3 - Skin & Soft Tissue Infections Flashcards
(75 cards)
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)
2
Q
Most common pathogen of skin abscesses
A
Staph aureus (75% of cases)
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
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.)
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
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
7
Q
What are the antibiotic options for skin abscesses?
A
- Cephalexin *preferred for bioavailability
- Cloxacillin (poorer bioavailability)
- [Clindamycin] for severe beta lactam allergy
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
9
Q
When would you empirically treat for MRSA?
A
If pt has a risk factor
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
11
Q
What are the oral antimicrobial options for treating MRSA skin abscesses?
A
- Doxycycline or TMP-SMX
- [Clindamycin]
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
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
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
15
Q
Most common pathogen in impetigo?
A
Staph aureus (less commonly S. pyogenes)
16
Q
What will a gram stain reveal for staph aureus?
A
Gram pos cocci in clumps
17
Q
What will a gram stain reveal for strep pyogenes?
A
Gram pos cocci in chains
18
Q
What is used for non-bullous impetigo w/ low risk of complications?
A
Topical Mupirocin 2% applied BID x 5 days
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
20
Q
What are the oral antimicrobial options for MSSA impetigo?
A
- Cloxacillin or cephalexin
- [Clindamycin]
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)
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
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
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
25
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)
26
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
27
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)
28
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
29
Important adjuvant non-pharms for cellulitis
- Immobilization
- Elevation
- Cool and warm dressings
30
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
31
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
32
What is the IV alternative to amoxicillin?
Ampicillin
33
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
34
Is staph aureus or S. pyogenes more susceptible to antibiotics?
S. pyogenes
35
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
36
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)]
37
Antimicrobial options for empirically treating severe cellulitis w/ rapid progression, hypotension, or immunocompromised?
- Pip-tazo + vanco
- Meropenem + vanco
- +/- clinda
38
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)
39
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
40
What is significant about necrotizing cellulitis?
Reaches fascia
41
Describe type 1 necrotizing cellulitis
- Associated w/ surgery or trauma
| - Polymicrobial mixed infection w/ gram pos, gram neg, and anaerobes
42
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
43
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
44
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)
45
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
46
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
47
When is IVIG used in tx of necrotizing cellulitis?
- Px w/ toxic shock syndrome
| - Giving extra Ab's from donors against group A strep
48
How long does it take for a dog/cat bite wound to become infected?
Normally 2-3 days
49
What are the common pathogens in dog/cat bite wounds?
Pasteurella multicoda (GNCB), then S. aureus and oral anaerobes
50
What is the susceptibility of P multicoda?
- Typically susceptible to pen, doxy fluoroquinolones, TMP-SMX
- Resistant to 1st gen cephalosporins and clinda
51
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
52
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
53
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
54
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
55
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
56
What are the common pathogens of human bite wounds?
- Viridans group streptococci (over 80%)
- Eikinella corrodens
- Staph aureus, oral anaerobes
57
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
58
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
59
What is used for a severe human bite infection?
- Pip-tazo
- Ceftriaxone + metro
- (Cipro/ levo/ moxi) + (clinda/ metro) - severe beta lactam allergy
60
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
61
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
62
What are some important adjuvant non-pharms for DFIs?
- Glycemic control
- Wound care (debridement, dressing changes)
- Pressure relief, off-loading, elevation
63
What are the clinical features of DFIs?
- Erythema, swelling, warmth, purulent discharge
| - Little to no pain or systemic signs of infection
64
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
65
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
66
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)
67
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
68
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
69
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
70
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
71
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
72
Which antimicrobials cover bacteroides anaerobes?
- Metronidazole (best)
- Amox-clav or pip-tazo
- Clindamycin (not the best; good for oral anaerobes)
- Carbapenem
- Cefoxitin (only cephalosporin)
73
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
74
What should be considered when dosing for DFIs?
- Creatinine clearance
- If bone is involved
- Diabetes = immunocompromised, so would give higher dose
- Body weight
75
What are some antimicrobial-related factors that could explain tx failure in DFIs?
- Penetration to site of infection
- Necrotic tissue
- Resistance
