Hospital acquired infection and antibiotic resistance Flashcards

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1
Q

What is the breakpoint?

A

The concentration of antibiotic that can be achieved in a clinical setting If the bacteria can divide at a concentration at or higher than the breakpoint, it is deemed resistant

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2
Q

Name some major antibiotic resistant Gram-negative bacterial pathogens.

A
  • Pseudomonas aeruginosa
  • E.coli
  • Klebsiella
  • Salmonella
  • Acinetobacter baumanii
  • Neisseria gonorrheae
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3
Q

Name some major antibiotic resistant Gram-positive bacterial pathogens.

A

-Staphylococcus aureus (MRSA) -Streptococcus pneumoniae -Clostridium dificile -Enterococcus spp. -Mycobacterium tuberculosis

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4
Q

Name 7 types of antibiotic.

A

Beta-lactams Aminoglycosides Chloramphenicol Tetracycline Quinolones Sulphonamides Macrolides

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5
Q

How do beta-lactams work?

Give some examples

A

Penicillin and Methicillin
-Interferes with synthesis of the peptidoglycan componenet of the bacterial cell wall, by binding to penicillin binding proteins- which catalyses a number of steps in peptidoglycan synthesis.

They have a beta-lactam ring that is a similar shape to a precursor of peptidoglycan in the bacterial cell wall and hence interferes with the synthesis of the cell wall

CELL WALL

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6
Q

How do aminoglycosides work? Give some examples.

A

Gentamicin and streptomycin.

  • Bactericidal: kills bacteria
  • Affects protein synthesis.
  • affects RNA proofreading which leasd to misfolded protein Some of these proteins get incorporated into the membrane and cause leakage so cells rupture
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7
Q

How does Rifampicin work?

A
  • bactericidal
  • targets subunit of RNA polymerase
  • makes secretions go orange/red: affects compliance
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8
Q

How does vancomycin work?

A

bactericidal
-targets Lipid II component of cell wall biosynthesis, and wall crosslinking via D-ala residues

CELL WALL

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9
Q

How does Linezolid work?

A
  • bacteriostatic
  • inhibits the initiation of protein synthesis by binding to 50S rRNA subunit.
  • gram-positive spectrum of activity
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10
Q

How does daptomycin work?

A
  • bactericidal
  • targets bacterial cell membrane
  • gram positive specturm
  • toxicity limits dose
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11
Q

How does tetracycline work?

A
  • bacteriostatic ( stops bacteria growing)
  • Prevents charged amino-acyl tRNAs from binding to the mRNA/ribosome complex, so prevents elongation
  • binds to 30S subunit

PROTEIN SYNTHESIS

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12
Q

How does chloramphenicol work?

A

Inhibits the peptidyl transfer step Binds to the 50S subunit

PROTEIN SYNTHESIS

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13
Q

How do quinolones work?

A

Quinolones inhibit the functioning of DNA gyrase (Gram-negative) and topoisomerase (Gram-positive) hence hampering the unravelling of DNA during replication

DNA REPLICATION

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14
Q

How do macrolides work? Give an example.

A

Erythromycin.
Only Gram-positive infections and some gram-negative Targets the 50S ribosomal subunit and prevents the aminoacyl transfer, causes truncation

PROTEIN SYNTHESIS

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15
Q

How do sulphonamides work?

A

Bacteriostatic

Inhibits the folate pathway

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16
Q

What are the four main mechanisms of antibiotic resistance?

A

Altered target site: acquire a gene that has same function but different structure
Inactivation of antibiotic :
gene codes for enzyme that kills antibiotic
Altered metabolism: to bypass the step that the antibiotic interferes with/ produce lots of enzymes to out-compete the AB
Decreased drug accumulation: reduce permeability of AB into bacterial cell, so drug doesn’t reach concentration to be effective

17
Q

What are the sources of antibiotic resistence genes?

A

-Plasmids: Lots of circular DNA, often carry multiple AB resistence genes, selection for one maintains resistence to all
-Transposons: integrate into chromosomal DNA. Allow transfer of genes from plasmid to chromosome
+vice versa
-Naked DNA. DNA from dead bacteria released into environment
-horizontal gene transfer allows rapid spread.
-Transformation (uptake of extracellular DNA)
-Conjugation ( DNA trasfer via pilus)
-Transduction ( DNA transfer using a virus as a vector to non offspring bacterium)

18
Q

What are non-genetic mechanisms of resistence?

A
  • biofilm
  • intraceulluar location
  • slow growth
  • spores
  • persisters
19
Q

Summarise some of the main approaches used to prevent the emergence of drug-resistant bacteria and nosocomial infections

A

Better prescribing practices. Infection control. Combination therapy. Narrow vs broad spectrum antibiotic therapy

20
Q

when does antibiotic resistance emerge/

A

resistance typically emerges soon after the arrival of a new antibiotic.