The treatment for people with active tuberculosis (TB) lasts six months and involves a combination of antibiotics. This is usually very effective if the person has a susceptible (non-resistant) strain of Mycobacterium tuberculosis, the causative organism of TB. Table 2.1 summarises one recommended treatment strategy that involves a combination of antibiotics. [Table 2.1]

Mark scheme

Marking points from the official mark scheme (Oct/Nov 2020). The mark or mark type is shown in brackets.

1. [4] any four from:
2. 1 (in combination treatment) antibiotics (in Table 2.1), act at different targets / have different modes of action / AW ;
3. A comparison of any two antibiotics from Table 2.1
4. A suggestion of how two antibiotics have different ways of killing
5. 2 idea that if resistance / mutation, occurs / exists, unlikely to be against all antibiotics / other antibiotics should still be effective;
6. 3 (in combination treatment) if resistance / mutation, occurs / exists, all bacteria will (still) be, killed / destroyed / AW ;
7. A no bacteria remain to develop resistance / no reservoir of resistant bacteria
8. 4 antibiotic resistance, not / less likely to be, spread to affect people because no bacteria surviving (with combination treatment) ; AW
9. 5 long treatment time / 6 months, with, combination treatment / AW, increases chance of killing all bacteria
10. or
11. long treatment time with a single antibiotic not effective in killing all bacteria if, resistance develops / a mutation occurs ;
12. 6 AVP; e.g.
13. combination treatment (is likely to) eliminate bacteria more quickly (so less chance of resistance occurring)
14. resistance to different antibiotics involves more genes so less chance of resistance occurring
15. gene for antibiotic resistance has more chance of being passed on if using single antibiotic (and not all killed) ora
16. if using single antibiotic (and not all killed) more chance of being passed on (to other bacteria) by horizontal / vertical / AW, transmission ora
17. [1] transcription ;
18. [3] any three from:
19. I stops transcription
20. 1 alters shape of /blocks, active site;
21. R enters / fits into, active site as it is not competitive
22. R ref. to choice of competitive or non-competitive
23. A alters shape of enzyme only if mp2 gained
24. 2 substrate / nucleotides, cannot, bind to / enter, active site;
25. A fewer/no, enzyme-substrate complexes / ESCs, form
26. allow ecf from mp1 if rifampicin described as, competitive /enters active site
27. 3 complementary (base) pairs / (complementary) base pairs, cannot form / form less easily (between DNA and RNA nucleotides) ;
28. 4, 5, 6 (in context of rifampicin binding to RNA polymerase)
29. prevents / AW, unwinding of DNA (double helix);
30. A uncoiling
31. I unzipping prevents / AW, attachment to DNA (strand)
32. A prevents / AW, attachment to promoter
33. prevents / AW, movement along DNA (strand);
34. prevents / AW, elongation (of polynucleotide) / formation of polynucleotide /nucleotides being joined ;
35. prevents / AW, phosphodiester bond formation ;
36. prevents / AW, proof reading ;
37. 7 AVP; e.g. prevents / AW, tRNA / rRNA, formation
38. [1] Phe
39. Tyr ; one mark for both correct
40. [1] BDFG ; in any order
41. [3] resistance
42. 1 shape / tertiary structure, of, β-subunit / enzyme, altered / AW ;
43. I active site changes shape
44. A quaternary structure of enzyme altered
45. 2 rifampicin / antibiotic, cannot / does not, bind (as well) ; AW
46. R if context is binding to active site
47. different levels of resistances
48. any two from:
49. 3 (because) other mutations are involved ; AW
50. A described from Table 2.1
51. e.g. C has 2 (other) mutations and D and E have 3
52. 4 mutations may result in different changes to, structure / shape of, β-subunit / enzyme, and result in different, effects / levels of resistance ;
53. 5 data from Table 2.2 to support mp 4; must be linked to concept of mp4
54. 6 AVP; e.g. ref. to different binding abilities (of rifampicin to enzyme)
55. some (of the other) mutations may cause more of a change to binding site for rifampicin
56. mutation(s) may make it harder to bind
57. lower resistance = binds, more strongly / for longer time
58. lower resistance = higher proportion of transcription events hindered
59. e.g. idea that mutations still, produce functioning enzyme / allow catalysis to occur