SSTIs Flashcards
Normal flora of the face, neck
Staph. epidermis
Normal flora of the axilla and groin
GNRs (acinetobacter spp.)
Primary infections
Usually involve areas of previously healthy skin and are typically caused by one pathogen
Secondary infections
Usually occur in areas of previously damaged skin and are often polymicrobic
cSSTIs
Complicated
Represents the more severe end of all SSTIs
Classification secondary to clinical decision
Impetigo definition
Superficial infection of stratum corneum
Impetigo epidemiology
Children
Poor hygiene
Impetigo causative organisms
S. aureus (including MRSA)
Group A streptococci
Impetigo clinical presentation
Purulent, localized vesicles/lesions
Mild pain, pruritis
Most common on exposed areas
Impetigo topical treatment
Wash affected area w/ soap and water
x 5 days if localized lesions
Mupiricin or Retapamulin
Impetigo oral treatment
Dicloxicillin, keflex, augmentin
If MRSA suspected: Doxy, Clinda, Bactrim
If streptococci alone is isolated: PCN G PO
Erysipelas definition
Cellulitis involving the more superficial layers of the skin and cutaneous lymphatics
Erysipelas epidemiology
Very young and very old
Erysipelas causative organisms
Group A streptococci
Erysipelas clinical presentation
- Raised, erythematous lesions with clear line of demarcation
- Typically associated with intense burning
- Orange peel appearance
- Often with systemic symptoms
- Most commonly affects the lower extremities
Erysipelas treatment
PCN G (any route) or Amoxil x 7-10 days
Purulent SSTIs
Furuncles
Carbuncles
Cutaneous abscess
Furuncles definition
Infection of the hair follicle that usually extends through the dermis into the SQ tissue resulting in small abscess
Carbuncles
Inflammatory nodule that extends through multiple adjacent follicles
Purulent SSTI epidemiology
Irritation/injury to hair follicle/skin
Purulent SSTI causative agent
S. aureus (if MRSA - angry looking w/black spot in the middle)
Furuncle clinical presentation
Inflammatory, draining nodule involving a hair follicle
Lesions start as a firm, tender, red nodule that becomes painful and fluctuant
Lesions often drain spontaneously
Lesions caused by CA-MRSA often have necrotic centers characteristic of “spider bites”
Carbuncle clinical presentation
Form broad, swollen, erythematous, deep, and painful follicular masses
Commonly develop on the back of the neck and are more likely to occur in patients with diabetes
General treatment of Purulent SSTIs
Incision and drainage, culture/sensitivity testing recommended for all carbuncles, large furuncles and abscesses
Purulent SSTI treatment: Mild infection
Localized; no systemic signs of infection
Mainly small furuncles
ABX not needed
Purulent SSTI treatment: Moderate infection
systemic signs of infection; use PO Rx x 5-10 days Empiric Rx: Bactrim or doxycycline Defined Rx: -MRSA: Bactrim -MSSA: Dicloxacillin/keflex
Purulent SSTI infection: Severe infection
If failed incision/drainage PLUS PO antibiotics, or if systemic inflammatory response syndrome is present; use IV rx x 5-10 days
Empiric Rx: MRSA coverage (Vanc, dapto, linexolid, telovancin, dalbovancin, oritavancin, ceftaroline)
Defined Rx:
-MRSA: same as above
-MSSA: Nafcillin/oxacillin/clindamycin
Cellulitis definition
Involves deeper dermis and SQ fat
Cellulitis epidemiology
Breaches in skin, obesity CA-MRSA: At higher risk if smoker, have DM, recurrent infections, IVDU, crowding, frequent skin contact, sharing contaminated personal care items, lack of cleanliness
Cellulitis causative organisms
Group A stretptococci and S. aureus are most common
Occasionally other G+ cocci, GNR and/or anaerobes
Cellulitis clinical presentation
Erythematous, nonelevated lesions without defined margins
Affected areas are edematous and warm to touch
Lesions may be associated with purulent drainage, exudates, and/or abscesses
Accompanied by systemic symptoms and lymphatic involvement
Cellulitis treatment: MSSA
5 days of Rx for uncomplicated cases IV: Nafcillin/oxacillin PO: Dicloxacillin IV (if PCN allergic): Cefazolin PO (if PCN allergic): Keflex
Cellulitis treatment: MRSA
7-10 days
IV: Vanc
Necrotizing fasciitis definition
Rare SQ infection that spreads rapidly along fascial planes
Results in progressive destruction of SQ fat, fascia, and uscle compartments
Necrotizing fasciitis risk factors
DM, penetrating trauma, crush injuries/interrupted blood supply
Necrotizing fasciitis type I causative agents
Mixed anaerobes, GNRs, enterococci
Mortality 20%
Necrotizing fasciitis type II causative agents
Group A streptococci
Associated systemic toxicity
Mortality 20-60%
Necrotizing fasciitis clinical presentation
Skin necrosis or ecchymosis with fever, constant pain
Systemic toxicity: fever, leukocytosis, delirium, renal failure
Necrotizing fasciitis general treatment
Surgical debridement +/- amputation
+ broad coverage
Necrotizing fasciitis type I treatment
Vancomycin/Linezolid PLUS
Pip/tazo or carbapenem or ceftriaxone (kids=cefotaxime [PLUS metronidazole/clinda if ceftriaxone/cefotaxime])
Necrotizing fasciitis type II treatment
Clindamycin PLUS PCN G (in cases of clinda resistance)
Diabetic Foot Infections Clinical Presentation
Swelling and erythema of the foot
Purulent secretions
Three distinct types (deep abscesses, cellulitis, ulcers)
Potential complication = osteomyelitis
Glucose control to optimize wound healing
Wound care
Mild diabetic foot infection clinical presentation
Local
Involves only the skin and SQ tissue
Mild diabetic foot infections causative organisms
MSSA
Streptococcus spp.
MRSA
Mild diabetic foot infections treatment: MSSA and Streptococcus
Keflex
Augmentin
Mild diabetic foot infections treatment: MRSA
Bactrim
Doxycycline
Moderate diabetic foot infections clinical presentation
Local infection
Erythema > 2cm
Involving structures deeper than skin and SQ tissue
AND
No signs of systemic inflammatory response
Severe diabetic foot infections clinical presentation
Local infection AND Signs of systemic inflammatory response + >/=2 of the following: Temp >38 or <36 HR > 90 RR > 20 or PaCO2 < 32 WBC > 12000 or < 4000 > 10% bands
Moderate-severe diabetic foot infections causative organisms
MRSA MSSA Streptococcus spp. Enterobacteriaceae Obligate anaerobes P. aeruginosa
Moderate-Severe diabetic foot infections treatment: MSSA, streptococcus spp., Enterobacteriaceae, Obligate anaerobes
Amp/sulbactam
Ertapenem
Moderate-severe diabetic foot infections treatment: MRSA
Linezolid
Vancomycin
Moderate-severe diabetic foot infections treatment: P. aeruginosa
Pip/tazo
Moderate-severe diabetic foot infections treatment: MRSA, Enterobacteriaceae, P. aeruginosa, obligate anaerobes
Vancomycin
PLUS Ceftazidime or cefepime
OR +/- anaerobic coverage if not using pip/tazo or carbapenem
Osteomyelitis definition
Infection of the bone
Osteomyelitis etiology
Prosthetic joint implants/orthopedic surgery Trauma Compromised circulation Bacteremia Diabetic foot infections
Osteomyelitis clinical manifestations
Pain
Swelling
Drainage after surgery or injury
Osteomyelitis diagnosis
Imaging
Laboratory tests (CBC, ESR, CRP)
Cultures
Osteomyelitis treatment
Early surgical intervention
Aggressive antibiotic therapy
IV therapy: 4-6 weeks
Osteomyelitis causative organisms
MSSA MRSA Streptococcus spp. Enterobacteriaceae P. aeruginosa
Osteomyelitis treatment: MSSA
Nafcillin, oxacillin, cefazolin, ceftriaxone
Osteomyelitis treatment: MRSA
Vancomycin
Linezolid
Daptomycin
Osteomyelitis treatment: Streptococcus spp.
PCN G
Ceftriaxone
Clindamycin
Osteomyelitis treatment: Enterobaccteriaceae
Pip/tazo
Ceftriaxone
Cipro
Osteomyelitis treatment: P. aeruginosa
Pip/tazp
Cefepime
Cipro
Imipenem/cilstatin
Animal bite causative organisms
Pasteurella multocida (most common)
Streptococci
Ctaphylococci
Animal bite preferred treatment
Augmentin
Animal bite treatment comments
Duration: 10-14 days
Cat bites have double infection rates compared to dog bites
Human bite causative organisms
Streptococci Staphylococci Eikenella corrodens PLUS Anaerobes (Fusobacterium, Peptostreptococcus, Prevotella, Perphyromonas)
Human bite preferred treatment
Augmentin
Amp/sulbactam
Ertapenem
Human bite comments
Duration: 10-14 days
Eikenella corrodens is resistant to 1st gen ceph, macrolides, clinda, and minoglycosides