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MMI > Lecture 8 - Antimicrobials > Flashcards

Lecture 8 - Antimicrobials Flashcards

1
Q

4 early syphilis treatments and their dates?

A
  1. Mercury (15th century)
  2. Arsenic (1910)
  3. Fever induced by Malaria (1917) dubbed ‘neurosyphilis’
  4. Penicillin (1929) (only used on prokaryotes)
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2
Q

What was the first synthetic antimicrobial substance to selectively act on bacteria?

A

SULFA aka Prontosil –> 1932

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3
Q

How did Alexander Flemming discover penicillin?

A

he cultured staphlococci in a petri dish and then accidentally left the lid off and exposed the surface to air
He then came back to notice that there was growth in the staphlococci but also mold growth in areas where staph was not growing

  • “zone of inhibition” –> areas where the mold was growing and the bacteria wasn’t
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4
Q

Which two scientists aided the discovery of penicillin based off Flemming’s work?

A

Florey and Chain

they isolated the mold and used it as a anti-biotic

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5
Q

If we wanted to create a antibiotic that has selective effect on bacteria but not on Eukaryotes, which two properties would we want to focus the most on?

A

Cell wall

and Folic Acid Synthesis

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6
Q

Which targets of antibiotic drugs would have side effects on human cells?

A

if they target the:

  • plasma membrane
  • ribosome 70s (mitochondria)
  • Cytosol
  • DNA
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7
Q

what are two non-drug ways we can protect and prevent ourselves from infections?

A
  1. Immunoactive substances like interferon (signalling proteins that are released by host cells when they detect viruses - which causes nearby cells to heighten their anti-viral defenses - this includes cytokines)
  2. maintenance of good hygiene and integrity
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8
Q

what is the anti-parasitic drug for malaria? what is the problem with them?

A

quinine and derivatives (i.e. chloroquinine)

the problem is that they are increasing resistance of malaria to the drug

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9
Q

What is the major problem with anti-fungal agents?

A

toxicity

because they are eukaryotic organisms and share alot of common characteristics with human cells (i.e. Nuclei, Ribosome 80S, organelles etc..)

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10
Q

What do the most successful anti fungal agents affect?

A

they affect the plasma membrane which contains ergosterol instead of cholestrol

ergosterol prevents the division of fungi which eventually kills it

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11
Q

which organ does the toxic effects of antifungals mostly affect in humans?

A

the kidney

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12
Q

What is the most common drug used for systemic fungal illness?

A

amphotericin B (inhibits ergosterol synthesis in the cytoplasmic membrane of the fungal cell)

it also has the least amount of complications in humans

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13
Q

What are the 6 targets for anti-virals?

A
  1. DNA/RNA synthesis inhibitors
  2. Entry inhibitors (blocking the attachment of the virus to the host cell)
  3. Uncoating inhibitor - M2 proton channel: i.e. for influenza ‘A” —> the M2 proton helps virus escape from phagosome so the antiviral uncoating inhibitor prevents the phagosome from uncoating by acidifying the environment so hat the virus cant get out
  4. Nucleoside analogue –> A,C,T,Gs that look like the real ones that tricks viruses into encoding it into their DNA/RNA
  5. Protease inhibitors –> prevents proteases from chopping up viral proteins into structured components
  6. Inhibiting reverse transcriptase –> inhibits synthesis of DNA from RNA
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14
Q

What is the role of Azidothymidine (AZT) and Zidovudine?

A

its a drug that is an analogue of the amino acid thymidine –> it inhibits reverse transcriptase
especially used for treating HIV –> it is NOT a cure because the person has to take it all the time

more recently, HIV has become resistant to Azidothymidine so it is used in a cocktail of HAART drugs to HIV patients

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15
Q

Bacteriostatic antibiotic?

A

stops replication of bacteria

does not kill bacteria that is already present

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16
Q

example of bacteriostatic antibiotic?

A

erythromycin (macrolides)

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17
Q

bactericidal antibiotic?

A

kills the bacteria

stops bacterial metabolism

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18
Q

example of bactericidal antibiotic?

A

penicillin (beta-lactam)

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19
Q

When do we opt to use bactericidal antibiotics? Why is it dangerous?

A

we use them when our WBCs are too weak to get rid of the infection or if the infection is way too severe

it is mostly avoided especially in gram negative bacteria infections because they release endotoxins when they die and that can further increase toxicity in the body

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20
Q

Which antibiotics inhibit cell wall synthesis?

A
  • Beta lactams (penicillin, and cephalosporin)

- Vancomycin (stops cell wall synthesis by prevent the joining of amino acids to make peptidoglycan)

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21
Q

Which antibiotics inhibit protein synthesis at the 50S ribosomal subunit of bacteria?

A
  • Macrolides
  • Clindamycin
  • Linezolid
  • Chloramphenicol
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22
Q

Which antibiotics inhibit protein synthesis at the 30S ribsomal subunit of bacteria?

A
  • Tetracyclines

- Aminoglycosides (gentamicin) [for serious infections only]

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23
Q

Which antibiotics cause injury to the plasma membrane?

A

Polymyxins (topical treatment)

  • toxic to ingest
  • used topically to disrupt the cell membrane of the bacteria
24
Q

Which antibiotics inhibit nucleic acid synthesis?

A
  • DNA Gyrase –> inhibits this enzyme that makes DNA –> Quinolones (Cyprofloxacin)
  • RNA Polymerase –> inhibits enzyme that makes RNA –> Rifampin
25
Q

which antibiotics inhibit synthesis of essential metabolites?

A

Folate synthesis –> antibiotics that prevent folate production which prevents DNA production –> Sulfonamides, and Trimethoprim which are both SEPTRA

26
Q

What is the difference between specific antibiotics vs. Broad-spectrum antibiotics? When are they used?

A

specific antibiotics: inhibit gram - or gram + organisms OR they inhibit certain bacterial species
- they are used when we know the type of bacteria we are dealing with

broad-spectrum antibiotics: inhibit both gram + and gram - bacteria

  • they are used in emergencies when we dont know the type of bacteria we are dealing with; we can switch to specific antibiotics after we test for which bacteria it is
  • Broad-spectrum antibiotics are a risk factor for developing c.diff as it disrupts normal gut flora
27
Q

What are narrow spectrum antibiotics?

A

an example of it is: penicillin G which is more specific than specific antibiotics
it is used specifically for streprococcus pneumoniae (gram +) which is the most common cause of pneumonia

28
Q

What are polymicrobial infections? how do we treat them?

A

polymicrobial infections are infections that could have been caused by a number of bacteria

a broad spectrum antibiotic is used to treat them (i.e. Amoxicillan –> both gram + and gram - bacteria

29
Q

What are three examples of polymicrobial infections?

A
  1. enterobacter
  2. staphylococcus
  3. streptococcus
30
Q

What are 5 groups of people who are most susceptible to bacterial infections?

A
  1. diabetics (hard to heal)
  2. Children (developing immunity)
  3. Elderly (immunosenescence –> decrease in immune system as you age)
  4. Burn wound: skin and soft tissue (tissues that are supposed to be sterile are exposed due to the burn)
  5. Immunocompromised (deficient immune system, neutropenia, and chemotherapy patients)
31
Q

What can cause infection in anyone?

A

lack of hygiene

32
Q

Which 4 groups are more at risk for developing side effects to antibiotics?

A
  1. People with allergies to antibiotics (i.e. penicillin allergy)
  2. Pregnant women (i.e. tetracycline will hinder bone and teeth development in fetus)
  3. Children (children have a different metabolism than adults and this will affect the pharmacokinetic and pharmacodynamic issues (how fast and how effective) the antibiotics are)
  4. Poeple with liver or kidney damage –> this is due to the detoxification of antibiotics and the build up of toxic by products
    i.e. for liver: fluoroquinolones and macrolides
    for kidney: aminoglycosides
33
Q

What are 4 things that occur when its too late to use antibiotics?

A
  1. too many bacteria
  2. too much tissue damage (antibiotics cant get to tissues because theres no blood supply to that tissue since its damaged)
  3. Formation of walled-off abscesses that cant be penetrated by antibiotics (wall around abscess that cant be penetrated and it must be drained or amputated)
  4. poor absorption of drug
34
Q

Why are IV antibiotics used instead of oral?

A
  1. GI problems
  2. Only drug possible i.e. for vancomycin, its only available for IV to treat c.diff patients
  3. rapid bioavailability (fastest way because it by-passes digestive system)

only used for serious infections like meningitis, septicaemia (sepsis), and endocarditis (infection of heart valves)

35
Q

What was the bacterial mutation that staphylococci went through to prevent being killed by penicillin?

A

the mutation produced the enzyme beta-lactamase or penicillinase –> which inactivated penicillin by breaking its beta-lactam ring

36
Q

How did scientists combat the beta-lactamase mutation by staphylococci?

A

they created semi-synthetic penicillin which had structures where the active portion of the antibiotic (the beta-lactam ring) was protected from the enzyme
- they did this by adding side chains on the beta-lactam ring, making it harder for beta lactamase to find it

37
Q

What are four ways in which bacteria become resistant to antibiotics?

A
  1. prevent penetration of antibiotic (i.e. gram - have the outer layer which prevents penetration of penicillin)
  2. destruction of the drug (i.e. destruction of the beta-lactame ring by beta-lactamase)
  3. Target site alteration (mutate or change their target site so the antibiotic cant bind)
  4. Ejection of the drug from the bacterium aka drug efflux (pumps located on bacterial cell wall bind to the antibiotic and pump it out)
38
Q

What are R-factors?

A

plasmids (small circular DNA pieces in the cytosol of bacteria) that transfer genes for resistance to antimicrobial to other bacteria via conjugation by sex pilus

R. factors are dangerous because they can be transferred between different bacterial species I.e. e.coli to shigella

39
Q

What are three reasons why bugs become resistant?

A
  1. over use–> the increase exposure of bacteria to the drug increases the chance of them developing resistance
  2. inappropriate treatment –> giving a patient antibiotics when its actually a viral infection
  3. incomplete treatment regimens –> stopping treatment too early; The bacteria is not completely wiped away while the treatment is still around so it develops resistance to the treatment and then replicates when the treatment is not given
40
Q

What are super bugs?

A

bacteria that cannot be controlled by antibiotics

41
Q

What are MRSA/MSSA?

A

MRSA’s are methicillin resistant S.aureus –> these are the variants of staphylococci that formed after the semisynthetic drugs began to be used

42
Q

what did MRSA do to inhibit the affect of penicillin (and the synthetic variants)?

A

it changed the penicillin binding site on the bacteria to produce a variant that was resistant to methicillin
- penicillin binding protein 2 (PBP 2) mutates to PBP2a (encoded by MecA) which has a low affinity for binding penicillin and beta-lactame anitbiotics

penicillin would not be effective for inhibiting the cross link of peptidoglycan for the bacteria

43
Q

what is the only remaining treatment for MRSA bacteria?

A

vancomycin –> doesnt bind to the penicillin binding protein

however, there is now a VRSA (vancomycin resistant s. aureus) which is resistant to both Methicillin and oxacillin

44
Q

What are VREs?

A

Vancomycin Resistant Enterococci –> genetic mutations of enterococci that are resistant to vancomycin and can be conjugated to streptococci and staphylococci via plasmids

  • it is a genetic mutation in Van A, Van B and Van C genes of the bacteria
45
Q

how did the Vancomycin resistance develop?

A

after the use of avoparcin (glycopeptide) in animal feed –> it was very similar to to vancomycin

46
Q

what are ESBLs?

A

extended spectrum beta-lactamase

  • enterobacteriacae (gram negative) like e.coli which have genetic mutations of many resistant genes (they can break any type of beta lactame bond)
  • causes the bacteria to be resistant to penicillins and cephalosporins
  • ESBL can inactivate the new beta-lactams as well like meropenem
  • increasing issue in the ICU and extended care
47
Q

what is NDM-1?

A

New Delhi Metallobetalactamase –> newest variant of ESBL carried from india

48
Q

What is XDR-TB?

A

it is a drug resistant version of tuberculosis (first and second line)
- it was first seen in south africa and killed 52/53 patients

49
Q

what is a new way to treat XDR-TB? what is the cure rate?

A

pretomanid + bedaquiline + linezolid for 6 months

it is a drug cocktail

it has 90-95% cure rate

50
Q

what is MIC? and why is it important to know?

A

Minimum Inhibitory Concentration

  • it is the minimum amount of antimicrobial that will inhibit the growth (not kill) the microorganism
  • every bacterial isolate must be tested and we must know the MICs for important bacteria
  • it is important to know MICs for appropriate dosing levels and intervals that the antibiotics must be taken
51
Q

What is the “drug of choice”? what is an example?

A

drug that is deemed to be the most effective with the least amount of toxicity for a specific infection

i.e. Penicillin is the drug of choice for streptococcal infections in the throat (pharyngitis)

52
Q

What is the Kirby-Bauer / Disk Diffusion test?

A

test done for antimicrobial susceptibility

  • test is used in the lab for rapidly growing bacteria by looking at how fast the bacteria takes up the antibiotics over time
  • spread bacteria on filter paper with antibiotic and measure the zone of inhibition and compare the diameter of the zone with a standard chart
  • DOES NOT MEASURE THE MIC VALUE
53
Q

what are the three categories of sensitivity in the disc diffusion test?

A 
S = sensitive or susceptible (best response to antibiotic) 
I = Intermediate 
R = Resistant (does not have an effect)
54
Q

What is the E-test?

A

Ellipse Test is used for MIC determination

  • you obtain a plate with bacteria spread on it, then use a plastic strip with antibiotic in increase concentration as you go up the strip
  • then you look to see where the bacteria is inhibited on the strip to determine the minimum amount of antibiotic needed in a person’s blood stream to kill the bacteria (you usually pick an amount 2X more than the MIC determined on the E-test)
55
Q

What are three reasons to monitor antimicrobial levels?

A
  1. To attain effective levels (over MIC)
  2. Prevent toxic side effects from too much drug
  3. Ascertain dosing intervals (i.e. every 8 hrs/ 12 hrs/ 24 hrs etc)

particularly important for aminoglycosides which is otoxic and nephrotoxicand can cause toxicity by deafness and kidney dysfunction
and
for vancomycin

MMI (18 decks)

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