Staphylococcus aureus Flashcards
How do you differentiate staph and strep?
- gram stain - both + and cocci
- catalase- staph will bubble and + (strep will not)
- latex agglutination for coagulase - staph will be + (confirmatory)
staph aureus characteristics
grape like, fac anaerobe, non-motile, skin and mucous membranes, carriers in nares
staph aureus epidemiology
opportunistic skin infection (unless coag negative); can survive on dry surfaces for a long time
staph aur. spreading
URI sneezing
protein A
a surface protein. coats surface of most SA, linked covalently to peptidoglycan; binds Fc receptor if IgG - prevents from recog. FAB region - masks staph from host
adherins
surface protein - collagen elastic and fibronectin binding protein
cytolytic enzymes
alpha and beta toxin gamma toxin and some have PVL
exfoliate enzymes
ETA AND ETB
enterotoxins
food poisoning. stable at 100 degrees for 30 min so sometimes cooking won’t even kill it. resistant to hydrolysis in GI and jejunum. some are super antigen. emesis is common and thought to be due to inflam mediators from mast cells
TSS-1
cause TSS. superantigen. heat and proteolysis resistant.
ETB
plasmid - proteases cleave a skin protein - cause SSS or bulleous impetigo
ETA
phage - proteases cleave a skin protein – SSSS and buleous impetigo
biofilms
an ECM (polysacc) - microorg hides inside. serves as a barrier to enviro. helps with resistance to abx. place to exchange genetic material. - common with OM CF UTI chronic lung infection and CVL infection
impetigo
localized pyogenic cutaneous infection. impetigo- young ppl - face and limbs - v. contagious
folliculitis
stye or hair follicle
faruncle
extension of folliculitis. may spont drain
carbuncle
coalesced faruncle, deeper, multiple sinuses
wound infections
s/p sx or foreign body, deeper than others and inc risk of cellulitis, after trauma possibly
consequences of deep tissue invasion
bacteremia, endocarditis (flu —-> rapid deterioration), pneu (aspiration, spread through blood), osteomylitis or trauma induced osteochondrosis, septic arthritis and joints (s/p injection or prosthesis)
SSSS staph scalded skin syndrome
happens in young. happens far away from initial infection. often on eyes. clear liquid. no exudate
staph food poisoning
enterotoxins. common if human carrier makes something and it sits out a while. creates toxin but organism need not be present. rapid onset and course – S+S GI (NO FEVER!!!!!!!) you C/S organism
TSS toxic shock syndrome
superantigen TSS1, tampons, abrupt onset of fever and then rapid deterioration (MODS and HYPOTENSION) - fatality 5%
peptidoglycan
cross linked gives rigidity. this also keeps it from drying out. endotoxin like activity - has techoic acids
pyrogens
peptidoglycans endotoxin like activity. endogenous - activate complement and release of IL-1 - activates aggregation of PMNs to make an abcess.
techoic acids
peptidoglycan - helps to attach to mucous membrane
importance of cytoplasmic membrane
important to maintain an osmotic barrier. anchors cellular enzymes
capsule
polysacc slime layer, 11 capsular serotypes, protective against chemotaxis and phagocytosis by PMNs, faceplates attachment to artificial surfaces.
coagulase
converts fibrinogen to fibrin - (only in + staph) - gives a protective layer to localise infection - via abcess
catalase
h2o2 to o2 and h2o
haluronidase
hydrolizes h. acid - helps spread into tissues
staphilokinase or fibrinolysin
dissolves clot to break abcess and help spread
lipases
hydrolyze fat - so once past dermis and epidermis it can spread into fatty areas and sebaceous glands etc. superficial skin infection in form of caruncle and feruncle
nuclease
when cells die they release nucleic acids - it helps chew it up and spread it
pcn-ase
facilitates resistance by cleaving beta lactam ring or mob in genetic elements
pcn binding protein PBP2a
makes resistance to oxicillian (MRSA)
communitiy aq. Staph A
scc mec gene, with increased virulence - remains susceptible to beta lactams, usually deem-necrotic and the most freq skin infection to present to the er
scc cassette chromosomes
mobile genetic component r/t abx resistance
resistance to oxicillian
pcn binding protein PBP2a
hospital aq Staph A
scc mec gene and abx resistence
MRSA resistance
pcn binding protein PBP2a
alpha toxin and beta toxin
cytolytic toxins, alpha can make a pore in RBCS, leuko, plots (alpha hemolysin)
(beta - sphyngomylinase C) - hydrolysis of lipids to get inside - RBCS, leuk, macrophages and fibroblasts)
beta and alpha toxin- what happens when they work together?
damage tissue and form abcess
gamma toxin
lyse macrophages and neutrophils via a pore
PVL
in some staph aureus - if high conc- NECROSIS and if low conc - APOPTOSIS
differentiate bulleous impetigo and SSSS and caused by _____?
caused by ETA AND ETB (exfoliative enzymes)
SSSS - systemic and clear fluid
BImpetigo - yellow and local
what do super antigens do? (ie. TSS1 in TSS)
- nonspecific cytokine release from macrophages and t cells
- inc hypersensitivy to endotoxin
- at low conc increase leakage of endothelial cells
- at inc conc - inc cytotoxic effects
- hypovolemic shock and mods cause death
quorem sensing
has to do with gene exp. up reg release of secreted toxins and down reg of surface proteins (which regulates super antigen) - this is because the organism uses up all nutrients as it continues to grow.
coag negative staph
staph epi
staph epi
normal flora in ALL ppl. ltd virulence but very abx resistance. good with biofilms.
staph epi - who is at risk?
immuno comp and preemies
what does staph epi cause?
endocarditis (not naive valves but if so its congenital)
CVL and shunt inf.
prosthetic joints
UTI from catheter
likes foreign bodies etc artificial things
how do you dx staph?
you scrape bottom/base of abcess and gram stain it.
use specific agar and C+S
biotype to differentiate type of staph
test for abx suscpetibily
NOOOOO SEROLOGY!!!!
