Skin/Soft Tissue Infections Flashcards
Erysipelas VS cellulitis?
Inflammation of the skin and subcutaneous tissues caused by infeciton
Erysipelas - upper dermis and superficial lymphatics
Cellulitis - involved deeper dermis and subcutaneous fat
Cellulitis presentations: (8)
variable presenations
Calor- warmth
Dolor - pain
Rubor - erythema
Tumor - swelling
Secretions - if abscess / ulcer
Systemic sx: fevers & chills (if more severe and not localized)
Lymphangitis
Pathogenesis of cellulitis:
**BREAK/DISRUPTION in skin barrier –> penetration, entry of causative
Predisposing factors: break in skin barriers, edema / water retention, skin conditions, DM-neuropathy can’t feel, other infections (athelete’s feet, chickenpox), immunosuppression, co-morbidities, procedures
BUGS!
Common bugs:
Less common bugs (4 + where they’re acquired from)
How are they identified on stain?
#1 GRAM POSITIVE ORGANISMS!
especially strep and staph
(because of virulence factors and they live on our skin)
Group A strep (strep pyogenes)
Other hemolytic strep species
Staph aureus (MSSA, MRSA)
Enterococcus (less commmon)
Less common:
gram negative bacteria
human bites- eikenella corrodens
Cat bites- pasteurella multocida
Dog bites - capnocytophaga canimorsus
Identification:
Gram + = stains purple
Gram - = stains red/pink
Strep- chains
Staph - clusters
DDx for cellulitis (3 broad groups + examples)
- Vascular disorder - thrombophebitis, lymphedema
- Dermatologic disorder - contact dermatitis, drug rxns, insect sting/bites, urticaria
- Immunologic / pheumatologic disorders - gouty arthritis, lupus, sarcoid
Purulent vs non-purulent cellulitis
common pathogens of each
Purulent Cellulitis: cellulitis associated with purulent drainage or exudate in absence of drainable abscess; some focus were purulent material is expressible or could be drainable
pathogens - MRSA more common (esp Community Acquired, no association with hospital - athelets, msm)
Non-purulent Cellulitis: cellulitis with no purulent drainage, exudate or abscess
Pathogens - CA-MRSA not as common of a pathogen, strep spp and MSSA
DZ?
common features
Purulent Cellulitis
area of purulence indulated (harder to palpate), erythema
Pathogens -likelihood of staph, MRSA, community acquired esp.
What is methicillin?
What causes methicillin resistance?..how does it work?
Methicillin is a semi-synthetic beta-lactamase-resistance penicillin
Resistanece is due to the presence of the mecA gene (mobile gene)
mecA is f_ound in the bacterial cell walls_ and prevents the ringlike structure of penicillin-like antibiotics to bind to the enzymes that help form the cell wall of the bacterium
MecA gene produces the penicillin binding protein 2a (PBP2a), which has a LOW AFFINITY for BETA-LACTAM antibiotics. PBPs arepeptidase enzymes important in cell wall synthesis
Seen in MSRA - difference between community acquired and hospital acquired MRSA
Hospital acquired typicically doesn’t have the purulent factors, likely due to different virulence factors SCCmec I,II,III
vs Community acquired typically due to SCCmec IV, V
What is a complication of diabetes in relation with dermatology?
What are common risk factors?
Diabetics commonly get lower extremity soft tissue infections (ulcers)
Neuropathy - poor sensation, often leads to breaks in skin that go unnoticed
Peripheral vasuclar disease - poor circulation prevents impt immunological factors from traveling to the site of infection
With ulcers, highly prone for infection
Usually poly-microbial
DX/TX dependent on severity and stage
What are some complications of cellulitis (3):
Sepsis
Toxic Shock Syndrome (staph or strep)
Necrotizing fascitis
Risk factors for TTS (9)
Mortality?
SX (2)
Clinical presentation (2)
menses, women (90%), wound infections, mastitis, sinusitis, osteo, burns, lesions, arthritis
Case fatality: 2%
SX: fever, HYPOtension (early stage)
Rash: diffuse macular erythema (faint early presentation), desquamation, often of palms/soles (1-2 weeks after presentation)
Multi-organ involvement: N/V, diarrhea, AKI, thrombocytopenia, delirium, alt levels of consciousness, transaminitis, mucosal surface hemorrhage / hyperemia
NEG blood cultures
Pathogenesis of TTS:
Staph releases TTS toxin -1 –> triggers intense immun respose –> massive cyokine production/release => severe presentation (fever, hypotension, rash….)
Staph TTS management (3)
- Supportive: fluids, vasopressor support
- Surgical: removal of any foreign body
- Antibiotics: relevant to bacteria
STREP TTS
Epi
Risk Factors
Pathogenesis
3.5 cases/100,000
case fatality: 30-40%
Risk factors: surgical procedures, injuries, trauma
Pathogenesis: Group A strep (s. pyogenes) –> exotoxins, which act as superantigens (pyrogenis exotoxin A and B - SPEA, SPEB), M protein (filamentous protein that confers virulence) –> inflammatory response by the body –> rxn
STREP TTS presentation (4)
- Localized Pain
- SKin - swelling, erythema, skin sloughing, (diffuse erythematous rash only in 10%)
- Evidence of multi-organ: N/V, HYPOtension, renal involvement, DIC, ARDS
Positive blood cultures in 50% of the time
Necrotizing Fasciitis:
Types
Clinical Presentation
= deep seated infection of subcut tissue with destruction of fascia and fat – making “necrotic” the lower layers
Type I: polymicrobials aerobic / anaerobic
often post surgery / would infection
FOURNIER’S GANGRENE (perineal area)
Type II: GAS or MRSA mono-microbial
Presentation: pain out of proportion to exam, rapidly evolving (pain, skin findings, systemic illess), skin changes (initial 0 minimal slight erythema; may become dark, bullae/vesicles, signs of necrosis/gangrene), systemic (fever hypotension )
- Fournier’s gangrene
Impetigo
Clinical presentation on who?
Where? (2)
Management:
= superficial bacterial infection
CONTAGIOUS
Commonly seen on: kids, face, sites of mild trauma
Micro-organisms: B-hemolytic strep species (groupA), staph aureus, polymicrobial
DX: clinical
Mtmg: topical and/or systemic antibiotics, antibiotics that cover strep and staph spps
