Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MCD - Microbiology > Hospital acquired infection and antibiotic resistance > Flashcards

Hospital acquired infection and antibiotic resistance Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name some major antibiotic resistant Gram-negative bacterial pathogens.

A
  • Pseudomonas aeruginosa
    cystic fibrosis
  • Klebsiella
    GI infection
  • Salmonella
    GI infection, typhoid fever
  • Acinetobacter baumanii
    UTI, wounds
  • Neisseria gonorrheae
    gonorrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name some major antibiotic resistant Gram-positive bacterial pathogens.

A
  • Staphylococcus aureus (MRSA)
    wound and skin infection
  • Streptococcus pneumoniae
    pneumonia
  • Clostridium dificile
    diarrhoea, colitus
  • Enterococcus spp.
    UTIs, bacteremia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Name 7 types of antibiotic.

A 
Beta-lactams
Aminoglycosides
Chloramphenicol
Tetracycline
Quinolones
Sulphonamides
Macrolides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do beta-lactams work? Give some examples.

A
  • Penicillin and Methicillin

They have a beta-lactam ring of similar structure to the precursor of peptidoglycan and hence interferes with the synthesis of the peptidoglycan cell wall

  • Binds to Penicillin Binding Proteins (PBP) - they catalyse a number of steps in
    peptidoglycan synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do macrolides work? Give an example.

A
  • Only Gram-positive infections
  • Targets the 50S ribosomal subunit and prevents the aminoacyl transfer step so there is no peptide bond
  • Erythromycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do aminoglycosides work? Give some examples.

A
  • bactericidal
  • affects protein synthesis
  • affects RNA proofreading which leads to misfolded proteins
  • Some of these proteins are incorporated into the membrane and allow leakage
    so the cells rupture.
  • hs some issues with being toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do sulphonamides work?

A
  • bacteriostatic
  • used to treat UTIs
  • interferes with the folate pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does tetracycline work?

A
  • bacteriostatic
  • inhibits protein synthesis
  • Prevents charged amino-acyl tRNAs from binding to the mRNA/ribosome complex
  • prevents the elongation of the polypeptide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does chloramphenicol work?

A
  • Bacteriostatic
  • Inhibits the peptidyl transfer step of protein synthesis
  • Binds to the 50S subunit and blocks the peptidyl transfer step
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the four main mechanisms of antibiotic resistance?

A
  • Altered target site
  • Inactivation of antibiotic
  • Altered metabolism
  • Decreased drug accumulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is bacteriostatic?

A

inhibits the growth of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is resistance?

A

the ability of an organism to replicate in the presence of an antibiotic at a particular concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is MIC? (minimal inhibitory concentration)

A

the lowest concentration of the antibiotic required to inhibit growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what were misconceptions formed at the dawn of the antibiotic era?

A
  • Resistance against more than one class of antibiotics could not occur
  • There is no horizontal gene transmission
  • Resistant organisms would be significantly less ‘fit’
17
Q

what is an exception to resistance of an antibiotic developing quickly?

why?

A

Erythromycin and Vancomycin

Vancomycin - is toxic and not hugely effective so it wasn’t used much at the
time of discovery so it took longer for resistance to develop

18
Q

what is the general mechanism of action of antibiotics?

A

Antibiotics generally tend to inhibit processes that are unique to bacteria -
SELECTIVE TOXICITY

19
Q

explain how altered active site gives rise to resistance?

A
  • the target site can change with a new gene that encodes for a target modifying enzyme
  • the new gene might have the same function but a new structure so it does not respond to the new antibiotic
20
Q

how does MRSA have an altered target site?

A

MRSA acquired a gene, which produces an alternative penicillin binding protein - it performs the same function but has lower affinity to beta- lactams so methicillin is ineffective.

21
Q

how is Streptococcus pneumoniae resistant?

A

Streptococcus pneumoniae is resistant to erythromycin because it has acquired a gene which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit - this changes its structure

22
Q

how does the inactivation of the antibiotic work?

A
  • Acquire gene for an enzyme which breaks down the antibiotic
  • eg. beta-lactamase (bla)
23
Q

how is the metabolism altered?

A
  • Re-engineer the metabolic pathways so you bypass the step that the antibiotic interferes with.
  • increased production of enzyme substrate can be used to outcompete antibiotic inhibitor
24
Q

how does decreased drug accumulation work?

A
  • Reduced permeability of Antibiotic into bacterial cell
  • Increase EFFLUX of antibiotic out of cell
  • the drug does not reach a sufficient concentration to be effective
25
Q

where is the source of antibiotic resistance genes?

and how does it happen?

A
  • plasmids
  • Transposons
  • naked DNA
  • horizontal gene transfer allows the rapid spread of antibiotic resistance
26
Q

what are other reasons for treatment failure?

A
  • inappropriate choice of organism
  • poor penetration of antibiotic
  • ## inappropriate dose
27
Q

what are risk factors for hospital acquired infections?

A
  • high numbers of ill people
  • crowded wards
  • presence of pathogens
  • broken skin
  • staff have contact with lots of sick patients
28
Q

how might antibiotic therapy impair commensal flora?

A
  • commensal organisms might outcompete pathogenic organisms
  • If the commensal organisms are removed due to use of antibiotics then the pathogen has less competition so can proliferate and cause disease
29
Q

how to prevent the emergence of drug resistant bacteria?

A
  • Tighter controls on prescription
  • Reduce use of broad spectrum antibiotics
  • Combination therapy
  • knowledge of resistance patterns
30
Q

how to overcome resistance?

A
  • Modification of existing medications

MCD - Microbiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions