what is the first line of defense for SSTIs
intact skin (physical barrier)
what are some ways bacteria can get in to skin?
loss of barrier via trauma of some sort
-ducts of skin
what are classical presentations of SSTIs
erythema, warmth, edema, tenderness
what is crepitus
caused by gas production of microbes
feels crunchy under the skin
-usually caused by C. perforingins
necrosis
death of tissue
Group A strep
fluctuance
fluid filled
purpura
leaking blood vessels
bullae
blisters
what are some other diseases that can mimic SSTIs
gout thrombophlebitis DVT contact dermatitis drug eruption (allergy to drug) foreign body reaction
folliculitis
minor infxn associated with friction and sweat gland activity
**number one cause is S. aureus
2nd is Group A strep
what causes hot tub folliculitis
Psuedomonas aeruginosa
what is the treatment of folliculitis
soap and water and topical ABX
Acne
inflammation of hair follicles and associated sebaceous glands
-casued by Propionibacterium acnes also can be S. aureus
what can cause acne
hormonal influences, organic acids produced by P. acnes
Soft tissue Abscesses
any breach in skin
-local superficial cellulitis->bacteria necrose/liquefy tissue->cellular debris+WBCs accumulate to make pus
description of abscesses
fluctuant, tender, erythematous nodule with surrounding erythema
most common cause of soft tissue abscesses
Staph aureus including MRSA
Tx for abscess
I and D with a possibility of systemic ABX
what is a furuncle
abscess in the area of a hair follicle
also called a boil
usually recurrent
what is a carbuncle
-multiloculated abscess
-spread of infection to subcutaneous tissue
-S. aureus
Tx=I and D
necrotizing fascitis
enzyme producing bacteria digest fascial barriers and cause tissue necrosis
-Rapid extension of infection
what are the common pathogens of necrotizing fascitis
Group A strep aka flesh-eating bacteria
Staph aureus
C. perforingins
polymicrobial of G+ and anaerobes
what is Fournier’s gangrene
polymicrobial infection of the genitals and perineum
patient characteristics of necrotizing fasciitis
usually a sick patient
edema(rare), erythema, pain, crepitus
**pain out of proportion to exam findings
surgical wound infections causes and sources
S. aureus most common
sources: pts own skin, trans by fomites, hands, air, and environment
* *hand hygiene very important as well as perioperative ABx
fungal infections of the superficial hair and nail infections
dermatophyte fungi-tinea cruris, corporis
what do dermatophyte fungi causes
ringworm
nail infections
keratinized layers of skin/nails
**superficial hair nail and skin
what is the most common yeast infections
Candida albicans
usually warm moist areas of the body
eg: mouth, vagina, butt
Tx for fungal infections
topical antifungals, systemic antifungals if severe
Candida albicans infections
diaper rash
intertrigo(under breasts)
thrush
Impetigo characteristics, causative agents
epidermis
honey crust
Group A strep, S. aureus
**highly contagious
treatment of impetigo
penicillin only for Group A, topical ABx
Erysipelas characteristics, causative agent
deep layers of dermis rapidly spreading rubor, calor, tumor, dolor maybe some systemic signs **Group A strep
Treatment of erysipelas
penicillin
cellulitis characteristics, causative agents
subcutaneous tissue
Group A strep, S. aureus
Gram negatives in immunocompromised pts, nosocomial, wounds, DM
Treatment of cellulitis
systemic ABx
not usually biopsied
what factors increase risk of wound infections
high number of organisms higher virulence of organisms Poor circulation near wound Poor general health Poor nutrition status Immunocompromised
staphylococcal toxins
alpha-toxin
exfoliatin
TSST-1
Enterotoxin
staphylococcal toxins
alpha toxin
scalded skin syndrome
staphylococcal toxins
exfolliatin
bullous impetigo
staphylococcal toxins
TSST-1
toxic shock syndrome
usually from old blood, sinus surgeries, tampons
staphylococcal toxins
enterotoxin
food poisoning
MRSA vs MSSA
MRSA strains acquire mecA gene which makes a new PBP with reduced affinity for beta lactams. resistant to all beta lactams
-MSSA use nafcillin, oxacillin, or cephalosporins
MRSA risk factors
close skin-skin contact
crowded living conditions
poor hygiene
IV drug users
MRSA treatment
trimethoprim-sulfa, doxycycline, vancomycin, linezolid, daptomycin
Group A strep ( strep pyogenes)
post strep sequelae
rheumatic fever or glomerulonephritis
over 100 serotypes based on antigenic differences in M protein
streptolysins O and S
cytotoxic
lyse leukocytes, tissue cells, platelets
pyrogenic exotoxins A and B
- superantigens (APC and T cells lock)
- causes major immune response and causes damage to human cells
- systemic illness, shock
- in about 10% Group A strep
streptokinase
protease
hyaluronidase
degrades carbohydrates and connective tissue
DNase
degrades DNA
Clostridium perfringens
anaerboic spore forming Gram + rod with square ends
found in soil and human colon
produces hydrogen and CO2 gas in tissue
lots of exotoxins
soft tissue infections with C. perfringens
wound infections
Gas gangrene
rapidly fatal
Pasteurella multocida
gram negative rod
animal bites
Pseudomonas aeruginosa
gram negative rod
non fermentor
environmental pathogen-water, hospital rooms
skin diseases of P. aeruginosa
hot tube folliculitis
secondary infection after burns
Vibrio vulnifcus
gram neg rod
in brackish salt water environments-colonize shellfish
Fever->sepsis->hemorrhagic bullae
associated with iron overload, cirrhosis
Mycetoma “madura foot”
bacterial- actinomyces, nocardia
Fungal-lots of molds
what bacteria causes cellulitis and erysipelas predominantly?
think Group A strep
abscess of skin are caused by what?
think Staph aureus
abscess of mouth/rectum/vagina caused by?
polymicrobial
G+, anaerobes, fungi
