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Medical Microbiology > Antibiotics > Flashcards

Antibiotics Flashcards

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1
Q
  1. Antibiotics are very widely prescribed drugs , but are they always prescribed correctly?
A

Nope

They are quite misused drugs

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2
Q
  1. There are 50 million antibiotic treatments per year and 80% of human use is in the community (eg GPs) , what are the two most common infections that GP’s prescribe antibiotics for?
A

50% - respiratory infections

15% - urinary tract infections

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3
Q
  1. What are antibiotics derived from?
A

Natural products of fungi and bacteria , these organisms develop mechanism to kill other bacteria (natural antagonism) this means they’ll target the bacteria not humans (selective toxicity)
These natural products are fermented and then chemically modified to increase pharmacological properties and antimicrobial effects

Whereas some are totally synthetic eg sulphonadmides

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4
Q
  1. How did we discover the effects of antibiotic effects of Penicillin ?
A

This scientist left an agar plate out that was growing colonies of Staphylococcus aureus and he noticed a big mould growing and a zone of inhibition around that zone, Big mould was Penicillium Notatum and it was the diffusion of Penicillin that was killing the other bacteria

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5
Q
  1. It is KEY that antibiotics have “Selective Toxicity” what is this?
A

Hurting the microorganism , not the host
Same species of bacteria can show differences in their response to antibiotics . So we have to access antibiotic susceptibility
There are lots of thing we can target that are only in bacteria = selective toxicity in antibiotics

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6
Q
  1. What is a therapeutic margin?
A 
active dose (MIC)  versus toxic effect
If the dose between the effective dose and the toxic dose is very narrow we call that a a narrow therapeutic margin/index
If drug is safe = wide margin/index
Dose given – enough to kill bacteria but not too much that the host is affected
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7
Q
  1. What are some examples of toxic antibiotics?
A

Aminoglycosides

Vancomycin( Cause kidney damage and hearing loss easily)

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8
Q
  1. What is MIC?
A

MIC- minimum inhibitory concentration and that’s the minimum conc of antibiotic needed for a drug to be effective,
Usually have to measure patient blood to maintain MIC but not to be toxic

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9
Q
  1. What is microbial antagonism and why is it important?
A

Microbial antagonism = one organism can produce something that inhibits growth of another

Important for maintaining flora = complex interactions
Competition between flora eg in our gut
Limits growth of competitors and PATHOGENS

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10
Q

Some antibiotics can mess up the balance of flora and cause a loss of flora, what is the consequence of this?

A

bacterial or pathogen overgrowth

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11
Q
  1. Give an example of an antibiotic that can cause pseudomembranous Colitis due to a loss of flora?
A

Antibiotic Associated Colitis :
(clindamycin, broad-spectrum lactams, fluoroquinolones)
trying to target C.Difficle (part of normal flora of 3% of the population) instead there is an overgrowth of C.Difficle
causes :
Ulcerations – inflammation
Severe diarrhoea
Serious hospital cross-infection risks

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12
Q
  1. What difference would needed to be made to antibiotic treatment for immunosuppressed patients?
A

Antibiotics need to be enhanced

As antibiotics AND immunity need to work together for bacterial clearance.

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13
Q
  1. Give some examples of immunosuppressed patients?
A 
cancer chemotherapy,
 transplantations,  
myeloma, leukaemias, 
HIV with low CD4
Neutropenics, asplenics, renal disease, 
diabetes, alcoholics,
Babies,  elderly
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14
Q
  1. What are the three main ways we can classify antibiotics (which is the best way)
A
  1. Type of activity
  2. Structure
  3. Target Site for Activity (best way)
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15
Q
  1. What are bacteriostatic antibiotics?
A

Bacteriostatic= only inhibit growth of bacteria eg tetracyclin . Allows immunity to come in and clear, ( so host defence mechanisms need to be intact) . If you give it at right dose and right time and immunity comes in and does it job , then the bacteria is cleared so that when you stop giving the bacteriostatic the bacteria doesn’t return.
Used for MANY infectious diseases

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16
Q
  1. What are bactericidal antibiotics?
A

Kill bacteria
Used when the host defense mechanisms are impaired
Required in endocarditis, kidney infection

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17
Q
  1. What is the difference between broad spectrum and narrow spectrum antibiotics?
    Give an example for each
A

Broad Spectrum Antibiotics:
Effective against many types
Example: Cefotaxime

Narrow Spectrum Antibiotics:
Effective against very few types
Example: Penicillin G

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18
Q
  1. How can we group different antibiotics together?
A

By their molecular structure –> Families of antibiotics

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19
Q
  1. What is a beta lactam?
A

Beta lactams are antibiotics that contain a beta lactam ring (this square structure with a double 0 bond and an N bond)
This ring acts as a natural competitor substrate for enzymes that are involved in making the bacterial cell wall

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20
Q
  1. What are some examples of antibiotics that are beta lactams?
A

Both penicillin’s and cephalosporins contain this beta lactam ring
So we tend to call them beta lactam
Really that is description of active compound in the drug, not the drug itself
Some organism have enzymes that destroy beta lactam – antibiotic resistance

21
Q
  1. What is the advantage of bacteria having quite complex structures?
A

Allows for many targets of antibiotics

22
Q
  1. Earlier we said that one of the ways of classifying bacteria is by their target site. What are the main target site for antibiotics?
A

Antibiotics can target:

  • > Cell Wall Synthesis
  • > Folic Acid metabolism
  • > Cell membranes
  • > Protein Synthesis
  • > DNA and RNA processing
  • > Free Radicals
23
Q
  1. Name two antibiotics that work by inhibiting the synthesises of cell walls?
A

Penicillins and Cephalosporins

24
Q
  1. Name two antibiotics that work by inhibiting the synthesis of 50s protein synthesis?
A

Clindamycin

Linezolid (new drug)

25
Q
  1. Name two antibiotics that work by inhibiting the synthesis of the 30s protein synthesis?
A

Tetracycline

Gentamicin

26
Q
  1. How do antibiotics that target DNA and RNA processing work?
    Give two examples of antibiotics that inhibit DNA and RNA processing
A

inhibit how bacteria replicates its DNA or how it makes its mRNA. Enzymes that do this process are targeted (these are different in bacteria than they are in humans – show good selective toxicity) .

Quinolones – very potent- inhibit DNA Gyrase- coiling/uncoiling enzyme – so different to eukaryotic - .

Rifampin- KEY DRUG, PROPHYLAXTIC for meningitis and the key drug for treating TB .- it targets enzyme that makes mRNA (DNA directed RNA polymerase) – inhibits bacterial mRNA – cant make proteins – cant live – will DIE

27
Q
  1. Why do some antibiotic target folic acid meabolism and give two examples of antibiotics we can use?
A

If bacteria cant make folic acid, looses its co-factor for multiple enzymes in metabolism and will die .Drugs that target this metabolic process – Trimethoprim and Sulfonamides (often used in synergistic ) Excellent selective toxicity as humans cant make folic acid.

28
Q
  1. How do antibiotics that target the cell membrane work and give two examples of antibiotics that do this?
A

damage cell membrane , damage eukaryotic membrane too so not great selective toxicity
We can use Colistin , but so toxic so dont want to use unless really need to - ie resistance from all other drugs except this one
Can use Daptomycin

29
Q
  1. What is the advantage of antibiotics that target free radicals and give two examples?
A

There are many different targets in the cell

classic example is Metronidazole (anaerobic conditions) and Nitrofurantoin (most used drug for UTI)

30
Q
  1. How does the type of bacteria (either + or -) affect cell wall inhibitor antibiotics?
A

Gram + :

  • > Massive structure of peptidoglycan
  • > Antibiotics that target cell wall synthesis target enzymes that make peptidoglycan structure. So enzymes that make this have to be on the outer side of the outer membrane
  • > Plenty of antibiotics can penetrate porous structure .Relatively easy

Gram - :
-> slightly difficult, because it has an outer membrane , impermeability membrane – has to go through porin’s . If the membrane doesn’t have transport mechanism to allow the antibiotic to get through (maybe its too big or its charged).many antibiotic you cant use on gram – because they cant get through this impermeable outer membrane

31
Q
  1. Briefly explain the structure of a peptidoglycan?
A

Made up of penta-peptides that are cross-linked together – hold this matrix together – long polysaccharide chain- whole thing is put together is by series of enzymes

32
Q
  1. Explain the process of how a bacteria makes a peptidoglycan
A

Precursor monomer of disaccharide – 5 peptides
Last 2 peptides of this disaccharide are alamines ( D-ala) – very specific to bacteria
Once its made , undergoes transport mechanism across the membrane by lipid transport molecule (can be inhibited by antibiotics)
Formation and transport of monomer, attatches by cross linking to 5 amino acids
Polymerised in the cell wall by enzymes
What an enzyme does is recognizes the D-ala, D-ala . And then cleaves off the terminal D-ala and then links it to a penta-peptide

33
Q
  1. Explain the different ways that antibiotics that inhibit cell wall synthesis can work?
A

Beta Lactam inhibit the enzymes that end the cross linking structure

Vancomycin binds to D-ala D-ala and binds to it to prevent enzymes from working on it

Some antibiotics block production of D-ala = cant make peptidglycan

Some antibiotics block the transport mechanism across the membrane of the peptidglycan

34
Q
  1. Antibiotics are often structural mimics

of natural substrates for bacterial enzymes. Give an example of this?

A

Beta lactum – almost identical to natural substate of D-ala, D-ala so they act as structural mimcs
If you break up beta lactum rings- antibiotic resistance

35
Q
  1. Explain the action of beta-lactams on PBP in Gram –ve bacteria?
A

Gram – so difficult to get through
Can only get through porin

PBP( penicillin binding protein) is making peptidoglycan sub units->peptidoglycan dimers

A beta-lactam comes in through the pore and binds to the PBP this stops in from making peptidoglycan
Instead there are autolytic enzymes – kill the bacteria

36
Q
  1. Explain the process of folic acid synthesis?
A
  1. Start with Dihydropteroate Diphosphate + PABA
  2. Then the enzyme Dihydropteroate Synthetase converts that to Dihydropteroic acid
  3. Becomes Dihydrfofolic acid
  4. Enzyme Dihydrofolate reductase converts this to tetrahydrofolic acid
37
Q
  1. Explain the process of how folic acid synthesis is targeted by antibiotics.
A

2 main enzymes that are targeted :

  • Dihydropteroate Synthetase
  • Dihydrofolate Reductase

Sulfonamides (eg Dapsone) acts as a competitor inhibitor of PABA and targets the enzyme Dihydropteroate to stop the process

Trimethoprim targets Dihydrofolate reductase . Humans DHFR is less inhibited –> Selective Toxicity

Sulfanomides and Trimethorpim work synergistically and are bactericidal

38
Q
  1. Explain the process of how protein synthesis is inhibited by antibiotics?
A

Binding fmet t-RNA
Initiation complex formation

Translocation of fmet t-RNA
to P site

Competition with new
Aminoacyl t-RNA
at the A site

Blocks formation of
peptide bond
peptidyl transferase

Block translocation of
peptidyl t-RNA

39
Q
  1. In what three main situations do we use antibiotics?
A
  1. Treatment (of bacterial infections)
  2. Prophylaxis ( close contact with infections, prevention, pre-operative for gut surgery, immunosuppressed )
  3. Inappropriate use (prescribing when not necessary eg sore throats)
40
Q
  1. What are some different route of administrations for certain bacterial infections?
A
  1. Orally
  2. Systemic treatment ( i.v)
  3. Topical (eg burns, skin infections)
41
Q
  1. What does the dose of antibacterial MIC depend on?
A

This will depend upon the age, weight, renal and liver function of the patient and the severity of infection

Depend on the susceptibility of the organism

Will also depend upon properties of the antibiotic i.e. enough to give a concentration higher than the MIC (minimum inhibitory concentration)

42
Q
  1. What is the difference between Basic Penicillins Anti-Staphylococcal Penicillin , broader spectrum penicillins?
A

Basic Penicillins :

  • > Active against streptococci, pneumococci, meningococci, treopnemes.
  • ->Most strains of Staphylococcus aureus are resistant
  • -> eg Pen G and PenV

Anti-Staphylococal Penicillins:

  • > narrow spectrum, G+ves, beta-lactamase resistant, less potent that PenG . Not MRSA
  • > eg Flucloxacillin

Broader Spectrum Penicillins:

  • > Spectrum of activity is similar to basic penicillins but also includes some Gram-negative organsims and also enterococci
  • > eg Ampicillin , Amoxiciilin
43
Q
  1. What are Anti-pseudomonal penicillins and Beta-lactam/beta-lactamase inhibitor combinations>
A

Anti-pseudomonal penicillins :

  • > extended spectrum
  • > G+ve , G-ve, anaerobes
  • > Piperacillin

Beta Lactam inhibitor combinations:

  • > Spectrum like amoxicillin plus activity against some Gram-negatives and Staph aureus
  • > eg Augmentin
44
Q
  1. What are Aminoglycosides?
A

These agents cannot be absorbed from the gut and must be given parenterally
They are active predominantly against Gram-ve bacteria including Pseudomonas aeruginosa
These agents are nephrotoxic and ototoxic and serum levels must be monitored

45
Q
  1. What are Macrolides?
A

Used to treat Gram-positive infections esp. in those allergic to beta-lactams

46
Q
  1. What is Glycopeptides?
A

Active only against Gram-positive organisms
Parenteral only
Usually reserved for situation when other agents cannot be used e.g. against MRSA

47
Q
  1. What are Tetracyclines?
A 
Broad spectrum
Used mainly for treating:
Chlamydia
Mycoplasma pneumoniae
Acne
48
Q
  1. What are Quinolones?
A

Older drugs such as ciprofloxacin active mostly against Gram-negatives
Useful for complicated UTIs and gastrointestinal infections

Newer agents have better anti-Gram-positive activity
Useful for some respiratory tract infections

Medical Microbiology (15 decks)

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