Staphylococcus Flashcards
(22 cards)
What do they look like
•gram positive cocci
•spherical, single or irregular clusters
•non motile, non spore forming
•facultative anaerobes
•mesophiles
•divide in multiple planes: irregular clumps (contrast to strep)
What are the basic metabolism stuff
•catalase positive
•oxidase negative (except s sciuri)
•high salt tolerance (<15%)
•high drying tolerance
Two major staph groups
Coagulase positive
•mostly pathogenic
•S aureus
Coagulase negative
•non pathogenic or opportunistic
•S epidermidis
Apart from S aureus, what are the other coagulase positive staph
•S intermedius
•S pseudintermedius
•S delphini
•S hyicus
•S lutrae
•S schleiferi
•S leei
S aureus disease
Skin and soft tissue
•impetigo
•boils, furunculosis
•scalded skin syndrome
•wounds, burns, surgical incisions
Food poisoning
•ingestion of pre-formed enterotoxin
Life threatening
•osteomyelitis, septic arthritis
•sepsis
•acute endocarditis
•pneumonia
•toxic shock syndrome
Cell associated S aureus virulence factors
•adhesins
•microcapsule- aids adhesion, immune evasion
•teichoic acids- aids adhesion
S aureus excreted factors
•coagulase, protease, lipase, hyaluronidase- tissue invasion, nutrients, allows spread
Exotoxins
•some are superantigens
No endotoxins (gram neg only)
How is coagulase a virulence factor
- Coagulase reacts with prothrombin
- Forms complex (staphylothrombin)
- Complex cleaves fibrinogen to fibrin
- Fibrin self assembles, polymerise, clot forms
•fibrin clot helps a aureus evade the immune system by protecting from phagocytosis
S aureus toxins
Produced by most:
•cytotoxins
•hemolysins
Produced by some:
•exfoliative A and B toxins
•toxic shock syndrome toxin
•enterotoxins
•Panton-Valentine leucocidin (PVL)
Hemolysins
Alpha- forms beta-barrel transmembrane pores
Beta- doesn’t form pores, hydrolyses sphingomyelin
Gamma- forms beta barrel
Delta- phenol soluble modulins, non specific membrane damage
S aureus enterotoxins
A, E- prophage
B, C- pathogenicity islands
D- plasmid
Superantigens
•SEA and SEB
•non specific T cell activation; bind directly to class II MHC
•stimulate 20-30% of all T cells, massive cytokine release
Toxic shock syndrome
•S aureus grow (menstrual products), release TSST
•TSST enters bloodstream, superantigenic activity
•cytokine release leads to shock, multi-organ failure
•30-70% mortality
•less than 10% of S aureus have the gene (on a pathogenicity island)
MRSA
•methicillin resistant staphylococcus aureus
•methicillin resistance on mecA gene
•carried on staphylococcal cassette chromosome mec (SCCmec)
•mecA encodes penicillin binding protein
S aureus antibiotic susceptibility
•vancomycin (glycopeptide) used
•glycopeptide resistance (VISA and VRSA) from vanA and vanB genes (from enterococci)
•vanA encoded on transposon Tn1546
Can either:
1 retain VRE conjugative plasmid or
2 transposon transferred into aureus
S aureus vancomycin resistance
•VANC binds to D-Ala-D-Ala
•disrupts peptidoglycan assembly
•alters cell wall intermediates:
D-Ala-D-Lac
D-Ala
Coagulase negative staphylococci (CoNS)
•basically not aureus
•commensal flora
•S epidermidis is 70% of CoNS on skin
•opportunistic
•mostly nosocomial infection
S epidermidis pathogenesis
•biofilm and slime production
•doesnt produce classic toxins
•produces phenol-soluble modulins (PSMS)
S epidermidis slime
•loosely adhered to bacteria, easily washed off
•allows bacteria to adhere to smooth surfaces
•inhibits neutrophil chemotaxis
•reduces antibiotic effectiveness
S epidermidis biofilm
•polysaccharide intercellular adhesin (PIA)
•extracellular DNA
•proteins, Sbp
S epidermidis antibiotic susceptibility
•susceptible to vancomycin
•methicillin resistance
•encoded on SCCmec (mecA gene)
•mecA encodes penicillin binding protein PBP2a
•epidermidis has CRISPR, aureus does not
CRISPR
Clustered regularly interspaced short palindromic repeat
