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antibacterial and antifungal agents Flashcards

1
Q

what is the aim of antimicrobials and how is this brought about?

A

killing microorganisms whilst preserving the life of the planet through: prophylaxis, treatment and selective toxicity whilst considering empiric theory, targeted therapy and susceptibility guided theories to chose the right ones

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2
Q

what is the empiric theory?

A

it is a best guest based on the predicted susceptibility of likely pathogens using local antimicrobial policies, knowledge of organisms site and ABs to use and the antibiotic guidelines

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3
Q

what is targeted therapy based on?

A

the predicted susceptibility of infecting organisms using local antimicrobial policies

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4
Q

what is the susceptibility guided theory?

A

it is based on susceptibility testing result by looking at the sensitivites and identifying the organism and antimicrobials

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5
Q

what is the relationship between knowledge and antimicrobial used?

A

as knowledge of infecting organism increases the spectrum of the antimicrobial decreases

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6
Q

what influences the right antimicrobrial?

A

the likely organism, the appropriate antimicrobial spectrum and the pharmacokinetics to the patient

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7
Q

what helps a clinical diagnosis?

A

organ system involved, endogenous or exogenous

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8
Q

what helps a lab investigation?

A

the infecting organism and likely antimicrobial susceptibility

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9
Q

what is an antibiotic?

A

chemical product of microbes that inhibit or kill other organisms

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10
Q

what comprises antimicrobial?

A

it could be antibiotics, synthetic compounds with similar properties, semi synthetic compounds or different antimicrobial spectrums with different pharmacological properties or toxicity

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11
Q

what is bacterio/fungistatic?

A

inhibiting growth such as protein synthesis inhibitors so the bodys immune system can deal with the rest of the microbes

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12
Q

what is bacteriocidal?

A

killing organisms which as cell wall active agents

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13
Q

what is the MIC?

A

minimum inhibitory concentration which is the minimum concentration of an antimicrobial that visible growth is inhibited at

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14
Q

what is the MBC?

A

the minimum bactericidal concentration - minimum concentration at which most of the organisms are killed

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15
Q

what interactions are there in antimicrobials?

A

there is synergy - when two antimicrobials given together have greater activity than when given separately - additive
antagonistic - when given together they will not work well as if given separately - inhibitory
Loewe additivity and Bliss independence

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16
Q

what is the antimicrobial spectrum?

A

it is the range of microbes that is specific to a particular antimicrobial - the narrowest spectrum (kills the least) should be used at all times

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17
Q

what is the result of an antimicrobial and the target?

A

killing of microbe

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18
Q

what are antimicrobial targets?

A

the inhibition of critical processes in microbes

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19
Q

what can be targeted by antimicrobials?

A

enzymes, molecules or physical structures (cell wall, DNA, RNA, protein synthesis or membrane function)

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20
Q

what do antimicrobials need to exhibit?

A

selective toxicity - the target should not be present on host cells or should not be accessible on host cells otherwise there is no use in the antimicrobial

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21
Q

what do cell wall synthesis inhibitors target?

A

peptidoglycan target - this is a major component of the bacterial cell wall that is made of polymers of glucose derivatives (N-acetyl muramic acid and N-acetyl glucosamine) that is very strong and not in animals as there is no cells wall - selective toxicity

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22
Q

what is the issue with B lactams?

A

some patients are allergic - therefore use glycopeptides as second line cell wall inhibitors

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23
Q

what are other cell wall inhibitors?

A

fosfomycin for UTI

cycloserine for antiTB

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24
Q

what was the first AB?

A

benzylpenicillin

beta lactams are most widely prescribed

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25
Q

what are beta lactamases?

A

they are ABs that all contain the four membered ring structure of CCCn. They interfere with the penicillin binding protein as they can affect the transpeptidases that cross link the peptidoglycan in the cell wall and also the carboxydases for this.

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26
Q

what is a characteristic of benzylpenicillin?

A

it is acid labile and therefore must be administered parenterally - same with ampicillin

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27
Q

what was the first AB against entereobacteriacae?

A

ampicillin

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28
Q

what is the oral equivalent of ampicillin?

A

amoxicillin

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29
Q

what is the anti-staphylococcal penicillin?

A

meticillin - had a side chain that prevents the hydrolysis of the drug by strep b-lactamase

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30
Q

what are the current common penicillins use?

A

cloxacillin and flucloxacillin

31
Q

what does the beta lactam AB do?

A

the ring forms an structural analogue of D-alanyl D alanine

32
Q

why are single ringed penicillins relatively narrow spectrum?

A

resistance

33
Q

what are cephalosporins?

A

they are double ringed beta lactams such as cerufoxime with a broad spectrum, that are arranged into generations with lots of drugs in each.

34
Q

what are carbapenems?

A

they are double ringed beta lactams such as meropenem which has high sensitivity with local infection. They have a broad spectrum but the use depends on resistance

35
Q

what are monobactams?

A

they are single ring structure such as aztreonam that are only active against gram negative bacteria. Safe use of this in allergies to double ring

36
Q

what are glycopeptides?

A

they are large molecules that bind to terminal amino acids of NAM (N-acetyl muramic acid) of pentapeptides. They inhibit the binding of transpeptidases and therefore peptidoglycan is not cross linked - cell wall cannot form and die. They can only be used on gram positive as cannot penetrate the gram negative outer membrane

37
Q

what are examples of glycopeptides?

A

vancomycin and teicoplanin

38
Q

what are protein synthesis inhibitors?

A

protein translation from RNA to protein takes place on the ribosome and the 50s (large) and the 30s (small) subunits will combine to make the 70s initiation complex. The ribonucleoprotein complex is made of 2 RNA and 1 protein. S - svedberg units - relative sedimentation rate
these ABs will inhibit the protein chain coming out of the ribosome or inhibit binding of the two parts - they have many processes

39
Q

what are the characteristics of protein synthesis inhibitors?

A

they are usually bacteriostatic not bactericidal

40
Q

what types of protein synthesis inhibitors are there?

A

aminoglycosides - gentamicin - toxic
macrolides - erythromycin and lincosamides - clindamycin
tetracycline and their synthetic derivatives tigecycline (similar mechanism, broader spectrum)

41
Q

what is linezoid?

A

it is a protein synthesis inhibitor used for gram positive infections

42
Q

what is mupirocin used for?

A

topical agent for staphylo/stretococcus infection - decolonisation of staphylococcus in nose for MRSA carriers

43
Q

what are trimethoprim and suphonamides?

A

they are DNA synthesis inhibitors that are both agens against folate synthesis - sulfonamides inhibit dihydropteroate synthesis and trimethoprim - dihydrofolate reductase inhibitor

44
Q

what is trimethoprim used for?

A

UTI treatment

45
Q

how is DNA synthesised in bacteria?

A

bacterial para amino benzoic acid - dihydropteroate - dihydrofolate - tetrahydrogolate - purine synthesis - DNA

46
Q

what does trimethoprim do to sulphonamides?

A

they potentiate it in in vitro tests but this synergy is not seen in treatment of bacterial infection

47
Q

what is folic acid for?

A

it is a precursor of purine synthesis and many bacteria make folic acid from para-amino benzoic acid

48
Q

why are sulphonamides rarely used?

A

toxicity and resistance

49
Q

what is co-trimoxazole used for?

A

effective against pneumocystis and toxoplasma

50
Q

what is the combination of trimethorpim and sulphonamides used for?

A

treatment of some protozoal infections, pneumocystis jirocevii infections and resistant bacterial infections

51
Q

what are fluoroquionolones?

A

they inhibit one or more of two related bacterial enzymes for DNA synthesis and remodelling inhibitors

52
Q

what are the two enzymes for fluoroquinolones?

A

the DNA gyrase and topoisomerase IV - involved in remodelling of DNA during DNA replication

53
Q

what are examples of fluoroquinolones?

A

ciprofloxacin or levofloxacin

54
Q

what are RNA synthesis inhibitors?

A

they are the corner stone of anti tuberculous chemotherapy and an example is rifampicin that is an RNA synthesis inhibitor that prevents synthesis of mRNA

55
Q

what are some cell membrane agents?

A

colistin or polymxin E for gram negative - these are to prevent cell membrane homeostasis but are nephrotoxic - now sue is increased due to resistance
daptomycin - gram positive
cyclic lipopeptides and are for the destruction of the outer membrane or cytoplasma membrane

56
Q

how are fungi classified?

A

as moulds/filamentous fungi or yeasts

57
Q

what are mycleium?

A

filamentous

58
Q

what does dimorphic mean?

A

several fungi are dimorphic - exist in both forms - exist with both features - endemic mycoses such as candida albicans and malassezia

59
Q

what are yeasts?

A

they are unicellular - budding

60
Q

what do yeasts cause?

A

cryptococcus causes meningitis in the immunocompromised

61
Q

what does pneumocystis jirovecii cause?

A

pneumonia in those with HIV - responds to very little

62
Q

what is the structure of fungi?

A

nucleus with chromosomes - they are similar to human cells more so than bacteria and therefore selective toxicity is difficult. They have a cell wall made of a glucose based polymer - beta-1,3-glucan

63
Q

what is a selective toxicity in fungi and why?

A

in their bilayered membrane they have ergosterol whereas we have cholesterol - selective toxicity, whereas their protein and DNA synthesis is very similar to humans

64
Q

what is another target for fungi?

A

cell wall - must keep forming and reforming as otherwise will die - no cell wall in animal cells and therefore is ideal for selective toxicity

65
Q

what is the fungal cell wall made of?

A

beta 1,3 glucan - large polymer of UDP glucose that is 50-60% of the dry weight of the fungal cell wall - forms a fibrous network on the inner surface of the cell that is synthesis by beta-1,3-glucan synthase

66
Q

what is on the inside and outside of B-1,3-glucan?

A

mannan on outside, B glucan, chitin on inside

67
Q

what are antifungal cell wall inhibitors?

A

echinocandins are enzyme inhibitors that inhibit B-1,3-glucan synthase that are selectively toxic and almost exclusively harmless to the host

68
Q

what are examples of antifungal cell wall inhibitors?

A

anidulafungin, caspofungin, micafungin - analogous to penicillin and exclusively harmless to host

69
Q

what is the largest group of cell membrane antifungal inhibitors?

A

azoles such as topical clotrimazole and fluconazole which is sytemic

70
Q

what is terbinafine?

A

it is a antifungal cell membrane inhibitor that inhibits the synthesis of ergosterol and has a wide use in lamicil for athletes foot and other superficial infections

71
Q

what is amphotericin B or nystatin?

A

it is a antifungal cell membrane agent that is used but carefully as there is a small therapeutic window - not too much for too long. This is because although it binds preferentially to ergosterol it also binds to cholesterol and is not selectively toxic

72
Q

what is the basis of amphotericin B?

A

it binds to ergosterol and therefore causes physical damage to the cell membrane and kills fungal cell

73
Q

what is the one agent that is a fungal protein/DNA synthesis inhibitor?

A

5-flurorcytosine

74
Q

what is the mechanism of action of 5-fluorocytosine?

A

entry into the cell requires fungal cytosine permease and it is then converted to 5-fluorouracil by cytosine deaminase - it is a fungus specific target that incorporates into fungal RNA and inhibits protein synthesis. It then is metabolised to 5-fluorodeoxyuridine monophosphate which inhibits DNA synthesis

CP (38 decks)

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