Skin and soft tissue infections Flashcards
most common pathgoen in skin abscesses
s.aureus
main types of skin abcesses
painful red nodule with erythema in dermis
furuncles -boils in hair follicle
inflammatory nodule with overlying pustule collection
carbuncles - collection of furuncles
common area for skin abcesses
back of the neck, face, axillae
first step in treating skin abcesses
drainage
moist heat compresses for 30 min 3-4 times daily
surgical incision for larger
what skin abscesses indicate antimicrobial therapy
>2cm multiple lesions extensive cellulitis systemic signs of infection indwelling medical device immunocompromised
two main drugs for skin abscesses
clox and ceph (iv)
drug for skin abscess in beta lactam allergy
clindamycin - increasing resistance to staph aureus and increased incidence of c.diff
risk factors for MRSA infection
MRSA colonization
close contact with MRSA infection
previous antimicrobials or saureus infection if failure with regimen that lacked mrsa coverage
mrsa mechanism of resistance
alters the penicillin binding protein
resistant to everything with beta lactam rings
how do you get mrsa in community
staph on the skin colonizes people in close contact
seen in daycares or athletic facilities
difference of mrsa in hospital
generally mor eserious infections, higher resistance rate
due to medical procedures, dialysis
oral options to treat MRSA skin abscesses
clinda - if macrolide resistant increase risk of clinda resistance developing during therapy
doxycycline
TMP-SMX
how to manage patients with recurrent furnucles or carbuncles
saureus colonized show in positive nasal swab
mupirocin 2% 2-3 times daily for 5 days every month
characteristics of impetigo
highest incidence in 2-5yoa
superficial infection of epidermis
pruritis with mild-mod erythema
common pathogens in impetigo
non bullous - saureus, spyogenes(group A strep)
bullous - saureus
why is antimicrobial therapy always warranted
even tho mild non bullous resolves spontaneously AM therapy reduces transmission, hastens ysmptoms and progression and prevent complications
when is impetigo treated topically
non bullous mild infections with limited area and number of lesions
low risk of complications
topical therapy for impetigo
mupirocin 2% twice daily for 5 days
inhibits RNA synthesis
oral options for empirically treating impetigo
clox
ceph
clinda in allergy
duration of empirically treating impetigo
7 days
oral option for impetigo thats MSSA
clox or ceph
clinda in allergy
oral option for impetigo thats MRSA
clinda,
doxy,
TMPSMX
oral options for impetigo thats s.pyogenes
pen V or amox
clinda in allergy
describe cellulitis
superficial infection involving upper dermis or superficial lymphatics with more delineated borders
is purulence present in cellulitis
can be
indicates a staph aureus
common pathogens in cellulitis
s.pyogenes and other bhemolytic strep
staph less common likely due to some sort of trauma and has pus
clinical representation of cellulitis
orange peel like vesicles bullae petechiae or ecchymoses phlenitis or lymphangitis local pain erythema warmth and edema sometimes systemic signs
cultures for cellulitis
needle aspirate
punch biopsy
blood cultures
not very reliable
differential diagnosis for cellulitis
contact derm - itchy
gout - severe pain, single joint swelling
DVT- risk factors, calf pain
stasis derm - bilateral, pitting edema, hyperpigmentation
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
cellulitis non pharms
immobilization
elevation
cool and warm dressings
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
empirically treating mild cellulitis orally suspected s.pyogenes
pen v
amoxicillin
clinda in allergy
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
empirical options for mod-sev cellulitis
clox
cephalexin po, cefazolin iv
clinda in allergy
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
compare clox vs. ceph
clox poor bioavailability, short half life so more frequent dosing
ceph better BA
oral treatment for mod cellulitis suspected s.pyogenes +MRSA
clinda
doxy + pen or amox
TMPSMX + pen or amox
*pen and amox for strep
iv treatment for sev cellulitis suspected s.pyogenes iv +MRSA
vanco
in intolerance or treatment failure - linezolid or dapto
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
typical response for uncomplicated cellulitis
clinical improvement within 24-48 hours
visible improvement may be delayed 72 hours
duration for uncomplicated cellulitis
5 days
14 days for severe infection, slow response, immunocompromised
why might you see initial worsening in treatment of cellulitis
toxin produced by strep pyogenes breaks open and releases toxins
type 1 necrotizing cellulitis
associated with surgery or trauma
polymicrobia lmixed infection with GP, GN, anaerobes
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
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
necrotizing cellulitus treatment
- emergency surgery for inspection, debridement and wound cultures
- empirical broad spectrum AM therapu
- pathogen directed therapy
what is the empirical therapy for necrotizing cellulitis
piptazo or meropenem ( want to save meropenem)
+ vanco
+/- clinda
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
pathogen directed therapy for necrotizing cellulitis clostridium
pen G + clinda +/- IVIG for toxic shock
pathogen directed therapy for necrotizing cellulitis aeromonas hydrophilia
TMPSMX or cipro or ceftriaxone or doxy as per susceptibilities
pathogen directed therapy for necrotizing cellulitis vibrio vulnificus
ceftriaxone + (doxy or cipro)
when do dog and cat bites usually develop infection
within 2-3 days
what bacteria is found in dog and cat bites
pasteurella multocida
streptococcus
s.aureus
oral anaerobes (bacteroides)
what is p.multocida susceptible to
pen doxy fluoroqinolone TMPSMX resistant to 1st GC, clinda
how long do you treat prophylaxis for animal bites
3-5 days
which animal bites should be treated prophylactically
mod-sev bite, on face, hands involving joints, sig edema, immunocompromised
antimicrobial therapy duration for animal bites
5-10 days
4-6 wks for spetic arthritis or osteomyelitis
first line antimicrobial therapy for animal bites
amoxi clav po
875/125 q12h
children 20mg/kg amox component q12h
allergy alternative for animal bite therapy
doxy + clinda or metro
cipro/levo/moxi + clinda or metro
TMPSMX + clinda or metro
animal bite therapy why the clinda or metro and which one is better
for anaerobe coverage
clinda bc it gets strep
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
antimicrobial therapy for severe infection of animal bite
iv
- piptazo
- ceftriax + metro
- cipro/levo/moxi + clinda or metro – allergies
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
pathogen in cat scratch disease
bartonella henselae
cat scratch disease presentation
papule or pustule with lympadenopathy within 3-30 days
cat scratch disease treatment
azithro 500mg po the 250 q24hrs for 4 days
pathogens in human bbites
bhemolytic strep (viridans)
eikenella corrodens (BNCB)
saureus
oral anaerobes
what is ecorrodens susceptible to
pens doxy fluoroquinolones TMPSMX resistant to 1dtGC, clinda, and metro
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
AM therapy duration to treat infection for animal bites
7-14 days
4-6 weeks for spetic arthritis or osteomyelitis
first line in humna bite wounds
oral amoxi clav
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
AM therapy for human bites in severe infection
same as animal
non pharms for human bites
tetanus toxoid
risk assessment for hepatitis and HIV transmission
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
important non pharms for diabetic foot ulcers
glycemic control
wound care - debridement and dressing changes
pressure relief, off loading, elevation
clinical features of diabetic foot infections
erythema swelling warmth purulent discharge little to no pain or systemic signs of infection
mild diabetic foot infections
superficial skin with erythema <2cm
swelling
heat or pain
no systemic signs
moderate diabetic foot infections
deep localized erythema >2cm abscess fasciitis septic arthrisi or osteomyelitis no systemic signs
severe diabetic foot infections
sig systemic signs of infection - tachycardia, tachypnea, leukocytosis, hypotension
DFI common pathogens in superficial acute cellulitis or infected ulcer not treated with AM in previous month
strep
staph
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
complications of DFI
hospitalization
contiguous spread to joints - septic arthritis
bone - oesteomyelitis
amputation
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
risk factors for AM resistance
chronic infections
repeat AM exposure
low AM concentrations at infection site
MDR pathogens
normally what is emperical therapy for DFI based on
patient history
suspected pathogens
local resistance rates
step down based on susceptibility
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
moderate acute or chronic DFI suspected mixed polymicrobial oral
greater than 2 weeks
amox clav +/- doxy or TMPSMX
clinda + fluoroquinolone in allergy
severe chronic extensive DFI suspected polymicrobial iv
pip tazo meropenem ceftriaxone + metro ceftazidime (pseudomonas) + metro alternative: moxi or cipro/levo +metro \+/- vanco if MRSA
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
