Medical Biotechnology Flashcards

1
Q

Resistance to penicillin was discovered how many years after its use began?
Resistance to vancomycin was discovered how many years after its use began?

A

For penicillin resistance was discovered around 2 years after usage began.
For vancomycin resistance was discovered around 15 years after it’s usage began.

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2
Q

What are the three methods a bacterium can gain resistance to an antibiotic?

A

Natural/producer immunity,
Mutation,
Acquisition of resistance genes.

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3
Q

Describe how bacterial interactions and their own DNA allow for a fast transmission of resistance throughout a population.

A

Bacterial conjugation allows for bacteria to share plasmids between them, sharing resistance genes that way. Integrons speed up resistance to their ability to capture and integrate gene cassettes via site specific recombination. Transposons jump segments of DNA around the genome of the organisms potentially creating mutations with resistance phenotypes. Finally transduction via phages also allows for resistance genes to spread.

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4
Q

What is the most common strain of salmonella Typhimurium isolated from humans?
One UK drug resistant isolate is resistant to what antibiotics?
Why is the zoonotic nature of DT104 thought to be the reason how it became resistant to so many antibiotics?

A

DT104.
Ampicillin, chloramphenicol, streptomycin, sulfonamide and tetracycline (ACSSuT).
Because many of these antibiotics are used in veterinary clinics.

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5
Q

How can antibiotic resistance be combatted?

A

New antibiotics can be developed,
Dosage can be directly observed,
Resistance could be tracked nationwide,
Antimicrobial use could be restricted,
Narrow spectrum antibiotics should be used,
Alternative therapies could be developed.

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6
Q

The efficacy of phage treatment is dependent on what?

A

The frequency of phage application,

The route of administration.

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7
Q

What are the benefits of using phage therapy?

A

They only target the pathogens of interest and not healthy flora,
They are effective against bacteria exhibiting multi drug resistance,
They represent a very useful last line of defence,
The initial dose increases exponentially once administered due to the replicative ability of bacteriophages,
They can penetrate poorly vascularised tissue and even cross the blood Brain barrier,
They are fast, cheap and easy to produce.

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8
Q

What are the problems with phage therapy?

A

They have a narrow host range,
Phages may not always remain lytic, bacteria can become resistant to them,
Phages can become inactivated by a neutralising antibody and there is the possibility of inducing an allergic reaction,
Sterilisation of phage preparations could inactivate them,
Pharmokinetics of phages is more complicated due to their self replicative nature,
Phages might endow bacteria with antibiotic resistance genes.

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9
Q

Describe inhibition of adhesins.

A

Adhesins are a virulence factor used by Yersinia pestis. They preferentially bind to oligosaccharides on host cells. If cells are treated with tunicamycin, which prevents oligosaccharide synthesis, then infection rates are reduced by more than 50%.

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10
Q

Describe the inhibition of type three secretion systems.

A

Kauppi et al 2003 found that inhibitors could target YopH, a protein tyrosine phosphatase or YopE, a GTPase activating protein.
Among such inhibitors are compounds such as sulfonamides.

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11
Q

What are probiotics?
What are prebiotics?
What are synbiotics?

A

Probiotics are products consisting of microbial cultures.
Prebiotics are ingredients that stimulate gut micro flora capable of modifying the GI environment which keeps the host healthy.
Synbiotics are a combination of one or more probiotics and prebiotics.

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12
Q

Health claims of probiotics include…?

A
Elimination of lactose intolerance,
Anti-diarrheal,
Immunomodulatory,
Anti diabetic,
Anti carcinogenic,
Hypocholesterolemic,
Antihypertensive.
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13
Q

How can antibiotics act against bacterial cells?

A

Inhibition of cell wall synthesis- beta lactams (penicillin), vancomycin.
Alteration of bacterial cell membrane activity- polymyxins.
Anti-metabolite activity- sulfonamides.
Inhibition of bacterial protein sythesis- aminoglycosides, chloramphenicol, tetracyclines.
Inhibition of bacterial nucleic acid synthesis- rifampin.

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