Lecture 14 - Evolution of Antibiotic Resistance

1. What is an antibiotic?

A chemical that kills or inhibits bacteria.

2. What is antibiotic resistance?

The ability of bacteria to survive or grow despite exposure to an antibiotic that would normally affect them.

3. Does a person become antibiotic-resistant after taking antibiotics?

No. Bacteria develop resistance; a person may experience an allergic reaction to a drug.

4. What are the three stages of bacterial infection described in the lecture?

Invasion, proliferation, and colonization; nonspecific host response; specific immunity.

5. How can bacteria naturally defend themselves against competing bacteria?

By producing and secreting chemicals or toxins that inhibit or kill other bacteria.

6. What ancient substance was used for its antibacterial properties?

Honey.

7. Who discovered penicillin, and when?

Alexander Fleming, in 1928.

8. What does a zone of inhibition around an antibiotic indicate?

Bacterial growth was inhibited in the area surrounding the antibiotic.

9. According to the lecture, what percentage of new TB cases were drug-resistant?

8.2%.

10. According to the lecture, what percentage of relapsed TB cases were drug-resistant?

21.5%.

11. A bacterium produces beta-lactamase. How can this cause penicillin resistance?

The enzyme breaks down or modifies the beta-lactam antibiotic, preventing it from working.

12. How can reduced permeability cause antibiotic resistance?

The antibiotic cannot enter the bacterial cell in sufficient amounts to affect its target.

13. How does an efflux pump help a bacterium resist antibiotics?

It pumps the antibiotic out of the cell, reducing its internal concentration.

14. How can changing an antibiotic's target cause resistance?

The drug can no longer bind effectively to the altered target.

15. Why can MRSA resist many beta-lactam antibiotics?

It has an alternative penicillin-binding protein, PBP2a, with low affinity for many beta-lactams.

16. A drug prevents bacteria from building cell walls. Which antibiotic classes in the lecture act this way?

Penicillins and cephalosporins.

17. A drug blocks bacterial folate synthesis. Which antibiotic class is involved?

Sulfonamides.

18. A drug interferes with bacterial DNA replication. Which class is involved?

Fluoroquinolones.

19. Which antibiotic classes listed in the lecture target bacterial protein synthesis?

Tetracyclines, aminoglycosides, and macrolides.

20. A bacterium pumps tetracycline out of its cell. Which resistance mechanism is this?

Efflux.

21. Why are antibiotic-resistant infections especially concerning for people undergoing transplants or dialysis?

These patients may be especially vulnerable to infections and complications.

22. A hospital patient develops an infection caused by MRSA or VRE. Why is this a concern?

These organisms can resist important antibiotics, making infections harder to treat.

23. How can unnecessary antibiotic prescriptions contribute to resistance?

They expose bacteria to antibiotics and favor resistant bacteria over susceptible ones.

24. Why can giving antibiotics to livestock without treating a diagnosed infection promote resistance?

It exposes large bacterial populations to antibiotics, selecting for resistant bacteria.

25. According to the lecture's estimate, how was antibiotic use divided between humans and animals?

Approximately 30% for humans and 70% for animals.

26. A mutation occurs in the bacterial rpoB gene. What resistance can it cause?

Rifampicin resistance.

27. How does natural selection spread rifampicin resistance in a bacterial population?

Rifampicin kills susceptible bacteria, while resistant bacteria survive and reproduce.

28. Which antibiotic is associated with resistance caused by mutations in rpoB?

Rifampicin.

29. What four evolutionary mechanisms are discussed in the lecture?

Mutation, natural selection, gene flow, and genetic drift.

30. Why can antibiotics select for resistant bacteria without directly causing the useful resistance mutation?

Resistance variants may already exist; antibiotics favor their survival and reproduction.

31. After antibiotic treatment, a population shifts from mostly susceptible bacteria to mostly resistant bacteria. Why?

Susceptible bacteria are removed more effectively, increasing the resistant bacteria's relative frequency.

32. How can antibiotics affect normal flora?

They can kill susceptible beneficial bacteria and select for resistant bacteria among the survivors.

33. What role does E. coli commonly play in the human gut, according to the lecture?

It is one of the bacteria that can live as part of the normal gut flora.

34. Where can Staphylococcus aureus be found as part of normal flora?

On the skin.

35. Why can normal flora act as a reservoir for antibiotic-resistance genes?

Resistance genes can persist in these bacteria and potentially transfer to disease-causing bacteria.

36. Why should patients follow the prescribed instructions for antibiotic treatment?

Incorrect use can contribute to treatment failure and resistance; patients should follow their prescriber's directions.

37. What may happen if a bacterial infection is not properly treated?

The infection may persist or return, and treatment may become more difficult.

38. Why don't antibiotics treat viral infections such as colds?

Antibiotics target bacterial structures or processes that viruses do not have in the same way.

39. Name three behaviors that help reduce antibiotic resistance.

Use antibiotics only when appropriately prescribed, follow medical instructions, and avoid unnecessary antibacterial products.

40. How can resistance genes move from one bacterium to another?

Through horizontal gene transfer.

41. How might using antibacterial products contribute to cross-resistance?

Exposure may select for bacteria with resistance mechanisms that also protect them against certain antibiotics.

43. What does nontherapeutic antibiotic use in agriculture mean?

Using antibiotics for purposes other than treating a diagnosed illness, such as growth promotion or routine prevention.

44. Why can high-density livestock production increase concern about antibiotic resistance?

Many animals and their bacteria are exposed in close quarters, creating opportunities for resistant bacteria to spread.

45. What did the lecture report about the proportion of U.S. antibiotics produced for agriculture?

It reported that more than 50% were produced for agricultural use.

46. How can antibiotic-resistant bacteria or genes from livestock reach humans?

Through food, direct animal contact, or environmental routes such as contaminated water or waste.

47. Why is agricultural antibiotic use relevant to human medicine?

Bacteria and resistance genes selected in animals can potentially reach humans.

48. What cross-resistance concern was associated with avoparcin in the lecture?

Avoparcin use was associated with selection for resistance that could also affect vancomycin, an important human antibiotic.

49. What relationship did the lecture describe between virginiamycin and Synercid?

Virginiamycin is related to Synercid, an antibiotic combination used in human medicine.

50. What is cross-resistance?

When one resistance mechanism makes a bacterium resistant to more than one related drug or compound.

51. What two trends contribute to the antibiotic-resistance crisis?

An increase in resistant organisms and a limited supply of new antimicrobial drugs.

52. Why might pharmaceutical companies invest too little in new antibiotics?

Antibiotics may offer lower financial returns than drugs used regularly for chronic conditions, while development is costly.

53. What does the phrase “post-antibiotic era” mean?

A situation in which resistant infections make antibiotics ineffective for conditions they once treated reliably.

54. Why could antibiotic resistance make a hip replacement more dangerous?

An infection after surgery could be harder to treat if the bacteria resist available antibiotics.

55. What cost comparison did the lecture make about drug-resistant infections?

It stated that such infections can cost at least twice as much as comparable non-resistant infections.

56. What was the purpose of the Davos Declaration mentioned in the lecture?

To encourage coordinated action and new efforts to address antimicrobial resistance.

57. What is the iChip, and why is it important?

A device that helps grow previously uncultured environmental microbes, supporting discovery of new antibiotics.

58. What was notable about teixobactin in the lecture?

It was presented as a promising antibiotic discovered using the iChip approach.

59. How does teixobactin act against bacteria, according to the lecture?

It binds lipid building blocks involved in bacterial cell-wall synthesis.

60. Why is discovering new antibiotic classes important?

New mechanisms of action may treat resistant bacteria that existing drugs cannot effectively control.

61. How are discovering an antibiotic and the evolution of resistance related but different processes?

Discovery provides a drug that inhibits bacteria; resistance evolves when heritable variants survive exposure and reproduce.

62. What two ingredients are needed for natural selection to increase antibiotic resistance?

Heritable variation in resistance and differential survival or reproduction under antibiotic exposure.

63. How can reducing unnecessary antibiotic prescriptions affect resistance evolution?

It reduces selective pressure favoring resistant bacteria.

64. Why might stopping nontherapeutic antibiotic use in animal growth promotion help?

It can reduce unnecessary selection for resistant bacteria in livestock and their environments.

65. A bacterium destroys a drug, pumps it out, or changes its target. What do these examples represent?

Different resistance mechanisms: antibiotic inactivation, efflux, and target alteration.

66. Why is taking antibiotics only when appropriate an evolutionary strategy against resistance?

It reduces unnecessary selection pressure that gives resistant bacteria a relative advantage.

67. A bacterial population contains 1% resistant bacteria before treatment and 40% afterward. Does that necessarily mean the antibiotic created the resistance?

No. Treatment may have selected for resistant bacteria that were already present or arose during the population's history.

68. Why is resistance in normal flora clinically important even if those bacteria are not causing disease?

They can act as a reservoir of resistance genes that may spread to pathogens.

69. How can overprescribing, livestock antibiotic use, and antibacterial products all contribute to resistance?

Each can expose bacterial populations to compounds that select for resistant bacteria; some mechanisms may also produce cross-resistance.

70. A patient develops a bacterial infection, receives an antibiotic, and resistant bacteria survive. Connect this outcome to the lecture's main concepts.

Antibiotics impose selection pressure; heritable resistance allows some bacteria to survive, reproduce, and increase in frequency.