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MLSCI 242 > LECTURE - Staphylococcus > Flashcards

LECTURE - Staphylococcus Flashcards

1
Q

Human-associated CoNS (negative staph)

A

S. epidermidis-like group:

  • S. epidermidis
  • S. saprophyticus + subsp
  • S. haemolyticus
  • S. capitis
  • S. hominis
  • S. pettenkoferi
  • S. simulans
  • S. warneri
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2
Q

T or F. S. lugdunensis is part of CoPS

A

F, CoNS

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3
Q

Human-associated CoPS

A
  • S. aureus + subsp
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4
Q

Diseases caused by S. aureus

A
  1. Skin infections
    - pyogenic
    - toxigenic
  2. Systemic infections
    - toxigenic
    - invasive disease
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5
Q

Skin infections caused by S. aureus: pyogenic

A
  • stye
  • boil (furuncle)
  • carbuncle (more serious!)
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6
Q

Staphylococcal skin infections: toxigenic

A
  • staphylococcal scalded skin syndrome (SSSS)

- bullous impetigo

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7
Q

Toxin-mediated systemic infections caused by S. aureus

A
  • food poisoning by staphylococcal enterotoxin (SE); causes vomiting + diarrhea
  • toxic shock by TSST
    • both are superantigens
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8
Q

Superantigens

A

(SAgs) are a class of antigens that result in excessive activation of the immune system. Specifically, it causes non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release

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9
Q

Systemic infections caused by S. aureus: invasive disease

A
  • pneumonia
  • acute endocarditis
  • sepsis
  • osteomyelitis
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10
Q

S. aureus virulence factors

A
  • adhesins: MSCRAMMs
  • toxins: superantigens, etc.
  • polysaccharide capsule
  • antibiotic resistance
  • regulation of surface adhesins (Quorum sensing)
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11
Q

What is the function of MSCRAMMs

A
  • microbial surface components recognizing adhesive matrix molecules
  • coat organism with host antigens: appear self-like to host
  • attack to host tissue or plastic implants
  • may misdirect antibody response (eg. to fibronectin-binding protein AFTER it has bound to fibronectin)
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12
Q

Four examples of MSCRAMMs

A
  • protein A (binds IgG)
  • collagen-binding protein
  • fibronectin-binding protein
  • clumping factor (binds fibrinogen)
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13
Q

MCRAMMs are proteins identified by unique AA motif:

A

LPXTG

- attached to the pentaglycine bridge in peptidoglycan by means of the sortase enzyme

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14
Q

protein A vs. regular MSCRAMM

A
  • it’s a special type of MCRAMM
  • it doesn’t bind a surface matrix molecule but it DOES have the LPTXG motif in its structure!
  • protein A binds IgG through the Fc region rather than the antigen-binding sites in the normal way
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15
Q

Toxins that work systemically

A
  • Superantigens: TSST, seven types of SE
    > bind to the outside of the TCR and the MHC II antigen
  • activate cytokine secretion in many cells (overproduction) and cause the typical consequences of shock
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16
Q

Toxins that work locally in skin infections

A
  • exfoliative toxins
  • SSSS and bullous impetigo
  • cleaves proteins exclusive to cells of the epidermis (ex: desmoglein-1)
17
Q

Toxic exoproducts of S. aureus

A
  • Staphylokinase or Sak binds to plasminogen to dissolve fibrin in clots but also extracellular matrix fibres, allows spread of infection (esp in combo with hyaluronidase and other proteases)
  • pore-forming toxins:
    > alpha-hemolysin: prototype of toxin family; 7 monomers form heptamer in cell membrane (like C9 in MAC)
    > leukocidin: PVL (panton-valentine leukocidin); S & F assemble in multiples (octamer) to form a pore
18
Q

S. aureus polysaccharide capsule

A
  • inhibits attachment + antiphagocytic

- conjugated vaccine use? 2/3 MRSA possess one of two capsule serotypes

19
Q

T or F. The S. aureus polysaccharide capsule is a critical virulence factor

A

F! Critical virulence determinant for other organisms but not S. aureus (not that significant)

20
Q

antibiotic resistant S. aureus

A
  • role of mecA and PBP2’
  • MRSA (community- vs. hospital-acquired)
  • VISA
21
Q

Organism detects a certain conctn of itself in the body which then triggers a chain in the type of virulence factors it produces

A

Quorum sensing

22
Q

S. aureus quorum sensing process

A 
regulation of surface adhesins!!!
- early growth phase = adhesins
- late exponential growth = adhesin genes OFF; exoprotein genes ON as AgrD accumulates w bacterial popln density
- AgrC (sensor) detects AgrD
- AgrC is phosphorylated
- AgrC-P phosphorylates AgrA (ACTIVATOR)
- AgrA-P transcriptionally activates virulence genes = EXPRESSED
=> pus formation
23
Q

endocarditis and other invasive infections

A

S. lugdunensis )CoNS)

24
Q

colonization of indwelling catheters, septicemia, endocarditis

A

S. epidermidis (CoNS)

25
Q

UTIs

A

S. saprophyticus (CoNS)

26
Q

T or F. S.lugdunensis is a constituent of the normal human skin flora

A

T!

27
Q

What’s so special about S. lugdunensis?

A
  • behaves clinically similar to S. aureus
  • causes fulminant native valve endocarditis
  • colonize skin and mucous more frequently than S. aureus
  • more virulent that other CoNS bc of several virulence factors including delta toxin-like hemolytic peptide, variety of adhesins, variety of enzymes (DNase + lipase), lysozyme resistance, biofilm formation, agr regulator
28
Q

T or F. S. epidermidis forms biofilm and contaminates indwelling catheters

A

T!

29
Q

Process of biofilm formation

A
  • adhesion and attachment
  • monolayer
  • accumulation, proliferation, intercellular adhesion processes
  • maturation
  • may disaggregate from macrocolony => bloodstream (metastatic + embolic complications)
30
Q

Most common gram + cause of UTI in the hospital

A

S. saprophyticus

- Propensity to attach makes it the most common gram + cause of urinary tract infection in the hospital

31
Q

S. saprophyticus virulence factors

A
  • surface protein that can bind fibronectin + erythrocyte membranes (hemaglutinin)
  • can assist colonization in different body sites (vagina + bladder)

MLSCI 242 (39 decks)

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