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Clinical 2 - Antibiotics > 3 - Skin & Soft Tissue Infections > Flashcards

3 - Skin & Soft Tissue Infections Flashcards

1
Q

What is an abscess?

A
  • pocket
  • contained
  • has fluid, inflammatory cells, could have bacteria
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2
Q

Describe the main types of skin abscesses

A
  • In dermis and deeper structures, painful red nodule with erythema; furuncles (boils) in hair follicle, inflammatory nodule with overlying pustule collection in dermis and deeper structures; carbuncles includes collection of furuncles
  • Most commonly back in neck, face, axillae
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3
Q

What is the most common pathogen of Skin Abscesses?

A

S. aureus (75% of cases)

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4
Q

What is the approach for treatment of a skin abscess?

A

1) Drainage +/- moist heat compresses x 30 min, 3-4 x daily for small lesions or surgical incision and drainage for larger lesions
2) Antimicrobial therapy for abscesses > 2 cm, multiple lesions, extensive cellulitis, systemic signs of infection, indwelling medical device or immunocompromised

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5
Q

What are systemic signs of infection?

A

temp > 38, tachypnea > 24/min, tachycardia > 90/min, WBC > 12000 or < 4000

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6
Q

What are the 2 antibiotics for 1st line therapy for Skin Abscesses ?

A

Cloxacillin

Cephalexin

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7
Q

What is 2nd line therapy for Skin Abscesses if they have a severe B lactam allergy?

A

Clindamycin

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8
Q

List 2 important points about Clindamycin

A
  • # 1 antibiotic associated with C. dif

- We are seeing increasing resistance in S. aureus

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9
Q

What would indicate a severe B lactam allergy?

A
  • anaphylaxis
  • severe rash
  • hives
  • angioedema (swelling of tongue, lips, face)
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10
Q

What are the risk factors for skin abscesses being MRSA?

A
  • MRSA colonization
  • close contact with MRSA infection
  • previous antimicrobials or S. aureus infection particularly if treatment failure with regimen that lacked MRSA coverage
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11
Q

When is CA-MRSA prevalent?

A

CA-MRSA contagion among close contacts in sites such as childcare centres and athletic facilities.

Increasing prevalence from 13% to >30% of CA-MRSA over recent years in Canada; 75% SSTIs

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12
Q

When is HCA-MRSA prevalent?

A

HCA-MRSA with medical procedures, dialysis, hospitalization, long-term care facilities; higher antimicrobial resistance rates than CA strains

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13
Q

What is MRSA resistant to?

A
  • penicillins
  • cephalosporins
  • carbapenems

(methicillin = penicillin, so they are resistant to anything with a B lactam ring)

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14
Q

What treatment do you chose for a CA-MRSA skin abscess?

A
  • Clindamycin
  • Doxycycline
  • TMP-SMX
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15
Q

Why would you not chose clindamycin for CA-MRSA?

A

**If macrolide-resistant, increased risk of inducible clindamycin resistance developing during therapy

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16
Q

Explain an approach to managing patients with recurrent furuncles or carbuncles

A

S. aureus lives in the nose

  • Try decolonizing the nose with:
  • Mupirocin 2% 2-3 times daily x 5 days every month
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17
Q

GAS

A

Group A Strep Pyogenes

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18
Q

Gram positive cocci in clumps

A

Staph

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19
Q

Gram positive cocci in chains

A

Strep

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20
Q

Impetigo:

Highest incidence in ?

A

Children 2-5 years old

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21
Q

What is Impetigo?

A
  • Superficial infection of the epidermis

- Pruritis with mild to moderate erythema

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22
Q

Impetigo:

___% non-bullous

A

90

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23
Q

Impetigo:

___% bullous

A

10

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24
Q

Impetigo:

Which form is more severe?

A

bullous

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25
Q

Impetigo:

What bugs cause non-bullous form?

A

S. aureus

S. pyogenes

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26
Q

Impetigo:

What bugs cause bullous form?

A

S. aureus

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27
Q

Impetigo:

Most common pathogen?

A

S. aureus or less common S. progenies (B-hemolytic Group A Streptococcus - GAS)

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28
Q

Impetigo:

Is antimicrobial therapy always indicated?

A

Yes:

  • For sure in moderate-severe non-bullous and bullous infections - should get oral AB
  • For mild, non-bullous infections often resolve spontaneously within weeks, however antimicrobial therapy reduces transmission, hastens symptoms and progression, prevents complications
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29
Q

Impetigo:
What is the treatment for non-bullous mild infections with limited area and number of lesions and low risk of complications?

*Hint - topical therapy

A

Mupirocin 2% applied twice daily x 5 days

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30
Q

MOA of Mupirocin?

A

monoxycarbolic acid inhibits RNA synthesis, more effective than alternatives (neomycin, polymyxin B, bacitracin, gentamicin) *increasing resistance to fusidic acid

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31
Q

What are the oral AB options for treating more serious cases of Impetigo?

A

Cloxacillin

Cephalexin

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32
Q

What is recommended if they have severe B lactam allergy?

A

Clindamycin

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33
Q

Impetigo:

Duration of oral AB therapy?

A

7 days

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34
Q

Impetigo:

What is the treatment for MSSA?

A

Cloxacillin or Cephalexin

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35
Q

Impetigo:
What is the treatment for MSSA if they have a severe B lactam allergy?

*Why don’t you use Doxy or TMP-SMX here?

A

Clindamycin

*Doxy and TMP-SMX do not cover Strep

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36
Q

Impetigo:

What is the treatment for MRSA?

A
  • Clinda
  • Doxy
  • TMP-SMX

*I guess you can use Doxy or TMP-SMX here because you know for sure it’s only Staph ????

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37
Q

Impetigo:

What is the treatment for S. pyogenes?

A
  • Pen V

- Amox

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38
Q

Impetigo:

What is the treatment for S. pyogenes if they have a severe B lactam allergy?

A

Clindamycin

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39
Q

Compare Clinda, Doxy and TMP-SMX?

A

Clinda:

  • lower susceptibility
  • highest incidence of C. dif

Doxy:

  • can’t be used in children or pregnancy
  • does not cover streptococcus

TMP-SMX:

  • does not cover streptococcus
  • high rate of adverse effects (allergy, hypersensitivity, rashes)
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40
Q

Compare Pen and Amox

A

Amox:

  • broader coverage
  • preferred in kids bc it tastes better than Pen

Pen:

  • QID
  • bitter taste
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41
Q

Describe Cellulitis

A

-Diffuse, superficial skin infection of epidermis and dermis that can extend to cutaneous lymphatics and subcutaneous fat

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42
Q

________ synonymous with cellulitis

A

erysipelas

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43
Q

Cellulitis:

Although purulence may be present, purulent discharge or pus is more consistent with ??

A

skin abscesses

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44
Q

Cellulitis:

Typically involves ______ (90% of cases) or upper extremities or face.

A

lower

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45
Q

Cellulitis:

Most common pathogen?

A

Strep pyogenes, less commonly S. aureus (typically associated with purulence, abscess, wound, trauma)

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46
Q

Describe the clinical presentation of cellulitis

A

-Orange-peel-like, vesicles, bull, petechiae or ecchymoses (discolouration of skin), phlebitis or lymphangitis (streaking)

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47
Q

What kind of symptoms (other than appearance) are associated with cellulitis

A
  • local pain
  • erythema
  • warmth
  • edema +/- systemic signs of infection (fever, chills, malaise)
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48
Q

Cellulitis:

How do you differentiate from contact dermatitis?

A

-contact dermatitis is pruritic

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49
Q

Cellulitis:

How do you differentiate from gout?

A

-gout has severe pain, single joint swelling

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50
Q

Cellulitis:

How do you differentiate from DVT?

A

-risk factors, calf pain

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51
Q

Cellulitis:
How do you differentiate from
stasis dermatitis?

A

-bilateral, venous insufficiency, pitting edema, hyper pigmentation

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52
Q

Cellulitis:

Risk factors?

A
  • skin disruption (abrasion, insect bite, ulcer)
  • inflammation (eczema, radiation)
  • advanced age
  • obesity
  • DM
  • Immunocompromised
  • PVD
  • lymphatic obstruction
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53
Q

Cellulitis:

Non-pharms

A
  • immobilization
  • elevation
  • cool and warm dressings
54
Q

_____ is used only in COMBO

A

Rifampin

*has a lot of SE and DI (drug interactions) too

55
Q

Why is Rifampin only used in combo?

A

When used alone - leads to RESISTANCE

56
Q

______ decrease vitamin K production and therefore increase bleeding with someone on anticoagulants

A

Antibiotics

57
Q

_______ interacts with warfarin and and spironolactone (increases K+ levels)

A

TMP-SMX

58
Q

What factors are considered in selecting PO versus IV antimicrobials for treating cellulitis?

A
  • severity of cellulitis based on location, area, progression
  • systemic signs of infection (fever, chills, confusion)
  • PO tolerability
59
Q

What is the treatment for Mild cellulitis? (remember you suspect S. pyogenes)

A

Pen V

Amox

60
Q

What is the treatment for Mild cellulitis if they have a B lactic allergy? (remember you suspect S. pyogenes)

A

Clindamycin

61
Q

Why is Doxy or TMP-SMX not a good choice for mild cellulitis?

A

they lack strep coverage !! (not effective for cellulitis at all then)

62
Q

How is staph resistant to penicillin?

A

Staph learned very quickly to produce beta lactamses so penicillin was not effective against Staph

63
Q

Why is cloxacillin effective against staph then?

A

Bc cloxacillin is penicillase stable (it has a stable ring)

64
Q

What is the treatment for moderate-severe cellulitis?

Remember you suspect S. progenies and/or MSSA

A

Cloxacillin (po)

Cephalexin (po) or Cefazolin (iv)

65
Q

Why can’t you give penicillin or amoxicillin for moderate-severe cellulitis?

A

Bc if you prescribe pen or amox and the bug turns out to be Staph, Pen/Amox will not kill it.

*in this scenario, you need something that will target strep and staph

66
Q

What is the treatment for moderate-severe cellulitis if they have a severe B lactam allergy?

A

Clindamycin

67
Q

What is the treatment for moderate cellulitis (Suspect S. pyogenes or MRSA)

A
  • Clindamycin
  • Doxy + (Pen or Amox) for strep coverage
  • TMP-SMX + (Pen or Amox) for strep coverage
68
Q

What are some risk factors for getting MRSA?

A
  • MRSA colonization
  • close contact with MRSA infection, previous antimicrobials or S aureus infection particularly if treatment failure with regimen that lacked MRSA coverage
69
Q

What is the treatment for severe cellulitis (suspect S. pyogenes or MRSA)

A

Vancomycin

70
Q

What is the treatment for severe cellulitis (suspect S. pyogenes or MRSA) if Vanco intolerance or treatment failure?

A
  • Linezolid

- Daptomycin

71
Q

Despite an approved indication for treating uncomplicated SSTIs, what are the potential disadvantages of using Levo or Moxi ??

A
  • less effective than alternatives due to unreliable streptococcal and staphylococcal activity from intrinsic or acquired resistance during therapy
  • unnecessarily broad GN coverage
  • increasing resistance and significant concern regarding collateral resistance
72
Q

What is the expected response for the treatment of uncomplicated cellulitis?

A

Clinical improvement within 24-48 hours, visible improvement may be delayed 72 hours

73
Q

What is the duration of therapy for uncomplicated cellulitis?

A

5 days (to 14 days for severe infection, slow response, immunocompromised)

74
Q

Necrotizing Cellulitis:

Describe Type 1 (80%)

A

-associated with surgery or trauma; polymicrobial mixed infection with GP, GN and anaerobes

75
Q

Necrotizing Cellulitis:

Describe Type 2 (streptococcal gangrene, “flesh-eating” bacteria)

A

-caused by virulent S. pyogenes, very rapid progression with severe systemic signs of infection including septic shock

76
Q

Necrotizing Cellulitis:

Describe Type 3 (clostridial gas gangrene - C. perfringes, myonecrosis - C. septicum)

A

-associated with surgery or trauma, very rapid progression with gas production and myonecrosis

77
Q

What is the general treatment for necrotizing cellulitis?

A

1) emergency surgery for inspection, debridement and wound cultures
2) empirical broad-spectrum antimicrobial therapy (pip-tazo or meropenem + vancomycin +/- clinda)

**start broad and then once you figure out exactly what it is, use pathogen-directed therapy

3) pathogen-directed therapy

78
Q

Necrotizing Cellulitis:

What is the therapy directed at S. pyogenes (necrotizing cellulitis)?

A

Pen G + Clinda +/- IVIG for toxic shock

79
Q

Necrotizing Cellulitis:

What is the therapy directed at Clostridium?

A

Pen G + Clinda +/- IVIG for toxic shock

80
Q

IVIG

A

intravenous immunoglobulin

81
Q

Necrotizing Cellulitis:

What is the therapy for Aeromonas hydrophila (fresh water) ?

A

TMP-SMX or Cipro or Ceftriaxone or Doxy (as per susceptibilities)

82
Q

Necrotizing Cellulitis:

What is the therapy for Vibro vulnificus (sea water) ?

A

Ceftriaxone + (Doxy or Cipro)

83
Q

What is the role of adding Clinda to Pen G in treating serious SSTI involving S. pyogenes?

A
  • it down regulates production or proteins and toxins

- it mitigates the toxin release that happens with beta lactam

84
Q

20% of dog and 50% of cat bites develop infection, typically within _____ days

A

2-3

85
Q

What is the main bug involved in dog/cat bite wounds?

A

Pasteurella multocida (GNCB)

  • 50% of dog bites
  • 75% of cat bites
86
Q

What other bugs can be involved in dog/cat bite wounds?

A
  • strep/staph in 40%

- anaerobes

87
Q

What is Pasteurella multicoda typically susceptible to?

A
  • Pen
  • Doxy
  • FQ
  • TMP-SMX
88
Q

What is Pasteurella multicoda resistant to?

A
  • 1st GC

- Clinda

89
Q

Describe the prophylactic treatment of dog/cat bite wounds

A

-antimicrobials for 3-5 days to prevent infection of high risk wounds from moderate-severe bite, on face, on hands involving joints, significant edema or immunocompromised

90
Q

Prophylactic duration for dog/cat bite wounds

A

3-5 days

91
Q

Treatment duration for dog/cat bite wounds

A

5-10 days
or
4-6 weeks for septic arthritis or osteomyelitis (involving bone or joint)

92
Q

What is the 1st line for dog/cat bite wounds?

A

Amox-clav (po) x 5-10 days

93
Q

What are some alternatives if someone has a severe B lactam allergy?

A
  • Doxy + (Clinda or Metro)
  • (Cipro/Levo/Moxi) + (Clinda or Metro)
  • TMP-SMX + (Clinda or Metro)
  • Macrolide/Azolide (if susceptible Pasteurella) + Clinda
94
Q

What if someone has a severe infection from a dog or cat bite wound?

A
  • pip-tazo
  • ceftriax + metro
  • (cipro/levo/moxi) + (clinda or metro)
95
Q

What option should be given to pregnant women and children?

A

Macrolide/Azolide (if susceptible pasteurella) + Clinda

96
Q

What are some additional considerations for someone with a dog/cat bite wound?

A
  • Tetanus toxoid (Tdap) if not vaccinated within 10 years + tetanus immunoglobulin if <2 primary immunizations
  • Risk assessment for rabies, post-exposure prophylaxis with hyper-immune globulin (40 IU/kg) infiltrated in and around wound, and serious of 5 vaccinations over 28 days
97
Q

What bug is responsible for cat scratch disease

A

Bartonella henselae

98
Q

How does Bartonella henselae present?

A

presents as papule or pustule with lymphadenopathy within 3-30 days

99
Q

What is the treatment for cat scratch disease (Bartonella henselae)?

A

Azithro

100
Q

______% of human bites develop infection, associated with severe infection and complications

A

10-50

101
Q

Human Bite Wounds:

B-hemolytic streptococcus (viridans group, S. anginosus) in >___%

A

80

102
Q 
Human Bite Wounds:
Eikenella corrodens (GNCB) in \_\_\_\_%
A

30

103
Q

Human Bite Wounds:

S. aureus, oral anaerobes such as fusobacteria, prevotella, porphyromonas, peptostreptococcus in > ___%

A

40

104
Q

What is E. corrodens susceptible to?

A
  • Pens
  • Doxy
  • FQ
  • TMP-SMX
105
Q

What is E. corrodens resistant to?

A
  • 1st GC
  • Clinda
  • Metro
106
Q

Human Bite Wounds:

Describe the prophylactic treatment

A

-Prophylaxis with pre-emptive antimicrobials x 3-5 days to prevent infection of high risk wounds from bites that penetrate the dermis

107
Q

Human Bite Wounds:

Treatment duration?

A

7-14 days

or 4-6 weeks for septic arthritis or osteomyelitis

108
Q

What is the 1st line treatment for human bite wounds?

A

Amox-clav (po)

109
Q

What are alternatives for human bite wounds if someone has a severe B lactam allergy?

A
  • Doxy + (Clinda or Metro)
  • (Cipro/Levo/Moxi) + (Clinda or Metro)
  • TMP-SMX + (Clinda or Metro)
110
Q

What are options for a severe human bite wound infection? (IV)

A
  • Pip-tazo
  • Ceftriax + metro
  • (Cipro/Levo/Moxi) + (Clinda or Metro)
111
Q

What are some additional considerations for human bite wounds?

A
  • Tetanus toxoid (as Tdap) if not vaccinated within 10 years

- Risk assessment for Hepatitis, HIV transmission

112
Q

DFI:

What diabetes-related factors increase the risk of diabetic foot ulcers and infections?

A
  • Angiopathy with PVD and ischemia
  • Neuropathy with sensory, motor, autonomic dysfunction
  • Immune dysfunction
113
Q

DFI:

List the important adjuvant (non-antimicrobial) measures for treating diabetic foot ulcers?

A
  • glycemic control
  • wound care including debridement, dressing changes
  • pressure relief, off-loading, elevation
114
Q

What are the clinical features of diabetic foot infections?

A
  • erythema, swelling (edema), warmth, purulent discharge

- little to no pain or systemic signs of infection in >50%

115
Q

Describe a Mild DFI

A

-superficial skin with erythema < 2 cm, swelling, heat or pain; no systemic signs of infection

116
Q

Describe a Moderate DFI

A

-deep localized with erythema > 2 cm, abscess, fascitis, septic arthritis or osteomyelitis; no systemic signs of infection

117
Q

Describe a Severe DFI

A

-significant systemic signs of infection (tachycardia, tachypnea, leukocytosis, hypotension)

118
Q

What pathogen is involved in:

Superficial, acute cellulitis and/or infected ulcer not treated with antimicrobials in previous month ??

A

streptococci, staphylococci

*therefore here we don’t have to go very broad - use same meds that we talked about earlier in cellulitis

119
Q

What pathogen is involved in:

Deep, chronic infected ulcer and/or treated with antimicrobials in previous month ?

A

mixed, polymicrobial with Gram positive aerobes in >40% (streptococci, staphylococci), gram positive aerobes in <20% (Proteus species, E. coli) and anaerobes in 25-40%, particularly if necrotic or gangrenous

**deep and chronic infections have a mixed amount of bugs, need broader treatment

120
Q

What are the complications of DFI’s?

A
  • 20% of diabetes-related hospitalizations
  • contiguous spread to joints (septic arthritis) or bone (osteomyelitis) in 25%
  • amputation in 10-20% of cases at one year and 25-50% at 5 years
121
Q

What factors are considered in using antimicrobials in treating DFI’s?

A
  • infected wound versus colonized ulcer
  • adequate wound debridement and care
  • severity of infection and clinical status
  • bone involvement
  • risk factors for antimicrobial resistance: chronic infections, repeat antimicrobial exposure, low antimicrobial concentrations at infection site, MDR pathogens that limit options for antimicrobial therapy
122
Q

What is the treatment for mild, acute infection suspected Gram positives (po) ?

A

Cloxacillin > 1-2 weeks of therapy
Cephalexin > 1-2 weeks of therapy

+/- Doxy or TMP-SMX for MRSA coverage

123
Q

What is the treatment for mild, acute infection suspected Gram positives (po) IF THEY HAVE A BETA LACTAM ALLERGY ?

A

CLINDAMYCIN

124
Q

What is the treatment for moderate, acute or chronic infection suspected mixed, polymicrobial (po) ?

A

Amox-clav for > 2 weeks of therapy (may require initial IV with po step-down)

+/- Doxy or TMP-SMX for MRSA coverage

125
Q

What is the treatment for moderate, acute or chronic infection suspected mixed, polymicrobial (po) ? IF THEY HAVE A BETA LACTAM ALLERGY ?

A

CLINDA +/- (Cipro/Levo/Moxi)

**this includes MRSA coverage

126
Q

What does clavulanic acid add to amoxicillin ?

A

covers beta lactamase

127
Q

What bugs produce beta lactase ?

A

E. coli, clebsiella (enteric gram negatives)

  • *Clavulanic acid tremendously expands coverage of gram negatives
  • *Clavulanic acid also covers anaerobes
128
Q

______ has a stable ring

A

Cloxacillin

129
Q

What is the treatment for severe, chronic, extensive infection suspected mixed polymicrobial (iv) ?

A

Pip-tazo
Meropenem
Ceftriazone + Metro
Ceftazadime + Metro

x > 2-4 weeks (initial broad-spectrum iv therapy with de-escalation and po step down)

130
Q

What is the treatment for severe, chronic, extensive infection suspected mixed polymicrobial (iv) ?

IF THEY HAVE A SEVERE BETA LACTAM ALLERGY

A

Moxi (also po)
Cipro/Levo + Metro (also po)

+/- Vancomycin for MRSA coverage

Clinical 2 - Antibiotics (14 decks)

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