs in infants younger than 6 months, because their immune responses are not fully developed, and it may also be seen in
adults with comorbidities such as diabetes or liver disease. For infantile cellulitis, presentations may include sepsis. [24]
Historically, facial cellulitis in children was frequently associated with H influenzae type B and S pneumoniae, but this is now generally considered a
rarity because of routine H influenza e type B and pneumococcal vaccines. However, a study of 500,000 pediatric hospitalizations demonstrated that,
although bacterial meningitis and epiglottitis diminished as a result of immunization for H influenzae type B and S pneumoniae, the incidence of facial
cellulitis was unaffected. [25] Nonetheless, another study noted that 96% of the serotypes that cause facial cellulitis were included in the heptavalent
conjugated pneumococcal vaccine that was routinely used at the time of the study.
Impetigo is commonly caused by strains of S aureus and/or S pyogenes, and erysipelas (acute infection of the upper dermis, characterized by a
sharply demarcated, raised border) is more commonly caused by streptococcal species such as S pyogenes.
Immunocompromised hosts may become infected from nontraditional cellulitis organisms, including gramnegative rods (eg, Pseudomonas, Proteus,
Serratia, Enterobacter, Citrobacter), anaerobes, and others (eg, Helicobacter cinaedi, Fusarium species). Although fungi (eg, Cryptococcus) and
herpes simplex virus may also cause cellulitis, these causes are rare.
Pneumococci may cause a particularly malignant form of cellulitis that is frequently associated with tissue necrosis, suppuration, and bloodstream
invasion. Two distinct syndromes are recognized: the first is marked by involvement of the extremities in patients with diabetes or substance abuse,
and the second is marked by involvement of the head, neck, and upper torso in patients with systemic lupus erythematosus, nephrotic syndrome, or
hematologic disorders. [26]
Mycobacterial infections may present as cellulitis. In contradistinction to the usual bacterial cellulitis, these presentations often range from subacute to
chronic and are typically unresponsive to short courses of antibiotics—which should then prompt further investigation. The diagnosis is made on the
basis of the presence of granulomas, multinucleated giant cells, and acidfast bacilli (AFB) from biopsy specimens or mycobacterial culture. [27, 28, 29]
S aureus is the leading cause of softtissue infections in injection drug users, [30] followed by Streptococcus species. [31]
Gramnegative bacteria may cause bullous cellulitis in patients with cirrhosis. [32] Early recognition is vital, because the course of the disease is rapid,
Gramnegative bacteria may cause bullous cellulitis in patients with cirrhosis. [32] Early recognition is vital, because the course of the disease is rapid,
typically progressing to septic shock and death. Gram stain and culture of fluid aspirated from the bullae may aid in management.
Recurrent staphylococcal cellulitis may occur in otherwise immunologically normal patients with nasal carriage of staphylococci and those with Job
syndrome.
Hospitalacquired infections
Various hospitalacquired infections following softtissue 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 betahemolytic 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
multidrugresistant pathogen in these scenarios. [33]
Cellulitis due to lymphatic obstruction or venectomy may be caused by non–group A streptococci (ie, groups B, C, and G). [22, 23] Postvenectomy
status following saphenous vein stripping can also result in cellulitis. [22] Cellulitis may also be associated with tinea pedis, and in such cases, culture
of toeweb spaces may help identify a bacterial pathogen. [34] Lymphadenectomy following tumor excision, such as mastectomy, is also a
predisposing factor for cellulitis.
Varicella
Cellulitis can complicate varicella and may be identified by larger margins of erythema surrounding the vesicles. One study identified patients with
invasive GAS cellulitis complicating varicella. [35] The median onset of GAS infection was day 4 of varicella, with fever, vomiting, and localized
swelling reported. This condition mandates antibiotic treatment and careful clinical followup. Untreated cellulitis in association with varicella may
progress to severe necrotizing softtissue infections requiring surgical intervention. [36]
MRSA
Although cellulitis can be complicated by abscess formation, it typically develops from an abscessogenic focus. One maxim in microbiology is the
following: "The hallmark of staph infection is abscess formation." This has become a significant concern because of changing patterns of antibiotic
resistance of S aureus, particularly MRSA. [37]
MRSA was first reported in 1968 [38] ; for years, MRSA infections were identified only in patients with recent hospitalization, surgery, renal dialysis,
residence in longtermcare facilities, or IV drug use. However, in recent years, isolates of S aureus have been found in patients without risk factors
for nosocomial disease. [39] These isolates, which mostly maintain susceptibility to antibiotics such as trimethoprimsulfamethoxazole or tetracycline,
have been termed CAMRSA to distinguish them from the previously identified hospital or healthcareassociated MRSA (HAMRSA). (See the
images below.)
View Media Gallery
Abscess and associated cellulitis caused by communityacquired methicillinresistant Staphylococcus aureus (CAMRSA). (Photo courtesy of Texas Dept. of Public
Health.)
View Media Gallery
Although reports have indicated that MRSA causes the majority of skin and softtissue infections (SSTIs), these studies are plagued by variability in
casefinding methodologies. [40] Furthermore, in the context of cellulitis, the finding is misleading in that these reports come from analysis of wound
cultures in cases in which abscess formation occurred. Cultures in cellulitis are difficult to perform and frequently do not yield positive results;
therefore, these tests are rarely done clinically. Consequently, the results of these studies cannot be generalized to cellulitis without abscess
formation. Studies are under way to determine the incidence of S aureus —in particular, CAMRSA in softtissue infection in which there is no
identifiable abscess. However, until results of those studies are available, treatment decisions must be made on clinical grounds. Because treatment
failures after empiric treatment may often occur, because of the emergence of resistantstrains,microbiologicinvestigations are strongly recommended.
Bite wounds, lacerations, and puncture wounds
Mammalian bite wounds represent a specific subset of cellulitis with unique pathogens. The infections are usually polymicrobial. [41] Human, dog, cat,
and wildanimal bites all predispose to cellulitis with unique pathogens, but dog bites are the most commonly encountered bite wound in both the
primary care and the emergency setting. [42] Several organisms are of particular interest in animal bites, including the following [41] :
Capnocytophaga canimorsus (dog)
Eikenella corrodens (human)
Pasteurella multocida (dog or cat)
Streptobacillus moniliformis (rat)
Puncture wounds, especially through the bottom of athletic shoes, may cause Pseudomonas osteomyelitis and/or cellulitis. However, lacerations and
puncture wounds sustained in an aquatic environment (eg, oceans, lakes, streams) may be contaminated with bacteria not typically found in land
based injuries, including Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, and
Mycobacterium marinum. [43] Individuals with chronic liver disease are particularly susceptible to V vulnificus infections (see the image below). [44]
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
View Media Gallery
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, [45] and no age predilection is usually
described. Nonetheless, studies have found a higher incidence of cellulitis in individuals older than 45 years. [17, 46, 47] Cellulitis was found to be more
common in geriatric patients in a retrospective study of international travelers by the GeoSentinel Surveillance Network. [48]
Certain age groups are at higher risk in some unique scenarios, such as the following:
Historically, buccal cellulitis caused by H influenzae type B was more common in children younger than 3 years; vaccination against this
organism may have decreased the incidence of buccal cellulitis, but recent data suggest that this source remains a consideration, even in
vaccinated cohorts [25]
Facial cellulitis is more common in adults older than 50 years; however, pneumococcal facial cellulitis occurs primarily in young children who are
at risk for pneumococcal bacteremia [26, 49]
Perianal cellulitis, usually with group A betahemolytic Streptococcus (GABHS), occurs in children younger than 3 years [50]
Elderly patients with cellulitis are predisposed to thrombophlebitis
A study of an insurance database in Utah found an incidence rate of 24.6 cases per 1000 personyears. [46] The incidence was noted to be higher in
males and in those individuals aged 4564 years. [46] In a large epidemiologic hospitalbased study on skin, softtissue, bone, and joint infections,
37.3% patients were identified as having cellulitis. [51]
Overall rates of visits increased for skin and softtissue infections (SSTIs) from 32.1 to 48.1 visits per 1000 population and reached 14.2 million by
2005, and visits for abscess and cellulitis increased from 17.3 to 32.5 visits per 1000 population and accounted for more than 95% of the increase,
according to the National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey. [52] The study provided data
regarding visits by patients with SSTIs to physician offices, hospital outpatient departments, and emergency departments in the United States. [52]
Cellulitis was found to account for approximately 3% of emergency medical consultations at one United Kingdom district general hospital.
Prognosis
Many cellulitis and softtissue infections can be treated on an outpatient basis with oral antibiotics and do not result in lasting sequelae. Most patients’
conditions respond well to oral antibiotics. When outpatient therapy is unsuccessful, or for patients who require admission initially, IV antibiotics are
usually effective.
Cellulitis may progress to serious illness by uncontrolled contiguous spread, including via the lymphatic or circulatory systems. Associated conditions
or complications include lymphangitis, abscess formation, and, rarely, gangrenous cellulitis or necrotizing fasciitis. [53] Certain species, most notably
group A betahemolytic Streptococcus (GABHS) and S aureus, produce toxins that may mediate a more severe systemic infection, leading to septic
shock and death. [54, 55]
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
overthecounter (OTC) pain medication such as acetaminophen (Tylenol) or ibuprofen (Advil, Motrin) for pain, if approved by their physician.
Patients should call their doctor's office or seek urgent evaluation if they have any of the following features:
Fever (>100.5°F), especially when associated with chills
Cellulitis with surrounding soft, fluctuant areas that are suggestive of abscess formation
Red streaking from an area of cellulitis or a fastspreading area of redness, which indicates that the infection may need closer observation,
change in antibiotic treatment, or inpatient supportive care
Significant pain not relieved by acetaminophen or ibuprofen
Inability to move an extremity or joint because of pain
Although any cellulitis infection may be severe, patients with diabetes, cancer, chronic lymphedema, or immunosuppression should be made aware
that they are more predisposed to serious infection. Patients with an underlying genetic condition, such as an immunodeficiency disease, are also at
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.
Clinical Presentation
References
1. Busch BA, Ahern MT, Topinka M, Jenkins JJ 2nd, Weiser MA. Eschar with cellulitis as a clinical predictor in communityacquired MRSA skin
abscess. J Emerg Med. Jul 8 2008.
2. [Guideline] Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, et al. Practice guidelines for the diagnosis and
management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014 Jul 15. 59
(2):14759. [Medline]. [Full Text].
3. Woo PC, Lum PN, Wong SS, Cheng VC, Yuen KY. Cellulitis complicating lymphoedema. Eur J Clin Microbiol Infect Dis. Apr 2000. 19(4):2947.
4. Swartz MN. Clinical practice. Cellulitis. N Engl J Med. Feb 26 2004. 350(9):90412.
5. Tayal VS, Hasan N, Norton HJ, Tomaszewski CA. The effect of softtissue ultrasound on the management of cellulitis in the emergency
department. Acad Emerg Med. Apr 2006. 13(4):3848.
6. Chao HC, Lin SJ, Huang YC, Lin TY. Sonographic evaluation of cellulitis in children. J Ultrasound Med. Nov 2000. 19(11):7439.
7. Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol. Mar 1998.
170(3):61520.
8. GabillotCarré M, Roujeau JC. Acute bacterial skin infections and cellulitis. Curr Opin Infect Dis. 2007 Apr. 20(2):11823. [Medline].
9. Stevenson A, Hider P, Than M. The utility of blood cultures in the management of nonfacial cellulitis appears to be low. N Z Med J. Mar 11
2005. 118(1211):U1351.
10. Sachs MK. The optimum use of needle aspiration in the bacteriologic diagnosis of cellulitis in adults. Arch Intern Med. Sep 1990. 150(9):1907
12.
11. Zahar JR, Goveia J, Lesprit P, BrunBuisson C. Severe soft tissue infections of the extremities in patients admitted to an intensive care unit. Clin
Microbiol Infect. Jan 2005. 11(1):7982.
12. Edlich RF, Cross CL, Dahlstrom JJ, Long WB 3rd. Modern Concepts of the Diagnosis and Treatment of Necrotizing Fasciitis. J Emerg Med. Dec
10 2008.
13. Kremer M, Zuckerman R, Avraham Z, Raz R. Longterm antimicrobial therapy in the prevention of recurrent softtissue infections. J Infect. Jan
1991. 22(1):3740.
14. Seaton RA, Bell E, Gourlay Y, Semple L. Nurseled management of uncomplicated cellulitis in the community: evaluation of a protocol
incorporating intravenous ceftriaxone. J Antimicrob Chemother. May 2005. 55(5):7647.
15. Lipsky BA. New developments in diagnosing and treating diabetic foot infections. Diabetes Metab Res Rev. MayJun 2008. 24 Suppl 1:S6671.
16. Roujeau JC, Sigurgeirsson B, Korting HC, Kerl H, Paul C. Chronic dermatomycoses of the foot as risk factors for acute bacterial cellulitis of the
leg: a casecontrol study. Dermatology. 2004. 209(4):3017.
17. Björnsdóttir S, Gottfredsson M, Thórisdóttir AS, Gunnarsson GB, Ríkardsdóttir H, Kristjánsson M, et al. Risk factors for acute cellulitis of the
lower limb: a prospective casecontrol study. Clin Infect Dis. Nov 15 2005. 41(10):141622.
18. Roberts S, Chambers S. Diagnosis and management of Staphylococcus aureus infections of the skin and soft tissue. Intern Med J. Dec 2005.
35 Suppl 2:S97105.
19. Kroshinsky D, Grossman ME, Fox LP. Approach to the patient with presumed cellulitis. Semin Cutan Med Surg. Sep 2007. 26(3):16878.
20. Lin JN, Chang LL, Lai CH, Lin HH, Chen YH. Clinical and molecular characteristics of invasive and noninvasive skin and soft tissue infections
caused by group A Streptococcus. J Clin Microbiol. 2011 Oct. 49(10):36327. [Medline]. [Full Text].
21. Miller LS, Cho JS. Immunity against Staphylococcus aureus cutaneous infections. Nat Rev Immunol. 2011. 11:50518. [Medline].
22. Baddour LM, Bisno AL. Recurrent cellulitis after saphenous venectomy for coronary bypass surgery. Ann Intern Med. Oct 1982. 97(4):4936.
23. Baddour LM, Bisno AL. Nongroup A betahemolytic streptococcal cellulitis. Association with venous and lymphatic compromise. Am J Med.
Aug 1985. 79(2):1559.
24. Kalliola S, VuopioVarkila J, Takala AK, Eskola J. Neonatal group B streptococcal disease in Finland: a tenyear nationwide study. Pediatr Infect
Dis J. Sep 1999. 18(9):80610.
25. Cieslak TJ, Rajnik M, Roscelli JD. Immunization against Haemophilus influenzae type B fails to prevent orbital and facial cellulitis: results of a
25year study among military children. Mil Med. Oct 2008. 173(10):9414.
26. Parada JP, Maslow JN. Clinical syndromes associated with adult pneumococcal cellulitis. Scand J Infect Dis. 2000. 32(2):1336.
27. Chin PW, Koh CK, Wong KT. Cutaneous tuberculosis mimicking cellulitis in an immunosuppressed patient. Singapore Med J. Jan 1999.
40(1):445.
28. Elkayam O, Gat A, Lidgi M, Segal R, Yaron M, Caspi D. Atypical cutaneous findings in a patient with systemic lupus erythematosus. Lupus.
2003. 12(5):4137.
29. Hsu PY, Yang YH, Hsiao CH, Lee PI, Chiang BL. Mycobacterium kansasii infection presenting as cellulitis in a patient with systemic lupus
erythematosus. J Formos Med Assoc. Aug 2002. 101(8):5814.
30. Bassetti S, Battegay M. Staphylococcus aureus infections in injection drug users: risk factors and prevention strategies. Infection. Jun 2004.
32(3):1639.
31. Sierra JM, Sanchez F, Castro P, et al. Group A streptococcal infections in injection drug users in Barcelona, Spain: epidemiologic, clinical, and
microbiologic analysis of 3 clusters of cases from 2000 to 2003. Medicine (Baltimore). May 2006. 85(3):13946.
32. Horowitz Y, Sperber AD, Almog Y. Gramnegative cellulitis complicating cirrhosis. Mayo Clin Proc. Feb 2004. 79(2):24750.
33. Sebeny PJ, Riddle MS, Petersen K. Acinetobacter baumannii skin and softtissue infection associated with war trauma. Clin Infect Dis. Aug 15
2008. 47(4):4449.
34. Semel JD, Goldin H. Association of athlete's foot with cellulitis of the lower extremities: diagnostic value of bacterial cultures of ipsilateral
interdigital space samples. Clin Infect Dis. Nov 1996. 23(5):11624.
35. Vugia DJ, Peterson CL, Meyers HB, et al. Invasive group A streptococcal infections in children with varicella in Southern California. Pediatr
Infect Dis J. Feb 1996. 15(2):14650.
36. Waldhausen JH, Holterman MJ, Sawin RS. Surgical implications of necrotizing fasciitis in children with chickenpox. J Pediatr Surg. Aug 1996.
31(8):113841.
37. Lowy FD. Staphylococcus aureus infections. N Engl J Med. Aug 20 1998. 339(8):52032.
38. Barrett FF, McGehee RF Jr, Finland M. Methicillinresistant Staphylococcus aureus at Boston City Hospital. Bacteriologic and epidemiologic
observations. N Engl J Med. Aug 29 1968. 279(9):4418.
39. Four Pediatric Deaths from CommunityAcquired MethicillinResistant Staphylococcus aureus Minnesota and North Dakota, 19971999. CDC.
August 20, 1999. 70710. [Full Text].
40. Furuya EY, Cook HA, Lee MH, Miller M, Larson E, Hyman S. Communityassociated methicillinresistant Staphylococcus aureus prevalence:
how common is it? A methodological comparison of prevalence ascertainment. Am J Infect Control. Aug 2007. 35(6):35966. [Medline].
41. Brook I. Microbiology and management of human and animal bite wound infections. Prim Care. Mar 2003. 30(1):2539.
42. Dendle C, Looke D. Review article: Animal bites: an update for management with a focus on infections. Emerg Med Australas. Dec 2008.
20(6):45867.
43. Noonburg GE. Management of extremity trauma and related infections occurring in the aquatic environment. J Am Acad Orthop Surg. JulAug
2005. 13(4):24353.
44. Dechet AM, Yu PA, Koram N, Painter J. Nonfoodborne Vibrio infections: an important cause of morbidity and mortality in the United States,
19972006. Clin Infect Dis. Apr 1 2008. 46(7):9706.
45. McNamara DR, Tleyjeh IM, Berbari EF, et al. Incidence of lowerextremity cellulitis: a populationbased study in Olmsted county, Minnesota.
Mayo Clin Proc. Jul 2007. 82(7):81721.
46. Ellis Simonsen SM, van Orman ER, Hatch BE, et al. Cellulitis incidence in a defined population. Epidemiol Infect. Apr 2006. 134(2):2939.
[Medline].
47. Lamagni TL, Darenberg J, LucaHarari B, et al. Epidemiology of severe Streptococcus pyogenes disease in Europe. J Clin Microbiol. Jul 2008.
46(7):235967. [Medline].
48. Lederman ER, Weld LH, Elyazar IR, et al. Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance
Network. Int J Infect Dis. Nov 2008. 12(6):593602.
49. Givner LB, Mason EO Jr, Barson WJ, et al. Pneumococcal facial cellulitis in children. Pediatrics. Nov 2000. 106(5):E61.
50. Kokx NP, Comstock JA, Facklam RR. Streptococcal perianal disease in children. Pediatrics. Nov 1987. 80(5):65963.
51. Lipsky BA, Weigelt JA, Gupta V, Killian A, Peng MM. Skin, soft tissue, bone, and joint infections in hospitalized patients: epidemiology and
microbiological, clinical, and economic outcomes. Infect Control Hosp Epidemiol. Nov 2007. 28(11):12908. [Medline].
52. Hersh AL, Chambers HF, Maselli JH, Gonzales R. National trends in ambulatory visits and antibiotic prescribing for skin and softtissue
infections. Arch Intern Med. Jul 28 2008. 168(14):158591. [Medline].
53. Davies HD, McGeer A, Schwartz B, et al. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study
Group. N Engl J Med. Aug 22 1996. 335(8):54754. [Medline].
54. Bisno AL, Cockerill FR 3rd, Bermudez CT. The initial outpatientphysician encounter in group A streptococcal necrotizing fasciitis. Clin Infect
Dis. Aug 2000. 31(2):6078. [Medline].
55. Francis JS, Doherty MC, Lopatin U, Johnston CP, Sinha G, Ross T. Severe communityonset pneumonia in healthy adults caused by methicillin
resistant Staphylococcus aureus carrying the PantonValentine leukocidin genes. Clin Infect Dis. Jan 1 2005. 40(1):1007. [Medline].
56. Durupt F, Dalle S, Ronger S, Thomas L. Does erysipelaslike rash after hip replacement exist?. Dermatology. 2006. 212(3):21620.
57. Simon MS, Cody RL. Cellulitis after axillary lymph node dissection for carcinoma of the breast. Am J Med. Nov 1992. 93(5):5438.
58. Masmoudi A, Maaloul I, Turki H, et al. Erysipelas after breast cancer treatment (26 cases). Dermatol Online J. Dec 1 2005. 11(3):12.
59. Zippel D, SiegelmannDanieli N, Ayalon S, Kaufman B, Pfeffer R, Zvi Papa M. Delayed breast cellulitis following breast conserving operation.
Eur J Surg Oncol. May 2003. 29(4):32730.
60. El Saghir NS, Otrock ZK, Bizri AR, Uwaydah MM, Oghlakian GO. Erysipelas of the upper extremity following locoregional therapy for breast
cancer. Breast. Oct 2005. 14(5):34751.
61. Lazzarini L, Conti E, Tositti G, de Lalla F. Erysipelas and cellulitis: clinical and microbiological spectrum in an Italian tertiary care hospital. J
Infect. Dec 2005. 51(5):3839.
62. Spear RM, Rothbaum RJ, Keating JP, Blaufuss MC, Rosenblum JL. Perianal streptococcal cellulitis. J Pediatr. Oct 1985. 107(4):5579.
63. Markham RB, Polk BF. Seal finger. Rev Infect Dis. MayJun 1979. 1(3):5679.
64. Crum NF, Higginbottom PA, Fehl FC, Graham BS. Sweet's syndrome masquerading as facial cellulitis. Cutis. Jun 2003. 71(6):46972.
65. Jenkins TC, Knepper BC, Sabel AL, Sarcone EE, Long JA, Haukoos JS, et al. Decreased Antibiotic Utilization After Implementation of a
Guideline for Inpatient Cellulitis and Cutaneous Abscess. Arch Intern Med. 2011 Jun 27. 171(12):10729. [Medline].
66. Perl B, Gottehrer NP, Raveh D, Schlesinger Y, Rudensky B, Yinnon AM. Costeffectiveness of blood cultures for adult patients with cellulitis. Clin
Infect Dis. Dec 1999. 29(6):14838.
67. Liu C, Bayer A, Cosgrove SE, et al. Clinical practice guidelines by the Infectious Diseases Society of America for the treatment of methicillin
resistant Staphylococcus aureus infections in adults and children. Clin Infect Dis. 2011 Feb. 52:138. [Medline].
68. Lipsky BA, Berendt AR, Cornia PB, et al. 2012 Infectious Diseases Society of America Clinical Practice Guideline for the Diagnosis and
Treatment of Diabetic Foot Infections. Clin Infect Dis. 2012. 54(12):31323172. [Full Text].
Treatment of Diabetic Foot Infections. Clin Infect Dis. 2012. 54(12):31323172. [Full Text].
69. Brown T. Recurrent Cellulitis: Penicillin Effective for Prevention. Medscape Medical News, May 1, 2013. Available at
http://www.medscape.com/viewarticle/803476. Accessed: May 8, 2013.
70. Thomas KS, Crook AM, Nunn AJ, Foster KA, Mason JM, Chalmers JR, et al. Penicillin to prevent recurrent leg cellulitis. N Engl J Med. 2013
May 2. 368(18):1695703. [Medline].
71. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. Methicillinresistant S. aureus infections among patients
in the emergency department. N Engl J Med. Aug 17 2006. 355(7):66674.
72. Cenizal MJ, Skiest D, Luber S, Bedimo R, Davis P, Fox P, et al. Prospective randomized trial of empiric therapy with trimethoprim
sulfamethoxazole or doxycycline for outpatient skin and soft tissue infections in an area of high prevalence of methicillinresistant
Staphylococcus aureus. Antimicrob Agents Chemother. Jul 2007. 51(7):262830.
73. Daum RS. Clinical practice. Skin and softtissue infections caused by methicillinresistant Staphylococcus aureus. N Engl J Med. Jul 26 2007.
357(4):38090.
74. Stryjewski ME, Chambers HF. Skin and softtissue infections caused by communityacquired methicillinresistant Staphylococcus aureus. Clin
Infect Dis. Jun 1 2008. 46 Suppl 5:S36877.
75. Davis SL, McKinnon PS, Hall LM, Delgado G Jr, Rose W, Wilson RF. Daptomycin versus vancomycin for complicated skin and skin structure
infections: clinical and economic outcomes. Pharmacotherapy. Dec 2007. 27(12):16118.
76. Krige JE, Lindfield K, Friedrich L, Otradovec C, Martone WJ, Katz DE. Effectiveness and duration of daptomycin therapy in resolving clinical
symptoms in the treatment of complicated skin and skin structure infections. Curr Med Res Opin. Sep 2007. 23(9):214756.
77. Hepburn MJ, Dooley DP, Skidmore PJ, Ellis MW, Starnes WF, Hasewinkle WC. Comparison of shortcourse (5 days) and standard (10 days)
treatment for uncomplicated cellulitis. Arch Intern Med. Aug 923 2004. 164(15):166974.
78. Wong CH, Khin LW, Heng KS, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing
necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004 Jul. 32(7):153541. [Medline].
79. King MD, Humphrey BJ, Wang YF, Kourbatova EV, Ray SM, Blumberg HM. Emergence of communityacquired methicillinresistant
Staphylococcus aureus USA 300 clone as the predominant cause of skin and softtissue infections. Ann Intern Med. Mar 7 2006. 144(5):30917.
80. Halilovic J, Heintz BH, Brown J. Risk factors for clinical failure in patients hospitalized with cellulitis and cutaneous abscess. J Infect. 2012 Mar
21. [Epub ahead of print]. [Medline].
81. Byl B, Clevenbergh P, Jacobs F, Struelens MJ, Zech F, Kentos A. Impact of infectious diseases specialists and microbiological data on the
appropriateness of antimicrobial therapy for bacteremia. Clin Infect Dis. Jul 1999. 29(1):606; discussion 678.
82. Chuang YC, Yuan CY, Liu CY, Lan CK, Huang AH. Vibrio vulnificus infection in Taiwan: report of 28 cases and review of clinical manifestations
and treatment. Clin Infect Dis. Aug 1992. 15(2):2716.
83. Fernandez JM, Serrano M, De Arriba JJ, Sanchez MV, Escribano E, Ferreras P. Bacteremic cellulitis caused by Non01, Non0139 Vibrio
cholerae: report of a case in a patient with hemochromatosis. Diagn Microbiol Infect Dis. May 2000. 37(1):7780.
84. US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when linezolid (Zyvox®) is given to
patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm265305.htm. Accessed: July 27, 2011.
85. Hurley HJ, Knepper BC, Price CS, Mehler PS, Burman WJ, Jenkins TC. Avoidable antibiotic exposure for uncomplicated skin and soft tissue
infections in the ambulatory care setting. Am J Med. 2013 Dec. 126(12):1099106. [Medline].
Media Gallery
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 seconddegree burn (left), and the smaller lesion is a firstdegree 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 communityacquired methicillinresistant Staphylococcus aureus (CAMRSA).
(Photo courtesy of Texas Dept. of Public Health.)
Abscess and associated cellulitis caused by communityacquired methicillinresistant Staphylococcus aureus (CAMRSA). (Photo courtesy of
Guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess. AFB = acidfast bacilli; BID = twice
daily; CRP = C reactive protein; CT = computed tomography scanning; DS = double strength; DM = diabetes mellitus; ESR = erythrocyte
sedimentation rate; ESRD = endstage 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 = methicillinresistant Staphylococcus aureus; NSAIDS = nonsteroidal antiinflammatory drugs; PO = by
mouth; SSTI = skin and softtissue 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):10729.
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.
of 14
Tables
Table 1. Empiric Antibiotic Therapy for Cellulitis by Etiology and Anatomic Location
Table 1. Empiric Antibiotic Therapy for Cellulitis by Etiology and Anatomic Location
Antibiotic Antibiotic Regimen
Complication/ Indication for
Location Likely Organisms Other Organisms Regimen Oral/ Parenteral/
Discussion Hospitalization
Outpatient Hospitalized
Cephalexin or
Cefazolin or oxacillin
dicloxacillin
Group A
streptococci much
Uncomplicated
more likely than
cellulitis or nafcillin
Staphylococcus or clindamycin
aureus
[(Cephalexin or
dicloxacillin or
clindamycin) plus Vancomycin
trimethoprim/
sulfamethoxazole]
Cellulitis,
concern for Daptomycin
Group A
methicillin
streptococci and S
resistant S or
aureus
aureus is a
concern Ceftaroline
Clindamycin
Dog bite Pasteurella species Staphylococci, Capnocytophaga Amoxicillin/ Deep wounds Thirdgeneration

(50% of wounds) streptococci canimorsus may clavulanate or severe cephalosporin
cause sepsis in wounds; (ceftriaxone
patients with [Rocephin]) plus
asplenia/hepatic metronidazole
S aureus Aerobes Moraxella disease. Penicillin allergic:
and Neisseria infections not
responding to
oral antibiotics or
Streptococcus Avoid firstgeneration Moxifloxacin
pyogenes Anaerobes cephalosporins/
Fusobacterium, erythromycin/
Bacteroides, dicloxacillin. betalactam/beta
Porphyromonas, lactamase inhibitor
and Prevotella (eg,
ampicillin/sulbactam)
High likelihood of or
infection –
fluoroquinolone plus
Prophylactic metronidazole
antibiotics indicated
for the following
wounds: deep
puncture, hands, or
requiring surgical
repair,
immunocompromised
host, venous or carbapenem
lymphatic (ertapenem)
compromise, crush
injury.
Requires close
followup care within
2448 h.
Thirdgeneration
cephalosporin
(Rocephin) plus
metronidazole
Amoxicillin/
clavulanate
or
Clenched fist
lacerations over
metacarpophalangeal Penicillin allergic:
Eikenella corrodens joints should be betalactam/beta
(gramnegative considered human lactamase inhibitor
facultative bites; anesthetize (eg,
anaerobe, 29% of wounds and irrigate; Moxifloxacin ampicillin/sulbactam)
wounds) reevaluate within 24
48 h.
48 h.
Human bite
or or
Aerobic gram
positive cocci, Intercanine distance
anaerobes >3 cm is likely bite
from adult; if wound (Clindamycin or fluoroquinolone plus
to child, consider metronidazole) metronidazole
abuse. plus (doxycycline
or cefuroxime or
trimethoprim/
sulfamethoxazole) or
carbapenem
(ertapenem)
Cat bite Pasteurella Staphylococci, Avoid firstgeneration Amoxicillin/ Deep wounds Thirdgeneration

multocida and P streptococci, cephalosporins/ clavulanate or severe cephalosporin
septica (75% of Bacteroides, erythromycin/ wounds; (Rocephin) plus
wounds) Peptostreptococcus, dicloxacillin infections not metronidazole
Actinomyces, responding to
Fusobacterium, Penicillin allergic oral antibiotics
Porphyromonas,
and Veillonella High likelihood of or
parvula infection
Prophylactic
antibiotics indicated Moxifloxacin
for the following betalactam/beta
wounds: deep lactamase inhibitor
puncture, hands, (eg,
requiring surgical or ampicillin/sulbactam)
repair, or
immunocompromised
host, venous or
lymphatic (Clindamycin or
compromise. metronidazole) fluoroquinolone plus
plus metronidazole
Requires close
followup care within (doxycycline or or
2448 h. cefuroxime or
trimethoprim/
sulfamethoxazole)
carbapenem
(ertapenem)
Nocardia
brasiliensis, Bacillus
Haemophilus anthracis, Largest study
influenzae type b, Pseudomonas indicates that H Age < 1 y/ more
Streptococcus aeruginosa, influenzae type b and Amoxicillin
Preseptal severe disease Thirdgeneration
pneumoniae, S Neisseria S pneumoniae not clavulanate,
(periorbital) require cephalosporin
aureus, other gonorrhoeae, diminished in facial cefpodoxime,
cellulitis intravenous (Rocephin)
streptococcal Proteus species, cellulitis as a result of cefdinir
antibiotic
species, and Pasteurella
anaerobes multocida, immunizations [25]
Mycobacterium
tuberculosis
No pathogen
identifiable in most
Lower Dicloxacillin or
infections, but it is
extremity cephalexin.
likely to be
Recurrent episodes
streptococcal (>
common; may be
staphylococcal)
associated with
Complicating rigors, extreme Add trimethoprim/ Firstgeneration
saphenous fatigue, myalgias, sulfamethoxazole cephalosporin
venectomy and hypotension; or tetracycline or (cefazolin);
Nongroup A beta
site after some associated with clindamycin if clindamycin;
hemolytic
coronary tinea pedis (toe web concern for vancomycin
streptococci most
bypass cultures may be methicillin
likely organism; S
grafting useful in establishing resistant S aureus
aureus less
probable pathogen)
common
Multiple regimens,
none clearly superior –
Piperacillin/tazobactam
or ceftazidime plus
aminoglycoside;
aminoglycoside;
No pathogen
Breast/arm
identifiable in most
(not mastitis) or
infections
Dicloxacillin,
cephalexin. Add
trimethoprim/
Complicating sulfamethoxazole Fever, recent ciprofloxacin plus beta
Group A or Non
breast cancer or tetracycline or chemotherapy, lactam
group A beta
surgery/lymph clindamycin if neutropenia
hemolytic
node concern for
streptococci most
dissection methicillin
likely organisms
resistant S aureus or
monotherapy with
piperacillin/tazobactam
or cefepime
Aquatic Aeromonas A hydrophila and Fluoroquinolone Third or fourth
environment hydrophila, Vibrio vulnificus may (eg, ciprofloxacin generation

Pseudomonas and produce rapidly or levofloxacin) cephalosporin (eg,
Plesiomonas progressive soft ceftazidime or
species, Vibrio tissue infection and cefepime) or
Fresh water/ species, sepsis fluoroquinolone (eg,
salt water/ Erysipelothrix Note: For M ciprofloxacin or
brackish rhusiopathiae, marinum levofloxacin)
water/ Mycobacterium infection, use
swimming marinum, and clarithromycin
pools/ others plus either
aquarium ethambutol or
rifampin
Puncture/
laceration
Amoxicillin/
clavulanate;
penicillin allergic:
Lacerations over
metacarpophalangeal
joints should be
Moxifloxacin
considered human
bites; anesthetize Failure to
E corrodens (gram wounds and irrigate; respond to oral
negative anaerobe, reevaluate within 24 therapy marked Betalactam/beta
or
Clenchedfist 29 % of wounds); 48 h by increasing lactamase inhibitor

injury aerobic gram pain and (eg,
positive cocci, swelling or ampicillin/sulbactam)
anaerobes purulent
(clindamycin or
Lacerations of drainage
metronidazole)
extensor tendon
plus (doxycycline
or cefuroxime or
trimethoprim/
sulfamethoxazole)
Aerobic and
facultative
organisms: group A Amoxicillin
Betalactam/beta
betahemolytic clavulanate
lactamase inhibitor
streptococci,
(eg,
Neisseria and
ampicillin/sulbactam)
Eikenella species
or
or
Odontogenic Require extraction or

facial cellulitis root canal
Anaerobes:
clindamycin
Prevotella and clindamycin
Peptostreptococcus
species
Back to List
Back to List
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 Ohio, Infectious
Diseases Society of America
Disclosure: Nothing to disclose.
Coauthor(s)
Subramanian Swaminathan, DNB, MD Fellow, Department of Infectious Diseases, Detroit Medical Center, Wayne State University School of
Medicine
Subramanian Swaminathan, DNB, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society
of America, International AIDS Society, HIV Medicine Association

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University
School of Medicine
Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for
Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America
Chief Editor
Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal
Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State
Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious
Acknowledgements
Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine,
Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine,
American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association,
American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy ofSciences,andSociety for Academic
Emergency Medicine
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
Dennis Cunningham, MD Assistant Professor of Pediatrics, Section of Infectious Diseases, Children's Hospital, Ohio State College of Medicine
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
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
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
Eric S Halsey, MD Head, Virology Department, Naval Medical Research Center DetachmentPeru (NMRCDPeru); 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
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
William D James, MD Paul R Gross Professor of Dermatology, ViceChairman, 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
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 PhysiciansAmerican Society of Internal
Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society
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
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
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
Maria R Nasca, MD, PhD Assistant Professor, Department of Dermatology, University of Catania School of Medicine, Italy
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
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; EditorinChief,
Medscape Drug Reference
Disclosure: Medscape Salary Employment

Cellulitis - Practice Essentials, Background, Pathophysiology

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Cellulitis - Practice Essentials, Background, Pathophysiology

Uploaded by

Copyright:

Available Formats

5/22/2017 Cellulitis: Practice Essentials, Background, Pathophysiology

Dog bite Pasteurella species Staphylococci, Capnocytophaga Amoxicillin/ Deep wounds Thirdgeneration

Cat bite Pasteurella Staphylococci, Avoid firstgeneration Amoxicillin/ Deep wounds Thirdgeneration

Aquatic Aeromonas A hydrophila and Fluoroquinolone Third or fourth

environment hydrophila, Vibrio vulnificus may (eg, ciprofloxacin generation

You might also like

Cellulitis - Practice Essentials, Background, Pathophysiology

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Cellulitis - Practice Essentials, Background, Pathophysiology

Uploaded by

Copyright:

Available Formats

5/22/2017 Cellulitis: Practice Essentials, Background, Pathophysiology

Dog bite Pasteurella species Staphylococci, Capnocytophaga Amoxicillin/ Deep wounds Third­generation

Cat bite Pasteurella Staphylococci, Avoid first­generation Amoxicillin/ Deep wounds Third­generation

Aquatic Aeromonas A hydrophila and Fluoroquinolone Third­ or fourth­

environment ­­ hydrophila, Vibrio vulnificus may (eg, ciprofloxacin generation

You might also like

Dog bite Pasteurella species Staphylococci, Capnocytophaga Amoxicillin/ Deep wounds Thirdgeneration

Cat bite Pasteurella Staphylococci, Avoid firstgeneration Amoxicillin/ Deep wounds Thirdgeneration

Aquatic Aeromonas A hydrophila and Fluoroquinolone Third or fourth

environment hydrophila, Vibrio vulnificus may (eg, ciprofloxacin generation