Quiz 4 (Lecture 18) Flashcards

1
Q

Who and when discovered penicillin?

A

Alexander Fleming and received the Nobel prize in 1945

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2
Q

When was penicillin resistance found?

A

same year (1945) Stanford found different strains of staphylococcus that do not respond to penicillin

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3
Q

What are antibiotics?

A
  • a heterogeneous class of molecules that interfere with the growth of bacteria
  • many antibiotics occur naturally and are isolated from bacteria & fungi
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4
Q

What are the three mode of actions in antibiotics?

A
  1. mimic a critical molecule
  2. bind irreversibly to an active site
  3. compete with a naturally occurring molecule for binding, passage or transport
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5
Q

What are the objectives of action in antibiotics?

A
  • to slow growth or kill target organisms
  • a therapeutic antibiotic needs to do this minimal toxicity to the host
    – usually accomplished by directing the antibiotic at a phylogenetically unique feature of the bacterial target
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6
Q

How do bacteria acquire resistance genes?

A
  1. mutations
  2. horizontal gene transfer
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7
Q

Do the genes for drug resistance exist in the pathogen population prior to infection or do they originate through mutation after infection?

A
  1. if the former, the strong, prolonged, antibiotic treatment selects for antibiotic resistance
  2. if the latter, treatment reduces the size of the pathogen population and the probability that a resistance mutation will ocur
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8
Q

What did traditional therapies wrongly assume that antibiotic resistance arises through?

A

mutation

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9
Q

What is a fix to antibiotic resistance?

A

use antibiotics to slow the rate of infection and control it rather than eliminate
- by letting immune system finish the job, we could slow/avoid the evolution of resistance

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10
Q

What does evidence suggest about most infections?

A

that they already contain pathogens with resistance genes

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11
Q

What was an example of the evolution of antibiotic resistance in a single patient?

A
  • JH acquired a staph infection after a heart valve operation
    -treated with rifampin and vancomycin
  • heart valved was replaced after 3 months
  • died 2 weeks later
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12
Q

What is the problem with using low levels of antibiotics?

A
  • only slows the growth of bacteria
  • bacteria w/ mutations that confer resistance to perform better; resistance genes will accumulate in the population
  • resistant bacteria then infect humans (spread and infects other animals too)
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13
Q

What were the results from the chickens who were fed with a sub-therapeutic dose of antibiotic v not at all?

A
  • after 2 weeks, 90% of experimental chicken excreted 100% resistant organisms in the feces
  • by 4 months, resistance was transferred to control chickens which now began to excrete resistant microbes
  • by 6 months, fecal samples of farmers also contained resistant bacteria
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14
Q

What was the result of farmers in Denmark reducing the amount of tylosin (antibiotic) in the feed of healthy pigs?

A

the prevalence of bacteria resistant to the drug dropped

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15
Q

In the 1990s the use of what dropped to less than 3% in the UK?

A

Sulfonamide (antibitoic)

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16
Q

What then happened to the frequency of sulfonamide resistant e. coli over this time period?

A

compensatory mutations arose in resistant strains, which eliminates the fitness costs associated with resistance

17
Q

What are ways to avoid or delay the evolution of resistance?

A
  • reduce the infection rate (avoid undercooked eggs and meat; wash hands to slow disease spread)
  • limit use of antibacterial soaps and cleaners
  • avoid prescribing antibiotics for viral infections
  • eliminate antibiotic use in animal feed
18
Q

Are the ways we avoid/delay evolution of resistance effective?

A

Only partially

19
Q

Nosocomial infections of multiply-resistant pathogens kill more patients each year than what?

A

breast cancer and HIV combined