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Microbiology Exam 3 > 2 - Control of Microbrial Growth (with LE Q's) > Flashcards

2 - Control of Microbrial Growth (with LE Q's) Flashcards

1
Q

microorganisms capable of causing disease (pathogens or potential pathogens)

A

infectious

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2
Q

unwanted microbes i.e. vegetative cells, endospores, protozoan cysts, fungal hyphae, viruses, etc

A

contaminant

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3
Q

hospital acquired infection

A

nosocomial infection

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4
Q

clean safe food prep, cleaning dirt/dust; personal hygien

A

normal household conditions

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5
Q

improved personal hygiene (handwashing); routine use of chemical disinfectants

A

general medical conditions

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6
Q

assume patients are infectious; use PPE; wash hands etc

A

Standard precautions

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7
Q

BSL-1

A

agents NO known potential for infection

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8
Q

BSL-2

A

clinical samples, including HIV and several more unusualy pathogens (not highly transmissible by respiratory route); PPE, lab access, special handling

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9
Q

BSL-3

A

more unusual or HIGHLY transmissible i.e. Mycobacterium tuberculossi, Brucella spp., infrequently encountered viruses, mold stages of fungi (highly transmissible respiratory. Precautions include Level 2 precautions HEPA filter mask, special lab design for control of air movement

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10
Q

BSL-4

A

agents highly infectious exotic microbes and toxins for which there is no vaccine or effective treatment requiring MAX containment

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11
Q

free of all microorganisms and their spores i.e. microbes have been destroyed or removed

A

sterile

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12
Q

use of physical procedures or chemical agents to destroy all microbial forms, including bacterial spores (kill or remove the microbes)

A

sterilization

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13
Q

procedures or chemical agents to destroy, inhibit, neutralize, or remove AT LEAST most of infect org

A

disinfect / decontaminate

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14
Q

agent or method (usually chemical) used to carry out disinfection; normally used on inanimate objects (levels of high, intermediate, low effects)

A

disinfectant agents

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15
Q

chemical agents on skin to eliminate or inhibit microorganisms (mild disinfectant)

A

antiseptic

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16
Q

-cide, -cidal

A

kills microbe e.g. bacteria, fungi, viruses (maybe not spores)

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17
Q

destroys spores & vegetative cells

A

sporicidal

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18
Q

-stat, -static

A

inhibiting growth (prevent) or multiplication of bacteria, but not killing

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19
Q

applying mild heat to kill, or reduce microbes that spoil food & beverage

A

pasteurization

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20
Q

free of contaminating or infectious microorg

A

aseptic

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21
Q

easily altered, decomposed, or destroyed by heat

A

thermolabile

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22
Q

not easily altered, decomposed or destroyed by heat

A

thermostable

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23
Q

Overall degree of microbial resistance to killing (most to least)

A

1) Bacterial Endospores
2) Mycobacteriam
3) Protozoan cysts
4) Non-enveloped small viruses
5) Vegetative bacteria
6) Fungi
7) Enveloped viruses

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24
Q

more resistant to antimicrobial control methods than all other microbial forms

A

Bacterial endospore

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25
Q

microbes are not killed instantly when exposed to lethal agents, but more dysfunctional and die over time. Vegetative cells die more rapidly than spores

A

microbial death

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26
Q

which die first… vegetative cells or spores?

A

vegetative die first

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27
Q

a larger quantity of contaminating microbes requires a longer exposure time to destroy

A

population size

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28
Q

usually increase chem concentration increase micro-org death. Some agents are more effective at lower concentrations

A

concentration/Intensity of antimicrobial

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29
Q

the longer a population is exposed to a microbicidal agent, the more organisms are killed

A

duration of exposure

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30
Q

High temps can inactivate enzymes and denature molecules— chem disinfectants may function better/faster at increased temps.

Strong acids can directly kill microbes; weak acid may enable chemicals to inactivate microbes faster

A

Temperature and pH

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31
Q

organic matter can protect micro-org from heating and chemical disinfectants

A

presence of protective or neutralizing matter

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32
Q

Modes of Action of Microbial Control Methods

A

Damage to cell wall
Disrupt cytoplasmic membrane
Inhibit synthesis of proteins and nucleic acids
Alter function of proteins & nucleic acids

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33
Q

a. Block its synthesis, digest it, or break down its surface b. Examples: antibiotics, lysozyme, detergents

A

Damage to cells wall

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34
Q

a. Cause loss of membrane integrity and selective permeability
b. Example: detergents (surfactants), heat

A

Disrupt cytoplasmic membrane

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35
Q

a. Interference with gene translation, thus preventing protein synthesis
b. Examples: antibiotics, radiation, formaldehyde

A

Inhibit synthesis of proteins and nucleic acids

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36
Q

a. Alter bonds that determine secondary and tertiary structure. Altered structure inactivates or denatures functions of enzymes and nucleic acids.
b. Examples: heat, strong organic solvents, phenolics, metallic ions, antibiotics

A

Alter function of proteins & nucleic acids

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37
Q

a. Refrigeration – slows metabolism of microbes, but does not kill most microbes. Used for prolonging storage and shelflife of foodstuffs, vaccines, blood, medications, etc.
b. Freezing (especially ultra-low, -70°C) – essentially stops metabolism, but does not kill microbes. Used for long-term storage of microbes and serum.

A

Cold Temperatures ( Physical Control Method)

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38
Q

Methods of PHYSICAL control of Microorganisms

A

Cold Temperatures
Heat
Radiation
Filtration

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39
Q

a. Heat kills cells by disrupting cell membrane functions, denaturing proteins, and inactivating nucleic acids.

(1) Cell membranes become more fluid at elevated temperatures, causing them to lose their
selective permeability.

(2) Proteins (e.g. enzymes) and nucleic acids are inactivated by breaking their hydrogen bonds,
which unfolds proteins and separates double-stranded nucleic acids.

b. Limited to heat-resistant materials. Sterilization depends on temperature, duration of heating, and
humidity.

c. Moist heat is more effective than dry heat
(1) Moist heat possesses greater heat energy than dry heat
(2) Boiling doesn’t kill bacterial endospores which may survive hours of boiling.

A

Heat (Physical Control of micro-org)

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40
Q

___ is more effective than dry heat

A

Moist heat

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41
Q

possesses greater heat energy: dry heat or moist heat?

A

moist heat

42
Q

how to attack proteins and nucleic acids?

A

breaking their hydrogen bonds (heat)

43
Q

(1) Conditions – 160 to 180°C for two hours.
(2) Disadvantages of dry heat oven
(a) Liquids cannot be heated above boiling point (100°C) without undergoing excessive evaporation and boil over.
(b) Organic compounds may denature above certain temperatures, e.g. 160°C.
(3) Used for thermostable non-liquid, e.g. metal or glass

A

Dry heat (hot air oven)

44
Q

hot air oven?

A

dry heat

45
Q

(1) Conditions
(a) 121°C for 15 minutes (minimum time required to ensure killing viable organisms and spores). Large loads may require more than 1 hour so that moist heat can penetrate to all items in the load.
(b) The high pressure in the autoclave counteracts vaporization (i.e. boiling) so that heat- stable liquids can be heated to 121°C under 15 lb of pressure without boiling over. High pressure does not cause the killing.
(2) Limitations
(a) Cannot be used for certain thermolabile substances
(b) Cannot be used for items adversely affected by moisture; i.e. surgical instruments with sharp cutting edges, dry chemicals, etc.
3) Uses
(a) Sterilization of clean, wrapped instruments, containers & microbial culture media
(b) To render contaminated materials biologically safe before they are discarded

A

Steam heat (steam under pressure, AUTOCLAVE)

46
Q

The burning of organic material destroys living cells; used for small metal or glass instruments in the laboratory and on medical wastes at the facility or installation level.

High temperature (e.g. 1800F) reduces waste to ash within several seconds; industrial size processes up to 1000 kg/hour.

A

incineration

47
Q

Heat methods:

A

Heat, moist heat, dry heat, steam heat, incineration

48
Q

a. Ionizing radiation – Gamma
(1) Nonspecifically alters cellular proteins and nucleic acids by penetrating deep into objects.
(2) Used to sterilize pharmaceuticals, medical/dental supplies, and items that cannot withstand the heat of steam sterilization or the effects of chemicals

b. Ionizing radiation – Electron Beam Radiation
(1) Alters nucleic acid
(2) Used to decontaminate packages, e.g. by Postal Service for mail, industry for medical items

c. Non-ionizing radiation – Ultraviolet
(1) Nucleic acids mutations that prevent normal gene expression and DNA replication.
(2) Optimum wave length – 240 to 280 nm (Optimum 254 nm).
(3) Low penetrating power - Must have direct contact with organism.
(4) Requires lengthy exposure, e.g. 10 seconds to 30 minutes depending on distance from UV
light source.

A

Radiation

Ionizing — Gamma and Electron Beam

Non-ionizing— Ultraviolet

49
Q

a. Membrane micropore filters – membrane of cellulose acetate & cellulose nitrate has complex
system of pores that trap microbes by pore size and chemical affinity to the matrix
(1) Pore size of 0.22 micron is usually effective in removing all bacteria (i.e. sterilization).
(2) Moderately effective on viruses, mycoplasma, chlamydia, and rickettsia.
(3) Used for sterilization of thermolabile liquids.
b. High-Efficiency Particulate Air (HEPA) filtration

(1) HEPA filters consist of randomly oriented glass and polymer fibers that effectively remove
99.97% of particles 0.3um and larger.
(a) They are also highly effective at containing particles between 0.3 and 0.1 um (100
nanometers) and smaller. (Highly effective for blocking bacteria; moderately effective for blocking viruses)
(b) Most bacteria and viruses exist in clumps, thus are larger than the pore size
(c) Removal of particles is accomplished by adherence of particles to the fibers rather than
by sieve in common paper filters.
(2) Uses
(a) Air filters for respiratory protection
i. Mask: N95, not routine surgical or painters mask ii. PAPR: Powered Air Purifying Respirator – includes HEPA filter, blower, hood

(b) Biological safety cabinet – A contained work area designed to prevent exposure to infectious aerosols and to protect materials and specimens from environmental contamination. Airflow carries particulate matter away from the user and into an area of filtration, and it prevents the outflow of infectious agents. (NOT same as chemical fume hood)

A

Filtration

50
Q

Table 2 - Physical Control

A

Learn it!

51
Q

Methods of Chemical Control of Microorganisms

A
  1. Levels of disinfectant activity (not a prefect classification)

a. High-level disinfectants – microbicidal and sporocidal, although some may do so slowly;
effectiveness approaches sterilization. Some may be sterilants under appropriate conditions.

b. Intermediate-level disinfectants – (effectiveness varies within category) – [Most commonly
employed products] - effective against vegetative forms of bacteria and may be effective against
fungi and viruses (microbicidal – tuberculocidal, fungicidal, virucidal), but few products will be sporocidal. A few are antiseptics.
Antiseptic – chemical disinfectant agent; method that may be safely used on skin; tissue

c. Low-level disinfectants – usually (but not always) bactericidal; not sporocidal or tuberculocidal,
often not fungicidal or virucidal.

  1. Soap
    a. Moderately effective as a disinfectant in infection control by mechanical removal of microbes
    through frequent handwashing
    b. Washing for at least 15 seconds with soap and water provides reasonable effectiveness.
    c. Bactericidal soap is not worthwhile, and several ingredients have been banned.
52
Q

Mechanisms of action of antimicrobics – note unique target sites of procaryotic cells
1. Introduction to antimicrobic concepts

a. Antibiotic / Antimicrobic agent (antimicrobic): a chemical substance of natural, semisynthetic, or
synthetic origin that inhibits or kills microorganisms and which can be used to treat or control
infection.

b. Selective toxicity – the antibiotic will affect only the target organism (microbe) without harming the
host (patient) [although mild toxicity or side effects are considered acceptable]

  1. Inhibitors of cell wall synthesis
    a. Beta-lactam antibiotics (use this mechanism of action)
    (1) The antibiotic activity of these compounds
    depends on the integrity of the beta-lactam ring
    (O=C-N). By altering the nature of the side
    chains (R), differences in antimicrobic properties
    can be obtained.
    (2) Examples
    (a) Penicillins (e.g. Pen G, ampicillin, methicillin,
    carbenicillin, piperacillin) (b) Cephalosporins (e.g. cephalothin, cefoxitin, ceftazadime)

(3) Principle of action – inhibits peptidoglycan synthesis by inhibiting the formation of crosslinks
between the polymers of the bacterial cell wall
(a) Peptidoglycan synthesis consists of about 30 enzymatic steps to synthesize long
polysaccharide chains of N-acetyl-glucosamine (NAG) & N-acetyl-muramic acid (NAM); and to cross link them by short peptides
(b) Penicillin binding proteins (PBP) are cell-membrane enzymes (proteins) responsible for
synthesizing peptidoglycan

(c) Beta-lactam antibiotics act by binding to PBPs. (d) Results in:
i. Inhibition of peptidoglycan synthesis
ii. Degradation of formed cell wall through the release of autolytic enzymes
iii. Weakened cell wall loses integrity and can no longer preserve osmotic pressure.
Results in cell death and increased phagocytosis.
(4) Major characteristics of Beta-lactams
(a) Acts poorly against existing peptidoglycan, so primarily effective against actively growing
bacteria
(b) Most effective against gram-positive bacteria because the outer membrane of gram-
negatives prevents some degree of antibiotic entrance (c) Very low toxicity (d) Generally bactericidal (e) Different groups/generations of antibiotics have different spectrums and resistance
(f) Resistance can occur due to:

i. Development of changes to pores thus preventing entrance of antibiotic
ii. Prevention of binding of antibiotic to PBP due to modified PBP structure
iii. Hydrolysis of antibiotic by beta-lactamases (penicillinase, cephalosporinase)

b. Vancomycin – binds onto the cross-link peptide, so that the link cannot be completed and peptidoglycan polymer cannot elongate

c. Bacitracin – blocks phospholipid carrier that helps carry subunits of peptidoglycan across membrane
to cell wall

d. Isoniazid (INH) – inhibits formation of mycolic acid in cell walls of mycobacterium (tuberculosis
organism)

A

Inhibitors of cell wall synthesis

53
Q

Inhibitors of cell wall synthesis

A

Beta-lactam antibiotics
Vancomycin
Bacitracin
Isonizid (INH)

54
Q

Inhibitors of protein synthesis

A

a. Principle – inhibits accurate translation of mRNA or polypeptide chain formation at the bacterial
ribosome

b. Examples and indications for use
(1) Chloramphenicol, clindamycin – inhibits the polypeptide elongation steps in translation by
binding to 50S ribosome subunit and blocking peptide bond formation
(a) Bacteristatic
(b) Broad-spectrum
(c) Resistance is primarily due to chemical alteration of either the antibiotic or the ribosomal molecule, thus preventing binding

(2) Macrolides (e.g. erythromycin) – binds to 50S subunit; prevents translocation (3) Aminoglycosides (e.g. gentamycin, tobramycin) – inhibit translation by binding to 30S ribosomal protein causing misreading of mRNA and incomplete synthesis of protein molecules
(a) Bactericidal
(b) Broad-spectrum, although predominately used against various systemic gram-negative
infections (c) Resistance most commonly results from enzymatic modification of the antibiotic

(4) Tetracyclines – inhibits translation into polypeptides (proteins) by blocking binding of tRNA to
the 30S ribosome-mRNA complex
(a) Bacteristatic
(b) Broad-spectrum
(c) Resistance most commonly results from active efflux of the antibiotic out of the cell or the
production of proteins that protect the 30S ribosome

55
Q

Inhibitors of cell membrane function

A

a. Principle – disrupts functional integrity of cytoplasmic membrane, allowing nucleotides and proteins to escape (detergent-like)
b. Polymyxins – active against gram-negatives, but nephrotoxicity limits them to external use
c. Amphotericin B (a polyene) – antifungal; binds with ergosterol in fungal membranes; somewhat toxic

56
Q

Inhibitors of nucleic acid

synthesis

A

a. Principle – competitive inhibition of essential nucleic acid precursor or binds essential enzyme (e.g. DNA gyrase)

b. Typical examples
(1) Quinolones (e.g. nalidixic acid) and Fluoroquinolones
(e. g. ciprofloxacin) – inhibit bacterial DNA gyrase (the enzyme that controls DNA coiling – if DNA is not tightly coiled, it will not fit into the bacterial cell)

(2) Rifampin – inhibits transcription by binding to RNA polymerase and inhibiting initiation of mRNA synthesis
(3) Metronidazole – causes breakage of microbial DNA (bacterial and parasitic DNA)
(4) Nucleoside analogues – antiviral antimicrobics

(a) Inhibit DNA or RNA synthesis by altering their composition using nucleic acid analogues (structurally similar chemicals which inactivate the DNA or RNA)
(b) Examples – Acyclovir, Ribavirin, Zidovudine

5) Flucytosine, 5-fluorocytosine (5FC) – incorporates into fungal RNA and interferes with DNA
and protein synthesis

c. Most are bactericidal and moderately narrow spectrum
d. Resistance is typically because of decreased uptake into the cells due to cell wall or cell membrane molecular changes

57
Q

Inhibitors of bacterial metabolism (antimetabolite)

A

Sulfonamides
Trimethoprim
Azoles

a. Sulfonamides (sulfamethoxazole) – inhibits folic acid synthesis by competing for precursor molecules
b. Trimethoprim – competitively interferes with folic acid production by inhibiting a metabolic enzyme c.

Azoles (fluconazole) – antifungal – inhibits synthesis of ergosterol, a key structural molecule of fungal cell membranes

58
Q

inhibitors of cell wall synthesis

A

Beta Lactam Abx
Vancomycin
Bacitracin
Isoniazad

59
Q

inhibitors of protein synthesis

A

Chloramphenicol & clindamycin
Macrolides (erythromycin)
Aminoglycasides (gentamycin, tobramycin)
Tetracyclines

60
Q

Inhibitors of cell membrane function

A

Polymyxins

Amphotericin B

61
Q

Inhibitors of nucleic acid sythesis

A 
Quinolones
Rifampin
Metronidazole
Nucleoside Analogues (Acyclovir, Ribavirin, Zidovudine)
Flucytosine, 5-fluorocytosine (5FC)
62
Q

inhibitors of bacterial metabolism (antimetabolite)

A

Sulfonamides (sulfamethoxazole)
Trimethoprim
Azoles (fluconazole)

63
Q

Non-enveloped or enveloped virus harder to kill?

why?

A

non-enveloped harder to kill!

Because enveloped virus have envelope made from human cell membrane or lipid bilayer…. which is easy to destroy with organic solvents

64
Q

which dies more rapidly, spores or vegetative cells?

A

vegetative cells die more rapidly than spores

65
Q

Abx Inhibitors of Protein synthesis sites of action

A

50S and 30S subunits

50S (CEC)
Chloramphenicol
Erythromycin
Clindamycin

30S (SAAT)
Streptomycin
Aminoglycosides
Amikacin
Tetracycline
66
Q

Cell membrane Abx

A

Polymyxins

Amphotericin B

67
Q

Cell Wall Abx (synthesis and repair blocking drugs)

A

Bacitracin
Beta Lactams - Cephalosporins / Penicillins
Isoniazid (INH)
Vancomycin

68
Q

DNA Abx

A 
Inhibit Gyrase (unwinding enzymes) (GQ)
Quinolones (ciprofloxacin)

Inhibit RNA polymerase
Rifampin

69
Q

Cytoplasm / metabolism Abx

A

Inhibit folic acid metabolism (ST)
SULFONamides (Sulfa drugs)
Trimethoprim

70
Q

Beta Lactam Abx means? differences between? Ex’s?

A

O=C-N

work differently by altering nature of side chains (R)

Penicillins & Cephalosporins

Penicillins
Pen G, ampicillin, methicillin, carbenicillin, piperacillin)

Cephalosporins
cephalothin, cefoxitin, ceftazadime

71
Q

Principle of Action for Beta Lactam Abx

A

inhibits peptidoglycan synthesis by inhibiting the formation for crosslinks between the polymers of the bacterial cell wall

a. Peptidoglycan 30 steps
b. PBP (penicillin binding proteins) - are cell-membrane enzymes (proteins) responsible for synthesizing Peptidoglycan
c. Beta-Lactam Abx act by binding to PBP’s

72
Q

Result of Beta-Lactam Abx binding to PBP’s

A

i. inhibtion of peptidoglycan synthesis
ii. degredation of formed cell wall through release of autolytic enzymes
iii. weakened cell wall loses integrity and can no longer preserve osmotic pressure –> cell death and increased phagocytosis

73
Q

Major characteristics of Beta-Lactams

A

a. Exists poorly against EXISTING peptidoglycan (targets GROWING bacteria)
b. MOST effective with Gram +
c. very LOW toxicity
d. generally bactericidal
e. Abx face resistance
f. resistance can occur due to:
i. development of changes to pores (preventing entrance of abx)
ii. prevention of binding of Abx to PBP (modified PBP structure)
iii. Hydrolysis of Abx by Beta-lactamases (penicillinase, cephalosporinase)

74
Q

Abx Beta Lactam resistance can occur due to:

A

i. development of changes to pores (preventing entrance of abx)
ii. prevention of binding of Abx to PBP (modified PBP structure)
iii. Hydrolysis of Abx by Beta-lactamases (penicillinase, cephalosporinase)

75
Q

binds to the cross-link peptide, so that the link cannot be completed and peptidoglycan polymer cannot elongate

A

vancomycin

76
Q

blocks phospholipid carrier that helps carry subunits of peptidoglycan across membrane to cell wall

A

bacitracin

77
Q

inhibits formation of MYCOLIC ACID in cell walsl of mycobacterium (TUBERCULOSIS organism)

A

Isoniazid (INH)

78
Q

inhibits accurate translation of mRNA or polypeptide chain formation at the bacterial ribosome

A

Inhibitor of protein synthesis (30S and 50S)

79
Q

inhibits the polypeptide elongation steps in translation by binding to 50S ribosome subunit and blocking peptide bond formation

A

Chloramphenicol, clindamycin

  • bacteriostatic
  • broad spectrum
  • resistance due to chemical alteration of ABX or ribosomal molecule (prevent binding)
80
Q

binds to 50S subunit; prevents TRANSLOCATION

A

Macrolides (erythromycin)

81
Q

Inhibits translation by binding to 30S ribosomal protein causing misreading of mRNA and incomplete proteins

A

Aminoglycosides (gentamycin, tobramycin)

  • bacteriocidal
  • broad spectrum
  • resistance from enzymatic modification of ABX
82
Q

inhibits translation into polypeptides (proteins) by blocking binding of tRNA to the 30S ribosome

A

Tetracyclines

  • bacteristatic
  • broad spectrum
  • resistance from active efflux of ABX out of the cell or production of proteins to protect 30S ribosome
83
Q

Inhibitors of cell membrane function abx

A

PA
Polymyxins (gram -, but NEPHROTOXIC to external use
Amphotericin B - antifungal - binds with ergosterol in fungal membranes

84
Q

Inhibitors of nucleic acid synthesis abx types

A 
QRMN (QueeR MeN)
Quinolones
Rifampin
Metronidazole
Nucleoside analogues
85
Q

Inhibitors of nucleic acid synthesis abx principle

A

competitive inhibition of essential nucleic acid precursor or binds essential enzyme

86
Q

inhibit bacterial DNA gyrase (enzyme controlling coiling)

A

Quinolones and Fluoroquinolones

87
Q

inhibits TRANSCRIPTION by binding to the RNA polymerase and inhibiting initiation of mRNA synthesis

A

Rifampin

88
Q

causes breakage of microbial DNA (bacterial and parasitic DNA)

A

Metronidazole

89
Q

antirviral antimicrobics (Nucleoside analogues) work by?

Ex’s?

A

inhibit DNA or RNA synthesis by altering their composition using nucleic acid analogues

Ex’s: Acyclovir, Ribavirin, Zidovudine

90
Q

Incorporates into fungal RNA and interferes with DNA and protein synthesis

A

Flucytosine, 5-flurocytosine (5FC)

91
Q

Inhibitors of bacterial metabolism (antimetabolite)

A

SAT
Sulfonamides
Trimethoprim
Azoles

Sulfonamides (sulfamethoxazole) – inhibits folic acid synthesis by competing for precursor molecules

Trimethoprim -competitively interferes with folic acid production by inhibiting a metabolic enzyme

Azoles (fluconazole) – antifungal - inhibits synthesis of ergosterol, key structural component of fungal cell membranes

92
Q

– inhibits folic acid synthesis by competing for precursor molecules

A

Sulfonamides (sulfamethoxazole)

93
Q

-competitively interferes with folic acid production by inhibiting a metabolic enzyme

A

Trimethoprim

94
Q

– antifungal - inhibits synthesis of ergosterol, key structural component of fungal cell membranes

A

Azoles (fluconazole)

95
Q

action: disrupts structural proteins & enzymes

kills vegetative bacteria within minutes & spores in 3-10 hr; active solution unstable

A

Glutaraldehyde, 2-5% aqueous - High disinfectant, Y Sterilant (Sporocidal)

96
Q

action: formation of hydroxyl free radicals which are toxic to cells

stays for several weeks. Vaporized sterilization – about 6 hr. Disinfection - about 2-30 minutes

A

hydrogen peroxide
vaporized, 25% (High disinfectant, Y Sporocidal)
Aqueous, 3% (Int disinfectant)

97
Q

Action: Disrupts cell walls & membranes; precipitates proteins

Kills vegetative bacteria within a few minutes; Stable. DIsinfection - about 2 - 30 minutes. Skin irritant.

A

Phenolic compounds

INT disinfectant, corrosive

98
Q

Action: inactivates enzymes; damages membranes

Fast action; Skin & lung irritant (Gas highly toxic); bleach decomposes w/ in a few dasy (prepare fresh every 2-3 days: High Level Disinfection - about 1-6 hrs. Normal disinfection 2-30 minutes.

A

chlorine compounds

  • gaseous, 100-1000 ppm
  • hypochlorite (1:10% dilution of bleach)
99
Q

when you see Mycobacterium tuberculosis, Brucella spp THINK

A

BSL-3

100
Q

Action: Metabolic enzymes (disrupts)

Disinfection: 2-30 min

A

Iodophors (eg 1-10% povidone-iodine)

Antiseptic & inactivated by organic material

101
Q

Action: dissolves membrane lipids; may coagulate protein

inactivated somewhat by organic matter; mild skin & lung irritant; dries skin; flammable. Disinfectant - about 1-10 min

A

Alcohol
70% isopropyl or ethyl
(including hand sanitizers)

102
Q

surfactant, destroys cell membrane; denatures proteins

A

Quarternary ammonium compounds (TOXIC if ingested)

Chlorhexidine, 4% (Low toxicity!)

Microbiology Exam 3 (15 decks)

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