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Microbiology > Antimicriobials 1 > Flashcards

Antimicriobials 1 Flashcards

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1
Q

What are the two main classes that inhibit cell wall synthesis?

A

B lactam antibiotics (pcc)

Glycopeptides

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2
Q

What beta lactam is becoming increasingly resistant?

A

Carbapenem

Lactam ring is active part

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3
Q

What bacteria do glycopeptides vanco and teico work on?

A 
Gram positive (can't get past outer membrane in negative) 
Became popular in rise of MRSA which are resistant to beta lactam a
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4
Q

What is bacteria protected from with cell wall?

A

Osmotic pressure, phagocytosis

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5
Q

How do beta lactams work?

A

Inactivate the enzymes that are involved in the terminal stages of cell wall synthesis (transpeptidases aka PBP)
B lactam is the structural analogue of the enzyme substrate
Bactericidal- active against rapidly dividing bacteria
Ineffective against bacterial that lack a peptidoglycan cell wall
DAUGHTER CELLS lyse

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6
Q

What happens when E. coli is exposed to b lactam antibiotic?

A

Weakened cell wall results in osmotic lysis of the bacterial cell

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7
Q

Which lactams are common ones?

A

Amox, piperacillin
Cefotaxime, ceftriaxone
Imipenem, meropenem

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8
Q

How does pencillin work?

A

Gram positive, strep, clostridium, staph aureus
Became resistant, broken down by b lactamase produced by s aureus
Hydrolysed lactam ring

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9
Q

How does amoxicillin work?

A

Broad spectrum, coverage to enterococcus and gram neg

Resistance- broken down by lactamase produced by s aureus and gram neg organisms

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10
Q

How does flucloxacillin work?

A

Similar to pencillin but less active

Stable to lactamase produced by s aureus

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11
Q

What is augementin or co amoxiclav?

A

Clavulanic acid added to amoxicillin
Clav protects it- b lactamase inhibitor, prevents enzymatic breakdown, increases coverage to include s aureus, gram neg and anaerobes

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12
Q

How does piperacillin work?

A

Similar to amoxicillin, extends coverage to pseudomonas, other non enteric gram negatives
Broken down by lactamase
Can add it to tazobactam, lactamase inhibitor TAZOCIN

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13
Q

How does the generations across cephalosporins work?

A

Becomes increasingly less active against positive, more against negative
1st- cephalexin
2nd- cefuroxime
3rd- cefotaxime, ceftriaxone, ceftazidime- acts on pseudo

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14
Q

What does cephalexin cover?

A

Some ecoli, rarely narrow spectrum

Ceftazidime covers many more neg, but doesn’t cover positives, treats bronchiectasis and CF

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15
Q

More about each cephalosporin?

A

Cefuroxime- stable to many b lactamases produced by negs. Similar cover to co amox but less active against anaerobes
Ceftriaxone- assoc with c diff, broad spectrum, wide resistance, 1st line with meningitis

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16
Q

What are ESBL?

A

Enzymes produced by organisms, makes it resistant to all cephalosporins regardless of in vitro results

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17
Q

What do surgeons typically use?

A

Cephalosporin plus metro to cover anaerobes

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18
Q

What is the 3rd main group of b lactams?

A

Carbapenem- stable to ESBL
Meropenem, imipenem, ertapenem
Very broad spectrum, pos, neg,anaerobes
Carbapenamase enzyme can break down pencillins, cephalosporin and carbapenem- resistance

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19
Q

What are the key features of b lactams?

A

Non toxic (renal impairment, huge doses can have convulsion)
Short half life
Will not cross in tact BBB
Cross allergenic- penicillins approx 10% cross reactivity with cephalosporins or carbapenems. Clarify nature of allergy

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20
Q

What are the features of glycopeptides?

A

Large molecules, unable to penetrate neg outer wall
Inhibit cell wall synthesis
Impt for treating serious MRSA infections iv only, when penicillin doesn’t work
Nephrotoxic- impt to monitor drug levels

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21
Q

What are examples of glycopeptides?

A

Vanco and teico
Oral vanco can be used to treat serious C. difficile infection (can’t be absorbed in gut but has good intra colonic levels)
Worse than b lactams

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22
Q

How do glycopeptides work?

A

Bind to amino acid d-ala on peptide cross link and block binding of transpeptidases and tranglycosidases

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23
Q

What are the 5 main classes of protein synthesis?

A 
Aminoglycosides
Tetracyclines
Macrolides
Chloramphenicol 
Oxazolidinones- linezolid (synthetic,took a year for resistance)
24
Q

How do aminiglycosides work?

A

Binds to amino acyl site of the 30S ribosomal subunit
Rapid, concentration dependant bacteriacidal action
Require specific transport mechanisms to enter cells (accounts for some intrinsic resistance eg strep)

25
Q

What are the side effects of aminiglycosides?

A

Ototoxic and nephrotoxic, must monitor
Gentamicin and tobramycin particularly active against pseudo
Synergistic combo with b lactams
No activity against anaerobes

26
Q

What is the specific MOA for aminiglycosides?

A

Prevents elongation of the polypeptide chain
Cause misreading of the codon along the mRNA
Doesn’t explain rapidity

27
Q

How do tetracyclines work?

A

Broad spectrum, activity against pathogen that doesn’t have cell walls eg chlamydia, rickettsiae, mycoplasma
Bacteriostatic
Widespread resistance via pump efflux apart from tiglacycline
Do not give to children/pregnant, bind to bone
Light sensitive rash- doxycline
Quite useful in multi drug resistance

28
Q

How do tetracyclines work?

A

Reversibly bind to ribosomal 30S subunit

Prevent binding of aminoacyl tRNA to ribosomal acceptor site, inhibiting protein synthesis

29
Q

What are macrolides?

A

Bacteriostatic, minimal against gram neg
Useful for treating mild staph or strep in pencillin allergic
Also active against camplyo and legionella (atypical pneumo, it’s intracellular so macro works)
Azithromycin- long half life

30
Q

How do macrolides work?

A

Bind to 50s subunit of ribosome

Interfere with translocation, stimulate dissociation of peptidyl tRNA

31
Q

How do chloramphenicol work?

A 
Bacteriostatic, very broad, meningitis 
Rarely used (used topically) aplastic anaemia, and grey baby syndrome, inability to metabolise drugs 
Some hospitals use it 1st line for pneumonia, for severe infection if allergic to b lactams
32
Q

What is the MOA for chloramphenicol?

A

Binds to peptidyl transferase of the 50S subunit and inhibits formation of peptide bonds during translation

33
Q

How do Oxazolidinones work?

A

Binds to 23s subunit of the 50s subunit to prevent formation of a functional 70s initiation complex, required for translation
Highly active against gram pos, including MRSA and VRE
Not active against most gram neg apart from bacterioides which is anaerobe
Expensive, cause thrombocytopenia

34
Q

What are the 2 main groups of DNA inhibitor synthesis?

A

Quinolones

Nitromidazoles

35
Q

How do fluoroquinonlones work?

A

Act on alpha subunit of DNA gyrase predominantly but together with other antibacterial actions are bacteriacidal

36
Q

What activity does fluoroquinonlones have?

A

Broad, especially gram neg including pseudo
Newer agents have increased activity against positives and intracellular bacteria like chlamydia, legionella
Well absorbed
UTI, pneumonia, atypical and gastroenteritis
Can develop resistance

37
Q

How do nitromidazoles work?

A

Metro and tinidazole, under anaerobic conditions an active intermediate is produced which causes DNA strand breakage
Rapidly bacteriacidal
Active against anaerobe and Protozoa edge giardia
Nitrofurans are related- useful for simple UTI

38
Q

What are the 2 main inhibitors of RNA synthesis?

A

Rifampicin and rifabutin

39
Q

How does rifampicin work?

A

Inhibits protein synthesis by binding to DNA dependant RNA polymerase thereby inhibiting initiation
Bacteriacidal
Active against certain bacteria, mycobacteria and chlaymidiae. Use in synergy with gram pos abx
Monitor lfts
Beware of interactions with other drugs that are metabolised in liver eg warfarin

40
Q

Why shouldn’t rifampicin be used as a single agent?

A

Except for short term prophylaxis eg meningococcal, resistance is due to chromosomal mutation
Causes single amino acid change in the B subunit of RNA polymerase which then fails to bind rifampicin

41
Q

What main abx are toxic to cell membrane?

A

Daptomycin- cyclic lipopeptide with activity limited to positive pathogens. Used as alternative to treat MRSA or VRE to linezolid and synercid

42
Q

What is the other cell membrane toxin?

A

Colistin- polymyxin antibiotic that is active against gram neg organisms. Not absorbed by mouth
Nephrotoxic, reserved for use against multi resistant organism
Resistance is increasing

43
Q

What are the 2 main inhibitors of folate metabolism?

A

Sulfonamides

Diaminopyridines eg trimethoprim

44
Q

How do folate inhibitors work?

A

Acts directly on DNA through interference with folic acid metabolism
Synergistic action between the 2 main ones, they act on sequential stages in the same pathway

45
Q

What can be used when there is sulphonamide resistance?

A

Use combo of sulphamethoxazole and trimethoprim- co trimoxazole, gee treating PCP
Trim can be used synergistically in MRSA

46
Q

Which 3 abx are inactivated?

A

B lactams, aminiglycosides, chloramphenicol

47
Q

Which 7 abx are affected by altered target?

A

B lactams, macrolides, quinolones, rifampicin, chloramphenicol, linezolid, glycopeptides

48
Q

Which 5 abx are affected by reduced accumulation?

A

Tetracyclines, b lactams, aminiglycosides, quinolones, chloramphenicol

49
Q

Which abx are affect by the bypass mechanism?

A

Trimethoprim

Sulphonamide

50
Q

How does inactivation in B lactam work?

A

B lactamases causes resistance in s aureus and gram neg bacilli
Not the mechanism of resistance in penicillin resistant pneumococci and MRSA
Pencillin resistance not reported in group A,B,C, or G beta haemolytic strep
Group a strep- nec fash

51
Q

How does altered target resistance work in b lactams?

A

MRSA- mecA gene encodes a novel PBP
Low affinity for binding B lactams
Substitutes for the essential functions of high affinity PBP at otherwise lethal concentrations of abx
S aureus resistance with flucloxacillin (pencillin is enzymatic inactivation)

52
Q

What is the issue with ESBL?

A

Able to break down cephalosporin
Becoming more common in E. coli and klebsiella species
Treatment failures reported in b lactam and lactamase inhibitor eg augementin and tazocin

53
Q

The beta lactamases break down pencillin,
ESBL
carbapenems
Difference in them ?

A

The original lactamases tended to move on genetic elements that just had the lactamase gene
ESBL and carbenempases, move on mobile genetic elements which encode resistance to multiple classes of abx

54
Q

Why has carbepenem usage gone up?

A

ESBL increase, so c resistance has gone up, causing e coli carbapenemase bacteraeima to go up

55
Q

How many classes of carbapenemases are there? And why is it difficult to treat?

A

5- oxa 48 big problem

No one knows how to treat

56
Q

How does altered target resistance in macrolides work?

A

Methyl transferase modifies 23s rRNA
Modification reduces the binding of MLS abx
Encoded by erythromycin ribosome methylation genes
If you have erythromycin resistance, be cautious in using clindamycin

57
Q

What are the examples of selective targets in bacteria? (Prokaryote vs eukaryotes)

A

Peptidoglycan layer of cell wall
Inhibition of bacterial protein synthesis
DNA gyrase and other prokaryote-specific enzymes

Microbiology (15 decks)

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