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Year 3 - Clinical > 3 - Skin & Soft Tissue Infections > Flashcards

3 - Skin & Soft Tissue Infections Flashcards

1
Q

What are the main types of skin abscesses?

A
  • Dermis and deeper structures, painful red nodules w/ overlying pustule and erythema
  • Furuncles (boils) in hair follicle
  • Carbuncles (collection of furuncles)
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2
Q

Most common pathogen of skin abscesses

A

Staph aureus (75% of cases)

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3
Q

What is a non-pharm for treating skin abscesses?

A

Drainage +/- moist heat compresses x 30 min applied 3-4x daily for small lesions, or surgical incision for larger lesions

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4
Q

Why are antimicrobials not often used for skin abscesses?

A

Can’t penetrate into the abscess and don’t work well in the environment of the abscess (anaerobic, low pH, etc.)

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5
Q

When are antimicrobials used for skin abscesses?

A
  • Abscess > 2 cm
  • Multiple lesions
  • Extensive cellulitis
  • Systemic signs of infection
  • Indwelling medical device (ex: catheter)
  • Immunocompromised
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6
Q

What are some common signs of infection?

A
  • Fever over 38 C
  • Tachypnea (shortness of breath) > 24/min
  • Tachycardia > 90/min
  • WBC > 12,000 or < 4,000 cells/uL
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7
Q

What are the antibiotic options for skin abscesses?

A
  • Cephalexin *preferred for bioavailability
  • Cloxacillin (poorer bioavailability)
  • [Clindamycin] for severe beta lactam allergy
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8
Q

What are some risk factors for an MRSA infection?

A
  • 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
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9
Q

When would you empirically treat for MRSA?

A

If pt has a risk factor

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10
Q

What is the significance of community-acquired MRSA compared w/ nosocomial infection?

A
  • 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
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11
Q

What are the oral antimicrobial options for treating MRSA skin abscesses?

A
  • Doxycycline or TMP-SMX

- [Clindamycin]

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12
Q

What are disadvantages to use of clindamycin?

A
  • Increasing resistance
  • Macrolide-resistance associated w/ increased risk of inducible clindamycin resistance developing during therapy
  • Highest risk of causing C. difficile infection
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13
Q

What are some severe reactions to a drug that would warrant not using it?

A
  • Anaphylaxis
  • Shortness of breath
  • Swelling of mucous membranes
  • Hives
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14
Q

Characteristics of impetigo

A
  • 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
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15
Q

Most common pathogen in impetigo?

A

Staph aureus (less commonly S. pyogenes)

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16
Q

What will a gram stain reveal for staph aureus?

A

Gram pos cocci in clumps

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17
Q

What will a gram stain reveal for strep pyogenes?

A

Gram pos cocci in chains

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18
Q

What is used for non-bullous impetigo w/ low risk of complications?

A

Topical Mupirocin 2% applied BID x 5 days

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19
Q

What are the oral antimicrobial options for empirically treating impetigo? Typical duration?

A
  • Cloxacillin or cephalexin (since not life threatening, difference in bioavailability isn’t really considered)
  • [Clindamycin]
  • Duration = 7 days
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20
Q

What are the oral antimicrobial options for MSSA impetigo?

A
  • Cloxacillin or cephalexin

- [Clindamycin]

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21
Q

What are the oral antimicrobial options for MRSA impetigo?

A
  • Doxycycline or TMP-SMX

- [Clindamycin] - for children (contraindication to doxy) w/ a sulfa allergy (contraindication to TMP-SMX)

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22
Q

What are the oral antimicrobial options for S. pyogenes?

A
  • Pen V or amoxicillin (amox has better kinetics and palatability but pen V has less adverse effects)
  • [Clindamycin] - severe beta lactam allergy
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23
Q

What is cellulitis?

A
  • 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
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24
Q

What is the difference between erysipelas and cellulitis?

A

Erysipelas is synonymous w/ cellulitis, but often superficial involving upper dermis or superficial lymphatics w/ more delineated borders

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25
Q

Where on the body does cellulitis commonly occur and what are the most common pathogens?

A
  • 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)
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26
Q

What is the clinical presentation of cellulitis?

A
  • 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
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27
Q

What are the differential diagnoses of cellulitis?

A
  • Stasis dermatitis (bilateral, venous insufficiency, pitting edema, hyperpigmentation)
  • Contact dermatitis (pruritic)
  • Gout (severe pain, single joint swelling)
  • DVT (risk factors, calf pain)
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28
Q

Risk factors for cellulitis

A
  • Skin disruption (abrasion, insect bite, ulcer, wound, trauma, IVDU) or inflammation (eczema, radiation)
  • Lymphatic obstruction
  • Advanced age, obesity
  • Peripheral vascular disease, diabetes mellitus
  • Immunocompromised
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29
Q

Important adjuvant non-pharms for cellulitis

A
  • Immobilization
  • Elevation
  • Cool and warm dressings
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30
Q

What should be considered when choosing oral vs. IV antimicrobials for cellulitis tx?

A
  • Severity of cellulitis based on location, area of involvement, and progression
  • Systemic signs of infection
  • Oral tolerability
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31
Q

Antimicrobial options for empirically treating non-purulent (mild) cellulitis w/ suspect S. pyogenes? Would it be oral or IV?

A
  • Oral
  • Pen V or amoxicillin
  • [Clinda] severe beta lactam allergy
32
Q

What is the IV alternative to amoxicillin?

A

Ampicillin

33
Q

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?

A
  • Can be either oral or IV
  • Cloxacillin (IV)
  • Cephalexin (po) or cefazolin (IV)
  • [Clinda (po or IV)] severe beta lactam allergy
34
Q

Is staph aureus or S. pyogenes more susceptible to antibiotics?

A

S. pyogenes

35
Q

Antimicrobial options for empirically treating purulent (mild to moderate) cellulitis w/ suspect MRSA +/- S. pyogenes? Would it be oral or IV?

A
  • Oral
  • Doxy + (pen or amox)
  • TMP-SMX + (pen or amox)
  • Pen or amox are added to cover strep
36
Q

Antimicrobial options for empirically treating purulent (moderate to severe) cellulitis w/ suspect MRSA +/- S. pyogenes? Would it be oral or IV?

A
  • IV
  • Vanco
  • [Linezolid (IV or po)] - vanco intolerance or tx failure
  • [Daptomycin (IV)]
37
Q

Antimicrobial options for empirically treating severe cellulitis w/ rapid progression, hypotension, or immunocompromised?

A
  • Pip-tazo + vanco
  • Meropenem + vanco
  • +/- clinda
38
Q

What is the typical response and duration of therapy for uncomplicated cellulitis?

A
  • 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)
39
Q

Why aren’t fluoroquinolones used for uncomplicated SSTIs?

A

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

40
Q

What is significant about necrotizing cellulitis?

A

Reaches fascia

41
Q

Describe type 1 necrotizing cellulitis

A
  • Associated w/ surgery or trauma

- Polymicrobial mixed infection w/ gram pos, gram neg, and anaerobes

42
Q

Describe type 2 necrotizing cellulitis

A
  • “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
43
Q

Describe type 3 necrotizing cellulitis

A
  • Associated w/ clostridium perfringens (trauma, surgery), C. septicum (spontaneous), and C. sordellii (gynaecological)
  • Very rapid progression w/ gas production and myonecrosis
44
Q

What is the tx approach for necrotizing cellulitis?

A
  • Emergency surgery for inspection, debridement, and wound cultures
  • Empirical broad spectrum antimicrobial therapy (pip-tazo + vanco; meropenem + vanco; +/- clinda)
45
Q

What are the antimicrobial options for pathogen-directed tx of necrotizing cellulitis?

A
  • 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
46
Q

Why is clinda added to the tx of necrotizing cellulitis?

A
  • 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
47
Q

When is IVIG used in tx of necrotizing cellulitis?

A
  • Px w/ toxic shock syndrome

- Giving extra Ab’s from donors against group A strep

48
Q

How long does it take for a dog/cat bite wound to become infected?

A

Normally 2-3 days

49
Q

What are the common pathogens in dog/cat bite wounds?

A

Pasteurella multicoda (GNCB), then S. aureus and oral anaerobes

50
Q

What is the susceptibility of P multicoda?

A
  • Typically susceptible to pen, doxy fluoroquinolones, TMP-SMX
  • Resistant to 1st gen cephalosporins and clinda
51
Q

When is prophylaxis given for dog/cat bite wounds and for how long?

A
  • Given for high risk wounds (moderate to severe bite, on face, on hands involving joints, immunocompromised)
  • Given for 3-5 days
52
Q

What is the antimicrobial therapy given for dog/cat bite wounds and for how long?

A
  • 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
53
Q

What is the antimicrobial therapy given for severe dog/cat bite wounds?

A
  • Pip-tazo
  • Ceftriaxone + metro
  • (Cipro/ levo/ moxi) + (clinda or metro) – severe beta lactam allergy
54
Q

What are some additional considerations for dog/cat bite wounds other than antimicrobials?

A
  • 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
55
Q

Describe cat scratch disease, the pathogen, and the antimicrobial tx

A
  • 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
56
Q

What are the common pathogens of human bite wounds?

A
  • Viridans group streptococci (over 80%)
  • Eikinella corrodens
  • Staph aureus, oral anaerobes
57
Q

What is the prophylaxis for human bite wounds?

A

Amox-clav x 3-5 days to prevent infection of high-risk wounds from bites that penetrate dermis

58
Q

What is the tx for human bite wounds? Duration?

A
  • Amox-clav (po) 875/125 mg q12h or 20 mg/kg amox component q12h for children
  • Alternatives = same as dog/cat bite wounds
59
Q

What is used for a severe human bite infection?

A
  • Pip-tazo
  • Ceftriaxone + metro
  • (Cipro/ levo/ moxi) + (clinda/ metro) - severe beta lactam allergy
60
Q

What else should be considered for a human bite wound besides antimicrobials?

A
  • Tetanus toxoid (Tdap) if not vaccinated w/in 10 years

- Risk assessment for hepatitis, HIV transmission

61
Q

What are some diabetes-related factors that increase the risk of DFIs?

A
  • Angiopathy w/ peripheral vascular disease and ischemia
  • Neuropathy w/ sensory, motor, autonomic dysfunction
  • Immune dysfunction
  • Poor vision
62
Q

What are some important adjuvant non-pharms for DFIs?

A
  • Glycemic control
  • Wound care (debridement, dressing changes)
  • Pressure relief, off-loading, elevation
63
Q

What are the clinical features of DFIs?

A
  • Erythema, swelling, warmth, purulent discharge

- Little to no pain or systemic signs of infection

64
Q

What are the classifications of DFIs?

A
  • 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
65
Q

What are the most common pathogens in DFIs?

A
  • 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
66
Q

What are some complications of DFIs?

A
  • 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)
67
Q

What should be considered when initiating antimicrobial therapy for DFIs?

A
  • Infected wound vs. colonized ulcer
  • Adequate wound debridement and care
  • Severity of infection and clinical status
  • Bone involvement
  • Risk factors for antimicrobial resistance
68
Q

What are some risk factors for antimicrobial resistance?

A
  • Chronic infections
  • Repeat antimicrobial exposure
  • Low antimicrobial concentrations at infection site
  • Multi-drug resistant pathogens that limit options for antimicrobial therapy
69
Q

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?

A
  • Given PO
  • Cloxacillin (+/- doxy or TMP-SMX)
  • Cephalexin (+/- doxy or TMP-SMX) – preferred for better PO absorption
  • [Clinda]
  • Duration = >/ 1-2 weeks
70
Q

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?

A
  • Given PO but may require initial IV therapy
  • Amox-clav (+/- doxy or TMP-SMX)
  • [Clinda] + (cipro/ levo/ moxi)
  • Duration = >/ 2 weeks
71
Q

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?

A
  • 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
72
Q

Which antimicrobials cover bacteroides anaerobes?

A
  • Metronidazole (best)
  • Amox-clav or pip-tazo
  • Clindamycin (not the best; good for oral anaerobes)
  • Carbapenem
  • Cefoxitin (only cephalosporin)
73
Q

Which antimicrobials cover pseudomonas?

A
  • Pip-tazo
  • Aminoglycosides
  • Carbapenems (not ertapenem)
  • Quinolones (cipro and levo) – only 2 oral options, but either must be combined w/ clinda
  • Ceftazidime
74
Q

What should be considered when dosing for DFIs?

A
  • Creatinine clearance
  • If bone is involved
  • Diabetes = immunocompromised, so would give higher dose
  • Body weight
75
Q

What are some antimicrobial-related factors that could explain tx failure in DFIs?

A
  • Penetration to site of infection
  • Necrotic tissue
  • Resistance

Year 3 - Clinical (30 decks)

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