manifestations from a distant infection site
toxin mediated
resident skin flora
mostly bacterial, includes staph epidermidis and p. acnes
transient skin flora
mostly staph aureus and strep pyogenes (group A)
spreading exogenous infection confined to epidermis
impetigo
spreading exogenous infection involving dermal lymphatics
erysipelas
spreading infection involving all the way down through subcutaneous layer
cellulitis
2 or more furuncles
carbuncle (abscess formation)
myonecrosis
muscle tissue death/infection
all streptococci are gram ___ and catalase ___
gram + and catalase -
all staphylococci are catalase ___
catalase + (distinguishes them from strep)
pyogenic cocci are obligate..?
obligate extracellular bacteria meaning they do not want to be inside cells
how do pyogenic cocci avoid being phagocytosed?
anti-phagocytic virulence factors
but sometimes cells have antibodies against these factors allowing uptake by PMNs
strep are classified by three things…
- hemolytic pattern (beta is clearing, alpha is partial)
- physiological traits and biochemical reactions
- antigenic composition (group A has A antigen in cell wall)
beta hemolytic strep
complete lysis of rbc around colony on blood agar
alpha hemolytic strep
partial hemolysis of rbc around colony on blood agar
gold standard detection method for group A strep?
culture
–strep is sensitive to bacitracin –> will be a clearing around bacitracin disc
group A strep
strep pyogenes
rapid looking for lancefield group A detection
strep test with great specificity but bad sensitivity
detects carbohydrate antigen that is part of cell wall murein layer, no virulence factor
major virulence factor in s pyogenes (group A)
M proteins
m protein
anti-phagocytic virulence factor in strep pyogenes
involved in binding to epidermis
why cant an antibody to hyaluronic acid be made against s pyogenes?
because humans have hyaluronic acid inour bodies so that would not be protective
components of streptococcal cell wall
capsule, m proteins, lipotechoic acid, phospholipid membrane
super antigens
stimulate excessive cytokine production –> lots of T cells
exotoxins involved in scarlett fever and toxic shock-like syndrome
extracellular virulence
exotoxins/super antigens streptolysin 0 DNAases streptokinase C5a peptidase
depolymerizes cell-free DNA in purulent lesions
DNAases
lyses blood clots helping bacteria spread
streptokinase
degrades complement component C5a that attracts PMNs
c5a peptidase
strawberry tongue, circum-oral pallor, desquamation
scarlet fever
purulent (pus) skin lesion
pyoderma
four pyodermas caused by s pyogenes
impetigo
erysipelas
cellulitis
necrotizing fasciitis
strep vs staph toxic shock syndrome
clinically the same except with strep patients are bacteremic(bacteria in blood) –>may have necrotizing fasciitis
autoimmune cross reaction between anti-M antibodies and the heart tissue
group A strep
rheumatic fever
renal injury due to deposition of antigen-antibody complexes on glomeruli
acute glomerulonephritis
PANDAS syndrome
pediatric autoimmune neuropsychiatric disorder associated with group A strep
5 criteria for PANDAS
prescence of OCD or tic pediatric onset abrupt/episodic GAS infections neurologic abnormalities (hyper, tics, etc)
how to treat pandas?
penicillin G or oral cephalisporins
if there is a co-infection with staph aureus, use penicillinase (will treat both)
penicillinase
resistant antibiotic to treat both strep pyogenes and staph aureus at the same time
what drug will treat both s pyogenes and s aureus simultaneously
penicillinase
gram +, catalase +, coagulase -
staph epidermidis or staph saprophyticus
gram +, catalase +, coagulase +
staph aureus
white nonhemolytic colony morphology
staph epidermidis
yellow beta hemolytic colony
staph aureus
gram +, catalase -
streptococci
catalase test
H2O2 plus bacteria
- ->bubbling = catalase + (staph)
- -> no bubbling = catalase - (strep)
hallmark of staph skin infections?
presence of pus
how to treat furuncle?
heat and or drainage
antibiotics if it invades subcutaneous layer
hydradentic suppurativa
infection of sweat glands
stye is what kind of infection and can progress to what?
folliculitis
can progress to cellulitis
impetigo is usually due to?
group A strep
binds fibronectin and induces shock
techoic acid
converts fibrinogen to fibrin
coagulase
hyaluronidase
acts on hyaluronic acids in CT facilitating dissemination through subcutaneous
potent pore former, toxic to many cell types
alpha hemolysin
also called spyngomyelinase C, kills cells via hydrolysis of membrane phospholipids
beta toxin
cytolytic, nonspecific detergent like action
delta toxin
poreforming toxins, lysis of neutrophils and macrophages
gamma toxin and panton-valentine leukocidin (PVL)
staph intermedius
coagulase/staph zoonotic pathogen
common from dog bite or exposure
common oral, nasal, skin flora in healthy dogs
food poisoning is caused by
staph enterotoxins
TSST1
staph aureus induced toxic shock syndrome
exfoliatin A/B cause…
staph aureus impetigo, Scalded skin syndrome, scarlet fever
exfoliatin
a serine protease that splits desmosomes in granulosum
major risk group for TSS
menstruating women
use ofcontraceptive devices
nasal surgery patients
semi-synthetic penicillin
resistant to penicillinase
methicillin
penicillinase-producing s aureus
generally plasmid encoded
transferred by conjuugation or transduction
treat with methicillin
MRSA
due to mecA gene (encodes PBP2 - altered penicillin binding protein)
methicillin resistance
what was developed to treat MRSA?
vancomycin - glycopeptide that binds to D-ala-D-ala residues of peptidoglycan precursors - stops chain
VISA
vancomycin intermediate of s aureus
VRSA
vancomycin resistant s aureus
acquisition of vanA gene
peptidoglycan precursor with D-ala-Dlactate terminus
hasnt spread as much as mrsa
what causes UTI, endocarditis, infections of foreign devices, endophthalmitis, osteomyelitis?
s epidermidis
biofilms
s epidermidis
irreversible adherence to device surfaces by extracellular polymers in a structural matrix
protects bacteria from antibiotics
nosocomial
detachment of bacteria can lead to sepsis
nosocomial
arising in a hospital
culprits of nosocomial skin infections
staph eureus
mRSA
acinetobacter baumanii
pseudomonas aeruginosa