This document defines and compares cellulitis and erysipelas, two types of skin infections caused by bacteria entering through breaks in the skin. Cellulitis affects deeper skin layers and fat, while erysipelas is more superficial. Diagnosis is clinical based on symptoms of redness, swelling and warmth. Treatment involves antibiotics, either orally or intravenously depending on severity. Factors like fever, rapid progression and underlying health issues determine need for intravenous antibiotics. Incision and drainage is sufficient for small skin abscesses without systemic involvement.

1. Cellulitis
Ni’maBader

2. Definition:
• Cellulitis (which includes erysipelas): skin infection that manifests
as an area of skin erythema, edema, and warmth; it develops as a
result of bacterial entry via breaches in the skin barrier.
• A skin abscess is a collection of pus within the dermis or
subcutaneous space.

3. Cellulitis Vs. Erysipelas
Similarities:
• Both manifest as areas of skin erythema, edema, and warmth; they develop as a result
of bacterial entry via breaches in the skin barrier
• Nearly always unilateral
• The lower extremities are the most common site of involvement

4. Differences:
*Purulent: Pus Discharge.
Cellulitis Erysipelas
Affects deeper dermis and SQ fats Affects the upper dermis and superficial
lymphatics
Purulent or non-purulent Non-purulent
Indolent course (few days) Acute onset
More localized symptoms Systemic symptoms (ex: fever and chills)
S.aureus (more w/ purulent) or β-hemolytic
strep (esp. GAS)
β-hemolytic strep

5. Non-purulent Cellulitis Vs. Erysipelas
• Erysipelas opposite to Non-purulent cellulitis, characterized by
raised lesions above the level of surrounding skin with clear
demarcation between involved and non-involved tissue.

6. Purulent Cellulitis Vs. Skin Abscess
• The discharges of skin abscess are drainable opposite to that of
Purulent cellulitis.

7. Cellulitis Risk Factors
1. Skin barrier disruption (abrasion, penetrating wound, pressure
ulcer, venous leg ulcer, insect bite, injection drug use)
2. Skin inflammation (eczema, radiation therapy)
3. Edema due to impaired lymphatic drainage or venous insufficiency
4. Obesity
5. Immunosuppression (diabetes, HIV infection…)
6. Preexisting skin infection (tinea pedis, impetigo)

8. Complications:
1. Bacteremia
2. Endocarditis
3. Osteomyelitis
4. Sepsis
5. Toxic shock syndrome.

9. Diagnosis and culture
• No specific lab test ( ↑inflammatory markers and WBCs)
• The diagnosis depends on clinical presentation.
• Skin abscess manifests as a painful, fluctuant, erythematous nodule, with or without
surrounding cellulitis.
• Lab testing is not required for patients with uncomplicated infection in the absence of
comorbidities or complications.
• Drainable abscess -----> incision & drainage -----> Cx and susceptibility test.
• Radiographic examination: US (skin abscess), MRI (osteomyelitis), CT (necrotizing faciatious)
• A skin biopsy if the diagnosis is uncertain
• Cultures of swabs from intact skin are not helpful.

10. Blood Cx If:
1. Systemic toxicity (fever, chills, HoTN and tachcardia)
2. Extensive skin or soft tissue involvement
3. Underlying comorbidities (lymphedema, malignancy, neutropenia,
immunodeficiency, splenectomy, diabetes)
4. Special exposures (animal bite, water-associated injury)
5. Persistent cellulitis

11. TREATMENT

12. When to give IV not PO?
• Patients with mild infection ------> oral antibiotics.
• IV if:
1. Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, or sustained
tachycardia)
2. Rapid progression of erythema
3. Progression of clinical findings after 48 hours of oral antibiotic therapy
4. Inability to tolerate oral therapy
5. Proximity of the lesion to an indwelling medical device (ex: prosthetic joint or
vascular graft)

13. When To Cover MRSA:
1. Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, or sustained
tachycardia)
2. Prior episode of MRSA infection or known MRSA colonization
3. Lack of clinical response to antibiotic regimen that does not include activity against
MRSA
4. Presence of risk factor(s) for MRSA infection (including recent hospitalization,
residence in a long-term care facility, recent facility, recent surgery, hemodialysis, and
HIV infection)
5. Proximity of the lesion to an indwelling medical device (eg, prosthetic joint or
vascular graft)

14. • Symptoms of infection resolve within 24-48 h
• Visible skin manifestation takes up to 72 h

15. Non-purulent Cellulitis:
PO options IV options
MRSA & β-hemolytic strep 1. Clindamycin
2. Amoxicillin PLUS TMP/SULF
3. Amoxicillin PLUS doxycycline
4. Amoxicillin PLUS minocycline
Vancomycin (preferred),
daptomycin
MSSA & β-hemolytic strep Cephalexin, dicloxacillin,
Cefadroxil, clindamycin
Cefazolin, clindamycin,
nafcillin, oxacillin.

16. Erysipelas
PO options IV options
β-hemolytic strep Penicillin, amoxicillin Cefazolin, ceftriaxone,
flucloxacillin

17. Purulent cellulitis and Skin Abscess
• Always cover MRSA
• When to cover gm-ve , gm+ve & anaerobes:
1. Pressure ulcer.
2. Peri-oral peri-rectal site of infection.
3. Prominent skin necrosis.
• Start IV Tx, Switch to PO once signs of infection resolved.

18. IV options PO options
MRSA Vancomycin (preferred) or
daptomycin
PLUS one of the following:
1. ampicillin/sulbactam
2. Piperacillin/tazobactam
3. Ticarcillin/clavulanate
4. Ceftriaxone + metronidazole
5. Ciprofloxacin +
metronidazole
6. Levofloxacin +
metronidazole
Clindamycin, TMP/SULF,
doxycycline, minocycline,
linezolid.
MRSA & GM+ve, GM-ve
bacilli and anaerobes.
Vancomycin (preferred) or
daptomycin

19. • PO options after s/s resolution:
• clindamycin, trimethoprim-sulfamethoxazole, or tetracyclines (doxycycline
or minocycline)

20. Skin abscess
 Role of antibiotic therapy — The role of antibiotic therapy for patients with abscess
depends on individual clinical circumstances. In general, antibiotic therapy is
warranted in the following circumstances:
• Single abscess ≥2 cm
• Multiple lesions
• Extensive surrounding cellulitis
• Associated immunosuppression or other comorbidities
• Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, or sustained tachycardia)
• Inadequate clinical response to incision and drainage alone
• Presence of an indwelling medical device (such as prosthetic joint, vascular graft, or
pacemaker)
• High risk for transmission of S. aureus to others (such as in athletes, military personnel)
 Management with incision and drainage alone (in the absence of antimicrobial
therapy) is generally sufficient for otherwise healthy adults with skin abscess <2 cm
in the absence of the above factors.

21. Duration of treatment:
• In general ----> 5 days
• Up to 14 days if:
1. Severe infection
2. Slow response to therapy
3. Immunosuppression.

22. Recurrent infection
• Usually in the same location
• Predisposing factors:
• Edema due to impaired lymphatic drainage, Venous insufficiency, Obesity,
Immunosuppression, Fissuring or maceration of the interdigital toe spaces and Tinea
pedis.
• treatment should be directed at both the infection and the predisposing condition if
modifiable
• Manage same as the initial episode.

23. Suppressive antibiotic therapy
• Used for patients with three to four episodes of cellulitis per year in the setting of predisposing
factors that cannot be alleviated.
• For patients with known or presumed beta-hemolytic streptococcal infection:
• Penicillin V
• Erythromycin
• Penicillin G benzathine IM
• For patients with known or presumed staphylococcal infection:
• Clindamycin
• Trimethoprim-sulfamethoxazole
• Suppressive therapy may be continued for several months with interval assessments for
efficacy and tolerance.