Unit Three : (CH 13) Contorlling Microbial Growth Flashcards

1
Q

define and distinguish sterilization and disinfection

A
  • sterilization is the process of killing or removing all forms of microbial life (including endoscopes) in a material or an object
  • disinfection reduces the number of disease-producing organims from inanimate surfaces; usually involves the removal of vegetative or non-endospore forming pathogens
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2
Q

what are the various forms of disinfection, based on surface/material being disinfected

A
  • sanitiation disinfection of surfaces, materials, liquids to reduce microbial content to levels deem safe for public health
  • antisepsis disinfection of living tissues (with solutions/materials generally called antiseptic, which are usually not as toxic)
  • pasteurization heat treatment of food aimed at killing potential pathogens
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3
Q

autoclave (moist heat)

A

• physical method

• chamber which is filled with hot steam (121 c) and pressure (15 lbs)

• preferred method of sterilization

• kills cells and endospores by denaturing proteins

• kills all microbes and endospores within 20 minutes

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4
Q

define and distinguish between bactericidal and bacteriostatic

A
  • bactericidal antibodies kill bacteria by inhibiting cell wall synthesis, bacterial enzymes or protein translation
  • (group includes: beta-lactum, daptomycin, aminoglycosides, metronidazole, fluroquinolones & vancomycin)
  • bacteriostatic antibiotics limit the growth of bacteria by interfering with bacterial protein production, dna replication, or other aspects of bacteria cellular metabolism
  • (group includes: tetracyclines, sulfonamides, spectinomycin, trimethoprim, chloramphenicol, macrolide & lincosamides)
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5
Q

define and distinguish between antibiotic and synthetic antimicrobial drugs

A
  • antibiotic is a natural substance produced by a microbe
  • synthetic is a substance that is chemically synthesized by humans in a lab
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6
Q

what contributions did ehrlich, fleming, florey, and chain make to the field of antimicrobial medicine?

A
  • enrlich (1910) synthesized salvarsan (arsenic derivative) that was used to treat syphilis
  • fleming (1928) discovered the first antibiotic (penicillin)
  • florey & chain produced first antibiotic as medication (penicillin)
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7
Q

which was the first antimicrobial drug? the first antibiotic?

A
  • first antimicrobial drug was salvarsan
  • first antibiotic drug was penicillin
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8
Q

what is the ecological role of antibiotics? (ie: why do bacteria and fungi produce them?)

A
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9
Q

define selective toxicity. (use the unity of life argument to explain the challenge involved in killing bacteria that are infecting us)

A
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10
Q

name and describe techniques that are used to measure the effectiveness of an antibiotic. for each technique, what are typical results and how are they interrupted?

A
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11
Q

what is chemotherapeutic index?

A

refers to the dosage range expected to achieve desire effects in the average individual

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12
Q

what is therapeutic does, and how does this relate to mic?

A
  • refers to the minimum concentration of antibiotics to kill/inhibit microbe in patients
  • it relates to mic because the higher concentration allows the mic to be maintain in host over a period of time
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13
Q

what is toxic dose?

A

refers to the maximum concentration of antibiotics that is effective without causing adverse drug reaction of negative side effects (which are more likely to increase as concentration of drug increases)

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14
Q

what do the terms broad-spectrum and narrow-spectrum antibiotics mean?

A
  • broad-spectrum act against an extensive range of disease-causing bacteria by targeting both gram-positive/negative bacteria groups
  • narrow-spectrum act against a limited group of gram positive/negative bacteria
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15
Q

pasteurization (moist heat)

A

• physical method

• developed by louis pasteur

• is disinfection (doesn’t kill all microbes but slows/halts microbial growth)

• targets pathogens typically found in food (salmonella, brucella, & mycobacterium)

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16
Q

incineration (dry heat)

A

• physical method

• kills cells and endospores by denaturing proteins (oxidation effects)

• effective way to sterilize disposable items (paper cups or dressings) & biological waste

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17
Q

refrigeration (low temperature)

A

• physical method

• temperatures from 0 to 7oC

• bacteriostatic effect

• reduces metabolic rate of most microbes to prevent toxin reproduction or production

• inhibits most microbial growth but doesn’t kill pathogens (mostly mesophiles)

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18
Q

filtration (physical separation)

A

• physical method

• removal of microbes by passage of a liquid or gas through screen like material with small pores

• sterilizes temperatures sensitive materials (vaccines enzymes, antibiotics & some culture media

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19
Q

irradiation

A

• physical method

• electromagnetic radiation includes: electron beams, gamma-rays, x-rays, uv lights, visible light & infrared lights

• kills microorganisms by damaging/mutating dna

• used as sterilization or disinfection (depends on time, intensity, type of material)

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20
Q

halogens (iodine, chlorine, bromine + fluorine)

A

• chemical method

• denatures proteins or lipid membranes

• found in common household products like bleach & iodine antiseptics

21
Q

alcohol (isopropanol & ethanol)

A

• chemical method

• kills bacteria & fungi, but not endoscopes or naked viruses

• acts by denaturing proteins and disrupting lipid-membranes

• found in common household products like clorox wipes & alcohol antiseptics

22
Q

ethylene oxide

A

• chemical method

• used to sterilize heat-sensitive, solid materials that can’t be autocalved

• kills all microorganisms and endospores by denaturing nucleic acids and proteins

23
Q

phenolics

A

• chemical method

• denatures protein or lipid membranes

• found in common household products like lysol & hand soaps

24
Q

detergent (surfactants)

A

• chemical method

• doesn’t kill microbe but does remove from surface

• found in common household products like laundry & dishwashing detergent

25
cell wall (peptidoglycan) inhibitors
- β-lactam antibiotics (penicillins, cephalosporins, vancomycin, and carbapenems) - these all share a common 4-member ring known as the β-lactam ring that mimics the critical D-Ala D-Ala needed for cross-linking D-Ala to L-Lys - these antibiotics inhibit transpeptidase enzymes from recognizing terminal D-Ala D-Ala in the 5 sidechain sequence of a NAM-NAG carbohydrate polymer.
26
explain in detail how penicillins (as well as semi-synthetic penicillins and cephalosporins) work to inhibit peptidoglycan synthesis. what is a beta-lactam ring?
27
what does the enzyme penicillinase (also called βeta-lactamase) do?
a bacterial enzyme that breaks the bond in the β-lactam ring of penicillin to disable the molecule
28
what are the disadvantages of the natural penicillins?
- narrow-spectrum: natural penicillins are mostly effective against gram-positive bacteria - susceptible to penicillinase
29
for what purposes were the semisynthetic penicillins (i.e.: oxacillin, ampicillin, methicillin, etc.) created?
semisynthetic penicillins and cephalosporins were structurally modified to over come weakness of natural penicillins
30
what does mrsa stand for? what characteristics does this bacterium possess?
- mrsa refers to methicillin-resistant staphylococcus aureus (or multiple-resistant s. aureus) - contains a gene in which allows s. aureus to be resistance to *multiple* natural/semisynthetic penicillins
31
what does the acronym vrsa stand for?
- vrsa refers to vancomycin-resistant staphylococcus aureus
32
what is the relevance of vancomycin? how does vancomycin differ from a beta-lactam antibiotic? how is it similar
33
explain in detail the mode of action of gramicidin
34
explain in detail the mode of action of Polymyxin B
35
explain in detail the mods of action of quinolones
36
explain in detail the mode of action of rifampicin
37
why are there so few useful antibiotics that disrupt membranes or inhibit nucleic acid synthesis? (another way to think about this is: what makes gramicidin, polymyxin b, quinolones, rifampicin, etc. selectively toxic?)
38
explain in detail how sulfa drugs (sulfonamides) prevent bacteria from synthesizing folic acid
39
what do organisms use folic acid for (i.e.: why do these drugs kill bacteria)?
40
explain in detail the modes of action of chloramphenicol, tetracyclines, streptomycin, and erythromycin
41
explain why protein synthesis inhibitors are less selectively toxic (cause more side effects) than peptidoglycan synthesis inhibitors
42
why is it even harder to target fungi and protozoans? What anti-fungal drug targets and options do we currently have available?
43
why don’t we have drugs that cure viral infections? what anti-viral drug targets and options do we currently have available?
44
when taking antimicrobial drugs, why are you instructed to take it at certain intervals (like every 4 hours)? what happens if you do not follow these instructions? (ie: how does that effect mic in the patient tissue/body?)
45
when taking antimicrobial drugs, why are you instructed to take it over a period of several days to weeks (like for 10 days)? what can happen if you do not follow these instructions?
- antimicrobial drug is meant to kill off most of pathogens, but some will survive due to resistance - those that survive through are few enough that the immune system can deal with them - if you stop taking antimicrobial drug before instructed, you are allowing more cells the time to spread their resistance via hgt
46
what is antibiotic resistance? how do antibiotic resistances originate? then, how are they typically passed from one bacterial cell to another?
47
name the strategies that bacteria can use/evolve to evade an antibiotic (give an example of each)
- bacteria can evolve an altered target molecule so that the antibiotic can no longer bind (ex. slightly modify ribosome so antibodies like tetracyclines can't attach or interact with 70S ribosome) - bacteria can produce enzymes that inactivate/degrade the antibiotic (ex: production of penicillinase that breaks the β-lactam ring of penicillins and some semi-synthetic penicillins to inactive the antibiotic) - bacteria can block entry of antibiotic (ex: cell wall of gram-negative bacteria) -bacteria can have efflux pumps that pump the antibiotic out of the cell (ex: an antibiotic enters the microbe, which then pumps the antibiotic back out of the cell)
48
what role(s) have humans played in the evolution of antibiotic resistances? what do the terms “misuse” and “overuse” mean?
- humans' role has increase the rate of the evolution of antibodies by due to the overuse and misuse of antibotics - **misuse** refers to the use of antibiotics for non-bacterial infections, whereas **overuse** refers is the use of antibiotics for mild infections (when the immune can eventually handle and clear the infection)
49
membrane inhibitors