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Genomes > Lecture 11: Antibiotic Resistance > Flashcards

Lecture 11: Antibiotic Resistance Flashcards

1
Q

What do all bacterial pathogens show?

A

Some degree of antibiotic resistance

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2
Q

Where is mycobacterium tuberculosis very drug resistant?

A

Asia

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3
Q

What are antibiotics?

A

Natural substances made by soil bacteria and fungi that inhibit the growth/proliferation of bacteria or kill them directly

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4
Q

What are the three ways antibiotics can work?

A

cell-wall synthesis inhibitors, protein synthesis inhibitors, DNA replication inhibitors

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5
Q

How do cell wall synthesis inhibitors work?

A

B-lactam antibiotics eg penicillins - methicillin amoxicillin and ampicillin bind to penicillin binding proteins (PBP) which play a role in cross-linking peptidoglycan and stop the synthesis of the cell wall. Glycopeptides such as vancomycin inhibit cell wall synthesis.

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6
Q

How do protein synthesis inhibitors work?

A

They bind the ribosome and inhibit protein synthesis

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7
Q

How do DNA replication inhibitors work and give an example.

A

Synthetic antibiotics that bind topoisomerase 2 blocking further DNA replication. eg quinones

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8
Q

How do resistance genes work? Give three ways

A
  1. Encode enzymes that inactivate the drugs by cleavage or chemical modification eg penicillinase.
  2. Encode products that modify or replace the target molecules in the cell to which antibiotics normally bind eg MRSA has alternative PBP so can still synthesise the cell wall.
  3. Can enable the cell to block entry of antibiotics or encode molecular pumps that export the drugs out the cell eg tetracycline resistance.
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9
Q

How can resistance genes be transferred?

A

Horizontally

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10
Q

What three things can give bacteria innate resistance?

A

Gram -ve bacteria have an outer membrane which acts as a permeability barrier. Bacteria may lack the transport system for getting the antibiotic into the cells. bacteria may lack the target or reaction hit by an antibiotic.

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11
Q

What is the difference between broad, narrow and limited spectrum?

A

broad antibiotics are effective against a range of different species. narrow are effective against a limited number of species. limited are effective against a single species.

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12
Q

Why can E.faecalis be fatal in hospitalised patients?

A

E.faecalis is normally present in the gut flora and is naturally resistant to cephalosporins. In hospitalised patients, the exposure to cephalosporins will reduce the competition from susceptible bacteria so e.faecilis can spread to the heart valves and other organs and be fatal.

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13
Q

What does clostridium difficile have?

A

innate resistance to broad spectrum antibiotics

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14
Q

How can we measure antibiotic resistance in bacteria?

A

place bacteria over surface of petri dish in culture medium. place disks of antibiotics onto petri dish and incubate over night. Bacteria will not grow in a zone around an antibiotic if it is susceptible to it.

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15
Q

What are antibiotics used for?

A

about 50% for medicine. In the US 40% are used in animal husbandry where low concs are administered over long periods of time to promote growth and resistant forms include salmonella. 10% for agriculture for spraying fruit trees.

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16
Q

When was penicillin rediscovered?

A

1928 by Alexander Flemming

17
Q

What was the first species to become resistant and when? 80% is what?

A

Staphylococcus aureus, 1946. The amount of S.aureaus that is resistant today.

18
Q

Why does resistance never get to 100%?

A

Because resistance can be lost so strains are sensitive to growth.

19
Q

$20-$30,000 is the cost of what?

A

The extra cost per patient in the US due to antibiotic resistnace

20
Q

How does it spread so quickly?

A

Overuse of antibiotics, non-medical uses, global movement of people, poor hygiene and environmental pollution, inadequate serveillance and monitoring

21
Q

How can they adapt and evolve quickly?

A

Large effective population size and very variable so natural selection has lots of raw materials. SHort generation times of about a day in the wild.

22
Q

What happens in many cases?

A

Resistance evolves before the antibiotic is used

23
Q

Why are resistance genes expected to be found in nature?

A

Because antibiotics are modified from natural compounds.

24
Q

What happens when antibiotics are present?

A

The previously rare resistant variants outcompete the sensitive strains.

25
Q

What did sequencing the genome of shigella reveal from a WW1 soldier in 1915?

A

It was alredy resistant to penicillin and erythromycin.

26
Q

How else can resistance genes be spread?

A

By being carried on mobile genetic elements eg plasmids or phage or via transformation resulting in exchange of chrDNA.

27
Q

How did S.aureus acquire multiple resistance?

A

By acquisition of a large piece of DNA which might come from a closely related species

28
Q

What are compensatory mutations? What is their impact?

A

Acquisition of resistance genes may confer a fitness cost to the cell but compensatory mutations will make up for this. Once they have evolved they remain in the population so resistance genes are more likely to emerge in the future again.

29
Q

What was there resistance to in 1953?

A

Streptomycin, chloramphenicol and tetracycline.

30
Q

In 1953 there was an outbreak of shigella in Japan and what did it have resistance to and what was bad about this?

A

Resistant to chloramphenicol, streptomycin, tetracycline and sulphonamides. They had multiple resistance due to acquisition of a single plasmid containing several resistance genes so using one antibiotic would select for resistance in all of them.

31
Q

What are homoplasies? How many SNPs appear independently on different branches and how many are associated with drug resistance?

A

Mutations that arise independently in different parts of the phylogenetic tree which is indicative of positive selection. 38 SNPs and 11.

32
Q

What is 2% and 40% and 20%

A

In 1992, MRSA accounted for 2% of S.aureus cases. in 2000, it was 40%. it declined in 2006 to 20%.

33
Q

What caused the rise of MRSA?

A

Hospital hygiene, bed occupancy, isolation wards, understaffing, management structure.

34
Q

What was put in place after the rise in MRSA?

A

Barrier nursing

35
Q

How was WGS used for resistance?

A

WGS of 308 clinical S.aureus isolates from 26 European countries. Looked for presence/absensce of each resistant determinant to make in silico prediction of resistance profile.

36
Q

What is Kelbsiella pneumoniae? What is the consequence?

A

Multidrug resistant to B lactams. Is difficult to treat and in Greece they have stopped doing bone marrow transplants because is too risky.

Genomes (12 decks)

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