Lecture 2: Gram-Positive Staphylococci

Question 1

What are the key features of S. aureus in lab tests?

Answer 1

Gram-positive cocci, beta-hemolytic, coagulase-positive, DNase-positive, Protein A-positive, golden colonies on blood agar.

Question 2

How does S. aureus become MRSA?

Answer 2

Acquires mecA gene (on SCCmec), encoding PBP2a with reduced affinity for beta-lactams (e.g., methicillin).

Question 3

Compare VISA and VRSA resistance mechanisms.

Answer 3

VISA: Thickened cell wall traps vancomycin (mecA + cell wall mutation).

VRSA: vanA gene alters D-ala-D-ala to D-ala-D-lac, blocking vancomycin binding.

Question 4

Name 3 virulence factors aiding colonization, evasion, and damage.

Answer 4

Colonization: MSCRAMMs (e.g., ClfA, FnbpA).

Evasion: Protein A (blocks phagocytosis), fibrin clots (avoid neutrophils).

Damage: α-hemolysin (pore-forming), exotoxins (e.g., TSST-1, enterotoxins).

Question 5

What does a positive tube coagulase test indicate?

Answer 5

Free coagulase enzyme converts fibrinogen to fibrin, forming clots (diagnostic for S. aureus).

Question 6

How does S. aureus appear on DNase agar with methyl green?

Answer 6

Yellow colonies (DNA breakdown clears methyl green); S. epidermidis remains agar-colored.

Question 7

How is S. aureus identified on BPA?

Answer 7

Black colonies (tellurite reduction) with halos (lecithinase activity); S. epidermidis lacks halos.

Question 8

Why are S. aureus exotoxins considered superantigens?

Answer 8

Bind non-specifically to MHC II/TCR, bypassing normal immune activation → cytokine storm (e.g., TSST-1).

Question 9

Name 3 infections caused by S. aureus.

Answer 9

Impetigo, endocarditis, cellulitis, abscesses, bacteremia, CRUTI.

Question 10

How was S. aureus named?

Answer 10

Latin for “golden” (golden colonies); S. epidermidis for skin (epidermis) colonization.