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Microbiology > Control of Micro Organisms. 2nd ppt (test 2) > Flashcards

Control of Micro Organisms. 2nd ppt (test 2) Flashcards

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Biology 101 flashcards
1
Q

Nystatin (a.k.a. mycostatin, achrostatin)

A
  • from Streptomyces bacteria
  • binds to sterols (fatty acid in cell membrane) in membrane of fungus and changes permeability (makes them leaky)
  • used to treat Candida albicans yeast infections (intestinal, oral, vaginal)
  • often combined with broad spectrum antibiotics to prevent Candida overgrowth later
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2
Q

Antifungal Chemotherapeutics.

A

Nystatin
Amphotericin B
Imidazoles

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3
Q

Amphotericin B

A

also from Streptomyces

- used for serious fungal infections (including those that become systemic)
- binds sterols and degrades (targets cell membrane)
- significant side effects (because of the class they are targeting, your cells contain sterols, you get leakiness in your cells and  toxicity)
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4
Q

Imidazoles.

A
  • synthetic
  • inhibits sterol synthesis (or biosynthetic pathway)
  • used topically (ointments) for Candida skin infections and invasive Cryptococossis**
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5
Q

Antiviral chemotherapeutics that block attachment.

A

most are synthetic
• amantadine (Symmetrel)
• vidarabine (Vira-A)
• enfuvirtide (Fuzeon)

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6
Q

Why don’t antibiotics work against viruses?

A

don’t grow or metabolize like cells (they also don’t have membranes or cell walls)

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7
Q

What are the 4 primary modes of action of antivirals?

A

1) inhibit attachment (from targeting and sticking to the cells)
2) disrupt genomic replication (base analogues mimic rungs of DNA or RNA ladder –very similar to DNA – specifically targeting when you are replicating the genome)
3) inhibit viral enzymes (some externally)
4) Interferons (generate antiviral proteins)

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8
Q

What does amantadine (Symmetrel) treat?

A

most influenza (no longer recommended due to resistance)

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9
Q

What does vidarabine (Vira-a) treat?

A

herpes zoster (chicken pox, shingles)

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10
Q

What does enfuvirtide (Fuzeon) treat?

A

HIV 1 (2003) (not HIV2)

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11
Q

What are some example son base analogues (mimic rung on DNA ladder)?

A

azidothymidine (AZT)

acyclovir (Zovirax)

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12
Q

What does azidothymidine (AZT) treat?

A

retroviruses (like HIV)

- also called the nonsense molecule (mimics the rung on DNA ladder)

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13
Q

What does acyclovir (Zovirax or valtrex) treat?

A

ointment for dental herpes or chicken pox

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14
Q

What are some examples of antiviral drugs that inhibit viral enzymes

A
  • protease inhibitors (saquinavier; Invirase)
  • Reverse transcriptase inhibitors (nevi rapine; Viramune)
  • neuraminidase inhibitor (oseltamivir; Tamiflu)
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15
Q

What is reverse transcriptase needed for?

A

enzyme needed for replication

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16
Q

What do protease inhibitors (saquinavir; Inverse) treat?

A

inhibit enzymes that process HIV proteins (needed to reassemble the capsid)

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17
Q

How do reverse transcriptase inhibitor (nevi rapine, Viramune) work?

A

inhibit the enzymes that converts viral RNA to DNA

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18
Q

How does neuraminidase inhibitor (oseltamivir; Tamil) work?

A

inhibits spike enzymes that allow penetration and exit from cell; prevents budding of virus

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19
Q

What are interferons?

A

secreted from cells in response to stimulation by a virus or foreign substance; stimulates the infected cells (remain infected) and those nearby to produce proteins (AVP) that prevent the virus from replicating within them

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20
Q

Describe Interferons (INF) treatment.

A
  • 20 different proteins
  • a, b, and g categories
  • g forms from tumor cells
  • mobilize natural killer cells
  • a and b form from virally infected cells (exclusively)
  • stimulate Anti-viral Protein (AVP) production which stop viral protein synthesis by binding viral mRNA (blocking protein)
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21
Q

What do g forms of interferon come from?

A

infected tumor cells

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22
Q

What do a and b forms of interferon come from?

A

virally infected cells

23
Q

What does INF-a treat?

A

hep B, genital warts, leukemia

24
Q

What is required to develop a drug?

A 
Laboratory  testing (in vitro)
Animal  testing (in vivo)
c) Clinical Trials
-3 phases
each phase increases
# of subjects
Statistical significance
Stringency of test
25
Q

In vivo.

A

in life

26
Q

In vitro.

A

in a test tube

27
Q

What is the first phase of clinical trials?

A

Phase I – aka “safety phase”

  • 20 to 100 HEALTHY subjects
  • tests different doses
  • judges SIDE EFFECTS, BIOAVAILABILITY (how much of the drug is in serum and circulating)
28
Q

What is the second phase of clinical trials?

A

Phase II

  • approx 500 patients with DISEASE(clinically)
  • continues to monitor side effects with (diff.) doses
  • COMPARES new drug to control / other drugs
29
Q

What is the third phase of clinical trials?

A
  • several thousand patients with disease

- tests drug against ESTABLISH METHOD

30
Q

Triple Blind study.

A

set-up so that people who analyze the data don’t know – barcodes and randomized. Codes assigned to each sample. Only when the codes are removed they will know at the end who got what. Removes last layer of bias.

31
Q

How do you establish statistics on efficacy and safety?

A

triple blind study

32
Q

How long do trials take?

A
  • trials take 7-15 years on average
  • 1/1000 drugs make it to humans
  • 1/5000 drugs make it through trials
33
Q

Superbugs.

A

resistant bacteria

34
Q

What do bacteria do to resist antibiotics?

A
  • Destruction of the drug (penicillinase)
  • Prevention of drug penetration
  • Alteration of the target site (or overproduction)
  • Rapid efflux of drug before it can act
35
Q

What contributes to super bugs?

A

• Misuse of antibiotics

  • Overprescription
  • self-medication – can be bought in corner stores over seas. Or even from vets!
  • Incomplete antibiotic regimens
  • use of antibiotics in livestock
36
Q

What percent of antibiotics are prescribed for the common cold (virus)?

A

50%

37
Q

How many prescriptions of antibiotics in NA/year?

A

150 million prescription in NA / year

38
Q

How much of the worldwide use of antibiotics is for animals?

A
  • more than 50% of all antibiotics used worldwide are used in
  • animals (Health Canada, 2002)
39
Q

slide 20 skipped?

A

slide 20 skipped?

40
Q

Horizontal gene transfer

A

sharing resistant genes among bacterial species

41
Q

What are the 3 major superbugs?

A
  1. MRSA (methicillin-resistant Staphylococcus aureus)
  2. Clostridium difficile (C. difficile)
  3. VRE (vancomycin resistant enterococcus)
42
Q

Describe MRSA.

A

-spread by direct contact – very close proximity to the person – fecal oral route

43
Q

How many people carry MRSA?

A

1 in 3 ppl (2billion)

44
Q

How many cases of MRSA per 1000 admissions in Canada?

A

5-6 cases

45
Q

Describe Clostridium difficile (C. difficile).

A

Gram +ve, sporeforming bacillus
Major cause of colitis** especially after use with broadspectrum antibiotics
Spread by fecal-oral route
Usually nosocomial (in NA)

46
Q

What is Clostridium difficile (C. difficile) treated with?

A
  • treated with vancomycin + antiprotozoal (metronidazole)
47
Q

Describes VRE (vancomycin resistant Enterococcus).

A

Gram +ve cocci
Part of normal flora
Developed by overuse of vancomycin
Spread by fecal-oral route

48
Q

What is VRE treated with?

A

Treated with high-dose, combintions (vancomycin, other streptomycin-like antibiotics, chloramphenicol)

49
Q

What is the prevalence of VRE?

A

Prevalence remains low in Canada (

50
Q

What is MDR Klebsiella pneumonia- carbapenemase producing (KPC)?

A

Gram-ve enterobacillus**
Causes pneumonia and UTIs
Spread by fecal-oral route

51
Q

What is the last resort antibiotic for MDR Klebsiella pneumonia- carbapenemase producing (KPC)?

A

Carbapenems are last-resort antibiotics; spread of resistance gene (NDM-1) could be catastrophic**

52
Q

How can we fight super bugs?

A

1) Educate front
- line health care professionals
- establish screening techniques
- stop the spread
2) Reduce overmedication
3) Generate new antibiotics (limitation-time)
4) Combination drugs
5) Vaccine development (need an antigen)
6) Alternative drugs
- bacteriophages
- herbs, spice and other drugs?

53
Q

What is the limitation of generating new antibiotics?

A
  • it takes up to 15 years for drug approval, it takes 4 years for bacteria to show resistance
  • not cost effective (research time, market flood, short regiment)

Microbiology (5 decks)

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