An ICU in a Gulf hospital screens all admissions for vancomycin-resistant enterococci (VRE) with a rectal-swab PCR for vanA and vanB and confirms positives by culture. Over 2 months, 14 patients are vanB positive (Ct 31-36) and vanA negative. Swabs reach the laboratory within 2 hours. Vancomycin enrichment broth subcultured to chromogenic VRE agar grows no enterococci from any of the 14 swabs, while vanA-positive swabs from the same period grow VRE. No-template controls are negative, and new swabs from the same patients are vanB positive again. The most likely explanation is:

vanB genes in gut anaerobes, not in enterococci

Amplicon contamination of the PCR work area

VRE killed by delays in swab transport

Intrinsic vanC of E. gallinarum detected as vanB

A Pseudomonas aeruginosa grows from the sputum of a ventilated patient who has received 10 days of imipenem in a Gulf hospital where carbapenemase producers are common. MICs (mg/L) with CLSI breakpoints: imipenem 16 (R ≥8); meropenem 2 (S ≤2); ceftazidime 4 (S ≤8); cefepime 4 (S ≤8); piperacillin-tazobactam 8 (S ≤16); aztreonam 8 (S ≤8). The mCIM is negative, and a lateral flow test for KPC, OXA-48, NDM, VIM and IMP enzymes is negative. The most likely resistance mechanism is:

Overexpressed MexAB-OprM efflux

Before cardiac surgery, a 64-year-old man is found to carry MRSA in his nose. He completes a 5-day course of nasal mupirocin with chlorhexidine body washes, but a nasal swab 2 weeks later still grows MRSA. The isolate is tested by disk diffusion. A 200 µg mupirocin disk shows no zone of inhibition; by CLSI, any zone around this disk excludes high-level resistance. A 5 µg mupirocin disk also shows no zone. QC with S. aureus ATCC 25923 is within range. What is the best interpretation?

High-level mupirocin resistance, usually mupA

Disk failure; susceptibility cannot be read

Low-level mupirocin resistance from ileS mutation

Recolonization by a mupirocin-susceptible strain

A meropenem-resistant Klebsiella pneumoniae from an ICU patient in Abu Dhabi was tested with the meropenem combination disks shown. By EUCAST guidance, synergy is a zone increase of at least 4 mm with phenylboronic acid (PBA) and at least 5 mm with EDTA or cloxacillin (CLX). The mechanism that best explains the result is:

Class A carbapenemase, such as KPC

AmpC with outer membrane porin loss

Metallo-β-lactamase, such as NDM

A Staphylococcus aureus blood isolate gives the cefoxitin disk result shown (CLSI: resistant ≤21 mm, susceptible ≥22 mm). Besides oxacillin, the report should list as resistant:

All other β-lactams except anti-MRSA cephalosporins

Cefoxitin only, as the surrogate marker

All β-lactams, including ceftaroline

Penicillin only; test cephalosporins separately

Resistance: MRSA, VRE, ESBL and carbapenemases

28 DOH Abu Dhabi (HAAD) lab licensing practice questions on Resistance: MRSA, VRE, ESBL and carbapenemases, part of Microbiology. The first 25 are below; the first 5 with answers and explanations (tap Show answer after you have chosen), the rest in Learn with a free account.

Question 1 · Hard
An ICU in a Gulf hospital screens all admissions for vancomycin-resistant enterococci (VRE) with a rectal-swab PCR for vanA and vanB and confirms positives by culture. Over 2 months, 14 patients are vanB positive (Ct 31-36) and vanA negative. Swabs reach the laboratory within 2 hours. Vancomycin enrichment broth subcultured to chromogenic VRE agar grows no enterococci from any of the 14 swabs, while vanA-positive swabs from the same period grow VRE. No-template controls are negative, and new swabs from the same patients are vanB positive again. The most likely explanation is:
1. AAmplicon contamination of the PCR work area
2. BVRE killed by delays in swab transport
3. CIntrinsic vanC of E. gallinarum detected as vanB
4. DvanB genes in gut anaerobes, not in enterococci
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Answer: D · vanB genes in gut anaerobes, not in enterococci
The vanB gene cluster is carried not only by enterococci but also by several gut anaerobes, such as Clostridium species and other commensals. A vanB-only PCR result on a rectal swab therefore has a low positive predictive value for VRE, especially at late Ct values, whereas vanA is much more specific. Contamination is unlikely, because no-template controls are negative and fresh swabs repeat the result, and transport is not the problem, because vanA-positive swabs from the same period grow VRE. Many laboratories therefore confirm vanB-only results by culture before a patient is labelled a VRE carrier. This avoids needless isolation and keeps single rooms for true carriers.
- A: Negative no-template controls and repeat positives on new swabs argue against contamination.
- B: Swabs arrived within 2 hours, and vanA-positive swabs from the same period grew VRE.
- C: vanB assays do not detect vanC, which differs in sequence.
Question 2 · Hard
A Pseudomonas aeruginosa grows from the sputum of a ventilated patient who has received 10 days of imipenem in a Gulf hospital where carbapenemase producers are common. MICs (mg/L) with CLSI breakpoints: imipenem 16 (R ≥8); meropenem 2 (S ≤2); ceftazidime 4 (S ≤8); cefepime 4 (S ≤8); piperacillin-tazobactam 8 (S ≤16); aztreonam 8 (S ≤8). The mCIM is negative, and a lateral flow test for KPC, OXA-48, NDM, VIM and IMP enzymes is negative. The most likely resistance mechanism is:
1. ADerepressed chromosomal AmpC
2. BVIM metallo-beta-lactamase
3. COverexpressed MexAB-OprM efflux
4. DLoss of the OprD porin
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Answer: D · Loss of the OprD porin
Resistance to imipenem alone, with meropenem, the cephalosporins, piperacillin-tazobactam and aztreonam still active, is the classic pattern of OprD porin loss. Imipenem enters P. aeruginosa mainly through OprD, and mutants lacking it are selected during imipenem therapy, as in this patient. Meropenem depends less on OprD, so its MIC rises only slightly. The negative mCIM and lateral flow test argue against a carbapenemase, which in P. aeruginosa is usually a metallo-beta-lactamase such as VIM or NDM that also hydrolyses ceftazidime and cefepime. Carbapenem-resistant isolates are still tested for carbapenemases, because the result guides infection control.
- A: Derepressed AmpC would make ceftazidime and piperacillin-tazobactam resistant.
- B: VIM would raise ceftazidime and cefepime MICs and give a positive mCIM and lateral flow test.
- C: MexAB-OprM efflux raises meropenem and aztreonam MICs but spares imipenem.
Question 3 · Hard
Before cardiac surgery, a 64-year-old man is found to carry MRSA in his nose. He completes a 5-day course of nasal mupirocin with chlorhexidine body washes, but a nasal swab 2 weeks later still grows MRSA. The isolate is tested by disk diffusion. A 200 µg mupirocin disk shows no zone of inhibition; by CLSI, any zone around this disk excludes high-level resistance. A 5 µg mupirocin disk also shows no zone. QC with S. aureus ATCC 25923 is within range. What is the best interpretation?
1. ADisk failure; susceptibility cannot be read
2. BLow-level mupirocin resistance from ileS mutation
3. CHigh-level mupirocin resistance, usually mupA
4. DRecolonization by a mupirocin-susceptible strain
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Answer: C · High-level mupirocin resistance, usually mupA
The 200 µg disk separates high-level from low-level mupirocin resistance: no zone means high-level resistance (MIC 512 µg/mL or more), and any zone rules it out. High-level resistance is usually carried on a plasmid gene, mupA (ileS2), which encodes an alternative isoleucyl-tRNA synthetase that mupirocin cannot block. Low-level resistance comes from point mutations in the native ileS gene and leaves a zone around the 200 µg disk. High-level resistance predicts failure of nasal decolonization, which fits this patient, so the surgical team should be told and another agent considered. Monitoring mupirocin resistance is useful wherever the drug is used widely.
- A: QC is in range and both disk strengths agree, so the test is valid.
- B: Low-level resistance leaves a zone around the 200 µg disk.
- D: A susceptible strain would give zones around both disks.
Question 4 · Hard
A meropenem-resistant Klebsiella pneumoniae from an ICU patient in Abu Dhabi was tested with the meropenem combination disks shown. By EUCAST guidance, synergy is a zone increase of at least 4 mm with phenylboronic acid (PBA) and at least 5 mm with EDTA or cloxacillin (CLX). The mechanism that best explains the result is:
Figure: MedExams
1. AAmpC with outer membrane porin loss
2. BOXA-48-like carbapenemase
3. CMetallo-β-lactamase, such as NDM
4. DClass A carbapenemase, such as KPC
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Answer: D · Class A carbapenemase, such as KPC
Compared with meropenem alone (10 mm), PBA enlarges the zone by 9 mm, EDTA by 1 mm and cloxacillin by 1 mm. Boronic acid inhibits both class A carbapenemases and AmpC, while cloxacillin inhibits AmpC only, so synergy with PBA alone points to a KPC-type enzyme. AmpC with porin loss would show synergy with both PBA and cloxacillin, and a metallo-β-lactamase would show synergy with EDTA. OXA-48-like enzymes show no synergy with any of these inhibitors, and a temocillin disk with little or no zone supports them.
- A: AmpC with porin loss would also show synergy with cloxacillin.
- B: OXA-48-like enzymes give no synergy, but PBA added 9 mm here.
- C: EDTA added only 1 mm, so there is no metallo-enzyme synergy.
Question 5 · Medium
A Staphylococcus aureus blood isolate gives the cefoxitin disk result shown (CLSI: resistant ≤21 mm, susceptible ≥22 mm). Besides oxacillin, the report should list as resistant:
Figure: MedExams
1. ACefoxitin only, as the surrogate marker
2. BAll β-lactams, including ceftaroline
3. CPenicillin only; test cephalosporins separately
4. DAll other β-lactams except anti-MRSA cephalosporins
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Answer: D · All other β-lactams except anti-MRSA cephalosporins
The 14 mm zone is in the resistant range, so the isolate carries mecA (or mecC) and is MRSA; cefoxitin is used because it induces and detects this resistance better than oxacillin. PBP2a binds almost all β-lactams poorly, so CLSI reports MRSA as resistant to penicillins, β-lactam/β-lactamase inhibitor combinations, cephems and carbapenems. The exceptions are the anti-MRSA cephalosporins, ceftaroline and ceftobiprole, which bind PBP2a and are tested separately. Cefoxitin itself is not reported as a treatment option.
- A: Cefoxitin is a surrogate marker; the resistance it detects covers the other β-lactams.
- B: Ceftaroline binds PBP2a and is tested and reported separately.
- C: MRSA is resistant to cephalosporins as well, apart from the anti-MRSA agents.
Question 6 · Medium
An Escherichia coli urine isolate resistant to cefotaxime and ceftazidime was tested with the CLSI combination disks shown. The result is interpreted as:
Figure: MedExams
1. AIndeterminate; repeat with cefepime
2. BAmpC production confirmed instead
3. CESBL not confirmed by either disk pair
4. DESBL confirmed by both disk pairs
Answer and explanation in LearnFree account
Question 7 · Easy
Which ESBL family is the most common in Escherichia coli worldwide, including in the Gulf countries?
1. ACTX-M
2. BSHV-1
3. CKPC
4. DTEM-1
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Question 8 · Hard
A nasal MRSA PCR that targets the SCCmec-orfX junction is positive. Culture grows only Staphylococcus aureus that is cefoxitin susceptible and PBP2a negative; on the isolate, the junction PCR is positive but mecA PCR is negative. The most likely explanation is:
1. AInducible clindamycin resistance in the isolate
2. BAn SCCmec remnant that has lost mecA (mecA dropout)
3. CA mecC strain missed by the cefoxitin disk
4. DContamination of the culture plate with MSSA
Answer and explanation in LearnFree account
Question 9 · Easy
A latex agglutination test for PBP2a performed on Staphylococcus aureus colonies detects:
1. ABeta-lactamase made by the blaZ gene
2. BProtein A and clumping factor
3. CThe protein product of the mecA gene
4. DVancomycin-binding cell wall precursors
Answer and explanation in LearnFree account
Question 10 · Hard
An Enterobacter cloacae complex isolate is resistant to cefotaxime and ceftazidime, and an ESBL is suspected. Why is a cefepime disk with and without clavulanate used for confirmation?
1. AClavulanate inactivates cefotaxime in Enterobacter
2. BEnterobacter cannot grow near ceftazidime disks
3. CCefepime is the only cephalosporin clavulanate can pair with
4. DCefepime is stable to AmpC, so AmpC does not mask the ESBL
Answer and explanation in LearnFree account
Question 11 · Hard
A Gulf hospital screens admissions with a chromogenic CRE agar evaluated mainly on KPC producers. A patient's rectal screen is negative, but a week later an OXA-48-like Klebsiella pneumoniae (meropenem MIC 0.25 mg/L) grows from urine, and the same strain grows when the stored swab is recultured on an OXA-48 medium. The most likely reason the screen missed it is:
1. AIts low carbapenem MIC let the medium inhibit it
2. BThe chromogenic medium inhibits all strains of Klebsiella
3. CRectal swabs are unsuitable for CRE screening
4. DOXA-48-like producers do not colonize the gut
Answer and explanation in LearnFree account
Question 12 · Easy
Among carbapenemase-producing Enterobacterales in the Gulf countries, including the UAE, the most commonly reported enzymes are:
1. AKPC and VIM
2. BSME and NMC-A
3. CIMP and GES
4. DOXA-48-like and NDM
Answer and explanation in LearnFree account
Question 13 · Hard
A Klebsiella pneumoniae isolate has a meropenem MIC of 0.5 mg/L and is mCIM positive. Combined-disk tests show no zone enhancement with phenylboronic acid, EDTA or cloxacillin, and there is no zone around the temocillin disk. The most likely enzyme is:
1. AAn NDM metallo-beta-lactamase
2. BA plasmid AmpC with porin loss
3. CAn OXA-48-like carbapenemase
4. DA KPC carbapenemase
Answer and explanation in LearnFree account
Question 14 · Medium
An ESBL-producing Escherichia coli typically remains susceptible in vitro to:
1. ACefotaxime
2. BCeftazidime
3. CCefoxitin
4. DAztreonam
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Question 15 · Medium
Why is the modified Hodge test no longer recommended by CLSI for carbapenemase detection?
1. AIt gives false positives and misses many NDM producers
2. BIt requires molecular equipment that most labs lack
3. CIt takes more than a week to give a result
4. DIt detects only KPC enzymes in Pseudomonas
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Question 16 · Medium
In the modified carbapenem inactivation method (mCIM), the meropenem disk that was incubated with the test isolate is then placed on a lawn of:
1. AThe test isolate itself
2. BCarbapenem-susceptible E. coli ATCC 25922
3. CA KPC-producing Klebsiella control strain
4. DPseudomonas aeruginosa ATCC 27853
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Question 17 · Hard
A Staphylococcus aureus isolate from a skin abscess has a cefoxitin zone of 16 mm (resistant ≤21 mm), but the PBP2a latex test and mecA PCR are both negative. The most likely explanation is:
1. AA vanA gene acquired from enterococci
2. BHyperproduction of blaZ penicillinase
3. CmecC-mediated methicillin resistance
4. DInducible clindamycin resistance
Answer and explanation in LearnFree account
Question 18 · Medium
When Enterobacterales are screened for possible carbapenemase production, the carbapenem with the highest sensitivity but lowest specificity is:
1. AImipenem
2. BMeropenem
3. CErtapenem
4. DDoripenem
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Question 19 · Hard
An Enterococcus faecium isolate from a liver transplant patient's blood has a vancomycin MIC of 64 µg/mL (resistant ≥32) and a teicoplanin MIC of 0.5 µg/mL (susceptible ≤8). Which resistance gene best explains this pattern?
1. AvanB
2. Bpbp5
3. CvanA
4. DvanC1
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Question 20 · Medium
Why do rapid MRSA assays on positive blood cultures not report MRSA from mecA detection alone?
1. ACoagulase-negative staphylococci also commonly carry mecA
2. BmecA detection is too slow for blood cultures
3. CmecA is also present in most enterococci
4. DmecA is lost when blood culture broth is stored
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Question 21 · Medium
Why is a cefoxitin disk preferred to an oxacillin disk for detecting mecA-mediated resistance in Staphylococcus aureus?
1. AOxacillin disks cannot be stored in the refrigerator
2. BCefoxitin also detects vancomycin-intermediate strains
3. CCefoxitin is the drug used to treat MRSA infections
4. DCefoxitin induces mecA more strongly, giving clearer zones
Answer and explanation in LearnFree account
Question 22 · Hard
An Escherichia coli blood isolate is ertapenem resistant but meropenem and imipenem susceptible. The mCIM is negative, and PCR for KPC, NDM, VIM, IMP and OXA-48-like genes is negative. What is the most likely mechanism?
1. AAn OXA-48-like carbapenemase variant
2. BA KPC carbapenemase
3. CAn NDM metallo-beta-lactamase
4. DESBL or AmpC production with porin loss
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Question 23 · Medium
The CLSI vancomycin agar screen for enterococci uses which medium and vancomycin concentration?
1. ABrain-heart infusion agar with 500 µg/mL
2. BBlood agar with 0.5 µg/mL
3. CMueller-Hinton agar with 32 µg/mL
4. DBrain-heart infusion agar with 6 µg/mL
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Question 24 · Hard
A carbapenem-resistant Acinetobacter baumannii from an ICU patient gives a negative mCIM. Why should this result not be used to rule out a carbapenemase?
1. AAcinetobacter cannot grow in the tryptic soy broth step
2. BAcinetobacter carbapenemases are all metallo-enzymes
3. CCLSI validated the mCIM only for Enterobacterales and P. aeruginosa
4. DThe indicator E. coli is killed by Acinetobacter
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Question 25 · Medium
OXA-48-like carbapenemase producers can be missed in routine testing mainly because:
1. AThey grow only under anaerobic conditions
2. BTheir enzyme is destroyed by EDTA in the medium
3. CTheir carbapenem MICs often stay in the susceptible range
4. DThey are inhibited by clavulanate in the ESBL test
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Resistance: MRSA, VRE, ESBL and carbapenemases

A Staphylococcus aureus blood isolate gives the cefoxitin disk result shown (CLSI: resistant ≤21 mm, susceptible ≥22 mm). Besides oxacillin, the report should list as resistant:

An Escherichia coli urine isolate resistant to cefotaxime and ceftazidime was tested with the CLSI combination disks shown. The result is interpreted as:

Which ESBL family is the most common in Escherichia coli worldwide, including in the Gulf countries?

A nasal MRSA PCR that targets the SCCmec-orfX junction is positive. Culture grows only Staphylococcus aureus that is cefoxitin susceptible and PBP2a negative; on the isolate, the junction PCR is positive but mecA PCR is negative. The most likely explanation is:

A latex agglutination test for PBP2a performed on Staphylococcus aureus colonies detects:

An Enterobacter cloacae complex isolate is resistant to cefotaxime and ceftazidime, and an ESBL is suspected. Why is a cefepime disk with and without clavulanate used for confirmation?

Among carbapenemase-producing Enterobacterales in the Gulf countries, including the UAE, the most commonly reported enzymes are:

A Klebsiella pneumoniae isolate has a meropenem MIC of 0.5 mg/L and is mCIM positive. Combined-disk tests show no zone enhancement with phenylboronic acid, EDTA or cloxacillin, and there is no zone around the temocillin disk. The most likely enzyme is:

An ESBL-producing Escherichia coli typically remains susceptible in vitro to:

Why is the modified Hodge test no longer recommended by CLSI for carbapenemase detection?

In the modified carbapenem inactivation method (mCIM), the meropenem disk that was incubated with the test isolate is then placed on a lawn of:

A Staphylococcus aureus isolate from a skin abscess has a cefoxitin zone of 16 mm (resistant ≤21 mm), but the PBP2a latex test and mecA PCR are both negative. The most likely explanation is:

When Enterobacterales are screened for possible carbapenemase production, the carbapenem with the highest sensitivity but lowest specificity is:

An Enterococcus faecium isolate from a liver transplant patient's blood has a vancomycin MIC of 64 µg/mL (resistant ≥32) and a teicoplanin MIC of 0.5 µg/mL (susceptible ≤8). Which resistance gene best explains this pattern?

Why do rapid MRSA assays on positive blood cultures not report MRSA from mecA detection alone?

Why is a cefoxitin disk preferred to an oxacillin disk for detecting mecA-mediated resistance in Staphylococcus aureus?

An Escherichia coli blood isolate is ertapenem resistant but meropenem and imipenem susceptible. The mCIM is negative, and PCR for KPC, NDM, VIM, IMP and OXA-48-like genes is negative. What is the most likely mechanism?

The CLSI vancomycin agar screen for enterococci uses which medium and vancomycin concentration?

A carbapenem-resistant Acinetobacter baumannii from an ICU patient gives a negative mCIM. Why should this result not be used to rule out a carbapenemase?

OXA-48-like carbapenemase producers can be missed in routine testing mainly because: