ICAR AICE-JRF/SRF (PhD) · India · NTA for ICAR
Original practice questions written to the published syllabus · not past papersICAR 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.
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.
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.
Methicillin resistance in Staphylococcus pseudintermedius is due to
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.
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?
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.
Which pair correctly names the two main acquired tetracycline-resistance mechanisms with an example gene for each?
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.
Macrolides reach higher concentrations in milk than in plasma after systemic dosing of a cow mainly because
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.
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?
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.
The colistin-resistance gene mcr-1, first reported in 2015 from pigs and people in China, is especially worrying because it
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.
The 'mutant selection window' for an antimicrobial is the concentration range
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.
A beta-lactam is time-dependent. Which change in regimen most improves its efficacy against a susceptible organism?
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.
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?
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.
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?
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.
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.
Read the manual chapters for these first and do every worked question you can find on them.
Aim for one sitting per unit, then mixed questions across them.
Learn the definitions, classifications and standard numbers; these units are more often recalled than worked.
Come back to these after a first pass, untimed, and read every explanation, including for the options you rejected.
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