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ICAR AICE-JRF/SRF Veterinary Chemotherapy & Antimicrobial Stewardship: practice questions

ICAR AICE-JRF/SRF (PhD) · India · NTA for ICAR

Original practice questions written to the published syllabus · not past papers
10worked here, free
26written to this exam in this subject
12syllabus units

About ICAR AICE-JRF/SRF

ICAR AICE-JRF/SRF (PhD) is a PhD, fellowship and lectureship exam run by NTA for ICAR, for candidates in India. Computer-based, 2 hours, 120 questions: Part A 20 (general agriculture, animal husbandry, current events), Part B 50 (core group), Part C 50 (specialised subject). +4 / -1, maximum 480.

Source: icar.org.in.

Checked against the exam body's published information. Formats and fees change; confirm the current edition there before you book.

Veterinary Chemotherapy & Antimicrobial Stewardship in ICAR AICE-JRF/SRF

PK/PD indices and the mutant selection window, resistance genes (mecA, erm, tet, qnr, mcr-1, CTX-M), horizontal gene transfer and integrons, FECRT and benzimidazole resistance genetics, WHO/WOAH importance lists, anticancer drug mechanisms.

Antibacterial, antifungal, antiprotozoal, anthelmintic, ectoparasiticide and anticancer drugs, and the prudent use that slows antimicrobial resistance.

Our 26 ICAR AICE-JRF/SRF questions in this subject: 0 easy, 10 medium, 16 hard, across 12 units.

10 practice questions, worked

Choose an answer, then open the working. Each explanation says why the right answer is right and why the others are not.

These 10 were written to ICAR AICE-JRF/SRF and are not shown on any other exam's page.

Question 1 · medium

Methicillin resistance in Staphylococcus pseudintermedius is due to

  1. loss of outer-membrane porins that admit beta-lactams to the cell
  2. erm methylation of 23S rRNA in the large ribosomal subunit
  3. mecA encoding PBP2a, a low-affinity penicillin-binding protein
  4. blaZ encoding a penicillinase that clavulanate cannot inhibit
Answer and working

C. mecA encoding PBP2a, a low-affinity penicillin-binding protein

mecA (sometimes mecC) encodes PBP2a, which continues cross-linking when beta-lactams have bound the normal PBPs, giving resistance to almost all beta-lactams. blaZ penicillinase is inhibited by clavulanate; staphylococci have no outer membrane.

Question 2 · hard

An E. coli isolate is resistant to ceftiofur and cefoxitin, and the resistance is not reversed by clavulanic acid. Which enzyme type is most likely?

  1. TEM-1 narrow-spectrum penicillinase
  2. CTX-M extended-spectrum beta-lactamase
  3. Plasmid-mediated AmpC such as CMY-2
  4. Staphylococcal blaZ penicillinase
Answer and working

C. Plasmid-mediated AmpC such as CMY-2

AmpC enzymes hydrolyse third-generation cephalosporins and cephamycins (cefoxitin) and are not inhibited by clavulanate. CTX-M ESBLs are inhibited by clavulanate and do not hydrolyse cefoxitin; TEM-1 does not touch third-generation cephalosporins.

Question 3 · hard

Which pair correctly names the two main acquired tetracycline-resistance mechanisms with an example gene for each?

  1. Enzymatic acetylation by cat; target methylation by erm
  2. Efflux by tet(M); ribosomal protection by tet(A)
  3. Efflux by tet(A); ribosomal protection by tet(M)
  4. Porin loss by ompF; target mutation in the gyrA gene
Answer and working

C. Efflux by tet(A); ribosomal protection by tet(M)

tet(A) and tet(B) encode efflux pumps; tet(M) and tet(O) encode ribosomal protection proteins. Swapping them is the classic trap; cat and erm belong to chloramphenicol and macrolides.

Question 4 · hard

Macrolides reach higher concentrations in milk than in plasma after systemic dosing of a cow mainly because

  1. mammary epithelium secretes them actively by P-glycoprotein
  2. they bind milk fat globules covalently and stay in the udder
  3. they are weak acids ion-trapped in slightly alkaline milk
  4. they are weak bases ion-trapped in slightly acidic milk
Answer and working

D. they are weak bases ion-trapped in slightly acidic milk

Milk (pH about 6.5-6.8) is more acidic than plasma, so lipid-soluble weak bases such as macrolides become ionised in milk and are trapped. Weak acids such as penicillins show the opposite, a lower milk-to-plasma ratio.

Question 5 · hard

An E. coli isolate's ciprofloxacin MIC is raised slightly; sequencing finds no gyrA or parC mutation but a plasmid gene. Which gene best explains this?

  1. mcr-1, encoding a lipid A phosphoethanolamine transferase
  2. mecA, encoding a low-affinity penicillin-binding protein
  3. erm(B), encoding a 23S rRNA methyltransferase enzyme
  4. qnr, encoding a protein that protects DNA gyrase
Answer and working

D. qnr, encoding a protein that protects DNA gyrase

Plasmid-mediated quinolone resistance (qnr, aac(6')-Ib-cr, qepA, oqxAB) gives low-level resistance that eases selection of high-level chromosomal mutations.

Question 6 · hard

The colistin-resistance gene mcr-1, first reported in 2015 from pigs and people in China, is especially worrying because it

  1. is plasmid-borne and so can spread horizontally between bacteria
  2. is a chromosomal mutation that cannot leave its host bacterium
  3. can only be expressed in Gram-positive bacteria such as enterococci
  4. also inactivates every beta-lactam including the carbapenems
Answer and working

A. is plasmid-borne and so can spread horizontally between bacteria

mcr-1 encodes a phosphoethanolamine transferase that modifies lipid A, and because it is plasmid-mediated it spread rapidly across species and continents; colistin is a last-resort human drug for carbapenem-resistant Enterobacterales.

Question 7 · hard

The 'mutant selection window' for an antimicrobial is the concentration range

  1. between the Cmax and the trough within one dosing interval
  2. below the MIC, where no bacteria are inhibited
  3. above the MPC, where all single-step mutants die
  4. between the MIC and the mutant prevention concentration
Answer and working

D. between the MIC and the mutant prevention concentration

Between MIC and MPC, susceptible cells are inhibited but first-step mutants survive and are enriched; regimens that pass quickly through this window slow resistance.

Question 8 · medium

A beta-lactam is time-dependent. Which change in regimen most improves its efficacy against a susceptible organism?

  1. Doubling the single dose but keeping the interval
  2. Giving the whole daily dose as one bolus
  3. Adding a bacteriostatic tetracycline to it
  4. Giving the same daily dose more frequently
Answer and working

D. Giving the same daily dose more frequently

For time-dependent drugs, %fT>MIC drives efficacy, so shorter intervals help more than higher peaks. A bacteriostatic partner may antagonise a beta-lactam.

Question 9 · medium

After an IV bolus a drug reaches 16 µg/mL and has a half-life of 2 h. For an MIC of 1 µg/mL and a 12-hour dosing interval, roughly what percentage of the interval is spent above the MIC?

  1. 50%
  2. 100%
  3. 33%
  4. 67%
Answer and working

D. 67%

16 to 1 µg/mL is four halvings (16-8-4-2-1), so 4 x 2 h = 8 h above the MIC; 8/12 x 100 = 67%. 33% is the time below the MIC; 50% assumes three half-lives.

Question 10 · hard

An E. coli isolate from a dog's urine has an MIC above the epidemiological cut-off (ECOFF) but below the clinical susceptible breakpoint for that drug at the urinary site. What does this mean?

  1. It likely has an acquired mechanism yet is still predicted to respond
  2. It must be reported as resistant because the ECOFF is exceeded
  3. It is wild-type and clinically resistant at the urinary site
  4. It is fully wild-type, as ECOFFs and breakpoints are identical
Answer and working

A. It likely has an acquired mechanism yet is still predicted to respond

ECOFFs separate wild-type from non-wild-type for surveillance; clinical breakpoints predict outcome for a given species, site and regimen. An isolate can be non-wild-type yet clinically susceptible, especially where urinary concentrations are high.

A study plan for Veterinary Chemotherapy & Antimicrobial Stewardship in ICAR AICE-JRF/SRF

This plan follows where our questions actually fall, so the time goes where the marks are likely to be. It is our reading of the syllabus, not the exam body's weighting.

  1. First, the heavy units (50% of the 26 questions): Mechanisms and problems of drug resistance (5, 19%); Critically important antimicrobials (3, 12%); Prudent use of antimicrobials (3, 12%); Aminoglycosides (2, 8%).

    Read the manual chapters for these first and do every worked question you can find on them.

  2. Then the middle band: Anthelmintics (2, 8%); Beta-lactam antibiotics (2, 8%); Ectoparasiticides (2, 8%); Fluoroquinolones (2, 8%).

    Aim for one sitting per unit, then mixed questions across them.

  3. Then the lighter units: Macrolides (2, 8%); Anticancer drugs (1, 4%); Antiprotozoal drugs (1, 4%); Tetracyclines (1, 4%).

    Learn the definitions, classifications and standard numbers; these units are more often recalled than worked.

  4. Leave time for the hard ones: Anthelmintics (2 hard of 2), Fluoroquinolones (2 hard of 2), Macrolides (2 hard of 2).

    Come back to these after a first pass, untimed, and read every explanation, including for the options you rejected.

  5. Finish timed. Sit the subject as a timed set without notes, mark it, and send each wrong answer back to its unit above.

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