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Acute cellulitis and erysipelas in adults: Treatment

authors: Denis Spelman, MBBS, FRACP, FRCPA, MPH, Larry M Baddour, MD, FIDSA, FAHA
section editor: Sandra Nelson, MD
deputy editor: Keri K Hall, MD, MS

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jun 2025.

This topic last updated: Jun 13, 2025.

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INTRODUCTION

Patients with skin and soft tissue infection may present with cellulitis, abscess, and other
forms of infection [1-3].

This topic will discuss treatment of cellulitis and erysipelas.

Clinical manifestations and diagnosis of cellulitis and erysipelas are discussed separately.
(See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and
diagnosis".)

Treatment of skin abscess is discussed elsewhere. (See "Skin abscesses in adults:

Treatment".)

DIFFERENTIATING CELLULITIS FROM ERYSIPELAS

Effective treatment of cellulitis and erysipelas depends on determining the most likely
microorganism causing the infection. Beta-hemolytic streptococci cause most cases of
cellulitis and erysipelas, but cellulitis is sometimes caused by Staphylococcus aureus and
occasionally by a multitude of other organisms.

Examination and clinical features cannot always differentiate cellulitis from erysipelas, so
we treat as if there is cellulitis whenever we are uncertain. Both cellulitis and erysipelas
manifest as areas of skin erythema, edema, and warmth. On physical examination,
cellulitis involves deeper layers of the skin, so it classically presents with indistinct borders
that are not raised ( picture 1 and picture 2). In contrast, classic erysipelas presents
as a bright red patch of skin with a clearly demarcated raised border ( picture 3 and
picture 4).

Details regarding the clinical presentation and diagnosis of cellulitis and erysipelas are
found elsewhere. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical
manifestations, and diagnosis", section on 'Cellulitis and erysipelas'.)

DETERMINING THE SITE OF CARE

Cellulitis and erysipelas can both cause rapidly progressive and severe illness. Initial
assessment of these infections should focus on determining the severity of illness and
whether hospitalization is indicated.

Hospitalization or admission to an observational unit is indicated for most individuals who

warrant parenteral antibiotics. All patients who are suspected of having high-risk "red-
flag" conditions should be hospitalized.

"Red-flag" conditions that warrant hospitalization — Red-flag conditions warrant

immediate hospitalization, and some require urgent surgical intervention. Findings that
increase suspicion for these conditions include severe sepsis or septic shock, rapidly
progressive infection, or pain out of proportion to examination findings. Because of high
morbidity and mortality, such conditions should be considered as part of the initial
assessment of every individual with skin and soft tissue infection. Diagnosis and
management of these conditions are discussed elsewhere.

● Toxic shock syndrome – (See "Invasive group A streptococcal infection and toxic shock
syndrome: Epidemiology, clinical manifestations, and diagnosis" and "Invasive group A
streptococcal infection and toxic shock syndrome: Treatment and prevention" and
"Staphylococcal toxic shock syndrome".)

● Necrotizing soft tissue infection (eg, necrotizing fasciitis) – (See "Necrotizing soft
tissue infections".)

● Joint involvement (with or without prosthesis) – (See "Septic arthritis in adults" and
"Prosthetic joint infection: Epidemiology, microbiology, clinical manifestations, and
diagnosis" and "Prosthetic joint infection: Treatment".)
● Involvement of vascular graft – (See "Overview of surgical site infection", section on
'Deep infection associated with implanted materials'.)

● Pyomyositis – (See "Primary pyomyositis".)

● Clostridial myonecrosis (gas gangrene) – (See "Clostridial myonecrosis".)

● Deep venous thrombosis – (See "Clinical presentation and diagnosis of the

nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

● Compartment syndrome – (See "Acute compartment syndrome of the extremities" and

"Pathophysiology, classification, and causes of acute extremity compartment
syndrome".)

Indications for parenteral therapy — The decision to initiate parenteral therapy is

typically based on the extent and severity of infection and patient comorbidities. Patients
who meet criteria for parenteral therapy are usually admitted to the hospital to ensure
prompt administration and close observation.

For individuals with cellulitis or erysipelas without suspicion for the conditions above, we
suggest initial treatment with parenteral antibiotics in the following circumstances:

● Systemic signs of toxicity such as fever >100.5°F/38°C, hypotension, or sustained

tachycardia (refractory hypotension should prompt consideration of toxic shock
syndrome).

● Rapid progression of erythema (eg, doubling of the affected area within 24 hours; in
particular, expansion over a few hours with severe pain should prompt consideration of
necrotizing fasciitis).

● Extensive erythema.

● High-risk neutropenia [4]. Patients with neutropenia are classified as low- or high-risk
based on scoring mechanisms that consider the anticipated duration of neutropenia,
comorbidities, and severity of illness; such scoring systems are discussed separately.
(See "Overview of neutropenic fever syndromes", section on 'Risk of serious
complications'.)

● Inability to tolerate or absorb oral therapy.

The need for parenteral antibiotics for acute lymphangitis accompanying cellulitis is
unknown. We consider parenteral therapy in the setting of rapid progression or concern
for incipient bacteremia.

For immunocompromised patients with low-risk neutropenia or a nonneutropenic form of

immunocompromise, we have a lower threshold for admission for intravenous (IV)
antibiotics than we do for immunocompetent patients.

Ultimately, clinical judgment is necessary and should consider the severity of infection,
type of underlying immunocompromise, and ability for close follow-up in the outpatient
setting in each case of cellulitis or erysipelas.

ACUTE CELLULITIS

The pillars of cellulitis treatment are antibiotic therapy and management of exacerbating
conditions, including the point of entry of infection. (See 'Considerations prior to selecting
antibiotics' below and 'Adjunctive treatments' below.)

Considerations prior to selecting antibiotics — At the time of presentation, selection of

empiric antibiotic therapy is based on determining the most likely pathogen. In most
cases, the causative pathogen is never identified. If a pathogen is identified, antibiotics
should be narrowed to target the pathogen.

Factors that should be considered when choosing antibiotics for acute cellulitis include the
severity and location of the cellulitis and whether coverage for methicillin-resistant S.
aureus (MRSA) or atypical organisms is necessary. These issues are discussed in the
sections that follow.

Pathogens to always cover — Empiric antibiotics for cellulitis should always cover
beta-hemolytic streptococci and methicillin-sensitive S. aureus (MSSA), which are the
most common pathogens of cellulitis [1-3]. Further details regarding the microbiology
of cellulitis are discussed elsewhere ( table 1). (See "Cellulitis and skin abscess:
Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Cellulitis
and erysipelas'.)

Indications for MRSA coverage — Empiric coverage for MRSA is indicated for patients
with severe sepsis, certain MRSA risk factors, and those who have increased morbidity if
suboptimal antibiotics are administered. Conditions that warrant MRSA coverage
include the following [2,5]:

● Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, sustained

 tachycardia)
● Cellulitis with purulent wound drainage
● Known MRSA colonization or infection
● Injection drug use
● High-risk neutropenia

Other risk factors are not as strongly associated with MRSA infection, so we individualize
the decision for MRSA coverage in such cases. For a complete list of risk factors for
MRSA, refer to the table ( table 2).

Wounds and exposures that warrant specific coverage — A broad range of

organisms can cause cellulitis in individuals with wounds, injuries, or certain
environmental exposures ( table 1). Antibiotic regimens for these conditions are
distinct and discussed in detail elsewhere.

● Wounds and injuries

• Diabetic foot ulcers – (See "Diabetic foot infection, including osteomyelitis: Clinical
manifestations and diagnosis", section on 'Microbiology' and "Diabetic foot
infections, including osteomyelitis: Treatment".)

• Animal bites – (See "Animal bites (dogs, cats, and other mammals): Evaluation and
management", section on 'Management'.)

• Human bites – (See "Human bites: Evaluation and management", section on

'Infected bites'.)

• Puncture wounds other than bites – (See "Infectious complications of puncture

wounds".)

• Pressure injury or pressure ulcer – (See "Infectious complications of pressure-

induced skin and soft tissue injury".)

• Surgical wound – (See "Overview of surgical site infection".)

● Environmental exposures

• Water exposure – (See "Soft tissue infections following water exposure".)

• Soil exposure – (See "Infectious complications of puncture wounds".)

• Travel-related skin infections – (See "Skin lesions in the returning traveler" and
 "Melioidosis: Epidemiology, clinical manifestations, and diagnosis", section on 'Skin
infection'.)

Anatomic site of infection — Cellulitis can occur on any part of the body. Depending
on the location of cellulitis, antibiotic selection and other interventions, including
surgery, can vary.

● Cellulitis of the extremities – The extremities are the most common site of cellulitis.
In the absence of a high-risk condition, red-flag finding, or other indication for
broadened antibiotic coverage, treatment focuses on beta-hemolytic streptococci and
S. aureus. (See 'Determining the site of care' above and 'Selecting an antibiotic
regimen' below.)

If cellulitis involves the hand, hospitalization is typically recommended along with

evaluation by a surgeon. Management of hand infections is discussed in depth
elsewhere. (See "Overview of hand infections".)

● Facial cellulitis – Facial skin infections are more often due to erysipelas than cellulitis.
Treatment of facial cellulitis focuses on beta-hemolytic streptococci and S. aureus. (See
'Selecting an antibiotic regimen' below.)

If the area around the eye is cellulitic, differentiation of preseptal (periorbital) from
orbital cellulitis is important. Preseptal cellulitis is generally a mild infection of the skin
around the eye, whereas orbital cellulitis involves the deeper tissues of the eye and
can lead to loss of vision. Rarely, infections involving the medial third of the face (ie,
the areas around the eyes and nose) can be complicated by septic cavernous
thrombosis, a life-threatening disease. More details regarding diagnosis and
management of preseptal and orbital cellulitis, as well as septic cavernous
thrombosis, are found elsewhere. (See "Preseptal cellulitis" and "Orbital cellulitis" and
"Septic cavernous sinus thrombosis".)

Severe external otitis may also be associated with facial cellulitis and is often caused
by Pseudomonas aeruginosa. More details regarding diagnosis and management of
external otitis are found elsewhere. (See "Acute otitis externa in adults: Treatment",
section on 'Severe disease'.)

● Neck cellulitis – Cellulitis of the neck is uncommon. When present, consideration

should be given to underlying deep neck space infection or submandibular space
infection (Ludwig angina), both of which require urgent evaluation and management.
Diagnosis and management of deep neck space infections are discussed elsewhere.
 (See "Deep neck space infections in adults" and "Ludwig angina".)

● Breast cellulitis – Breast cellulitis is usually due to beta-hemolytic streptococci or S.

aureus and is managed similarly to uncomplicated cellulitis unless the patient has an
underlying breast implant, as described below (see 'Selecting an antibiotic regimen'
below). Additional considerations regarding the management of breast cellulitis are
found elsewhere. (See "Breast cellulitis and other skin disorders of the breast", section
on 'Treatment'.)

● Cellulitis of the abdominal wall – Most reports of abdominal-wall cellulitis of adults

are in individuals with surgical site infection, abdominal-wall mesh infection, or intra-
abdominal conditions such as appendicitis. In each of these situations, both surgical
intervention and antibiotic therapy are usually necessary for management [6-17].
Management of these conditions is discussed elsewhere. (See "Overview of surgical
site infection" and "Wound infection following repair of abdominal wall hernia".)

Few reports of idiopathic abdominal-wall cellulitis exist, but the infection is probably
more common than the medical literature suggests. In a case series of 260 patients
with cellulitis and severe obesity between 1998 and 2003, 24 (9 percent) had
idiopathic abdominal-wall cellulitis [18]. Of those 24 patients, 17 (71 percent) had a
remote history of healed abdominal surgery, 10 (42 percent) had diabetes mellitus, 7
(29 percent) experienced recurrences, and 3 (13 percent) underwent surgical
debridement and/or panniculectomy. Eleven (46 percent) had an underlying
dermatologic condition of the abdominal wall, most commonly lymphedema and/or
intertrigo.

No studies have evaluated treatment of idiopathic abdominal-wall cellulitis. We use

the same approach as for cellulitis in general. (See 'Selecting an antibiotic regimen'
below.)

We suggest treating underlying dermatologic and other contributing conditions, such

as intertrigo, while the patient is receiving antimicrobial therapy.

● Cellulitis of the perineum or genitalia – Cellulitis of the perineum and genitals may
be confused with Fournier gangrene, a polymicrobial necrotizing fasciitis of the
perineum that can involve the lower abdominal wall, the penis and scrotum in males,
and the labia in females. Fournier gangrene is a medical and surgical emergency that
requires empiric broad spectrum antimicrobial therapy. Details regarding diagnosis
and management of Fournier gangrene are found elsewhere. (See "Necrotizing soft
 tissue infections".)

● Cellulitis overlying a prosthetic joint or vascular graft – In this situation, the

cellulitis may be a consequence or cause of infection of the prosthesis or graft. Details
regarding these infections are found elsewhere. (See "Prosthetic joint infection:
Epidemiology, microbiology, clinical manifestations, and diagnosis" and "Prosthetic
joint infection: Treatment" and "Overview of surgical site infection", section on 'Deep
infection associated with implanted materials'.)

Selecting an antibiotic regimen — The first step when selecting an initial antibiotic
regimen for cellulitis is to determine whether providing coverage beyond beta-hemolytic
streptococci and S. aureus is necessary. Certain conditions, exposures, or anatomic sites
often require broader antibiotic coverage than standard regimens, and antibiotic selection
for those conditions is discussed elsewhere ( table 1). (See 'Determining the site of care'
above and 'Considerations prior to selecting antibiotics' above.)

For most patients with cellulitis who don't have features that warrant specific
management, our approach depends on the severity of illness, patient's immune status,
and risk for MRSA, as outlined below and in the algorithm ( algorithm 1).

Dosing of antibiotics may be influenced by the presence of obesity, which is a risk factor
for the development of cellulitis, though data on efficacy and optimal antimicrobial dosing
for cellulitis in obesity are lacking [19].

In general, our antibiotic recommendations match those of expert guidelines [2].

Patients with severe sepsis — In the setting of severe sepsis, rapid administration of
empiric broad-spectrum antibiotics is indicated because delay or lack of adequate
coverage increases mortality [20,21]. Of note, patients with septic shock, manifested by
refractory hypotension, may have toxic shock syndrome or another high-risk condition
and should be managed accordingly, as discussed elsewhere. (See 'Determining the site
of care' above.)

● Initial therapy – We suggest the following antibiotic regimen for patients with severe
sepsis ( algorithm 1):

• Intravenous (IV) vancomycin (see table for dosing ( table 3))

plus

Cefepime 2 g IV every eight hours

 Other regimens may be more appropriate in certain situations:

• For patients who are known or suspected of having an infection due to an organism
with an extended-spectrum beta-lactamase, we suggest using an empiric
carbapenem (eg, meropenem 1 g IV every eight hours) in conjunction with
vancomycin.

• For patients with reported beta-lactam allergies, empiric antibiotic selection

depends on the type and severity of the reaction ( algorithm 2). Patients with
mild, nonimmunoglobulin (Ig) E-mediated reactions to penicillins (eg,
maculopapular rash) can usually safely receive cephalosporins; carbapenems are
typically safe in patients who cannot take penicillins or cephalosporins (see "Choice
of antibiotics in penicillin-allergic hospitalized patients"). For patients who cannot
take any beta-lactam agent, we suggest IV vancomycin ( table 3) paired with
either levofloxacin (750 mg IV once daily) or aztreonam (2 g IV every eight hours;
dosing up to 2 g every six hours may be reasonable for weight >120 kg). Note that
individuals with a history of life-threatening or anaphylactic reaction to ceftazidime
should not be given aztreonam, but levofloxacin is generally safe.

• If alternative high-risk red-flag conditions have not been ruled out, broader empiric
regimens may be appropriate. As an example, for patients with suspected toxic
shock syndrome, IV clindamycin or linezolid may be added to the above regimens.
Anaerobic coverage may be added in patients with suspected necrotizing fasciitis.
(See "Necrotizing soft tissue infections".)

● Oral step-down therapy – Once clinical improvement and resolution of sepsis occurs,
it is generally appropriate to transition to an oral regimen. If a pathogen is identified
during the course of therapy, antibiotics should be narrowed to coverage specific for
that pathogen.

If a pathogen is not identified, stable patients who are not immunocompromised can
generally be transitioned to one of the narrower oral agents described below. (See
'Immunocompetent patients without severe sepsis' below.)

The rationale for using a spectrum that covers pathogens in addition to streptococci
and S. aureus is the risk of poor outcomes with a narrower spectrum of empiric therapy
in severely ill patients if other pathogens are involved.

Immunocompetent patients without severe sepsis — We typically divide this group

of patients into those who warrant MRSA coverage and those who do not (
 algorithm 1). Indications for MRSA coverage are described above. (See 'Indications
for MRSA coverage' above.)

Without an indication for MRSA coverage — For most patients, antibiotic regimens
that cover beta-hemolytic streptococci and MSSA are effective, and coverage for MRSA
is not necessary [2,5,22,23]. We suggest one of the following regimens (
algorithm 1):

● Oral antibiotic regimens – Many patients with cellulitis of the lower extremity can
be managed with oral antibiotics in the outpatient setting [24]. For such patients,
we suggest one of the following regimens:

• Dicloxacillin 500 mg orally every six hours

• Flucloxacillin 500 to 1000 mg orally every six hours (not available in the United
States)
• Cephalexin 500 mg orally every six hours
• Cefadroxil 500 mg orally every 12 hours or 1 g orally once daily

● Parenteral antibiotic regimens – Parenteral antibiotics are recommended for

higher risk patients (see 'Indications for parenteral therapy' above). For such
patients, we suggest one of the following regimens:

• Cefazolin 1 to 2 g IV every eight hours

• Nafcillin 1 to 2 g IV every four hours
• Oxacillin 1 to 2 g IV every four hours
• Flucloxacillin 2 g IV every six hours (not available in the United States)

For cefazolin, nafcillin, and oxacillin, we usually favor the higher doses listed above
(ie, 2 g) for treatment of these infections.

Once there is evidence of clinical improvement, parenteral antibiotics should be

switched to one of the oral regimens listed above [25].

Studies suggest that most patients with cellulitis do not need MRSA coverage:

● A randomized trial of adults with nonpurulent cellulitis in five emergency

departments in the United States noted similar clinical cure rates among those
treated with cephalexin plus trimethoprim-sulfamethoxazole (TMP-SMX) and those
treated with cephalexin plus placebo [22]. In the per-protocol analysis, 182 (84
percent) of 218 individuals in the cephalexin plus TMP-SMX group achieved cure
versus 165 (86 percent) of 193 in the cephalexin group (difference -2 percent, 95%
 CI -9.7 to 5.7 percent). The modified intention-to-treat analysis suggested a possible
trend favoring the cephalexin plus TMP-SMX group, but those results are difficult to
interpret due to a large number of patients in both groups who did not complete
the full course of therapy.

● Another randomized trial of 153 patients with cellulitis without abscess noted
comparable cure rates among those treated with cephalexin and TMP-SMX (85
percent) and those treated with cephalexin and placebo (82 percent; difference 2.7
percent, 95% CI -9.3 to 15 percent) [23].

With an indication for MRSA coverage — MRSA coverage is indicated if certain

conditions are present (see 'Indications for MRSA coverage' above). We suggest one of
the following regimens ( algorithm 1):

● Oral antibiotic regimens – For many patients, treatment in the outpatient setting
with oral antibiotics is effective [24]. We suggest one of the following regimens:

• TMP-SMX (one to two double-strength tablets orally twice daily; for patients who
weigh more than 70 kg and have normal kidney function, we favor two double-
strength tablets twice daily).

TMP-SMX has activity against both beta-hemolytic streptococci and S. aureus,

including MRSA. Cellulitis cure rates with TMP-SMX range from 78 to 83 percent
[26,27].

• Amoxicillin (875 mg orally twice daily) plus doxycycline (100 mg orally twice daily).

Doxycycline provides coverage for S. aureus, including most MRSA isolates;

amoxicillin is added to it for streptococcal coverage. Support for doxycycline for
MRSA skin and soft tissue infection is based on observational data, as discussed
elsewhere. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults:
Treatment of skin and soft tissue infections", section on 'Oral antibiotic therapy'.)

Linezolid (600 mg orally every 12 hours) is acceptable if the above agents cannot be
used. Meta-analyses, systematic reviews, and randomized trials suggest that
linezolid has at least equivalent outcomes for skin and soft tissue infections
(including MRSA infections) when compared with IV vancomycin [28-31]. The
analyses also found elevated rates of nausea, vomiting, and thrombocytopenia
when linezolid was administered; we suggest weekly complete blood counts if a
patient receives linezolid for longer than two weeks. Linezolid is discussed in more
 detail elsewhere. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults:
Treatment of skin and soft tissue infections", section on 'Linezolid and tedizolid'.)

Clindamycin (450 mg orally every eight hours) may have activity against both
Streptococcus and S. aureus and is an alternative if no other options exist; we avoid
its use due to risk for Clostridioides difficile infection and the possibility of
streptococcal and staphylococcal resistance. Local rates of resistance to clindamycin
should be considered before prescribing, as described below. (See 'Alternatives for
serious beta-lactam allergy' below.)

● Parenteral antibiotic regimen – For patients who meet criteria for parenteral
antibiotics, we suggest the following regimen (see 'Indications for parenteral
therapy' above):

• IV vancomycin (see table for dosing ( table 3))

• Daptomycin 4 to 6 mg/kg IV every 24 hours (alternative)

Vancomycin is the preferred option because of extensive experience with this

agent. When daptomycin is used, we usually favor the higher dose (ie, 6 mg/kg). For
patients who cannot take vancomycin or daptomycin, alternative agents can be
used and are listed in the table ( table 4), and their efficacy is discussed
elsewhere. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults:
Treatment of skin and soft tissue infections".)

Once there is evidence of clinical improvement, parenteral antibiotics should be

switched to one of the oral regimens listed above.

Alternatives for serious beta-lactam allergy — Although many patients have

reported beta-lactam allergies, most do not have allergies that would prohibit the use
of beta-lactams. In particular, many with penicillin allergies can still take a
cephalosporin ( algorithm 2). Evaluation and management of reported penicillin
allergies are discussed in detail elsewhere. (See "Choice of antibiotics in penicillin-
allergic hospitalized patients" and "Allergy evaluation for immediate penicillin allergy:
Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam
antibiotics".)

For immunocompetent patients without severe sepsis who have serious allergies
that preclude use of beta-lactams, we suggest one of the following regimens (
algorithm 1):
● Oral antibiotic regimen – If no indication for parenteral antibiotics is present, we
suggest either of the following:

• TMP-SMX (one to two double-strength tablets orally twice daily).

• Linezolid (600 mg orally every 12 hours). More detail regarding this agent is
discussed above. (See 'With an indication for MRSA coverage' above.)

An alternative is clindamycin (450 mg orally every eight hours), but we generally

avoid it due to risk of C. difficile infection and the possibility of streptococcal and
staphylococcal resistance [26,32]. Local rates of resistance to clindamycin should be
considered before prescribing. Data from the United States Centers for Disease
Control and Prevention (CDC) found that 26 percent of group A Streptococcus
isolates were resistant to clindamycin in 2023, and 47 percent of MRSA isolates were
resistant to clindamycin in 2017 [33-36]. In Australia in 2019, clindamycin resistance
was reported in 7 percent of group A Streptococcus and 30 percent of MRSA isolates
[37].

Data suggest that TMP-SMX and clindamycin are equally effective for management
of cellulitis [38]. In one randomized trial of outpatients with cellulitis, 110 (81
percent) of 136 individuals who received clindamycin achieved cure versus 110 (76
percent) of 144 who received TMP-SMX (difference -4.5 percent, 95% CI -15.1 to 6.1
percent) [26]. Susceptibility testing of group A streptococcus to TMP-SMX in the
United States is not routinely performed.

We avoid monotherapy with doxycycline and other tetracyclines because of unclear

susceptibility of streptococcal species and lack of clinical randomized trial data
[35,39,40]. Surveillance data from the CDC found that 32 percent of invasive group
A Streptococcus isolates were resistant to tetracycline in 2023 [36].

We do not recommend macrolides, such as azithromycin, due to high resistance

rates among beta-hemolytic streptococci [2,33,41]. The CDC reported that 27
percent of group A streptococci were resistant to macrolides in 2023 [36].

● Parenteral antibiotic regimen – For patients with an indication for parenteral

therapy, we suggest IV vancomycin ( table 3). (See 'Indications for parenteral
therapy' above.)

For patients who cannot take vancomycin, alternative parenteral agents can be
used and are listed in the table ( table 4).
 Once there is evidence of clinical improvement, parenteral antibiotics should be
switched to one of the oral regimens listed above.

Immunocompromised patients without severe sepsis — Patients who have certain

immunocompromising conditions are at risk for a wide range of pathogens. However,
there is a spectrum of immunocompromising conditions, and some do not substantially
increase risk. Ultimately, choosing an antibiotic regimen for immunocompromised
patients should depend on the type of underlying immunocompromise, severity of
infection, and ability for close follow-up in the outpatient setting.

● Patients with high-risk neutropenia – We hospitalize these patients for prompt

administration of IV broad-spectrum antibiotics that cover gram-negative pathogens
(including Pseudomonas spp) in addition to streptococci and S. aureus. Our preferred
regimen is vancomycin plus cefepime ( table 5). (See "Treatment of neutropenic
fever syndromes in adults with hematologic malignancies and hematopoietic cell
transplant recipients (high-risk patients)", section on 'Initial regimen'.)

● Patients with immunocompromise other than high-risk neutropenia – In our

experience, many patients in this group can be treated with IV or oral therapy using
the same regimens as the immunocompetent population. (See 'Immunocompetent
patients without severe sepsis' above and 'Indications for parenteral therapy' above.)

Some immunocompromising conditions can be associated with specific pathogens (

table 1). For example, patients with cirrhosis can develop cellulitis from enteric
gram-negative bacilli (eg, Klebsiella spp), so some experts select a regimen that covers
those organisms (eg, amoxicillin-clavulanate). As another example, patients with low-
risk neutropenia are at risk for pseudomonal infection, so many experts administer
combination therapy (eg, amoxicillin-clavulanate plus ciprofloxacin).

Ultimately, the decision to broaden coverage beyond beta-hemolytic streptococci and

S. aureus is nuanced and requires clinical judgment.

Duration of antibiotic therapy — The duration of therapy should be individualized

depending on clinical response. In general, five to six days of therapy is appropriate for
patients with uncomplicated cellulitis whose infection has improved [2,42,43]. Extension of
antibiotic therapy (up to 14 days) may be warranted in the setting of severe infection, slow
response to therapy, or immunocompromise.

The above suggested duration is supported by a meta-analysis of eight randomized

controlled trials totaling almost 1500 adults with cellulitis that found no difference in
response rates between short (five to six days) and longer courses of antibiotics (relative
risk [RR] 0.99, 95% CI 0.96-1.03) [24]. The only trial that assessed outcome beyond 30 days
was a trial of 151 individuals hospitalized with nonpurulent cellulitis who were randomized
to treatment with a 6-day or 12-day course of flucloxacillin [44]. Cure rates were similar
between the groups (74 versus 67 percent); relapse rates after 90 days were higher in the
six-day group (6 versus 24 percent), but most relapses in the six-day group were in
patients with a history of at least one prior episode of cellulitis.

Adjunctive treatments — When treating cellulitis of the lower extremities, management

of exacerbating conditions and any points of entry for microorganisms is paramount.

Elevation and edema management — Edema, a common manifestation of cellulitis,

can impair antibiotic penetration into infected tissue and prevent resolution of infection.
For lower extremity cellulitis, elevation of the affected limb hastens improvement by
allowing gravity drainage of edema and inflammatory substances [2]. To optimize the
effect of gravity, we instruct patients to elevate the heel of the foot above the knee and
the knee above the hip.

Lymphedema and venous insufficiency are commonly associated with lower extremity
cellulitis, especially in individuals who are obese. In addition to elevation, compression
therapy can be used to treat both lymphedema and venous insufficiency. While
compression therapy has been shown to be effective for preventing recurrences of
cellulitis in individuals with lymphedema, the efficacy of compression therapy during
acute cellulitis is uncertain, and clinical practice varies, including among UpToDate
contributors. Traditionally, compression therapy was felt to be contraindicated during
episodes of acute cellulitis for fear of compromising vascular function, although no data
support this contraindication. Limited data suggest that individualized compression
therapy applied by specialized lymphedema physiotherapists may not be harmful and
does not compromise microcirculation in patients with active cellulitis [45,46].
Compression therapy should be avoided in individuals with known or suspected arterial
insufficiency. Details regarding the management of lymphedema and venous
insufficiency are found elsewhere. (See "Pathophysiology, classification, and causes of
lymphedema" and "Management of peripheral lymphedema" and "Overview of lower
extremity chronic venous disease" and "Compression therapy for the treatment of
chronic venous insufficiency".)

Skin management — Treatment of skin conditions and the point of microorganism

entry can expedite resolution of cellulitis.
The point of entry of microorganisms should be sought and managed at the time of
diagnosis of cellulitis. Common points of entry include intertrigo in the toe webs of the
feet, tinea pedis, onychomycosis, and lower extremity ulcers. Details regarding
diagnosis and management of these issues are found elsewhere. (See "Intertrigo" and
"Dermatophyte (tinea) infections", section on 'Tinea pedis' and "Onychomycosis:
Management" and "Approach to the differential diagnosis of leg ulcers".)

As cellulitis evolves, skin can begin to weep, blister, flake, or crack. Dermatologists and
wound care specialists can provide assistance with management of these conditions.
More details regarding the cutaneous progression of cellulitis are found below. (See
'Monitoring response to therapy' below.)

Numerous underlying skin conditions are risk factors for the development of cellulitis
including atopic dermatitis (eczema) and psoriasis. Such conditions should be optimally
managed in conjunction with standard cellulitis treatment. Details regarding skin
conditions that predispose to cellulitis are discussed elsewhere. (See "Cellulitis and skin
abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on
'Epidemiology'.)

Interventions that are not recommended — We do not recommend the following

therapies. These recommendations generally match those of expert guidelines [2].

● Anti-inflammatory medications – We suggest not using nonsteroidal anti-

inflammatory drugs (NSAIDs) or corticosteroids when there is concern for moderate
to severe cellulitis. These drugs can mask signs and symptoms of inflammation in
patients with necrotizing soft tissue infection, and their use may be associated with
delay in diagnosis.

For patients with mild infection, anti-inflammatory medications may reduce

symptoms of pain. While some data suggest that use of NSAIDs or corticosteroids
may hasten healing among patients with cellulitis or erysipelas, these results are
inconclusive and are limited by small sample size [47-49]. (See "Necrotizing soft tissue
infections".)

● Topical antibiotics – Although topical antibiotics are effective for some skin infections
(eg, impetigo, folliculitis), topical antibiotics are unlikely to be effective for cellulitis or
erysipelas due to involvement of the layers of skin below the epidermis.

● Hyperbaric oxygen therapy – For cellulitis, hyperbaric oxygen therapy has not been
shown to be effective [2]. Further information on hyperbaric oxygen therapy is found
 elsewhere. (See "Hyperbaric oxygen therapy".)

TREATMENT OF ERYSIPELAS

Management of erysipelas primarily consists of antibiotic therapy along with the

adjunctive therapies described above. (See 'Adjunctive treatments' above.)

Oral antibiotics for erysipelas — Most cases of erysipelas can be managed with oral
antibiotics in the outpatient setting. For patients with unambiguous erysipelas who do not
meet criteria for parenteral antibiotics, empiric oral antibiotics active against beta-
hemolytic streptococci should be administered (see 'Indications for parenteral therapy'
above). We suggest one of the following regimens:

● Penicillin V potassium 500 mg orally every six hours

● Amoxicillin 875 mg orally every 12 hours
● Cephalexin 500 mg orally every six hours
● Cefadroxil 500 mg orally every 12 hours or 1 g orally once daily

For patients with serious beta-lactam allergies that preclude use of the above regimens,
oral options are the same as those listed above for cellulitis. (See 'Alternatives for serious
beta-lactam allergy' above.)

Parenteral antibiotics for erysipelas — We suggest antibiotics that cover beta-hemolytic

streptococci and S. aureus for patients with erysipelas who have an indication for
parenteral therapy (see 'Indications for parenteral therapy' above). Differentiating
erysipelas from cellulitis is not always straightforward, so we believe that adding
staphylococcal coverage is prudent in individuals who are ill enough to warrant parenteral
therapy.

For such patients, appropriate regimens include those described in the above discussion
about antibiotic therapy for cellulitis.

If a microbiologic diagnosis of beta-hemolytic Streptococcus is subsequently established

(eg, by a positive blood culture), then we recommend switching to parenteral aqueous
crystalline penicillin G (2 to 4 million units intravenously [IV] every four to six hours).

For patients in whom outpatient parenteral antibiotic is desired, ceftriaxone (1 to 2 g IV

once daily) is an alternative that allows for convenient once-daily outpatient
administration.
Once there is evidence of clinical improvement, parenteral antibiotics should be switched
to oral antibiotics that cover streptococci. Appropriate oral antibiotics for erysipelas are
described above. (See 'Oral antibiotics for erysipelas' above.)

Duration of antibiotic therapy — In general, the duration of therapy for erysipelas is

analogous to the duration used for cellulitis. (See 'Duration of antibiotic therapy' above.)

MONITORING RESPONSE TO THERAPY

Patients with cellulitis or erysipelas typically have symptomatic improvement within 24 to

48 hours of beginning antimicrobial therapy, although visible improvement of skin
manifestations can take 72 hours or longer [50,51]. In some cases, we monitor patients
remotely by having patients send daily pictures of their infection to our clinic; we advise
patients to take photographs from the same angle and in the same environment, with
particular attention to lighting.

It is useful to document the baseline appearance of the physical findings at the start of
antibiotic therapy. We obtain a baseline digital photograph to help monitor progress.
Some experts outline the area of infection with an indelible marker at the time of
treatment initiation to allow objective monitoring of progress. Others do not outline the
infection because patients sometimes experience unnecessary anxiety if the infection
appears to extend beyond the line as the infection dissipates. In the early stages of
treatment, erythema may expand beyond the initial margins of infection as the infection
dissipates. Deepening of erythema may be observed due to destruction of pathogens that
can enhance local inflammation. These findings should not be mistaken for therapeutic
failure. Clues that the infection is improving include reductions in fever, pain, brightness
or intensity of erythema, peripheral white blood cell count, and other signs of infection.

As cellulitis evolves, skin can begin to weep, blister, flake, or crack. None of these findings
are necessarily indications of worsening infection. As discussed elsewhere, wound care
specialists or dermatologists can help to manage these conditions. (See 'Skin
management' above.)

Residual skin inflammation is a common finding after completion of effective therapy

[44,50,52]. In a study of 216 patients hospitalized for cellulitis, more than half had residual
inflammation at the end of therapy and 40 percent still did two weeks after completion of
therapy [51].

In patients with lower extremity cellulitis, residual erythema and swelling during
dependent positioning may be due to ongoing venous stasis or lymphedema instead of
infection [52]. In such patients, a history of improvement with elevation and positional
examination of the affected limb may help differentiate infection from noninfection; signs
of cellulitis persist with leg elevation but often improve in patients with stasis or
lymphedema.

REFRACTORY INFECTION

Significant progression of erythema or persistence of systemic symptoms after 24 to 48

hours should prompt a search for possible reasons for treatment failure.

Failure to respond to appropriate therapy should prompt consideration that the initial
diagnosis of cellulitis is incorrect. Cellulitis is often confused with other infectious and
noninfectious illnesses, and misdiagnosis is perhaps the most common cause of lack of
response to therapy [53,54]. The differential diagnosis of cellulitis and erysipelas is broad
and is discussed in detail elsewhere.

Additional evaluation should consider multiple possibilities:

● Red-flag condition – Any time cellulitis progresses rapidly or clinical symptoms,

especially pain, seem to be out of proportion to physical examination, red-flag
conditions such as necrotizing skin and soft tissue infection should be considered. A low
threshold for surgical consultation to evaluate for these conditions is prudent. A list of
red-flag conditions is provided above. (See 'Determining the site of care' above.)

● Inadequate dosing or tissue penetration of antibiotics – Conditions at the site of

infection, such as edema or peripheral artery disease, can markedly reduce the ability of
antibiotics to penetrate into soft tissue. To optimize tissue penetration of the antibiotics,
management of these conditions is paramount. (See 'Adjunctive treatments' above.)

In patients failing oral antibiotics, switching from oral to intravenous antibiotics may
increase antibiotic delivery to the site of infection, especially for antibiotics with poor
oral bioavailability (such as some beta-lactam agents) or for patients whose ability to
absorb oral medications is uncertain.

In select situations, using higher antibiotic doses may be beneficial. Obesity can
increase drug clearance from circulation and thereby limit the amount of antibiotic that
reaches the site of infection [55]. Moreover, certain bacteria, such as Pseudomonas spp,
require higher antibiotic doses to achieve bacterial killing. Consultation with an
 infectious disease specialist or pharmacist may be helpful in these cases.

● Abscess – As cellulitis responds to antibiotic therapy, sometimes the infection can

coalesce to form an abscess below the surface. Abscess should be suspected when focal
tender fluctuance is found on examination, and ultrasound can aid in detection. If
present, surgical consultation for incision and drainage is recommended. Detailed
discussion of skin abscess management is found elsewhere. (See "Skin abscesses in
adults: Treatment".)

● Resistant pathogen – Re-evaluating for the possibility of resistant microorganisms and

reviewing past culture data can help guide antibiotic change. Methicillin-resistant S.
aureus (MRSA) or other organisms associated with certain conditions or environmental
exposures should be considered. (See 'Considerations prior to selecting antibiotics'
above.)

In immunocompromised individuals, cellulitis can be due to a multitude of organisms

including atypical bacteria, fungi, viruses, and parasites. If these individuals fail to
respond to broad-spectrum antibiotic therapy, a dermatologic evaluation and skin
biopsy can be beneficial. Nodular or ulcerative lesions should be biopsied early during
the clinical course in highly immunocompromised individuals, especially for those who
are septic or have rapidly progressive illness. Further discussion of skin infection in
neutropenic individuals is found elsewhere. (See "Diagnostic approach to the adult
cancer patient with neutropenic fever", section on 'Skin and mucous membranes'.)

● Inadequate adherence to the treatment plan – Adherence to the antibiotic regimen

and nonantibiotic interventions, including elevation, should be assessed.

RECURRENT INFECTION

Recurrent erysipelas and cellulitis are not uncommon. Recurrences have been reported to
occur in 14 percent of cellulitis cases within one year and up to 45 percent of cases within
three years, usually in the same location [3,56,57]. In one review of over 400,000
admissions for cellulitis, the readmission rate was 10 percent and most readmissions were
due to recurrent cellulitis [58].

Management of recurrent infection — During the active stage of infection,

management of recurrent episodes is the same as the approach for initial episodes (see
'Acute cellulitis' above). For individuals who have frequent or severe recurrences, prefilled
prescriptions for treatment doses of antibiotics can be provided so that patients can self-
initiate antibiotic therapy at the onset of symptoms while seeking immediate medical
attention.

Prevention of recurrences — Potential tools for prevention of recurrent cellulitis include

alleviation of predisposing conditions (such as use of compression therapy for
management of edema), antibiotic prophylaxis, and S. aureus decolonization. These are
discussed below.

Alleviation of predisposing conditions — Predisposing conditions should be identified

and treated, if possible [3]. Examples of modifiable predisposing conditions include the
following:

● Edema. Elevation of the affected area and diuretic therapy can help to alleviate
edema. Compression therapy has been shown in studies to be highly effective for
lymphedema and venous insufficiency and is discussed in detail below. (See
'Compression therapy' below.)

● Foot infections including intertrigo in the toe webs of the feet, tinea pedis, and
onychomycosis. (See "Intertrigo" and "Dermatophyte (tinea) infections" and
"Onychomycosis: Management".)

● Lower extremity ulcers. (See "Approach to the differential diagnosis of leg ulcers".)

● Chronic skin conditions, such as eczema and psoriasis. (See "Treatment of atopic
dermatitis (eczema)" and "Chronic plaque psoriasis in adults: Overview of
management".)

● Obesity. (See "Obesity in adults: Overview of management".)

● Immunosuppression.

Compression therapy — For patients with recurrent episodes of cellulitis in the setting
of chronic lower extremity venous insufficiency or lymphedema, compression therapy is
an essential component of management that has been shown to be effective in
reducing episodes of recurrent cellulitis [59].

In a randomized trial involving 84 patients with chronic lower extremity edema and ≥2
prior episodes of cellulitis, daily use of compression therapy reduced the rate of
recurrent cellulitis compared with no compression therapy (15 versus 40 percent,
respectively, at a median follow-up of six months; hazard ratio [HR] 0.23, 95% CI 0.09-
0.59) [59]. The compression therapy was provided by specialized lymphedema
physiotherapists and usually consisted of prescription knee-high stockings that included
the foot and were worn throughout the day. The compression therapy was provided
only when no active cellulitis was present, and no adverse events related to
compression therapy were observed. Of note, the trial was stopped early for benefit,
which tends to overestimate treatment efficacy.

Additional details regarding compression therapy in patients with chronic venous

insufficiency and lymphedema are provided separately. (See "Pathophysiology,
classification, and causes of lymphedema" and "Management of peripheral
lymphedema" and "Compression therapy for the treatment of chronic venous
insufficiency".)

Antibiotic prophylaxis for selected patients — For select patients who optimize
predisposing conditions but still develop recurrent cellulitis in the same anatomic site,
we suggest prophylactic antibiotic therapy [2]. Although infrequent, there are scenarios
(eg, complicated bacteremia in patients with a prosthetic device) when initiation of
suppressive therapy after an initial bout of cellulitis may be warranted; consultation of
clinicians with experience in these cases is suggested.

For prophylactic therapy, we suggest one of the following antibiotic regimens:

● For patients with known or presumed recurrent beta-hemolytic streptococcal infection

[60-62]:

• Penicillin V (250 to 500 mg orally twice daily)

• Penicillin G benzathine intramuscular (IM) injections (1.2 to 2.4 million units IM
every four weeks; shorten interval to every two weeks if longer interval is not
effective)
• Amoxicillin (500 mg twice daily)
• Cefadroxil (500 mg orally once or twice daily)
• Cephalexin (500 mg twice daily)

● For patients with known or presumed recurrent staphylococcal infection:

• Cefadroxil (500 mg orally once or twice daily)

• Cephalexin (500 mg orally two to four times daily)
• Trimethoprim-sulfamethoxazole (TMP-SMX; one double-strength tablet orally once
or twice daily)

Cefadroxil and cephalexin have no activity against methicillin-resistant S. aureus

 (MRSA) and should only be used if recurrent methicillin-sensitive S. aureus (MSSA)
infection is suspected.

For patients with reported beta-lactam allergies, we suggest referral to an allergist. If

beta-lactam allergy is confirmed and TMP-SMX is not an option, we consider a trial of
doxycycline (100 mg orally twice daily), recognizing that this may be less effective
against beta-hemolytic streptococci. We avoid clindamycin (150 mg orally once daily)
unless there are no other options, due to risk of C. difficile infection and increasing
resistance among beta-hemolytic streptococci [63].

Other than penicillin and clindamycin, minimal data exist to support the options listed
above as prophylactic agents. Amoxicillin and cephalexin are more bioavailable than
oral penicillin and may be considered either as initial prophylaxis or if there is
breakthrough infection despite penicillin. The optimal dosing for these antibiotics when
used as prophylaxis is unknown. Titration to lower doses over time may allow
determination of the best dose for individual patients.

Serologic testing for beta-hemolytic streptococci may be a useful diagnostic tool to help
guide the choice of prophylactic antibiotic therapy. Such tests include the anti-
streptolysin-O reaction and the anti-deoxyribonuclease B test (anti-DNAse B). Further
information regarding serologic testing for beta-hemolytic streptococci is found
elsewhere. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical
manifestations, and diagnosis", section on 'Diagnosis'.)

Support for prophylactic antibiotic therapy for prevention of recurrent cellulitis comes
from multiple trials:

● In a randomized trial that included 274 patients with two or more episodes of lower
extremity cellulitis, penicillin (250 mg orally twice daily) nearly halved the risk of
recurrence during 12 months of prophylaxis (HR 0.55, 95% CI 0.35-0.86), but the
protective effect diminished rapidly after the prophylaxis period ended [60]. A lower
likelihood of response was observed among patients with a body mass index ≥33
kg/m2, multiple previous episodes of cellulitis, or lower extremity edema.

● Two separate meta-analyses of five trials totaling over 500 patients with recurrent
cellulitis concluded that prophylactic antibiotics substantially reduce the risk of
subsequent cellulitis (relative risk [RR] 0.46, 95% CI 0.26-0.79, and RR 0.31, 95% CI 0.13
to 0.72, respectively) [64,65]. Findings from two of the included studies also
demonstrated that antibiotic prophylaxis is cost-effective [62,66].
 In the trials and meta-analyses, no significant differences in adverse effects were found
between the groups that received antibiotics and those that did not.

Prophylactic therapy may be continued for several months to years with interval
assessments for efficacy and tolerance. Patients in whom recurrent cellulitis occurs
while on suppressive therapy should undergo re-evaluation of predisposing conditions
and antimicrobial agents. (See 'Prevention of recurrences' above.)

S. aureus decolonization — For patients with suspected recurrent S. aureus infection,

we suggest an attempt at S. aureus decolonization. Detailed discussion of S. aureus
decolonization is found elsewhere. (See "Methicillin-resistant Staphylococcus aureus
(MRSA) in adults: Prevention and control", section on 'Decolonization' and "Methicillin-
resistant Staphylococcus aureus (MRSA) in children: Prevention and control".)

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

regions around the world are provided separately. (See "Society guideline links: Skin and
soft tissue infections".)

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the
Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview
and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces
are longer, more sophisticated, and more detailed. These articles are written at the 10th to
12th grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to
print or email these topics to your patients. (You can also locate patient education articles
on a variety of subjects by searching on "patient education" and the keyword(s) of
interest.)

● Basics topics (see "Patient education: Cellulitis and erysipelas (skin infections) (The
Basics)" and "Patient education: Cellulitis (skin infection) in adults – Discharge
 instructions (The Basics)")

● Beyond the Basics topic (see "Patient education: Skin and soft tissue infection (cellulitis)
(Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

● Overview – Patients with skin and soft tissue infection may present with cellulitis,
erysipelas, or abscess. This topic addresses management of cellulitis and erysipelas in
adults. The management of skin abscess is discussed separately. (See "Skin abscesses in
adults: Treatment".)

● Identify conditions treated differently than cellulitis ( algorithm 1)

• "Red-flag" conditions – These warrant immediate hospitalization and often surgery.

Examples include ( table 6):
- Toxic shock syndrome
- Necrotizing soft tissue infection (eg, necrotizing fasciitis, including Fournier's
gangrene)
- Clostridial myonecrosis
- Pyomyositis
- Deep venous thrombosis
- Compartment syndrome

(See 'Determining the site of care' above.)

• Specific exposures and anatomic sites – Some exposures or anatomic sites may
require distinct antibiotic coverage, surgical intervention, or specific radiographic
imaging:

- Involvement of the hand, periorbital space, periauricular tissue, or neck

- Location over a joint (native or prosthetic), vascular graft, or other foreign body
- Infection of a diabetic foot ulcer, pressure ulcer, animal or human bite, puncture
wound, or surgical wound
- Infection following exposure to water, soil, or recent travel

(See 'Wounds and exposures that warrant specific coverage' above and 'Anatomic site
of infection' above.)

● Antibiotic selection for cellulitis in immunocompetent patients without severe

 sepsis

• Determine risk for methicillin-resistant Staphylococcus aureus (MRSA) or adverse

outcomes – Antibiotic selection depends on the risk for MRSA or adverse outcomes.
Features that increase those risks in this population include (see 'Indications for MRSA
coverage' above):

- Systemic toxicity (eg, fever, hypotension, sustained tachycardia)

- Purulent wound drainage
- Known MRSA colonization or infection
- Injection drug use
- Immunocompromise

• Antibiotic regimens

For immunocompetent patients with one of the above features, we suggest a regimen
that covers beta-hemolytic streptococci, methicillin-sensitive S. aureus (MSSA), and
MRSA ( algorithm 1) (Grade 2C) (see 'With an indication for MRSA coverage' above):

- Oral – Trimethoprim-sulfamethoxazole, amoxicillin plus doxycycline, or linezolid

- Intravenous (IV) – Vancomycin
- Other risk factors ( table 2) may not be as strongly associated with MRSA infection
so we individualize the decision for MRSA coverage in such cases.

For immunocompetent patients without the above features, we suggest a narrower

regimen with coverage for beta-hemolytic streptococci and MSSA ( algorithm 1)
(Grade 2C). (See 'Without an indication for MRSA coverage' above.)

- Oral – Dicloxacillin, flucloxacillin, cephalexin, or cefadroxil

- IV – Cefazolin, nafcillin, oxacillin, or flucloxacillin

Intravenous therapy is warranted for patients with systemic toxicity (eg, fever,
tachycardia), rapidly progressive or extensive erythema, or inability to absorb oral
therapy. (See 'Indications for parenteral therapy' above.)

● Antibiotic regimens for cellulitis in patients with severe sepsis or an

immunocompromising condition

• For patients with severe sepsis (eg, evidence of tissue hypoperfusion or organ
dysfunction) or high-risk neutropenia ( table 5), we suggest initial therapy with
vancomycin plus cefepime (Grade 2C). This regimen provides broad coverage against
 MRSA, MSSA, beta-hemolytic streptococci, and gram-negative organisms for patients
at highest risk for poor outcomes. (See 'Patients with severe sepsis' above.)

• For patients with other immunocompromising conditions (and without severe sepsis),
we often use the same regimens as for immunocompetent patients. The decision to
cover additional pathogens associated with specific conditions should be
individualized ( table 1). (See 'Immunocompromised patients without severe sepsis'
above.)

● Antibiotic regimens for erysipelas – For patients with unambiguous erysipelas (eg,
bright red erythema with distinct raised borders), we suggest antibiotics that primarily
target streptococci (Grade 2C).

Oral options include penicillin V potassium, amoxicillin, cephalexin, and cefadroxil.

Parenteral options include cefazolin, nafcillin, and flucloxacillin. (See 'Treatment of
erysipelas' above.)

● Duration of antibiotic therapy – We suggest five to six days of therapy rather than
longer durations (Grade 2C). However, extended regimens (ie, up to 14 days) may be
appropriate for severe or slowly responding cellulitis. Parenteral antibiotics should be
switched to an oral option once clinical improvement has occurred. (See 'Duration of
antibiotic therapy' above.)

● Adjunctive therapy – We instruct patients with cellulitis of the limb to elevate it to allow
drainage of edema and hasten improvement.

Areas of skin breakdown are potential points of entry that should be identified and
managed. Common points of entry include intertrigo in the toe webs, tinea pedis,
onychomycosis, lower extremity ulcers, atopic dermatitis, and psoriasis. (See 'Adjunctive
treatments' above.)

● Expected response – Symptomatic improvement typically occurs within 24 to 48 hours,

although visible improvement of skin manifestations can take 72 hours or longer. (See
'Monitoring response to therapy' above.)

● Refractory infection – Significant progression of erythema or continued systemic

symptoms should prompt a search for possible reasons for treatment failure.
Considerations include deeper infection, inadequate antibiotic penetration (eg, due to
edema), or incorrect diagnosis. (See 'Refractory infection' above.)

● Recurrent infection – During the active stage of infection, management of recurrent

 episodes is the same as the approach for initial episodes.

There are multiple tools to prevent recurrences (see 'Recurrent infection' above):

• Treating points of entry (eg, intertrigo, chronic skin conditions). (See 'Alleviation of
predisposing conditions' above.)

• Managing predisposing conditions – For patients with lymphedema or venous

insufficiency, we suggest compression therapy (Grade 2B). (See 'Compression
therapy' above.)

• Antibiotic prophylaxis for select patients – For patients who optimize predisposing
conditions but still have recurrent cellulitis in the same anatomic site, we suggest
prophylactic antibiotics (Grade 2B). For most patients, our preferred initial regimen is
penicillin V (250 to 500 mg orally twice daily). (See 'Antibiotic prophylaxis for selected
patients' above.)

• S. aureus decolonization – For patients with suspected recurrent S. aureus infection,

some experts attempt decolonization. (See "Methicillin-resistant Staphylococcus
aureus (MRSA) in adults: Prevention and control", section on 'Decolonization' and
"Methicillin-resistant Staphylococcus aureus (MRSA) in children: Prevention and
control".)
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Contributor Disclosures
Denis Spelman, MBBS, FRACP, FRCPA, MPH No relevant financial relationship(s) with ineligible
companies to disclose. Larry M Baddour, MD, FIDSA, FAHA No relevant financial relationship(s)
with ineligible companies to disclose. Sandra Nelson, MD Equity Ownership/Stock Options:
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listed have been mitigated. Keri K Hall, MD, MS No relevant financial relationship(s) with ineligible
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