3 - Skin & Soft Tissue Infections Flashcards
What are the main types of skin abscesses?
- Dermis and deeper structures, painful red nodules w/ overlying pustule and erythema
- Furuncles (boils) in hair follicle
- Carbuncles (collection of furuncles)
Most common pathogen of skin abscesses
Staph aureus (75% of cases)
What is a non-pharm for treating skin abscesses?
Drainage +/- moist heat compresses x 30 min applied 3-4x daily for small lesions, or surgical incision for larger lesions
Why are antimicrobials not often used for skin abscesses?
Can’t penetrate into the abscess and don’t work well in the environment of the abscess (anaerobic, low pH, etc.)
When are antimicrobials used for skin abscesses?
- Abscess > 2 cm
- Multiple lesions
- Extensive cellulitis
- Systemic signs of infection
- Indwelling medical device (ex: catheter)
- Immunocompromised
What are some common signs of infection?
- Fever over 38 C
- Tachypnea (shortness of breath) > 24/min
- Tachycardia > 90/min
- WBC > 12,000 or < 4,000 cells/uL
What are the antibiotic options for skin abscesses?
- Cephalexin *preferred for bioavailability
- Cloxacillin (poorer bioavailability)
- [Clindamycin] for severe beta lactam allergy
What are some risk factors for an MRSA infection?
- MRSA colonized or close contact of MRSA infection
- Previous antimicrobials or S. aureus infection particularly if tx failure w/ regimen lacking MRSA coverage
- Medical procedures
- Chronic dialysis
- Hospitalization
- ICU admission
- Resident of long-term care facility
When would you empirically treat for MRSA?
If pt has a risk factor
What is the significance of community-acquired MRSA compared w/ nosocomial infection?
- Contagion among close contacts (ex: childcare centres, athletic facilities) and IV drug users
- Increasing prevalence
- Generally more susceptible to other antimicrobials
- Associated w/ SSTI in 75% of cases
What are the oral antimicrobial options for treating MRSA skin abscesses?
- Doxycycline or TMP-SMX
- [Clindamycin]
What are disadvantages to use of clindamycin?
- Increasing resistance
- Macrolide-resistance associated w/ increased risk of inducible clindamycin resistance developing during therapy
- Highest risk of causing C. difficile infection
What are some severe reactions to a drug that would warrant not using it?
- Anaphylaxis
- Shortness of breath
- Swelling of mucous membranes
- Hives
Characteristics of impetigo
- Highest incidence in children 2-5 y/o
- Superficial infection of epidermis
- 90% non-bullous/ crusty scabs (S. aureus, S. pyogenes); 10% bullous/ blisters (S. aureus)
- Pruritus w/ mild to moderate erythema
Most common pathogen in impetigo?
Staph aureus (less commonly S. pyogenes)
What will a gram stain reveal for staph aureus?
Gram pos cocci in clumps
What will a gram stain reveal for strep pyogenes?
Gram pos cocci in chains
What is used for non-bullous impetigo w/ low risk of complications?
Topical Mupirocin 2% applied BID x 5 days
What are the oral antimicrobial options for empirically treating impetigo? Typical duration?
- Cloxacillin or cephalexin (since not life threatening, difference in bioavailability isn’t really considered)
- [Clindamycin]
- Duration = 7 days
What are the oral antimicrobial options for MSSA impetigo?
- Cloxacillin or cephalexin
- [Clindamycin]
What are the oral antimicrobial options for MRSA impetigo?
- Doxycycline or TMP-SMX
- [Clindamycin] - for children (contraindication to doxy) w/ a sulfa allergy (contraindication to TMP-SMX)
What are the oral antimicrobial options for S. pyogenes?
- Pen V or amoxicillin (amox has better kinetics and palatability but pen V has less adverse effects)
- [Clindamycin] - severe beta lactam allergy
What is cellulitis?
- Diffuse, superficial skin infection of epidermis and dermis that can extend to cutaneous lymphatics and subcutaneous fat
- Purulence may be present, but more consistent w/ skin abscesses
What is the difference between erysipelas and cellulitis?
Erysipelas is synonymous w/ cellulitis, but often superficial involving upper dermis or superficial lymphatics w/ more delineated borders
Where on the body does cellulitis commonly occur and what are the most common pathogens?
- Lower (90%) or upper extremities or face
- S. pyogenes and other beta-hemolytic streptococcus including Group B, C, F or G
- Less commonly staph aureus (typically associated w/ purulence, abscess, wound, trauma)
What is the clinical presentation of cellulitis?
- Orange-peel-like appearance, vesicles, bullae, petechiae (hemorrhages under the skin) or ecchymoses (bruising)
- Phlebitis (inflammation of vein) or lymphangitis (streaking)
- Local pain, erythema, warmth, edema, +/- systemic signs of infection
What are the differential diagnoses of cellulitis?
- Stasis dermatitis (bilateral, venous insufficiency, pitting edema, hyperpigmentation)
- Contact dermatitis (pruritic)
- Gout (severe pain, single joint swelling)
- DVT (risk factors, calf pain)
Risk factors for cellulitis
- Skin disruption (abrasion, insect bite, ulcer, wound, trauma, IVDU) or inflammation (eczema, radiation)
- Lymphatic obstruction
- Advanced age, obesity
- Peripheral vascular disease, diabetes mellitus
- Immunocompromised
Important adjuvant non-pharms for cellulitis
- Immobilization
- Elevation
- Cool and warm dressings
What should be considered when choosing oral vs. IV antimicrobials for cellulitis tx?
- Severity of cellulitis based on location, area of involvement, and progression
- Systemic signs of infection
- Oral tolerability
Antimicrobial options for empirically treating non-purulent (mild) cellulitis w/ suspect S. pyogenes? Would it be oral or IV?
- Oral
- Pen V or amoxicillin
- [Clinda] severe beta lactam allergy
What is the IV alternative to amoxicillin?
Ampicillin
Antimicrobial options for empirically treating non-purulent (moderate to severe) or purulent cellulitis w/ suspect S. pyogenes or S. aureus? Would it be oral or IV?
- Can be either oral or IV
- Cloxacillin (IV)
- Cephalexin (po) or cefazolin (IV)
- [Clinda (po or IV)] severe beta lactam allergy
Is staph aureus or S. pyogenes more susceptible to antibiotics?
S. pyogenes
Antimicrobial options for empirically treating purulent (mild to moderate) cellulitis w/ suspect MRSA +/- S. pyogenes? Would it be oral or IV?
- Oral
- Doxy + (pen or amox)
- TMP-SMX + (pen or amox)
- Pen or amox are added to cover strep
Antimicrobial options for empirically treating purulent (moderate to severe) cellulitis w/ suspect MRSA +/- S. pyogenes? Would it be oral or IV?
- IV
- Vanco
- [Linezolid (IV or po)] - vanco intolerance or tx failure
- [Daptomycin (IV)]
Antimicrobial options for empirically treating severe cellulitis w/ rapid progression, hypotension, or immunocompromised?
- Pip-tazo + vanco
- Meropenem + vanco
- +/- clinda
What is the typical response and duration of therapy for uncomplicated cellulitis?
- Response = clinical improvement w/in 24-48h, visible improvement may be delayed 72 h
- Duration = 5 days (up to 14 days for severe infection, slow response, or immunocompromised)
Why aren’t fluoroquinolones used for uncomplicated SSTIs?
Aren’t used for staph or strep infections b/c although the body may seem susceptible in the first few days, it can quickly gain resistance
What is significant about necrotizing cellulitis?
Reaches fascia
Describe type 1 necrotizing cellulitis
- Associated w/ surgery or trauma
- Polymicrobial mixed infection w/ gram pos, gram neg, and anaerobes
Describe type 2 necrotizing cellulitis
- “Flesh-eating” bacteria
- Caused by virulent S. pyogenes or less commonly staph aureus, aeromonas hydrophila, or vibrio vulnificus
- Very rapid progression w/ severe systemic signs of infection including septic shock
- Only diagnosed through surgery
Describe type 3 necrotizing cellulitis
- Associated w/ clostridium perfringens (trauma, surgery), C. septicum (spontaneous), and C. sordellii (gynaecological)
- Very rapid progression w/ gas production and myonecrosis
What is the tx approach for necrotizing cellulitis?
- Emergency surgery for inspection, debridement, and wound cultures
- Empirical broad spectrum antimicrobial therapy (pip-tazo + vanco; meropenem + vanco; +/- clinda)
What are the antimicrobial options for pathogen-directed tx of necrotizing cellulitis?
- IV treatment
- S. pyogens or clostridium species = Pen G + clinda
- A. hydrophila (fresh water) = Doxy + (cipro or ceftriaxone, as per susceptibilities)
- V. vulnificus = doxy + ceftriaxone
Why is clinda added to the tx of necrotizing cellulitis?
- Clinda reduces function of ribosomes in the cells (static) and penicillin attacks cell walls (cidal)
- Toxins are proteins, so clinda winds down production of exotoxin so when penicillin goes in and rapidly kills it and cells burst, the toxin load being released is reduced
- Staph aureus and strep pyogenes are most common associated w/ toxic shock syndrome
When is IVIG used in tx of necrotizing cellulitis?
- Px w/ toxic shock syndrome
- Giving extra Ab’s from donors against group A strep
How long does it take for a dog/cat bite wound to become infected?
Normally 2-3 days
What are the common pathogens in dog/cat bite wounds?
Pasteurella multicoda (GNCB), then S. aureus and oral anaerobes
What is the susceptibility of P multicoda?
- Typically susceptible to pen, doxy fluoroquinolones, TMP-SMX
- Resistant to 1st gen cephalosporins and clinda
When is prophylaxis given for dog/cat bite wounds and for how long?
- Given for high risk wounds (moderate to severe bite, on face, on hands involving joints, immunocompromised)
- Given for 3-5 days
What is the antimicrobial therapy given for dog/cat bite wounds and for how long?
- Amox-clav (po) 875/125 mg q12h, children 20 mg/kg amox component q12h
- Alternatives
- Doxy + (clinda or metro)
- (Cipro/ levo/ moxi) + (clinda or metro)
- TMP-SMX + (clinda or metro)
- Macrolide/ azolide (if susceptible Pasteurella) + clinda (in children & pregnancy)
- Given 5-10 days to treat infections or 4-6 weeks for septic arthritis or osteomyelitis
What is the antimicrobial therapy given for severe dog/cat bite wounds?
- Pip-tazo
- Ceftriaxone + metro
- (Cipro/ levo/ moxi) + (clinda or metro) – severe beta lactam allergy
What are some additional considerations for dog/cat bite wounds other than antimicrobials?
- Tetanus toxoid (Tdap) if not vaccinated w/in 10 years + tetanus IG if <2 primary immunizations
- Risk assessment for rabies; post-exposure prohylaxis w/ hyper-immune globulin (40 IU/kg) in & around wound and series of 5 vaccinations over 28 days
Describe cat scratch disease, the pathogen, and the antimicrobial tx
- Papule or pustule w/ lymphadenopathy w/in 3-30 days
- Bartonella henselae (gram neg)
- Azithromycin (PO) 500 mg x1 the 250 mg q24h x4 days
What are the common pathogens of human bite wounds?
- Viridans group streptococci (over 80%)
- Eikinella corrodens
- Staph aureus, oral anaerobes
What is the prophylaxis for human bite wounds?
Amox-clav x 3-5 days to prevent infection of high-risk wounds from bites that penetrate dermis
What is the tx for human bite wounds? Duration?
- Amox-clav (po) 875/125 mg q12h or 20 mg/kg amox component q12h for children
- Alternatives = same as dog/cat bite wounds
What is used for a severe human bite infection?
- Pip-tazo
- Ceftriaxone + metro
- (Cipro/ levo/ moxi) + (clinda/ metro) - severe beta lactam allergy
What else should be considered for a human bite wound besides antimicrobials?
- Tetanus toxoid (Tdap) if not vaccinated w/in 10 years
- Risk assessment for hepatitis, HIV transmission
What are some diabetes-related factors that increase the risk of DFIs?
- Angiopathy w/ peripheral vascular disease and ischemia
- Neuropathy w/ sensory, motor, autonomic dysfunction
- Immune dysfunction
- Poor vision
What are some important adjuvant non-pharms for DFIs?
- Glycemic control
- Wound care (debridement, dressing changes)
- Pressure relief, off-loading, elevation
What are the clinical features of DFIs?
- Erythema, swelling, warmth, purulent discharge
- Little to no pain or systemic signs of infection
What are the classifications of DFIs?
- Mild - superficial skin w/ erythema <2 cm, swelling, heat or pain; no systemic signs of infection; likely staph or strep
- Moderate - deep localized w/ erythema >2 cm, abscess, fasciitis, septic arthritis or osteomyelitis; no systemic signs of infection; likely staph or strep
- Severe - systemic signs of infection; likely polymicrobial
What are the most common pathogens in DFIs?
- Superficial, acute cellulitis and/or infected ulcer NOT treated w/ antimicrobials in previous month = strep, staph
- Deep, chronic infected ulcer and/or treated in previous month or previous hospitalization = mixed, polymicrobial w/ gram pos (staph, strep), gram neg (proteus, E. coli) and anaerobes, particular if necrotic or gangrenous
What are some complications of DFIs?
- 20% of diabetes related hospitalizations
- Contiguous spread to joints (septic arthritis) or bone (osteomyelitis)
- Amputation (10-20% at 1 year; 25-50% at 5 years)
What should be considered when initiating antimicrobial therapy for DFIs?
- Infected wound vs. colonized ulcer
- Adequate wound debridement and care
- Severity of infection and clinical status
- Bone involvement
- Risk factors for antimicrobial resistance
What are some risk factors for antimicrobial resistance?
- Chronic infections
- Repeat antimicrobial exposure
- Low antimicrobial concentrations at infection site
- Multi-drug resistant pathogens that limit options for antimicrobial therapy
What are the antimicrobial options to empirically treat mild, acute DFI w/ suspected gram pos pathogen? Is it given PO or IV? What is the duration?
- Given PO
- Cloxacillin (+/- doxy or TMP-SMX)
- Cephalexin (+/- doxy or TMP-SMX) – preferred for better PO absorption
- [Clinda]
- Duration = >/ 1-2 weeks
What are the antimicrobial options to empirically treat moderate, acute or chronic DFI w/ suspected polymicrobial pathogen? Is it given PO or IV? What is the duration?
- Given PO but may require initial IV therapy
- Amox-clav (+/- doxy or TMP-SMX)
- [Clinda] + (cipro/ levo/ moxi)
- Duration = >/ 2 weeks
What are the antimicrobial options to empirically treat severe, chronic, extensive DFI w/ suspected polymicrobial pathogen? Is it given PO or IV? What is the duration?
- Given IV
- Pip-tazo
- Meropenem
- Ceftriaxone + metro (preferred b/c ceftriaxone has long t1/2 and only needs q24h dosing)
- Ceftazidime + metro
- Severe beta lactam allergy = moxi (po); cipro/ levo + metro (po)
- Duration = >/ 2-4 weeks
Which antimicrobials cover bacteroides anaerobes?
- Metronidazole (best)
- Amox-clav or pip-tazo
- Clindamycin (not the best; good for oral anaerobes)
- Carbapenem
- Cefoxitin (only cephalosporin)
Which antimicrobials cover pseudomonas?
- Pip-tazo
- Aminoglycosides
- Carbapenems (not ertapenem)
- Quinolones (cipro and levo) – only 2 oral options, but either must be combined w/ clinda
- Ceftazidime
What should be considered when dosing for DFIs?
- Creatinine clearance
- If bone is involved
- Diabetes = immunocompromised, so would give higher dose
- Body weight
What are some antimicrobial-related factors that could explain tx failure in DFIs?
- Penetration to site of infection
- Necrotic tissue
- Resistance