IC14 SSTI Flashcards
How do SSTIs come about? (Pathogenesis)
Disruption of normal host cell defenses (eg. skin break) –> allows overgrowth & invasion of skin and soft tissue by pathogenic microorganisms
What are the risk factors for SSTIs?
- disruption of skin barrier
- traumatic causes (lesions, abrasions, burns, surgery, bites from humans/animals/insects, IV drug use)
- nontraumatic causes (ulcers, tinea pedis, dermatitis, chemical irritants)
- impaired venous & lymphatic drainage
- peripheral artery disease - conditions that predispose to infection
- DM, cirrhosis, neutropenia, HIV, transplant, immunosuppression - history of cellulitis
How do you prevent SSTIs?
- management of risk factors
- good wound care
- treat tinea pedis
- prevent dry, cracked skin
- good foot care for DM patients to prevent wounds & ulcers
- removal of foreign objects, irrigation, tissue debridement
How do you diagnose a SSTI?
physical exam & patient history
Where should you and should you NOT take samples for cultures for SSTIs from?
do NOT take cultures from:
- open, draining wounds (v likely contaminated)
- wound swabs
take cultures from:
- deep in the wound after surface cleansed
- base of closed abscess
- curettage > wound swab/irrigation (debridement of top layers before taking tissue sample)
Do you need to take blood samples for SSTIs?
Only for severe SSTI or immunocompromised patients
Describe impetigo
erythematous papules that develop into vesicles and pustules that rupture, with the dried discharge forming a honey-colored crust on a erythematous base
Describe ecthyma
ulcerative form of impetigo that occurs in deeper skin layers (not a progression of impetigo; they are diff SSTIs)
Describe furuncles and carbuncles
furuncle (boil) - infection of hair follicle
carbuncle - group of furuncles
Describe skin abscesses
collection of pus within dermis and deeper skin tissue; painful, tender and red nodules
Describe erysipelas
fiery red painful plaque (raised above surrounding skin) with well-demarcated edges; common on face and lower extremities
Describe cellulitis
involves deeper and subq fats; acute, diffuse, spreading, non-elevated, poorly demarcated area of erythema, mostly unilateral (on one limb); typically in lower extremities
What are the likely pathogens for each SSTI?
- impetigo: Staph, strep pyogenes
- ecthyma: Strep pyogenes (GAS)
- nonpurulent (cellulitis, erysipelas): Strep pyogenes
- purulent (purulent cellulitis, furuncles, carbuncles, skin abscesses): Staph aureus, Strep pyogenes
What are the two kinds of MRSA that can cause SSTIs?
community-acquired MRSA
healthcare-associated MRSA
How are the two MRSAs different?
CA-MRSA and HA-MRSA are genetically different
1. PVL (Panton-Valentine leucocidin) [cytotoxin]
2. SCCmec (CA: IV, HA: II) [mobile genetic element for novel specific PBP2a]
Describe the prevalence of the two MRSAs involved in SSTIs
CA-MRSA: More common in USA
HA-MRSA: Usually almost always HA-MRSA in SG, so have to treat as long as patient has MRSA risk factors
Define HA-MRSA
patient develops MRSA infection within
1. 2 days of being in hospital
2. 12 months of being discharged from hospital
What are the risk factors for HA-MRSA?
- antibiotic use
- recent hospitalization/surgery (for a decent duration; doesn’t count if just visiting etc)
- prolonged hospitalization
- ICU
- hemodialysis
- MRSA colonization
- close proximity to MRSA colonized/infected people
Describe the treatment for mild impetigo (limited lesions)
Likely pathogen: Staph (MSSA), strep
THEORY: Topical mupirocin BD x 5/7
NOT recommended; reserved for MRSA decolonization in hospitals
IN PRACTICE: no need to treat as self-limiting
Describe the EMPIRIC treatment for impetigo/ecthyma (multiple lesions)
Likely pathogens:
impetigo: Staph (MSSA), strep
ecthyma: grp A strep
- PO beta lactams
- Cloxacillin
- Cephalexin - PO Clindamycin (penicillin allergy)
Describe the CULTURE-DIRECTED treatment for impetigo/ecthyma (multiple lesions) if it is caused by
1. Strep pyogenes (Grp A strep)
2. MSSA
Strep pyogenes:
1. PO penicillins
- Pen V
- Amoxicillin
MSSA:
1. PO beta lactams
- Cloxacillin
- Cephalexin
What is the typical treatment duration of impetigo & ecthyma for
1. mild infection
2. moderate to severe infection
- 5-7 days
- moderate to severe: 10-14 days
What is the main treatment for purulent SSTIs (purulent cellulitis, furuncles, carbuncles, skin abscesses)?
incision & drainage (source control)
When do we use antibiotics for purulent SSTIs?
- unable to drain completely
- lack of response to I&D
- extensive disease involving many sites
- extreme ages (v young/old)
- immunosuppressed
- signs of systemic illness (2/4 of SIRS criteria)
- IV abx for severe disease state
Describe the SIRS criteria
SIRS = systemic inflammatory response syndrome
1. temp (>38 or <36)
2. WBC (>12 or <4)
3. HR (>90)
4. RR (>24)
Describe the treatment to be given for purulent SSTIs that are
1. mild
2. moderate
3. severe
Likely pathogens: Staph aureus (MSSA)
- I&D + warm compress
- I&D + PO abx
- Cloxacillin
- Cephalexin
- Clindamycin (Penicillin allergy) - I&D + IV abx
- Cloxacillin
- Cefazolin
- Clindamycin
- Vanco
Describe the empiric treatment to be given for purulent SSTIs that involve MRSA
PO
- co-trimoxazole
- doxycyline
- clindamycin
IV
- vanco
- daptomycin
- linezolid
(daptomycin & linezolid reserved for VRE/vanco allergy)
What happens if purulent SSTI occurs near perioral/perirectal/ vulvovaginal areas?
add G(-) anaerobic coverage
Describe the empiric treatment to be given for purulent SSTIs that involve G(-) anaerobes
amoxicillin-clavulanate (Augmentin)
pip-tazo (if risk of resistant strain)
carbapenem (if super duper sick)
What is the typical treatment duration for purulent SSTIs?
5-10 days
Describe the treatment to be given for nonpurulent SSTIs that are
1. mild
2. moderate
3. severe
Likely pathogen: Grp A strep
- PO abx
- Pen V
- Amoxicillin
- Cloxacillin
- Cephalexin
- Clindamycin (penicillin allergy) - moderate = signs of systemic ifxn + some purulence; IV abx
- Ampicillin
- Cloxacillin
- Cefazolin
- Clindamycin (penicillin allergy) - severe = signs of systemic ifxn/failed oral therapy/immunocompromised; broader coverage + possibility of necrotizing fasciitis
IV
- Pip-tazo
- Cefepime (4th gen)
- Meropenem
if MRSA risk factors
- Vanco, daptomycin, linezolid
Describe the treatment to be given for non-purulent SSTI in a patient with a history of water exposure
+ Cipro to cover Aeromonas, Vibrio & Pseudomonas
What is the typical duration of treatment for nonpurulent SSTIs?
5-10 days
14 days for immunocompromised
What are some other things to do when treating nonpurulent SSTIs?
- rest
- limb elevation to promote drainage of edema
- treat underlying conditions (eg. tinea pedis, skin dryness, limb edema)
What are the monitoring parameters when monitoring for therapeutic response of SSTI treatment?
- improvement within 2-3 days (won’t resolve so fast)
- no progression of lesions/development of complications
- reassess indication/choice of abx if no improvement within 2-3 days
How do DFIs (diabetic foot infections) come about? (Pathogenesis)
- risk factors
- neuropathy (loss of sensation)
- vasculopathy (poor circulation)
- immunopathy - ulcer formation/wound
- bacterial colonize, penetration, proliferation
- DFIs
What constitutes DFIs?
- wounds
- ulcers
When do we treat wounds and ulcers found in diabetic patients?
if infected (ie. true DFI)
criteria for infection:
1. purulent discharge, or
2. at least 2 signs of inflammation
- erythema
- warmness
- tender
- pain
- induration (thickening/hardening of skin)
What are the microbes involved in DFIs?
typically polymicrobial
G(+)
- Staph, Strep
G(-) (for wet/chronic wounds)
- Proteus, Klebsiella, E Coli
Anaerobes (for deep/ischemic/necrotic wounds)
- Peptostreptococcus (Finegolda magna in SOA table)
- Veillonella
- Bacteroides
When and how do we take cultures for DFIs?
no need for mild DFI
need for moderate to severe DFI
take deep tissue cultures after cleansing + before starting empiric abx
- avoid skin swabs
- do not culture uninfected wounds
What is the criteria for mild DFI?
- involves skin + SQ tissue, AND
- erythema ≤2cm, AND
- no signs of systemic infection
What are the organisms to cover for mild DFI?
- Staph aureus
- Strep species
What are the antibiotics to use for mild DFI?
PO abx
- Cloxacillin
- Cephalexin
- Clindamycin
if MRSA risk factors (PO)
- Co-trimoxazole
- Doxycyline
- Clindamycin
What is the criteria for moderate DFI?
- involves deeper tissues (eg. bones, joints), OR
- erythema >2cm
- no signs of systemic infection (compulsory)
What are the organisms to cover for moderate DFI?
G(+)
- Staph
- Strep
G(-)
- +/- PA
anaerobes
What are the antibiotics to use for moderate DFI?
IV abx
- Amox/clav (Augmentin)
- Cefazolin/Ceftriaxone + Metronidazole
if MRSA risk factors (IV)
- Vanco
- Daptomycin
- Linezolid
What is the criteria for severe DFI?
- involves deeper tissues (eg. bones, joints) OR
- erythema >2cm
- signs of systemic infection (compulsory)
What are the organisms to cover for severe DFI?
G(+)
- Staph, strep
G(-)
- PA
anaerobes
What are the antibiotics to use for severe DFI?
IV abx
- Pip-tazo
- Cefepime + metronidazole
- Meropenem
- Cipro + clindamycin
if MRSA risk factors (IV)
- Vanco
- Daptomycin
- Linezolid
What is the recommended duration of therapy for DFIs
1. not involving bones (mild, moderate, severe)
2. involving bones
A: surgery - infected tissue completely removed, residual infected tissue left, residual viable bone left
B: no surgery
Not involving bones
* mild: 1-2 wks
* moderate: 1-3 wks
* severe: 2-4 wks
Involving bone
* surgery, complete removal: 2-5 days
* surgery, residual infected tissue: 1-3 wks
* surgery, residual viable bone: 4-6 wks
* no surgery: ≥3 months
What are some adjunctive measures for DFIs?
- wound care
- foot care
- glycemic control
What are some risk factors for pressure ulcers?
- reduced mobility
- impaired immunity
When do we treat pressure ulcers with antibiotics?
when it becomes infected, meaning
1. purulent discharge
2. ≥2 signs of inflammation (erythema, warmness, tender, pain, induration)
What are some adjunctive measures for pressure ulcers?
- debridement of infected/necrotic tissue
- local wound care
- relief pressure
