Staphylococcus aureus Flashcards by alexandra brennan

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)

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staph aureus characteristics

grape like, fac anaerobe, non-motile, skin and mucous membranes, carriers in nares

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staph aureus epidemiology

opportunistic skin infection (unless coag negative); can survive on dry surfaces for a long time

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staph aur. spreading

URI sneezing

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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

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adherins

surface protein - collagen elastic and fibronectin binding protein

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cytolytic enzymes

alpha and beta toxin gamma toxin and some have PVL

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exfoliate enzymes

ETA AND ETB

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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

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TSS-1

cause TSS. superantigen. heat and proteolysis resistant.

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ETB

plasmid - proteases cleave a skin protein - cause SSS or bulleous impetigo

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ETA

phage - proteases cleave a skin protein – SSSS and buleous impetigo

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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

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impetigo

localized pyogenic cutaneous infection. impetigo- young ppl - face and limbs - v. contagious

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folliculitis

stye or hair follicle

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faruncle

extension of folliculitis. may spont drain

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carbuncle

coalesced faruncle, deeper, multiple sinuses

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wound infections

s/p sx or foreign body, deeper than others and inc risk of cellulitis, after trauma possibly

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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)

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SSSS staph scalded skin syndrome

happens in young. happens far away from initial infection. often on eyes. clear liquid. no exudate

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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)

1. nonspecific cytokine release from macrophages and t cells 2. inc hypersensitivy to endotoxin 3. at low conc increase leakage of endothelial cells 4. at inc conc - inc cytotoxic effects 5. 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

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!!!!