skin and soft tissue infections

Question 1

epidermis

Answer 1

the thin, outermost non-vascular layer composed of continuously dividing (shed) cells and the stratum corneum

Question 2

dermis

Answer 2

the layer directly beneath the epidermis consisting of connective tissue, blood vessels, lymphatics, sensory nerve endings, sweat and sebaceous glands, hair follicles, and smooth muscle fibers.

Question 3

subcutaneous tissue

Answer 3

layer of loose connective tissue primarily containing adipose cells (of variable thickness).

Question 4

fascia

Answer 4

The fascia is located beneath the subcutaneous tissue layer and separates the skin from underlying muscle. Superficial fascia is located immediately beneath the skin, while deep fascia forms sheaths that surround muscles.

Question 5

importance of obtaining a thorough history

Answer 5

While most SSTIs are caused by β-hemolytic Streptococci** or Staphylococcus aureus**, other organisms (such as additional bacteria, fungi, mycobacteria, and/or spirochetes) are capable of causing these infections depending on the epidemiologic setting and patient risk factors.
A careful history should be obtained from all patients with a SSTI that includes information about the patient’s immune status, living situation, PMH, obesity, IV drug use, water exposure, geographic locale, travel history, recent trauma or surgery, lifestyle, hobbies, animal exposure/bites, previous antimicrobial therapy, etc in order to develop an adequate differential diagnosis including risk for specific etiologic organisms.

Question 6

Impetigo

Answer 6

A superficial skin infection involving the epidermis consisting of multiple, coalescing erythematous papules that evolve into pustules/vesicles that rupture and form a dried, honey-colored crust**/discharge on an erythematous base; most often involves the skin of the face (nares, perioral) and extremities.

Question 7

impetigo symptoms

Answer 7

Maculopapular lesions/vesicles that rupture leaving superficial erosions that are occasionally pruritic or painful with honeycolored crusts.
clinical features: Non-bullous (70%) versus bullous (separation of dermal-epidermal layers to form fragile, thin-roofed vesiclopustules); can become secondarily infected.

Question 8

impetigo pathogenesis

Answer 8

The organism can directly invade healthy skin (primary) or can be introduced into superficial layers of the skin (epidermis) during trauma or abrasions (secondary); non-bullous form is highly contagious.

Question 9

impetigo risk factors

Answer 9

Children***, skin trauma, hot/humid climates, poor hygiene, day care settings, crowding, malnutrition, diabetes

Question 10

impetigo bacteriology

Answer 10

The majority of cases are caused by Staphylococcus aureus** and/or Streptococcus pyogenes** (Group A streptococcus)

Question 11

impetigo diagnosis

Answer 11

Clinical – Diagnosis is most often made clinically based on the characteristics appearance of the lesions.
Laboratory
-Culture – Not routinely performed; may be considered in patients not responding to first-line therapy (culture the pus/bullous fluid).

Question 12

impetigo treatment overview

Answer 12

Topical: Mupirocin 2% or retapamulin 1% ointment BID x 5 days
Systemic: Recommended for patients with numerous lesions or during outbreaks affecting several people to help decrease transmission; 7 days of therapy is recommended

Question 13

impetigo systemic treatment options

Answer 13

dicloxacillin 500 mg q6h
cephalexin 500 mg q6h
erthytromycin 500 mg q6h
clindamycin 300 mg q8h
amox/clav 875 q12h

Question 14

cellulitis

Answer 14

An acute, diffuse, spreading infection that involves the epidermis, dermis, and subcutaneous tissue, without involvement of the fascia; most commonly occurs on the lower extremities**, but can occur in other areas of the body depending on site of trauma or other risk factors.

Question 15

cellulitis sxs

Answer 15

Rapidly spreading area of erythema, edema, tenderness, and warmth in the skin with a poorly defined border.
other clinical features: Fever, malaise, leukocytosis, lymphangitis, regional lymphadenopathy

Question 16

cellulitis pathogenesis

Answer 16

The organism is typically introduced into the skin during trauma, lacerations, abrasions, puncture wounds, fissured toe webs from fungal infections of the feet**, cracks in dry skin, bite wounds, skin ulcers, or surgery (altered integrity of the protective barrier).

• Breaks in the skin are often small and clinically unapparent.
• Patients with diabetes are at increased risk for the development of skin infections due to neuropathy, dry skin, and altered blood supply (micro- and macrovascular changes).

Question 17

patients at risk of cellulitis

Answer 17

Infection can occur in normal hosts; but is commonly seen in injection drug users, patients with arterial or venous insufficiency (peripheral vascular disease), patients with diabetes mellitus, obese patients (poor lymphatic drainage), patients with chronic lymphedema, and patients who are immunocompromised.

Question 18

erysipelas

Answer 18

is a variant of cellulitis caused by β-hemolytic streptococci** involving only the upper dermis and superficial lymphatics with intense erythema with clearly defined borders and a peau d’ orange (orange peel) appearance due to superficial cutaneous edema surrounding the hair follicles; often involves the face**.

Question 19

bacteriology of cellulitis

Answer 19

depends on the host Majority of cases are caused by Staphylococcus aureus** or Streptococcus pyogenes** (Group A streptococcus); other common organisms include Group C or Group G streptococci*
infants and children - strep pyogenes (group A)
adults; post op patients - S. aureus (including MRSA), S. pyogenes
Inj drug users - S. aureus (including MRSA), S. pyogenes
diabetics - S. aureus, S. pyogenes

Question 20

cellulitis in immunocompromised patients

Answer 20

Cellulitis due to Methicillin-Resistant Staphylococcus aureus
There is an increasing prevalence of skin and soft tissue infections caused by community-associated MRSA (CA-MRSA).
CA-MRSA differs from hospital-acquired MRSA strains with respect to their risk factors for acquisition, virulence factors and antibiotic susceptibility.
-Acquisition of CA-MRSA is not associated with hospital or long-term care facility exposure, but rather from close contact to other patients with CA-MRSA. Cases (and even outbreaks) of CA-MRSA have been reported among patients with recent tattoos, inmates, injection drug users, Native American populations, gay men, participants in contact sports, and children.
-CA-MRSA contains a type IV SCCmec cassette and genes for Panton-Valentine leukocidin, a virulence factor that has been associated with tissue necrosis, abscess formation, and subsequent mild to severe infections. Patients with skin infection due to CA-MRSA often have cellulitis AND abscess/pustules.
-CA-MRSA is often susceptible to doxycycline, clindamycin, and trimethoprim-sulfamethoxazole.
CA-MRSA should be suspected as the cause of cellulitis in the populations listed above, especially if the cellulitis is accompanied by an abscess. CA-MRSA should also be considered in patients with skin infections not responding to β-lactam therapy.
Skin abscesses should be drained and cultured.

Question 21

diagnosis of cellulitis

Answer 21

Clinical – The diagnosis of cellulitis is most often made clinically based on the clinical presentation of the patient in addition to the physical examination findings. On presentation, physicians will often use a pen to outline the borders of cellulitis on a patient’s skin to serve as an objective method to monitor the response to antibiotic therapy over time (looking for extension or recession from original pen marking).

b. Laboratory
- Elevated white blood cell count
- Culture (often unnecessary in most cases) – aspiration of leading edge of cellulitis (yield is low); swab culture or needle aspiration of abscess, if present; blood cultures (positive in less than 5%)

Question 22

treatment of cellulitis overview

Answer 22

Prompt antimicrobial therapy is necessary to prevent the spread of the infection through the lymphatic system and into the bloodstream.
The choice of a particular antibiotic will depend upon the infection type; most probable causative organism based on patient risk factors; the Gram stain, culture, and susceptibility results (if available); the PK and PD characteristics of the antibiotic; the allergy history of the patient; underlying medical conditions; the severity of infection; etc.
-Patients with mild infections can receive oral therapy.
-Patients with moderate to severe infections (with systemic symptoms) should initially receive parenteral antibiotic therapy, which may be switched to oral therapy once the patient is clinically stable and the infection is resolving.
If the patient does not have an abscess within the cellulitis or if Gram stain and culture results are unavailable or inconclusive (which is most often the case), empiric therapy should be directed against both Group A streptococcus AND Staphylococcus aureus since the clinical features are indistinguishable
If an organism is isolated and identified, therapy should be directed against the causative pathogen.
-Streptococcus pyogenes→ Penicillin
-MRSA → Vancomycin, clindamycin or TMP/SMX
-Gram-negative bacilli → 3rd generation cephalosporin, extended spectrum penicillin (piperacillin), fluoroquinolone
-Polymicrobial with anaerobes → β-lactamase inhibitor combination (Zosyn® = piperacillin/ tazobactam) OR 3rd generation cephalosporin or fluoroquinolone with metronidazole OR carbapenem alone
Non-pharmacologic treatment of cellulitis includes elevation and immobilization of involved area to decrease swelling; surgical incision and drainage (usually only for abscess).
Duration of therapy = Minimum of 5 days, but should be
extended if not resolved within this timeframe.
-Include IV and oral days of therapy.
-May be longer in patients with vascular insufficiency, lymphedema, obese patients, or chronic cellulitis.

Question 23

empiric antibiotic regimens for mild infection

Answer 23

Dicloxacillin 500 mg PO every 6 hours OR Cephalexin 500 mg PO every 6 hours

Question 24

empiric antibiotic regimens for mild infection if MRSA is suspected

Answer 24

Trimethoprim-Sulfamethoxazole 2 DS PO every 12 hours OR Clindamycin 300 to 450 mg PO every 6 hours OR Linezolid 600 mg PO every 12 hours

Question 25

empiric antibiotic regimens for moderate to severe infection

Answer 25

Nafcillin 1 to 2 grams IV every 4 to 6 hours OR Cefazolin 1 to 2 grams IV every 8 hours

Question 26

empiric antibiotic regimens for moderate to severe infection is MRSA is suspected

Answer 26

Vancomycin 15 mg/kg IV every 12 hours OR Linezolid 600 mg IV or PO every 12 hours
Other treatment options include daptomycin and telavancin (in adults)

Question 27

empiric antibiotic cellulitis regimen in patients with a severe pen allergy

Answer 27

For patients with severe penicillin allergy, use clindamycin, vancomycin, or linezolid

Question 28

when MRSA is suspected in cellulitis

Answer 28

In patients whose cellulitis is associated with penetrating trauma, evidence of MRSA infection elsewhere, nasal colonization with MRSA, injection drug use, purulent cellulitis (abscess), or SIRS.

Question 29

necrotizing soft tissue infections overview

Answer 29

An aggressive subcutaneous infection that also involves the fascia (all tissue between the skin and underlying muscle) characterized by progressive destruction** of superficial fascia, subcutaneous fat and muscle due to toxins elaborated by the infecting organism(s).

Question 30

sxs/other clinical features of necrotizinf fasciitis

Answer 30

In addition to the cellulitis symptoms** mentioned above, patients may also experience intense pain (out of proportion to physical exam findings), bullae, crepitus, cutaneous gangrene, cutaneous anesthesia, “wooden-hard”** induration, and systemic toxicity** (high fever, mental status changes, hypotension), which rapidly progresses. Mortality rate of Group A strep necrotizing fasciitis with systemic symptoms and organ failure is 30-70%!

Question 31

pathogensis/risk factors for nec fasc

Answer 31

same as cellulitis

Question 32

bacteriology of nec fasc

Answer 32

Monomicrobial – Streptococcus pyogenes** (group A strep), Staphylococcus aureus, Vibrio vulnificus, or Aeromonas hydrophila.
Polymicrobial (perianal abscess, penetrating abdominal trauma, bowel surgery, decubitus ulcer, nearby genital infection, IDUs) – mixed infection involving organisms from GI or GU tract (gram negative aerobes and anaerobes).

Question 33

diagnosis of nec fasc

Answer 33

Clinical – Cellulitis (usually in lower extremities, genital area or abdomen) with clinical features and systemic symptoms suggesting deeper infection listed above; swollen and gray fascia with areas of necrosis during surgical debridement/exploration.
Laboratory – Gram stain and culture of tissue aspirate or deep tissue obtained during surgical debridement; blood cultures
Radiography – CT or MRI may be performed to document the presence of fascial edema but should not delay the diagnosis.

Question 34

treatment of nec fasc

Answer 34

considered an ID Medical Emergency!!
SURGICAL INTERVENTION – Repeated surgical debridement (every 24 to 36 hours until infected/ necrotic material is no longer present) is the primary therapeutic modality for the management of necrotizing fasciitis.
Antibiotic therapy
-Empiric therapy: Vancomycin + piperacillin/ tazobactam, meropenem, ceftriaxone/metronidazole OR FQ/metro
-Directed therapy:
—Streptococcus pyogenes, Clostridium spp. → penicillin + clindamycin** (suppresses toxin production)**
—Staphylococcus aureus → nafcillin or cefazolin (MSSA); vancomycin (MRSA)
—Aeromonas hydrophila → doxycycline + ciprofloxacin
—Vibrio vulnificus → doxycycline + ceftriaxone
-Therapy should be administered until further surgical debridement is no longer necessary, the patient has shown clinical improvement, and fever has been absent for 48-72 hours.

Question 35

diabetic foot infection overview

Answer 35

Infected foot ulcers are one of the most serious and devastating infections in diabetic patients, as they may lead to significant morbidity, hospitalization, osteomyelitis, and/or amputation.

Question 36

diabetic foot infection epidemiology

Answer 36

DFI are increasing in prevalence due to a larger number of patients with diabetes mellitus (DM), the increasing body weight of patients with DM, and the increasing longevity of patients.

Question 37

diabetic foot infection pathogenesis

Answer 37

Patients with diabetes are prone to the development of DFIs due to the presence of neuropathy, angiopathy with ischemia, immune system defects, and decreased wound healing. Patients with neuropathy experience a diminished sensation of pain so that they are often unaware of ulcers or traumatic injuries. A DFI occurs when the organisms invade the wound and cause tissue damage to illicit a host response.
increased blood glucose, decreased neutrophil fxn

Question 38

diabetic foot infections symptoms

Answer 38

Not all diabetic ulcers/wounds are infected. Infection is diagnosed based on the presence of at least 2 classic signs and symptoms of inflammation such as redness, warmth, swelling/induration, tenderness or pain (latter 2 may not be present in patient with significant neuropathy), and purulent secretions. Patients may also experience systemic signs and symptoms of infection depending on the extent of infection.

Question 39

diagnosis is diabetic foot infection

Answer 39

Wound Classification should be performed in all patients after necrotic tissue and surrounding callous have been debrided. - Positive probe to bone test may indicate osteomyelitis.
Laboratory – Elevated WBC, elevated ESR or C-reactive protein - Wound Culture – Only infected wounds should be cultured; deep wound cultures should be obtained after wound has been debrided and before empiric antibiotic therapy.
Radiographic – X-ray, MRI, or other imaging to determine the presence of osteomyelitis, if necessary.
Other tests: Once a DFI has been documented and classified, the affected limb and foot should be assessed for arterial ischemia* (ABIs), venous insufficiency, the presence of protective sensation, and biomechanical problems.

Question 40

bacteriology of diabetic foot infections

Answer 40

Depends on wound severity
Mild DFI → aerobic Gram positive cocci such as β-hemolytic Streptococci** and Staphylococcus aureus**
Moderate DFI → aerobic Gram positive cocci such as β- hemolytic Streptococci** and Staphylococcus aureus; also consider Enterobacteriaceae (not Pseudomonas aeruginosa) if on antibiotic therapy within the past 30 days; also consider obligate anaerobes if patient has a necrotic wound that has not been debrided
c. Severe DFI → aerobic Gram positive cocci such as β-hemolytic Streptococci** and Staphylococcus aureus** (including MRSA); Enterobacteriaeceae; Pseudomonas aeruginosa; and anaerobes**
d. MRSA – Prevalence in DFI ranges from 5 to 30%. Empiric therapy directed at MRSA should be considered in patients with a previous history of MRSA infection or colonization within the past year, in areas where the local prevalence is high and there is a reasonable probability of MRSA, and the infection is sufficiently severe that failing to empirically cover MRSA while waiting for culture results poses an unacceptable risk.
e. Pseudomonas aeruginosa – Recent studies of complicated SSTI (including DFI) have reported that P. aeruginosa is isolated in less than 10% of wounds. Empiric antibiotic therapy directed at P. aeruginosa should be considered in patients who have been soaking their feet, patients failing therapy without pseudomonal activity, and in patients with severe infection.
f. Obligate anaerobes – Isolated from many chronic, previously treated or severe infections; however, they are not thought to be major pathogens in most mild to moderate infections. There is limited evidence supporting the need for antibiotics with anaerobic activity in DFIs that have been adequately debrided.

Question 41

nonpharm treatment of diabetic foot infections

Answer 41

Overall management requires a multifaceted approach.

• The goal of therapy is to preserve limb function while limiting the spread of infection.*
• *Non-pharmacologic Treatment
• Appropriate wound care – debridement, appropriate dressing changes, off-loading, bed rest with elevation)
• Tight glycemic control
• Optimizing Blood flow – stents, revascularization, smoking cessation

Question 42

pharmacologic treatment

Answer 42

antibiotics alone are insufficient for management of DFI and must be combined with nonpharmacologic treatment
Clinically uninfected wounds should NOT be treated with antibiotic therapy.
Empiric antibiotic therapy* should be selected based on the severity of the infection, the likely causative pathogen(s), available microbiologic data including recent culture results/antibiotic use, and the local prevalence of pathogens (especially antibiotic-resistant strains).
-Mild DFI → Agents with relatively narrow spectrum that cover β-hemolytic Streptococci and Staphylococcus aureus such as PO Cephalexin, PO Dicloxacillin or PO Amoxicillin/Clavulanate
-Moderate DFI → Agents with relatively narrow spectrum that cover β-hemolytic Streptococci and Staphylococcus aureus such as IV Cefazolin; use IV ceftriaxone if Enterobacteriaceae suspected (previous antibiotic use within 30 days); add PO metronidazole if obligate anaerobes suspected (undebrided necrotic tissue)
-For mild to moderate DFI, empiric therapy directed at MRSA and/or P. aeruginosa is usually unnecessary except for patients with risk factors for true infection with these bacteria.
-Severe DFI → Broad-spectrum agents covering all possible bacteria (including MRSA and Pseudomonas aeruginosa) until culture and susceptibility results are available
Directed antibiotic therapy should be utilized based on the results of adequately-obtained cultures.

Question 43

minimum duration of therapy for diabetic foot infections

Answer 43

should be extended if patient
experiences a slow response to therapy***
Mild infections – 1 to 2 weeks
Moderate infections – 1 to 3 weeks
Severe infections – 2 to 4 weeks

Question 44

empiric therapy for mild diabetic foot infections**

Answer 44

description: Cellulitis extends less than 2 cm around ulcer, infection limited to skin/superficial tissue; patient without SIRS; Usually treated with PO antibiotics
likely causative organism: B-hemolytic Streptococcus** and/or Staphylococcus aureus** (MSSA unless patient has MRSA risk factors); MRSA suspected - Consider providing empiric therapy directed against MRSA in patients with a prior history of MRSA infection/colonization, when the local prevalence of MRSA is high, or in patients with severe infection
empiric therapy: PO Cephalexin or PO Dicloxacillin or PO Amoxicillin/clavulanate
MRSA suspected? PO Clindamycin or PO TMP/SMX

Question 45

empiric therapy for moderate diabetic foot infections**

Answer 45

Description: Cellulitis extending over 2 cm or involving structures deeper than skin/SC tissue (e.g., abscess, septic arthritis, osteomyelitis, fasciitis); patient without SIRS; May be treated with PO or initial IV therapy
Likely causative organism: B-hemolytic Streptococcus** and/or Staphylococcus aureus**
(MSSA unless patient has MRSA risk factors), Also consider Enterobacteriaceae** if on antibiotics within past 30 days (Consider providing empiric therapy against Pseudomonas aeruginosa in patients with frequent exposure of the foot to water, in patients who failed therapy with nonpseudomonal agents, or in patients with severe infection.), Also consider obligate anaerobes** if patient has necrotic wound that has not been debrided
empiric therapy: IV Cefazolin (or vancomycin if patient has MRSA risk factors: Consider providing empiric therapy directed against MRSA in patients with a prior history of MRSA infection/colonization, when the local prevalence of MRSA is high, or in patients with severe infection), Use IV ceftriaxone alone if Enterobacteriaceae suspected, Add PO metronidazole if anaerobes suspected

Question 46

empiric therapy for severe diabetic foot infections**

Answer 46

Description: Local infection with signs of SIRS manifested by ≥ 2 of the following: temp over 38°C or under 36°C, heart rate over 90 beats/min, respiratory rate over 20 breaths/min, WBC over 12,000 or under 4,000 cells/µL or over 10% immature (band) forms; Usually treated with IV therapy
Likely causative organism: β-hemolytic Streptococcus, Staphylococcus aureus (MSSA and MRSA), Enterobacteriaceae, P. aeruginosa, anaerobes
empiric therapy: Vancomycin PLUS Piperacillin/ tazobactam; meropenem; ceftazidime/cefepime with PO metronidazole; OR levofloxacin/ciprofloxacin with PO metronidazole