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Clinical 2.0 > Skin and soft tissue infections > Flashcards

Skin and soft tissue infections Flashcards

1
Q

most common pathgoen in skin abscesses

A

s.aureus

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2
Q

main types of skin abcesses

A

painful red nodule with erythema in dermis
furuncles -boils in hair follicle
inflammatory nodule with overlying pustule collection
carbuncles - collection of furuncles

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3
Q

common area for skin abcesses

A

back of the neck, face, axillae

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4
Q

first step in treating skin abcesses

A

drainage
moist heat compresses for 30 min 3-4 times daily
surgical incision for larger

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5
Q

what skin abscesses indicate antimicrobial therapy

A 
>2cm
multiple lesions
extensive cellulitis
systemic signs of infection
indwelling medical device
immunocompromised
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6
Q

two main drugs for skin abscesses

A

clox and ceph (iv)

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7
Q

drug for skin abscess in beta lactam allergy

A

clindamycin - increasing resistance to staph aureus and increased incidence of c.diff

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8
Q

risk factors for MRSA infection

A

MRSA colonization
close contact with MRSA infection
previous antimicrobials or saureus infection if failure with regimen that lacked mrsa coverage

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9
Q

mrsa mechanism of resistance

A

alters the penicillin binding protein

resistant to everything with beta lactam rings

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10
Q

how do you get mrsa in community

A

staph on the skin colonizes people in close contact

seen in daycares or athletic facilities

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11
Q

difference of mrsa in hospital

A

generally mor eserious infections, higher resistance rate

due to medical procedures, dialysis

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12
Q

oral options to treat MRSA skin abscesses

A

clinda - if macrolide resistant increase risk of clinda resistance developing during therapy
doxycycline
TMP-SMX

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13
Q

how to manage patients with recurrent furnucles or carbuncles

A

saureus colonized show in positive nasal swab

mupirocin 2% 2-3 times daily for 5 days every month

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14
Q

characteristics of impetigo

A

highest incidence in 2-5yoa
superficial infection of epidermis
pruritis with mild-mod erythema

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15
Q

common pathogens in impetigo

A

non bullous - saureus, spyogenes(group A strep)

bullous - saureus

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16
Q

why is antimicrobial therapy always warranted

A

even tho mild non bullous resolves spontaneously AM therapy reduces transmission, hastens ysmptoms and progression and prevent complications

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17
Q

when is impetigo treated topically

A

non bullous mild infections with limited area and number of lesions
low risk of complications

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18
Q

topical therapy for impetigo

A

mupirocin 2% twice daily for 5 days

inhibits RNA synthesis

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19
Q

oral options for empirically treating impetigo

A

clox
ceph
clinda in allergy

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20
Q

duration of empirically treating impetigo

A

7 days

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21
Q

oral option for impetigo thats MSSA

A

clox or ceph

clinda in allergy

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22
Q

oral option for impetigo thats MRSA

A

clinda,
doxy,
TMPSMX

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23
Q

oral options for impetigo thats s.pyogenes

A

pen V or amox

clinda in allergy

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24
Q

describe cellulitis

A

superficial infection involving upper dermis or superficial lymphatics with more delineated borders

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25
Q

is purulence present in cellulitis

A

can be

indicates a staph aureus

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26
Q

common pathogens in cellulitis

A

s.pyogenes and other bhemolytic strep

staph less common likely due to some sort of trauma and has pus

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27
Q

clinical representation of cellulitis

A 
orange peel like
vesicles
bullae
petechiae or ecchymoses
phlenitis or lymphangitis 
local pain erythema warmth and edema
sometimes systemic signs
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28
Q

cultures for cellulitis

A

needle aspirate
punch biopsy
blood cultures
not very reliable

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29
Q

differential diagnosis for cellulitis

A

contact derm - itchy
gout - severe pain, single joint swelling
DVT- risk factors, calf pain
stasis derm - bilateral, pitting edema, hyperpigmentation

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30
Q

risk factors for cellulitis

A 
skin disruption ex bug bite
inflammation 
advanced age
obesity - not as much vascularization 
diabetes - decreased IS
peripheral vascular disease
lymphatic obstruction
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31
Q

cellulitis non pharms

A

immobilization
elevation
cool and warm dressings

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32
Q

what factors should you consider when selecting oral vs iv for treating cellulitis

A

severity based on location, area, and progression
systemic signs of infection
oral tolerability

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33
Q

empirically treating mild cellulitis orally suspected s.pyogenes

A

pen v
amoxicillin
clinda in allergy

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34
Q

what pathogens are suspected in mod-sev cellulitis that you want to treat for

A

s.pyogenes and MSSA becuase dont want to miss staph or the patient could be hospitalized

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35
Q

empirical options for mod-sev cellulitis

A

clox
cephalexin po, cefazolin iv
clinda in allergy

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36
Q

ceftriaxone used for severe cellulitis in out patient antimicrobial programs - adv and dis?

A

once daily
increase pneumoniae and gram negative
iv only
CI in neonates

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37
Q

compare clox vs. ceph

A

clox poor bioavailability, short half life so more frequent dosing
ceph better BA

38
Q

oral treatment for mod cellulitis suspected s.pyogenes +MRSA

A

clinda
doxy + pen or amox
TMPSMX + pen or amox
*pen and amox for strep

39
Q

iv treatment for sev cellulitis suspected s.pyogenes iv +MRSA

A

vanco

in intolerance or treatment failure - linezolid or dapto

40
Q

levo or moxi approved indication for treating uncomplicated SSTI adv and dis

A

less effective due to unreliable strep and staph from intrinsic or acquired resistance during therapy
unnecessarily broad gram - coverage
increasing resistance and sig concern regarding collateral resistance
lead to more virulent strains of c.diff

41
Q

typical response for uncomplicated cellulitis

A

clinical improvement within 24-48 hours

visible improvement may be delayed 72 hours

42
Q

duration for uncomplicated cellulitis

A

5 days

14 days for severe infection, slow response, immunocompromised

43
Q

why might you see initial worsening in treatment of cellulitis

A

toxin produced by strep pyogenes breaks open and releases toxins

44
Q

type 1 necrotizing cellulitis

A

associated with surgery or trauma

polymicrobia lmixed infection with GP, GN, anaerobes

45
Q

type 2 necrotizing cellulitis

A

streptococcal gangrene
flesh eating bacteria
caused by virulent s.pygenes
very rapid progression with severe systemic signs of infection including septic shock

46
Q

type 3 necrotizing cellulitis

A

clostridial gas gangrene
c.perfringens, c.septicum, myonecrosis
associated with surgery or trauma
very rapid progression with gas production and myonecrosis

47
Q

necrotizing cellulitus treatment

A
  1. emergency surgery for inspection, debridement and wound cultures
  2. empirical broad spectrum AM therapu
  3. pathogen directed therapy
48
Q

what is the empirical therapy for necrotizing cellulitis

A

piptazo or meropenem ( want to save meropenem)
+ vanco
+/- clinda

49
Q

pathogen directed therapy for necrotizing cellulitis s.pyogenes

A

pen G + clinda +/- IVIG for toxic shock

clinda because when bacteria is killed it releases toxins, downregulates the production of the toxin

50
Q

pathogen directed therapy for necrotizing cellulitis clostridium

A

pen G + clinda +/- IVIG for toxic shock

51
Q

pathogen directed therapy for necrotizing cellulitis aeromonas hydrophilia

A

TMPSMX or cipro or ceftriaxone or doxy as per susceptibilities

52
Q

pathogen directed therapy for necrotizing cellulitis vibrio vulnificus

A

ceftriaxone + (doxy or cipro)

53
Q

when do dog and cat bites usually develop infection

A

within 2-3 days

54
Q

what bacteria is found in dog and cat bites

A

pasteurella multocida
streptococcus
s.aureus
oral anaerobes (bacteroides)

55
Q

what is p.multocida susceptible to

A 
pen 
doxy 
fluoroqinolone
TMPSMX
resistant to 1st GC, clinda
56
Q

how long do you treat prophylaxis for animal bites

A

3-5 days

57
Q

which animal bites should be treated prophylactically

A

mod-sev bite, on face, hands involving joints, sig edema, immunocompromised

58
Q

antimicrobial therapy duration for animal bites

A

5-10 days

4-6 wks for spetic arthritis or osteomyelitis

59
Q

first line antimicrobial therapy for animal bites

A

amoxi clav po
875/125 q12h
children 20mg/kg amox component q12h

60
Q

allergy alternative for animal bite therapy

A

doxy + clinda or metro
cipro/levo/moxi + clinda or metro
TMPSMX + clinda or metro

61
Q

animal bite therapy why the clinda or metro and which one is better

A

for anaerobe coverage

clinda bc it gets strep

62
Q

animal bite therapy what is used in pregnant women and children and why

A

macrolide/azolide is susceptible to pasteurella + clinda
quinolones - tendon affects
tmp - affects folic acid production
sulfa - can displace bilirubin

63
Q

antimicrobial therapy for severe infection of animal bite

A

iv

  1. piptazo
  2. ceftriax + metro
  3. cipro/levo/moxi + clinda or metro – allergies
64
Q

non pharms for animal bites

A

Tdap if not vaccinated within 10yrs + tetanus immunoglobulin if <2 primary immunization
risk assessement for rabies - hyperimmuni globulin 40IU/kg infiltrated in and around wound, 5 vaccines over 28 days

65
Q

pathogen in cat scratch disease

A

bartonella henselae

66
Q

cat scratch disease presentation

A

papule or pustule with lympadenopathy within 3-30 days

67
Q

cat scratch disease treatment

A

azithro 500mg po the 250 q24hrs for 4 days

68
Q

pathogens in human bbites

A

bhemolytic strep (viridans)
eikenella corrodens (BNCB)
saureus
oral anaerobes

69
Q

what is ecorrodens susceptible to

A 
pens
doxy 
fluoroquinolones
TMPSMX
resistant to 1dtGC, clinda, and metro
70
Q

when how long do you give AM prophylaxis in human bites

A

3-5 days

prevent infection of high risk wounds from bites that penetrate the dermis

71
Q

AM therapy duration to treat infection for animal bites

A

7-14 days

4-6 weeks for spetic arthritis or osteomyelitis

72
Q

first line in humna bite wounds

A

oral amoxi clav

73
Q

antimicrobial therapy in allergy for human bite wounds

A

doxy + clinda or metro
cipro/levo/moxi + clinda or metro
TMPSMX + clinda or metro
*azithro not effective

74
Q

AM therapy for human bites in severe infection

A

same as animal

75
Q

non pharms for human bites

A

tetanus toxoid

risk assessment for hepatitis and HIV transmission

76
Q

what diabetes related factors increase the risk of diabetic foot ulcers and infections

A

angiopathy with peripheral vascular disease and ischemia
neuropathy with sensory, motor, autonomic dysfunction
immune dysfunction

77
Q

important non pharms for diabetic foot ulcers

A

glycemic control
wound care - debridement and dressing changes
pressure relief, off loading, elevation

78
Q

clinical features of diabetic foot infections

A 
erythema
swelling 
warmth 
purulent discharge 
little to no pain or systemic signs of infection
79
Q

mild diabetic foot infections

A

superficial skin with erythema <2cm
swelling
heat or pain
no systemic signs

80
Q

moderate diabetic foot infections

A 
deep localized erythema >2cm
abscess
fasciitis 
septic arthrisi or osteomyelitis 
no systemic signs
81
Q

severe diabetic foot infections

A

sig systemic signs of infection - tachycardia, tachypnea, leukocytosis, hypotension

82
Q

DFI common pathogens in superficial acute cellulitis or infected ulcer not treated with AM in previous month

A

strep

staph

83
Q

DFI common pathogens in deep chronic infected ulcer or treated with AM in previous month

A

mixed
polymicrobial with gram + aerobes
gram - aerobes
anaerobes - in gangrenous

84
Q

complications of DFI

A

hospitalization
contiguous spread to joints - septic arthritis
bone - oesteomyelitis
amputation

85
Q

factors considered in using AM in treating DFIs

A 
infected wound vs colonized ulcer 
adequate wound care and debridement 
severity of infection adn clinical status 
bone involvement 
risk factors for AM resistance
86
Q

risk factors for AM resistance

A

chronic infections
repeat AM exposure
low AM concentrations at infection site
MDR pathogens

87
Q

normally what is emperical therapy for DFI based on

A

patient history
suspected pathogens
local resistance rates
step down based on susceptibility

88
Q

mild acute DFI suspected gram positive oral

A

clox or ceph +/- doxy or TMPSMX
*TMPSMX or doxy for MRSA
1-2 weeks or more
clinda in allergy

89
Q

moderate acute or chronic DFI suspected mixed polymicrobial oral

A

greater than 2 weeks
amox clav +/- doxy or TMPSMX
clinda + fluoroquinolone in allergy

90
Q

severe chronic extensive DFI suspected polymicrobial iv

A 
pip tazo 
meropenem 
ceftriaxone + metro 
ceftazidime (pseudomonas) + metro 
alternative: moxi or cipro/levo +metro
\+/- vanco if MRSA
91
Q

clinda is not as good for anaerobes as metro but why can you use clinda instead in DFI

A

anaerobes are seldom alone

often aerobes use up the oxygen and let anaerobes come in so when aerobe dies anaerobes will too

Clinical 2.0 (24 decks)

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