Resistance: genetic determinants (mecA, vanA, blaKPC)

6 ASCP MLS practice questions on Resistance: genetic determinants (mecA, vanA, blaKPC), part of Microbiology. The first 6 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

1. Question 1 · Easy

   The mecA gene of Staphylococcus aureus encodes:

   1. AAn altered binding protein, PBP2a
   2. BA methylase that blocks macrolide binding
   3. CA penicillinase that hydrolyses oxacillin
   4. DAn efflux pump for beta-lactam drugs

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   Answer: A · An altered binding protein, PBP2a

   mecA sits on the mobile SCCmec element and encodes PBP2a, a penicillin-binding protein with very low affinity for beta-lactams. Cell wall synthesis therefore continues in the presence of oxacillin and almost every other beta-lactam. A mecA-positive isolate is reported resistant to the whole class apart from the anti-MRSA cephalosporins. The protein can also be detected directly by a PBP2a latex agglutination test.

   • B: Methylases encoded by erm genes cause macrolide and clindamycin resistance.
   • C: Staphylococcal penicillinase (blaZ) causes penicillin resistance, not methicillin resistance.
   • D: Efflux is not the mechanism of methicillin resistance.

2. Question 2 · Hard

   A vancomycin-resistant gram-positive coccus from urine has a vancomycin MIC of 8 micrograms/mL, is motile and yellow pigmented, and is negative for vanA and vanB. The best explanation is:

   1. AA vanA gene that the assay failed to amplify
   2. BIntrinsic vanC resistance in E. casseliflavus
   3. CA vanA-positive strain of Enterococcus faecium
   4. DPlasmid loss during the overnight subculture

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   Answer: B · Intrinsic vanC resistance in E. casseliflavus

   E. casseliflavus and E. gallinarum carry the chromosomal vanC gene, which gives low-level vancomycin resistance with MICs of about 8 to 16 micrograms/mL. Motility and yellow pigment point to E. casseliflavus, and both species are vanA and vanB negative. These isolates are not reported as VRE for infection control, so correct identification avoids needless isolation. vanA strains give MICs of 64 micrograms/mL or more.

   • A: A vanA strain would give a much higher MIC, and the gene is detected whether or not it is expressed.
   • C: E. faecium is non-motile and unpigmented, and its vanA PCR would be positive.
   • D: van genes are not lost during a single overnight subculture.

3. Question 3 · Medium

   A rapid multiplex panel on a positive blood culture reports Staphylococcus aureus with mecA detected. The therapeutic implication is:

   1. AThe organism is a coagulase-negative species
   2. BThe isolate is also resistant to vancomycin
   3. CVancomycin should be continued because the isolate is MRSA
   4. DNafcillin can be started because the isolate is MSSA

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   Answer: C · Vancomycin should be continued because the isolate is MRSA

   Detecting mecA together with an S. aureus target identifies MRSA hours before culture-based susceptibility results. An anti-staphylococcal beta-lactam such as nafcillin or cefazolin would fail, so vancomycin or another anti-MRSA agent is continued. If the S. aureus target is positive and mecA is not detected, the isolate is MSSA and a beta-lactam is preferred because it performs better. Conventional susceptibility testing still follows for confirmation and other agents.

   • A: The panel reported an S. aureus target, not a coagulase-negative species.
   • B: mecA says nothing about vancomycin, which is tested separately.
   • D: mecA detected means methicillin resistance, so nafcillin would fail.

4. Question 4 · Easy

   How does the vanA gene make Enterococcus faecium resistant to vancomycin?

   1. AIt alters the ribosome so the drug can no longer bind
   2. BIt thickens the capsule so the drug cannot reach the wall
   3. CIt makes an enzyme that cleaves the vancomycin molecule
   4. DIt ends precursors in D-alanyl-D-lactate instead of D-alanyl-D-alanine

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   Answer: D · It ends precursors in D-alanyl-D-lactate instead of D-alanyl-D-alanine

   vanA encodes enzymes that build peptidoglycan precursors ending in D-alanyl-D-lactate rather than D-alanyl-D-alanine. Vancomycin binds this altered terminus about a thousand times less well, so cell wall synthesis continues. vanA gives high-level resistance to both vancomycin and teicoplanin and is carried on a transferable plasmid. E. faecium carries vanA far more often than E. faecalis.

   • A: Vancomycin acts on cell wall precursors, not on the ribosome.
   • B: Capsule changes are not a glycopeptide resistance mechanism.
   • C: No enzyme that destroys vancomycin has been described in enterococci.

5. Question 5 · Medium

   A carbapenem-resistant Klebsiella pneumoniae isolate is blaKPC positive by PCR. How does this differ from an NDM producer?

   1. AKPC leaves aztreonam reliably active
   2. BKPC is a serine enzyme inhibited by avibactam
   3. CKPC is a zinc-dependent metallo-beta-lactamase
   4. DKPC is carried only on the chromosome

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   Answer: B · KPC is a serine enzyme inhibited by avibactam

   KPC is a serine carbapenemase, so it is inhibited by the newer inhibitors avibactam, vaborbactam and relebactam. NDM is a metallo-beta-lactamase that requires zinc and is not inhibited by them, which changes treatment and is why the genotype is reported. Both genes are usually plasmid borne and spread among Enterobacterales. Aztreonam escapes hydrolysis by metallo-enzymes but is destroyed by KPC and by the ESBLs that often accompany these strains.

   • A: KPC hydrolyses aztreonam, so activity cannot be assumed.
   • C: The zinc-dependent metallo-enzymes are NDM, VIM and IMP, not KPC.
   • D: blaKPC is usually carried on a transferable plasmid.

6. Question 6 · Medium

   Compared with vanB, vanA-mediated resistance in enterococci is characterized by:

   1. AResistance confined to Enterococcus gallinarum
   2. BResistance to teicoplanin with vancomycin susceptibility
   3. CHigh-level resistance to both vancomycin and teicoplanin
   4. DLow-level resistance that is lost on subculture

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