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Microbiology > Antimicrobial chemotherapy 1 > Flashcards

Antimicrobial chemotherapy 1 Flashcards

1
Q

What is antimicrobial chemotherapy?

A

-Using drugs to control infection
-Target organisms are causing infection

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2
Q

How do microbes avoid immune response - when divide rapidly?

A

-Immunosuppressed
-Very unwell

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3
Q

When are you given antimicrobials?

A

Symptoms of infection when required

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4
Q

What removes lasting infection?

A

Own body (as antimicrobials can’t get everywhere & some organisms = resistant), unless are immunosuppressed

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5
Q

What is chemotherapy & how does it work?

A

-Based on - selective toxicity - against targets (not self-cells) –> applies to invading organism (infection) & abnormal body cells (cancer)
-How? -> kills/stops rep of cells so immune cells can work on cancer/infection

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6
Q

What is selective toxicity?

A

-Identify something to organism not seen in host & binds to this target
= more harm to microorg than host

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7
Q

When might antimicrobials not show selective toxicity?

A

Once metabolise = toxic waste
Could accumulate in organs

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8
Q

What is the chemotherapeutic index?

A

-Conc of drug to kill target vs conc of drug can cause damage to host (own cells)
-Toxic dose = to us
-Therapeutic dose = kills bacteria
-High index (1000s) = +ve (unlikely toxicity to us)
-Low index = -ve –> small diff in dose kills microorg & us (when is 5 or 10 fold diff)

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9
Q

Why take more than therapeutic dose?

A

Must absorb, metabolise, excrete - take more than need to kill target

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10
Q

What is chemotherapeutic agent?

A

Drug based molecule used to target specific cells

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11
Q

What are antimicrobial drugs?

A

Drug used to control bacteria, viruses, fungi, parasites (microbial infections)

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12
Q

What are the 4 types of antimicrobial drugs?

A

-Antibacterial drugs
-Antifungal drugs
-Antiprotozoan drugs
-Anthelminthic drugs

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13
Q

What enzymes can sulphonamides (synthetic antimicrobial) target in folic acid metabolism?

A

-Dihydropteroate synthase

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14
Q

Which enzyme is a unique target for sulphonamides to target?

A

Dihydropteroate synthase - as this enzyme is specific to folic acid metabolism in bacteria (i.e., not in humans)

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15
Q

What is the folic acid pathway important for?

A

Biosynthesis of:
-Purines –> DNA, RNA
-Methionine, glycine, fMet-tRNA –> proteins
-Thymidine –> DNA

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16
Q

How do humans obtain folate & why is this important?

A

From diet (nutritionally) - means sulphonamides have little effect on human metabolism, only on bacteria

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17
Q

How can dihydrofolate reductase be targeted by antimicrobial/bacterial drugs when is in human & bacteria folic acid metabolism?

A

Enz in bacteria is v. diff to humans even though have same function - target this diff w/ drugs

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18
Q

What antimicrobial (antibacterial) drugs target dihydrofolate reductase?

A

-Trimethoprim
-Methotrexate
-Pyrimethamine

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19
Q

What are 5-Flurouracil & flucytosine used for?

A

Drugs to control paths to cancer & human growth - not used now
-5-Fluorouracil = topical control some infections - take internally (oral/IV) will affect us but if use on skin will only target here (localised)

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20
Q

What is IC50?

A

Conc of drug inhibiting 50% of the enzyme’s activity (that target) - therapeutic index values

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21
Q

What is the therapeutic index like for trimethoprim?

A

VERY high
-V. low conc kills bacteria (selective toxicity)
-V. high conc kills human cells
-BUT not as useful for protozoal/fungal (as is antibacterial) - as need higher conc to kill these

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22
Q

What is pyrimethamine most effective against (selective toxicity)?

A

Protozoal/fungal - as v. low conc kills these & high conc kills humans
-BUT not useful for bacteria - as conc need to kill these is higher than humans

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23
Q

Why does methotrexate have no real selective toxicity?

A

Conc that kill human cell, bacteria & protozoal/fungal = v. similar

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24
Q

What is the folic acid metabolism pathway in humans & bacteria?

A
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25
Q

What do antimicrobials often cause?

A

Cell death (killing cells)

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26
Q

What are static drugs?

A

Stop cell growth

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27
Q

What type of drug is trimethoprim?

A

Diaminopyrimadine

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28
Q

What is the target of trimethoprim?

A

Dihydrofolate reductase

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29
Q

What is the PHARMACOLOGY of trimethoprim?

A

-Inhibits dihydrofolate reductase
-Is a structural analogue of dihydrofolate (substrate)
-H bonding between enz & sub

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30
Q

What is the PHYSIOLOGY of trimethoprim?

A

-Stops converting dihydrofolate -> tetrahydrofolate
= inhibits biosyn of purines, thymidylate, methionine, glycine, fMet-tRNA
-So inhibits DNA rep –> toxic decline (cidal activity) –> cell death

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31
Q

What is the CLINICAL aspect of trimethoprim?

A

-Often use w/ sulfamethoxazole - for UTIs, GI & respiratory infections
-Also treat parasitic infections - malaria
-Anti-proliferative effects (cancer)

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32
Q

Why combine 2 drugs?

A

-Reduce amount each drug needed - controls for toxicity
-Used to reduce resistance developing

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33
Q

How do drugs target DNA rep & protein syn?

A

-Target enzymes - as these are diff in humans, bacteria, fungi, parasites

34
Q

What antibacterial drug targets RNA polymerase?

A

Rifampicin

35
Q

What is DNA gyrase?

A

-Enzyme that ‘cuts’ DNA for DNA to be unpacked
-Catalyses -ve super-coiling (unwinding) of double-stranded closed-circular DNA = to replicate this DNA

36
Q

What antibacterial drug targets DNA gyrase?

A

Quinolones

37
Q

What antibacterial drug targets cell wall integrity?

A

β-lactams

38
Q

What antibacterial drugs target cell wall biosynthesis?

A

-D-cycloserine
-Vancomycin
-Bacitracin
-Penicillins
-Cephalosporins
-Cephamycins

39
Q

What antibacterial drugs target protein synthesis - translation?

A

50s ribosome inhibitors
-Erythromycin
-Chloramphenicol
-Clindamycin
-Lincomycin

30s ribosome inhibitors
-Tetracyclines
-Streptomycin
-Spectinomycin
-Kanamycin

40
Q

Why are there few antimicrobial drugs that target cell membs?

A

Few differences between cell membs of microorganisms & human cells

41
Q

What antibacterial drug targets cell membs?

A

Polymyxins

42
Q

What is another term for peptidoglycan?

A

Murein

43
Q

What is in mycobacteria in place of peptidoglycan?

A

Arabinogalactan

44
Q

What is the structure of mycobacteria?

A
45
Q

What is the structure of gram +ve bacteria?

A
46
Q

What is the structure of gram -ve bacteria?

A
47
Q

How do antibacterial inhibit cell wall biosynthesis?
-β-lactams (e.g., penicillins)
-Bacitracin
-Cycloserine
-Vancomysin

A

*β-lactamases
-Stops AAs & carbs cross-linking by inhibiting transpeptidase enzyme
Cell wall forms BUT = not rigid - so will burst due to cytoplasmic pressure - osmosis in
-Inhibiting synthesis of peptidoglycan (carb)

*Bacitracin = binds to carbs & AAs so not moved from int to ext - no cell wall synthesis (as need to form outside cell)
-Inhibiting N-acetylmuramic acid-pentapeptide units

*Cycloserine = stops adding D-AAs onto chain - so chains of AAs not cross-link (won’t transpeptidase)

-Vancomycin = no enz target - binds to terminus of peptide chain = stops further cross linking

48
Q

What are PBPs?

A

Penicillin binding proteins - catalyse cross-linking of amino acids & carbs in cell wall of bact - forming mesh-like peptidoglycan

49
Q

Name some β-lactams?

A

-Penicillins
-Cephalosporins
-Carbapenems
-Monobactam

Ampicillin
Amoxicillin

50
Q

What is D-Ala-D-Ala?

A

-Last 2 AAs on AA chain dropping down from peptidoglycan structure
-Needed for binding - cross-linking (peptide transpeptidation )

51
Q

What is the normal process of cell wall synthesis?

A

-Transpeptidase enz binds to D-Ala-D-Ala (H bonds)
-Cleaves D-Ala-D-Ala = x1 alanine
= binds to 2nd peptide chain - so 2 peptide chains are linked by this alanine

52
Q

What do β-lactams do to inhibit cell wall synthesis - common mechanism?

A

-Penicillin has β-lactam ring = so is planar
-Penicillin = mimics D-Ala-D-Ala dimer (similar structure)
-Pen forms complex w/ transpeptidase enz (covalent)
-Enz can’t cleave drug = ‘dead-end’ complex
–> NO cross-linking (peptide transpeptidation)

53
Q

What type of drug is amoxicillin?

A

β-lactam

54
Q

What is the target of amoxicillin?

A

Bacterial penicillin-binding protein - transpeptidase enzyme

55
Q

What is the structure (CHEMISTRY) of Amoxicillin?

A

B-lactam ring (mimicking D-ala-D-ala)

56
Q

What is the PHARMACOLOGY of amoxicillin?

A

-Inhibits transpeptidases
–> by mimicking D-Ala-D-Ala

57
Q

What is the PHYSIOLOGY of amoxicillin?

A

-Competitively inhibits penicillin binding prots
-High affinity = binds covalently w/ transpeptidase enz
-So = unable to cross-link
-Cells lyse (as drug = cidal) - autolytic enzs = upregulated

58
Q

What is the CLINICAL aspect of amoxicillin?

A

-Treat ENT, GI, skin, lower resp tract - infections
-Can combine w/ omeprazole - for Helicobacter pylori infections

59
Q

How are β-lactams made selectively toxic?

A

Divide into targeting gram +ve & -ve bacteria - look at which are most common types of transpeptidases in each group (+/-)

60
Q

Why is ribosome biosynthesis a good target for antibacterials?

A

Ribosomes are diff in prok vs euk
-Prok = 50s & 30s subunits = 70s
-Euk = 60s & 40s subunits = 80s

61
Q

Why might drugs targeted to ribosomal biosynthesis cause some toxicity to human?

A

Mitochondria = prok ribosomes

62
Q

What drugs target ribosomal biosynthesis?

A

30s subunit
-Aminoglycosides - e.g., gentamicin*
-Tetracyclines

50s subunit
-Macrolides - e.g., clarithromycin*
-Fusidic acid

63
Q

What do aminoglycosides do?

A

Cause misreading - stops protein synthesis @ high concs

64
Q

What do tetracyclines do?

A

Block aminoacyl tRNA binding

65
Q

What do macrolides do?

A

Inhibit translocation

66
Q

What type of drug is clarithromyocin?

A

Macrolide

67
Q

What is the target of clarithromycin?

A

23s ribosomal RNA of the 50S ribosomal subunit

68
Q

What is the structure (CHEMICAL) of clarithromycin?

A

-Semi-synthetic macrolide derived from erythromycin

69
Q

What is the PHARMACOLOGY of clarithromycin?

A

-Binds to 23s rRNA of 50s subnit
= inhibits translocation of aminoacyl tRNA –> stops elongation of peptide chain

70
Q

What is the PHYSIOLOGY of clarithromycin?

A

-Inhibits prot syn (translocation) - no new prots
= cell death
-Drug = cidal

71
Q

What is the CLINICAL aspect of clarithromycin?

A

-Treats upper/lower resp tract, skin & soft tissue infections
-Treat Lyme disease, Helicobacter pylori, strep throat, prevents bacterial endocarditis
-Treat Cryptosporidium & Toxoplasma infections (parasitic ribosomes)

72
Q

How is DNA folded in proks?

A

-Folds lots = supercoiled chromosomal like structure - uses DNA gyrase
-Needed for DNA to rep

73
Q

What is an antimicrobial drug (quinolone type) used to target DNA unfolding for DNA rep?

A

Ciprofloxacin

74
Q

What type of drug is ciprofloxacin?

A

Fluroquinolone

75
Q

What is the target of ciprofloxacin?

A

Bacterial topoisomerase I V gyrase

76
Q

What is the structure (CHEMISTRY) of ciprofloxacin?

A

-Fully synthetic antimicrobial drug

77
Q

What is PHARMACOLOGY & PHYSIOLOGY of ciprofloxacin?

A

-Binds to DNA gyrase
-Causes cleavage of 2 DNA strands - double strand DNA breakage –> causes more DNA cleavage
= cell death

78
Q

What is the CLINICAL aspect of ciprofloxacin?

A

-Treats skin, bone, joint, intra-ab, lower resp tract, infections, chronic bacterial prostatitis., complex UTIs (children), acute sinusitis
-Eye drop form = for bacterial corneal ulcers & conjunctivitis

79
Q

How do antibacterial drugs target cell memb?

A

e.g., polymyxins
-Last resort for gram -ve
-Detergent-like action on phospholipids - only in gram -ve
-reduce bacterial harmfulness (as neut lipopolysaccharides)

80
Q

What is spectrum activity of antimicrobials?

A

-Narrow spectrum antibiotics = target v. specific groups of organisms - GI side-effects less likely & residual drug-resistant strains
-Broad-spectrum antibiotics = best when causative microorganism = not known but probs in a certain category - might disrupt normal microflora

Microbiology (6 decks)

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