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mcd > Antimicrobial Therapies > Flashcards

Antimicrobial Therapies Flashcards

1
Q

What is an antibiotic?

A

antimicrobial angetnt prodiced by a microorganism that kills or inhibits other microorganisms

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2
Q

How do antibiotics with a beta latcam ring work?

A

Interfere with synthesis of peptidoglycan component of bacterial cell wall

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3
Q

Examples of antibiotics that with a beta lactate ring

A

Penicillin and methicillin

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4
Q

How do aminoglycosides work?

A

toxic
Bactericidal
Inhibit protein sunthesis
Incroectly produces unfolded r

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5
Q

Examples of bactericidal antibiotics:

A 
Rifampiccin - Targets RNA polymerase
Vancomycin - targets cell wall, toxic 
Daptomycin - Targets bacterial cell membrane.
Gram-positive spectrum of activity.
Toxicity limits dose.
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6
Q

Examples of bacteriostatic antibiotics:

A

Linezolid

Inhibits the initiation of protein synthesis by binding to the 50S rRNA subunit.
Gram-positive spectrum of activity.

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7
Q

What are 4 mechanisms of antibiotic resistance?

A
  • Altered target site
  • Inactivations of antibiotic
  • Altered metabolism
  • Decreased drug accumulation
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8
Q

How does altering the target site work:

A

gene that codes for target modifin enzyme. EG. MRSA codes for alternative PBP w low affinity for beta lactams. EG. Strep resistane to erythromycin, gene that codes for an enzyme that methylates AB target site in ribiosome.

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9
Q

How does inactivations of antibiotics work?

A

beta lactamases stopped. Targets beta lactam ring

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10
Q

How does Altered metabolism work?

A

increased production of enzyme substrate to outcompete antibiic inhibitor. OR Swich to other metabolic pathway

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11
Q

How does decreased drug accumulation work?

A

selective pumps in bacteril wall. Can pump out antibiotic

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12
Q

List 5 resistance mechanisms:

A
  • Plasmid transformation (penicillinases)
  • point mutation (target site modicfication)
  • Plasmid conjugation (efflux pump)
  • Transposons (integrate into chromosomal DNA, allow transfer of genes from plsmid to chromosome)
  • Naked DNA – DNA from dead bacteria released into environment
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13
Q

How are resistant AB genes spread?

A

Transformation – taking up other DNA
- Conjugation – Pilus DNA
- Transduction (phage – move DNA from one organism to other)
New antibiotic resistance makes new antibiotics
Genes for resistance already exist

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14
Q

List some non genetic mechanisms of bacteria:

A
  • Biofilm (covered in slime/carbs)
  • Intracellular location (hide in cells)
  • Slow growth (less susceptible to antibiotics, as they don’t use processes like most)
  • Spores
  • Persisters (don’t replicate)
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15
Q

Why don’t some antibiotics work?

A
  • Wrong dose
  • Bacteria causing infection protected by micro biota
  • Inappropriate administration (oral vs IV)
  • Inappropriate choice for organism
  • Poor penetration of AB into target site
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16
Q

What are some risk factors for HAI (hospital acquired infection):

A
  • High no of ill people
  • Crowded wards
  • Pathogens
  • Broken skin
  • Transmission by staff
  • AB supress normal flora
  • Lots of vulnerable paties
  • High antibiotic usage
17
Q

How do we address resistance?

A
  • Strategies (tighter control)
  • Reduce broad specrrum antibiotics
  • Quicker identifying infection caused by resistant strains
  • Combinration therapy
  • Knowing local strains resistance patters
  • Modify existing medicdines
  • Beta lactams with inhibitors
  • Reactive approach
  • new vaccines
  • better screening and decolonisation
  • using non pathogenic competitor strains
18
Q

What is meant by selectively toxic?

A

Antibiotics that target many different bacterial processes

19
Q

What are macrolides?

A

E.g. Erythromycin, azithromycin.
Gram-positive and some Gram-negative infections.
Targets 50S ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides.

20
Q

What are quinolones?

A

Synthetic, broad spectrum, bactericidal.

Target DNA gyrase in Gm-ve and topoisomerase IV in Gm+ve.

21
Q

What is prontosil?

A
  • A sulphonamide antibiotic
  • Bacteriostatic.
  • Synthetic
  • Examples include sulpha-methoxazole. Sometimes used together with Trimethoprim (co-trimoxazole).
  • Used to treat UTIs, RTIs, bacteraemia and prophylaxis for HIV+ individuals.
  • Becoming more common due to resistance to other antimicrobials, despite some host toxicity.
22
Q

Give some examples of gram negative antibiotic resistant bacteria:

A
  • E.coli (sepsis, neonatal meningitis)
  • salmonella (typhoid fever)
  • gonorrhoea
23
Q

Give some examples of gram positive bacteria that are antibiotic resistant:

A
  • MRSA
  • C.difficile
  • TB

mcd (5 decks)

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