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Clinical 2.0 > Skin and soft tissue infections > Flashcards

Skin and soft tissue infections Flashcards

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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
is purulence present in cellulitis
can be | indicates a staph aureus
26
common pathogens in cellulitis
s.pyogenes and other bhemolytic strep | staph less common likely due to some sort of trauma and has pus
27
clinical representation of cellulitis
``` orange peel like vesicles bullae petechiae or ecchymoses phlenitis or lymphangitis local pain erythema warmth and edema sometimes systemic signs ```
28
cultures for cellulitis
needle aspirate punch biopsy blood cultures not very reliable
29
differential diagnosis for cellulitis
contact derm - itchy gout - severe pain, single joint swelling DVT- risk factors, calf pain stasis derm - bilateral, pitting edema, hyperpigmentation
30
risk factors for cellulitis
``` skin disruption ex bug bite inflammation advanced age obesity - not as much vascularization diabetes - decreased IS peripheral vascular disease lymphatic obstruction ```
31
cellulitis non pharms
immobilization elevation cool and warm dressings
32
what factors should you consider when selecting oral vs iv for treating cellulitis
severity based on location, area, and progression systemic signs of infection oral tolerability
33
empirically treating mild cellulitis orally suspected s.pyogenes
pen v amoxicillin clinda in allergy
34
what pathogens are suspected in mod-sev cellulitis that you want to treat for
s.pyogenes and MSSA becuase dont want to miss staph or the patient could be hospitalized
35
empirical options for mod-sev cellulitis
clox cephalexin po, cefazolin iv clinda in allergy
36
ceftriaxone used for severe cellulitis in out patient antimicrobial programs - adv and dis?
once daily increase pneumoniae and gram negative iv only CI in neonates
37
compare clox vs. ceph
clox poor bioavailability, short half life so more frequent dosing ceph better BA
38
oral treatment for mod cellulitis suspected s.pyogenes +MRSA
clinda doxy + pen or amox TMPSMX + pen or amox *pen and amox for strep
39
iv treatment for sev cellulitis suspected s.pyogenes iv +MRSA
vanco | in intolerance or treatment failure - linezolid or dapto
40
levo or moxi approved indication for treating uncomplicated SSTI adv and dis
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
typical response for uncomplicated cellulitis
clinical improvement within 24-48 hours | visible improvement may be delayed 72 hours
42
duration for uncomplicated cellulitis
5 days | 14 days for severe infection, slow response, immunocompromised
43
why might you see initial worsening in treatment of cellulitis
toxin produced by strep pyogenes breaks open and releases toxins
44
type 1 necrotizing cellulitis
associated with surgery or trauma | polymicrobia lmixed infection with GP, GN, anaerobes
45
type 2 necrotizing cellulitis
streptococcal gangrene flesh eating bacteria caused by virulent s.pygenes very rapid progression with severe systemic signs of infection including septic shock
46
type 3 necrotizing cellulitis
clostridial gas gangrene c.perfringens, c.septicum, myonecrosis associated with surgery or trauma very rapid progression with gas production and myonecrosis
47
necrotizing cellulitus treatment
1. emergency surgery for inspection, debridement and wound cultures 2. empirical broad spectrum AM therapu 3. pathogen directed therapy
48
what is the empirical therapy for necrotizing cellulitis
piptazo or meropenem ( want to save meropenem) + vanco +/- clinda
49
pathogen directed therapy for necrotizing cellulitis s.pyogenes
pen G + clinda +/- IVIG for toxic shock | clinda because when bacteria is killed it releases toxins, downregulates the production of the toxin
50
pathogen directed therapy for necrotizing cellulitis clostridium
pen G + clinda +/- IVIG for toxic shock
51
pathogen directed therapy for necrotizing cellulitis aeromonas hydrophilia
TMPSMX or cipro or ceftriaxone or doxy as per susceptibilities
52
pathogen directed therapy for necrotizing cellulitis vibrio vulnificus
ceftriaxone + (doxy or cipro)
53
when do dog and cat bites usually develop infection
within 2-3 days
54
what bacteria is found in dog and cat bites
pasteurella multocida streptococcus s.aureus oral anaerobes (bacteroides)
55
what is p.multocida susceptible to
``` pen doxy fluoroqinolone TMPSMX resistant to 1st GC, clinda ```
56
how long do you treat prophylaxis for animal bites
3-5 days
57
which animal bites should be treated prophylactically
mod-sev bite, on face, hands involving joints, sig edema, immunocompromised
58
antimicrobial therapy duration for animal bites
5-10 days | 4-6 wks for spetic arthritis or osteomyelitis
59
first line antimicrobial therapy for animal bites
amoxi clav po 875/125 q12h children 20mg/kg amox component q12h
60
allergy alternative for animal bite therapy
doxy + clinda or metro cipro/levo/moxi + clinda or metro TMPSMX + clinda or metro
61
animal bite therapy why the clinda or metro and which one is better
for anaerobe coverage | clinda bc it gets strep
62
animal bite therapy what is used in pregnant women and children and why
macrolide/azolide is susceptible to pasteurella + clinda quinolones - tendon affects tmp - affects folic acid production sulfa - can displace bilirubin
63
antimicrobial therapy for severe infection of animal bite
iv 1. piptazo 2. ceftriax + metro 2. cipro/levo/moxi + clinda or metro -- allergies
64
non pharms for animal bites
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
pathogen in cat scratch disease
bartonella henselae
66
cat scratch disease presentation
papule or pustule with lympadenopathy within 3-30 days
67
cat scratch disease treatment
azithro 500mg po the 250 q24hrs for 4 days
68
pathogens in human bbites
bhemolytic strep (viridans) eikenella corrodens (BNCB) saureus oral anaerobes
69
what is ecorrodens susceptible to
``` pens doxy fluoroquinolones TMPSMX resistant to 1dtGC, clinda, and metro ```
70
when how long do you give AM prophylaxis in human bites
3-5 days | prevent infection of high risk wounds from bites that penetrate the dermis
71
AM therapy duration to treat infection for animal bites
7-14 days | 4-6 weeks for spetic arthritis or osteomyelitis
72
first line in humna bite wounds
oral amoxi clav
73
antimicrobial therapy in allergy for human bite wounds
doxy + clinda or metro cipro/levo/moxi + clinda or metro TMPSMX + clinda or metro *azithro not effective
74
AM therapy for human bites in severe infection
same as animal
75
non pharms for human bites
tetanus toxoid | risk assessment for hepatitis and HIV transmission
76
what diabetes related factors increase the risk of diabetic foot ulcers and infections
angiopathy with peripheral vascular disease and ischemia neuropathy with sensory, motor, autonomic dysfunction immune dysfunction
77
important non pharms for diabetic foot ulcers
glycemic control wound care - debridement and dressing changes pressure relief, off loading, elevation
78
clinical features of diabetic foot infections
``` erythema swelling warmth purulent discharge little to no pain or systemic signs of infection ```
79
mild diabetic foot infections
superficial skin with erythema <2cm swelling heat or pain no systemic signs
80
moderate diabetic foot infections
``` deep localized erythema >2cm abscess fasciitis septic arthrisi or osteomyelitis no systemic signs ```
81
severe diabetic foot infections
sig systemic signs of infection - tachycardia, tachypnea, leukocytosis, hypotension
82
DFI common pathogens in superficial acute cellulitis or infected ulcer not treated with AM in previous month
strep | staph
83
DFI common pathogens in deep chronic infected ulcer or treated with AM in previous month
mixed polymicrobial with gram + aerobes gram - aerobes anaerobes - in gangrenous
84
complications of DFI
hospitalization contiguous spread to joints - septic arthritis bone - oesteomyelitis amputation
85
factors considered in using AM in treating DFIs
``` infected wound vs colonized ulcer adequate wound care and debridement severity of infection adn clinical status bone involvement risk factors for AM resistance ```
86
risk factors for AM resistance
chronic infections repeat AM exposure low AM concentrations at infection site MDR pathogens
87
normally what is emperical therapy for DFI based on
patient history suspected pathogens local resistance rates step down based on susceptibility
88
mild acute DFI suspected gram positive oral
clox or ceph +/- doxy or TMPSMX *TMPSMX or doxy for MRSA 1-2 weeks or more clinda in allergy
89
moderate acute or chronic DFI suspected mixed polymicrobial oral
greater than 2 weeks amox clav +/- doxy or TMPSMX clinda + fluoroquinolone in allergy
90
severe chronic extensive DFI suspected polymicrobial iv
``` pip tazo meropenem ceftriaxone + metro ceftazidime (pseudomonas) + metro alternative: moxi or cipro/levo +metro +/- vanco if MRSA ```
91
clinda is not as good for anaerobes as metro but why can you use clinda instead in DFI
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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