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Microbiology > Exam 2 pt. 2 > Flashcards

Exam 2 pt. 2 Flashcards

1
Q

What are the methods of microbial control used outside of the body designed to result in 4 possible outcomes.

A

Sterilization
Disinfection
Decontamination (sanitation)
Antisepsis

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2
Q

Sterilization

A

The complete removal or destruction of all viable microorganisms (including viruses)
- Used on inanimate objects.

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3
Q

Disinfection

A

The destruction or removal of vegetative pathogens but not bacterial endospores.

  • inanimate objects
  • physical process or chemical agent

ex. lowering number of organisms on countertop, silverware

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4
Q

Decontamination (sanitation)

A

The mechanical removal of most microbes.

ex. Wiping down counter; physical removal

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5
Q

Antisepsis

A

Chemicals applied to body surfaces to

destroy or inhibit vegetative pathogens.

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6
Q

Antiseptics

A

Applied directly to exposed body surfaces to destroy or inhibit vegetative pathogens (lowers the number)

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7
Q

Sepsis

A

The grown of microorganisms in the blood or other tissues

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8
Q

Asepsis

A

Any practice that prevents the entry of infectious agents into sterile tissues

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9
Q

Do anti-septics work on spores?

A

no

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10
Q

Primary targets of microbial control

A

Microorganisms that can cause infection or spoilage that are constantly present in the external environment

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11
Q

What is the goal of any sterilization process?

A

Destruction of bacterial endospores

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12
Q

Any process that kills endospores will invariably kill _____.

A

all less resistant microbial forms

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13
Q

What are the most resistant living things?

A

Bacterial endospores

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14
Q

What is the gold standard for sterilization?

A

Bacterial endospores

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15
Q

Can you sterilize things against prions

A

no

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16
Q

What are more resistant, prions or bacterial endospores?

A

Prions

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17
Q

Bactericide

A

Chemical that destroys bacterial (not endospores)

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18
Q

Fungicide

A

A chemical that can kill fungal spores, hyphae, and yeasts

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19
Q

Virucide

A

A chemical that inactivates viruses

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20
Q

Sporicide

A

Can destroy bacterial endospores

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21
Q

Bacteristatic

A

Prevent the growth of bacteria

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22
Q

Fungistatic

A

inhibit fungal growth

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23
Q

microbiostatic

A

material used to control microorganisms in the body,

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24
Q

-cide

A

to kill

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25
Q

-stasis/-static

A

to stand still

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26
Q

What is microbial death?

A

When various cell structures become dysfunctional. cell sustains irreversible

  • cell can no longer reproduce under ideal environment
  • death begins when a certain threshold of microbial agent is met, and continues in a logarithmic manner
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27
Q

What take longer to kill, vegetative endospores or the spore?

A

spore

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28
Q

Microbe death by chemical agents : Damage to cell wall

A

You can achieve this by blocking synthesis, digesting it, breaking down its surface –> the cell becomes fragile and is lysed easily

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29
Q

When trying to chemically kill a microbe, if the phospholipid bilayer will lyce if the bilayer is…

A

hydrophobic, hydrophilic, hyper/hypo tonic

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30
Q

Microbe death by chemical agents: change cell wall permeability

A

Mode of action of surfactants on the cell membrane

ex. soap

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31
Q

Microbe death by chemical agents: Damage cell synthesis (nucleotides)

A

Binding to ribosomes to stop translation

  • bind irreversibly to DNA preventing transcription and translation
  • mutagenic agents
  • you can mutate it so that there are so many point mutations in it that the proteins are no longer functional
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32
Q

Microbe death by chemical agents: Damage protein

A

Most common

  • -> denaturing proteins by adding heat or changing pH
  • -> change conformational shape so active site no longer works, you can use heavy metals to block active site

No enzyme function in bacteria cell – no glycolysis, not APT/E and cell dies

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33
Q

What are the 3 ways in which you can control microbes

A

Physical, chemical and mechanical agents

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34
Q

Physical control of microbes: Heat

A

Generally, elevated temperatures are microbicidal and lower temperatures are microbiostatic
– can use moist or dry heat

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35
Q

Heat treatment of perishable substances must render the product free of agents of spoilage or disease without affecting what?

A

the speed and cost of processing

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36
Q

Thermal death time (TDT)

A

shortest length of time required to kill all test microbes at a specified temperature

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37
Q

Thermal death point (TDP)

A

the lowest temperature required to kill all microbes in a sample in 10 minutes

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38
Q

What is better? moist or dry heat?

A

moist heat – it takes shorter time to kill than dry heat

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39
Q

Method of Moist Heat Control: Steam under pressure

A

Pressure raises the temperature of steam
- Autoclave is used

results in STERILIZATION!!!!

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40
Q

Most efficient pressure-temperature combination for sterilization

A

15 psi which yields 121°C for 15 minutes

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41
Q

Moist heat sterilization is used for what

A

surgical instruments, packs, fluids

- microbiological media

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42
Q

Pasteurization

A

Used to disinfect beverages

–> heat is applied to liquids to kill potential agnets of infection and spoilage (lowers overall #s)

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43
Q

Does pasteurization kill endospores of thermoduric microbes

A

no

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44
Q

Does pasteurization sterilize

A

no

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45
Q

any food w an expiration date is not _____

A

sterile

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46
Q

Boiling water is used for _____ and not _____

A

disinfection; not sterilization

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47
Q

Dry heat: Incineration

A

Ignites and reduced microbes to ashes and gas

  • destroys bio-hazard waste
  • large scale
  • sterilizes (even prions)
  • common in microbiology labs (incineration of inoculating loops and needles)
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48
Q

Dry heat sterilization: oven

A

Used for glass and metal objects

–> used for heat resistant items that do not sterilize well with moist heat

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49
Q

What impacts do cold environments have on microbes?

A

Slow growth of cultures and microbes in food during processes and storage

  • cold does not kill
  • freezing can preserve
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50
Q

Desiccation

A

Dehydration of vegetative cells when directly exposed to normal room air

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51
Q

Lyophilization

A

A combination of freezing and drying; used to preserve microorganisms and other cells in a viable state for many years

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52
Q

Radiation

A

Energy emitted from atomic activities and dispersed at high velocity through matter or space

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53
Q

What kind of radiation is used for microbial control

A

gamma rays, X rays, UV radiation

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54
Q

Ionizing radiation

A

Gamme rays, X rays, Cathode rays

  • cold sterilization
  • dosage of radiation
  • measured in Grays
  • -> causes DNA breakages
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55
Q

Used of ionizing radiation

A

food and medical products

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56
Q

Explain how ionizing radiation crosses a barrier

A

if you take medical supplies and put them in a bag and radiate it, the supplies will be clean

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57
Q

Non-ionizing radiation

A

UV rays

  • Not as penetrating as ionizing radiation
  • does not kill bacterial spores
  • does not cross barrier
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58
Q

What are some examples of when non-ionizing radiation are used

A

disinfection of hospital rooms, operating rooms, schools, food prep areas, dental offices, treats drinking water is purify liquids

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59
Q

Mechanical techniques for removing microbes: filtration

A

Removes microbes from air and liquids

- fluids strained through filter with openings large enough for fluid but too small for microorganisms

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60
Q

What are filters made of

A

Usually thin membranes of cellulose acetate materials

- pore size can be standardized

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61
Q

What are things to keep in mid when choosing a disinfectant

A
  • nature of microbe being treated (what are you trying to get rid of)
  • nature of material being treated (skin, counter top, operating room)
  • degree of contamination
  • time of exposure
  • strength and chemical action of the germicide
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62
Q

Halogen Antimicrobial Chemicals

A

Fluorine, bromine, chlorine, iodine

  • halogens denature proteins
  • halogens are microbicidal and sporicidal with longer exposure
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63
Q

Chlorine compoinds

A

liquid and gaseous chlorine, hypochlorites, chloramines
- kills bacterial and endospores, fungi and viruses (slowly)

ex. chlorox bleach

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64
Q

Iodine compounds

A

Free iodine and iodophors

  • topical antiseptic
  • disinfectant
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65
Q

Why are halogens good for antiseptics and disinfectants?

A

you can use on objects and people

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66
Q

why is hydrogen peroxide dangerous to bacteria?

A

it is an oxygen radical; one of the molecules that gets created from aerobic respiration, and one of the molecules that gets created from bacteria –> had to have an enzyme to combat

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67
Q

Germicide effects are due to what

A

direct and indirect actions of O2

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68
Q

Hydrogen peroxide is -cidal to what microbes

A

bactericidal, virucidal, and fungicidal

–> in higher concentration is it sporicidal

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69
Q

How does hydrogen peroxide cause damage to your tissues at high concentrations

A

burns skin and turns it white

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70
Q

Hydrogen peroxide is a good _____

A

disinfectant

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71
Q

Explain how aldehydes can act as germicides

A
  • CHO functional group on end C
  • disinfectants (not used on humans –> carcinogen)
  • protein denaturization and reacting with the amine group in the cells, this acting as a cytotoxic agent

ex. glutaraldehydes and formaldehydes most often used in microbial control

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72
Q

What is the aqueous solution for most aldehydes

A

formalin

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73
Q

Gaseous Sterilants and Disinfectants: Ethylene oxide (ETO) and hydrogen peroxide

A

a. ETO
- Used to sterilize heat sensit
- kills spores

b. Hydrogen peroxide
- plasma sterilizers

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74
Q

Gaseous Ethylene oxide (ETO) and hydrogen peroxide are used on what

A

objects only

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75
Q

Phenol coefficiant

A

Compares a chemical’s antimicrobial properties to those of phenol

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76
Q

High concentrations of phenol

A

Cellular poison

- denaturation of the bacterial proteins and lysis of the cell membrane

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77
Q

Lower concentrations of phenol

A

inactivate certain critical enzyme systems

- destabilized enzyme

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78
Q

what are some examples of how phenol can be used on humans

A

listerine mouth wash and lysol (for disinfection)

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79
Q

Chlorahexidine – Avagard

A

Contains chlorine and two phenolic tings

  • denatures cell membranes and disrupts protein structure
  • mild, low toxicity, rapid action
  • hand sanitizers used in hospitals
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80
Q

Describe Chlorahexidine – Avagard at moderate to high concentrations

A

Bactericidal for both gram-positive and gram-negative bacterial but inactive against spores

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81
Q

Downside to hand sanitizers

A
  • does not kill spores

- C Diff. is a spore (should never just use this between c fid. pt.)

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82
Q

Alcohols as antimicrobial agents

A

Only ethyl and isopropyl alcohols

- doesn’t destroy bacterial spores at room temp but can destroy resistant vegetative forms

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83
Q

Alcohols as antimicrobial agents are more effective at inactivating ____ than ____

A

enveloped viruses than nonenveloped viruses

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84
Q

What is the foundational chemical for many hand sanitizers

A

OH based

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85
Q

explain how Alcohols as antimicrobial agents mechanisms depend on its concentration

A

a. 50% dissolve membrane lipids, disrupt cell surface tension and compromise membrane integrity
b. 50%-90% denatures proteins through coagulation
c. 100% (absolute alc.) dehydrates cells and inhibits their growth

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86
Q

Detergents

A

Act as surfactants (soap)

- soaps are weak microbicides; work better when mixed with chlorhexidine or iodine

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87
Q

Cationic detergents

A

effective because the positively charged end binds well with the predominantly negatively charged bacterial surface proteins

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88
Q

explain how detergents work

A

They take a hydrophobic membrane and make it hydrophilic and break it up

89
Q

The only heavy metal compounds that still have a significance as germicides are

A

Hg (mercury) and Ag (silver)

90
Q

When are Hg (mercury) and Ag (silver) effective

A

exceedingly small amounts

91
Q

How do Hg (mercury) and Ag (silver) work as gemicides?

A

bind functional groups of proteins and inactivated them

92
Q

What are drawbacks to using Hg (mercury) and Ag (silver) as germicides

A

a. toxic to humans (inactivate OUR proteins)
b. allergic reactions
c. biological fluids and wastes neutralize them
d. microbes develop resistance to silver

93
Q

What is the primary source of drugs used in chemotherapy

A

Dyes as antimicrobial agents

94
Q

What are some examples of dyes as antimicrobial agents

A

Crystal violet (inhibits gram pos,) and malachite green are very active gram-postives

95
Q

What are yellow acridine dyes used for

A

antisepsis and wound treatment

96
Q

Goal of antimicrobial chemotherapy

A

Administer a drug to an infected person that destroys the infective agent without causing harm to host cells

97
Q

A drug must be able to

A
  • easy administer
  • reach infectious agent anywhere in body
  • toxic to infectious agent
  • nontoxic to host
  • remain in body as long as needed
98
Q

Prophylaxis

A

Use of a drug to prevent imminent infection of a person at risk

99
Q

Antimicrobials

A

All-inclusive term for any antimicrobial drug regardless of its origin

100
Q

Antibiotics

A

substances produced by the natural metabolic process of some microorganisms that can inhibit or destroy other microorganisms

101
Q

Narrow spectrum (limited spectrum)

A

Antimicrobials effective against a limited array of microbial types
ex. a drug effective mainly in gram-positive bacteria

102
Q

Broad spectrum (extended spectrum)

A

Antimicrobials effective against a wide variety of microbial types
ex/ a drug effective against both gram-positive and gram-negative bacteria

103
Q

Antibiotics are common metabolic products of what

A

aerobic bacteria and fungi
bacterial are: streptomyces and bacillus
molds are: Penicillium and cephalosporium

104
Q

How have chemists created new drugs?

A

by altering the structure of naturally occurring antibiotics (penicillin made from penicillium)

105
Q

Antimicrobials that affect the BACTERIAL CELL WALL (peptidoglycan)

A

Active bacterial cells must constantly synthesize new peptidoglycan and transport it to the proper place in the cell envelope (if you don’t make peptidoglycan its getting small fast because it multiplies every 10 minutes)

106
Q

Cephalosporin and Pencillin belong to a group of antibiotics call

A

Beta Lactam antibiotics –> they are BL because they have a BL ring

  • Cephalosporin 6 c ring
  • Pencillin 5 C ring
107
Q

Beta-Lactam Drug covalently links to what?

A

Cytoplasmic membrane Regulatory Enzymes (aka Penicillin bring proteins / PBP)

108
Q

Penicillin bring proteins / PBP function in cell

A

catalyze cross linking of peptidoglycan chains

109
Q

Penicillin bring proteins / PBP is a targer of wat

A

Beta-lactam antibiotic

110
Q

MIC

A

Minimum inhibitory concentration

  • how to identify the effectiveness of antibiotic
  • the lowest concentration that the antibiotic works at
111
Q

Beta-lactam antibodies bind to what and then do what

A

Bind to PBP and distrupt peptidoglycan synthesis which results in the release autolytic enzymes that degrade the cell wall and cause the cell to lyse and the bacteria is effectively killed

112
Q

The penicillin group consists of three parts

A

thiazolidine ring, beta lactam ring, variable side chain

113
Q

Beta-lactamases

A

Enzymes produced by bacteria that break the beta-lactam ring
- about 80 dif. beta-lactamases that bacteria make

114
Q

Subgroups and uses of cephalosporins

A
  • broad spectrum
  • resistant to most beta-lactamases (penicillinases)
  • cause fewer allergic reactions than penicillins
115
Q

How many generations of cephalosporins exist based on their antimicrobial activity?

A

4

116
Q

Cephalosporins have how many functional groups

A

2 –> R1 and R2

117
Q

What are other beta-lactam antibiotics?

A

Carbapenems

  • imipenem
  • aztreonam
118
Q

What another drug that targets the cell wall but is not apart of the beta-lactam family?

A

Vancomycin (important for treating MRSA)

  • targerts cell wall (not beta-lactam)
  • totally resistant to all beta-lactamases and all other means of antibiotic resistance of that group
  • used to treat MRSA (last bet)
119
Q

How do antimicrobial drugs block protein synthesis

A

a. Inhibit translation by reacting with the ribosome-mRNA complex
- they have 70s ribosomes = good target

b. Tend to be broad spectrum because GP and GN all have 70s ribosome

120
Q

Sulfonamides and trimethoprim are what

A

competitive inhibitors of enzymes

121
Q

Competitive inhibitors of enzymes

A

When something comes into active site that is ALMOST the substrate but not quite, it gets in the active site and since it never makes a product, it never leaves –> it’s permanent and you have inactivated an enzyme

122
Q

how are Sulfonamides and trimethoprim supplied to cells

A

high concentrations to make sure the enzyme is constantly occupies with the metabolic analog rather than the true substrate

123
Q

Folic acid is what kind of inhibitor?

A

competitive inhibitor

124
Q

What does folate make

A

purines, pyrimidines and amino acids

125
Q

Explain how drugs act synergistically

A

2 drugs often give in combination to enhance effectiveness

126
Q

Explain how antimicrobial drugs effect nucleic acids

A
  • block synthesis of nucleotides
  • inhibit replication
  • stop transcription
  • inhibit DNA synthesis
127
Q

Quinolones

A

An antimicrobial drug that affects nucleic acids

ex. fluoroquinolones (very common)

128
Q

Metronizadole

A

A broad spectrum antimicrobial drug that affects nucleic acids
ex. parasites, anaerobes

129
Q

Explain when the function of Metronizadole occurs

A

only occurs when Metronizadole is partially reduced, and because this reduction usually happens only in anearobic cells, it has relatively little effect upon human cells or aerobic bacteria

130
Q

If you have super coiled DNA and not going to uncoil it, are you going to replicate that bacterial chromosome if its all coiled up?

A

No –> and this is how some of the flouroquinolones work

131
Q

Explain how some drugs disrupt the cell membrane

A

Damaged membrane invariably results in death from disruption in metabolism or lysis
–> specificity for particular microbial groups based on differences in the types of lipids in the cell membranes

They do not make the cell wall leaky, but they make the cell wall of GP out the outer membrane and inner membrane of DN damaged

132
Q

Why are some fungal cells hard to target when trying to kill with drugs

A

can be hard to target because they are euk. cells and so are we so some drugs can be toxic to us

133
Q

Majority of chemotherapeutic drugs are designed to act on what

A

bacteria and are ineffective for fungal infections

134
Q

What are the 4 main groups of anti-fungals

A
  1. Macrolide Polyene antibiotics
  2. Griseofulvin
  3. synthetic azoles
  4. flucystosine
135
Q

What are fungal cell walls made out of

A

Chitin –> chitin is different than what our cell walls are made out of so this is a good target when trying to kill with drugs

136
Q

What is an antiparasitic chemotherapy method

A

Metronizadole (Flagyl)

  • amoebicide
  • treating mild and severe intestinal infections by Entamoeba histolytica
  • orally can also apply to infections by Giardia lamblia and Trichomonas vaginalis
137
Q

Why is selective toxicity almost impossible to achieve when using antiviral chemotherapeutic agents?

A

because a single metabolic system is responsible for the well being of both virus and host because viruses use our cells to live

138
Q

Several antiviral drugs have been developed to target what in viruses

A

specific points in the infectious cycle of viruses

139
Q

What are the 3 modes of action in antiviral chemotherapeutic agents

A
  • . Barring penetration of the virus into the host cell
  • Blocking the transcription and translation of viral molecules
  • Preventing the maturation of viral particles
140
Q

What is something to remember about antiviral drugs

A

you have to take the at the beginning of the illness –> 24-48 hours to act after the onset of symptoms
- if taken at the beginning, it will only lessen the severity or shorten the duration of the illness

141
Q

Interferon (INF)

A

An alternative to artificial drugs

  • -> glycoprotein produced by fibroblasts and leukocytes in response to various immune stimuli
  • -> produced to recombinant DNA technologies
142
Q

What are the known therapeutic benefits of Interferon (IFN) drugs

A
  • reduced time of healing and complications in certain infections
  • prevent some symptoms of cold and papillomaviruses
  • slow progress of some cancers
  • treat rare cancers
143
Q

How do Interferon (IFN) drugs result in serious side effects

A

when you start putting something into your body that you make in unregulated amounts, there is always a side effect

144
Q

Do we make interferon

A

yes –> this is why serious side effects can occur is you take IFN drugs

145
Q

Drug resistance

A

an adaptive response in which microbes begin to tolerate an amount of drug that would ordinarily be inhibitory

146
Q

Drug resistance can be ___ or ___

A

intrinsic or acquired

147
Q

Microbes become newly resistant to a drug after…

A

Spontaneous mutations
- Acquisition of entire new genes or sets of genes via transfer from another species (plasmids called resistance [R] factors)

148
Q

How does a bacterial cell get antibiotic resistance?

A

conjugation, transformation, transduction

- these are ways that bacteria will pick up the resistant plasmid

149
Q

Mechanisms of drug resistance

A
  1. drug inactivation
  2. Decreased permeability / Activation of drug pumps
  3. change in drug binding site
  4. use of alternative metabolic pathways
150
Q

Drug inactivation: Beta-lactamases

A

Breaks beta lactam ring and inactivates the antibacterial drug and now the antibacterial drug will not bind to the binding protein
–> you will not stop the protein peptide synthesis between NAMs and NAGs because they are intact and strong

151
Q

Drug inactivation: decreased permeability / Activation of drug pumps

A
  • make it harder for things to get inside infectious cell
  • drug comes into infectious cell and cell pumps it back out

both of these DONT allow antibiotic into cell so the antibiotic can not do its job

152
Q

Drug inactivation: change in drug binding site

A

infectious cell changes the amino acid sequence so the binding site is gone and the antibiotic is completely ineffective

ex. MRSA

153
Q

What are common side effects of drugs

A
  • direct damage to tissues
  • allergic reactions
  • disruption of normal biota (flora)
154
Q

what percent of people taking an antimicrobial drug will experience an adverse side effect

A

5%

155
Q

Drug inactivation: use of alternative metabolic pathways

A

this is what microbes do with triclosan resistance

The drug has blocked the usual metabolic pathway, so the microbe avoids this by using an alternate, unblocked pathway

156
Q

What organs can be threatened by antimicrobial drugs

A

liver, kidneys, GI tract, CV system and blood forming tissues, nervous system, respiratory tract, skin, bones and teeth

157
Q

Allergy

A

heightened sensitivity

–> the drug acts as antigen and stimulates allergic response

158
Q

Normal flora

A

normal colonists or residents of health body surfaces

  • usually harmless or beneficial
  • small number can be pathogens
159
Q

What can happen to normal flora is a broad spectrum antimicrobial drug is used

A

the drug will destroy both infectious agents but also some beneficial species which act as barrier to infection

160
Q

Superinfection

A

When beneficial species are destroyed, microbes that were once kept in small numbers can begin to overgrow and cause disease

161
Q

What types of drugs can lead to superinfection

A

broad spectrum
–> this is why narrow spectrum antibiotics and knowing the gramstain is very important because it helps us decrease the damage to our normal flora

162
Q

What 3 factors must be known when considering and selecting antimicrobial drugs

A
  1. nature of the microbe causing infection
  2. degree of microorganisms susceptibility to various drugs
  3. overall medical condition of pt.
163
Q

What are 2 things to consider when identifying the infectious agent when you are making considerations in selecting antimicrobial drugs

A
  1. direct examination of body fluids, sputum or stool is a rapid initial method
  2. the choice of drug will be based on experience with drugs that are known to be effective against the microbe (the “informed” guess)
164
Q

infectious disease

A

disruption of a tissues or organism caused by microbes or the products

165
Q

what is the rule for disease

A

contamination without colonization and colonization without disease

166
Q

what is the ratio for cell for cell in body

A

microbes on the human body equal human cells

167
Q

Many times bacterial biota benefit the host by preventing the overgrowth of harmful organisms –> what is this process called

A

microbial antagonism

168
Q

Endogenous infections

A

caused by flora that are already present in the body getting to the wrong place
ex. UTI

169
Q

Anatomical sites and fluids that are thought to be sterile

A

all internal organs and tissues and fluids within an organ or tissues
- if closed, it is sterile

170
Q

Since all babies are sterile in the womb, where do their normal flora come from

A

passage from mothers birth canal, breast milk, what they eat, caretakers

171
Q

Pathogen

A

a microbe whose relationship with its host is parasitic (they benefit, we lose) and results in infectious and disease

172
Q

Pathogenicity

A

an organism’s potential ability to cause infection or disease (some are better than others)

173
Q

True pathogen

A

only present in disease

  • aka frank pathogens
  • do not ever belong on body unless you are in diseased state
174
Q

opportunistic pathogens

A
  • present elsewhere in body
  • can be present on body or environment
    ex. dirt
175
Q

virulence of a microbe is determined by what

A
  • its ability to establish itself in a host and cause damage
176
Q

virulence factor

A

any characteristic or structure of the microbe contributes to its ability to establish itself on host and cause damage

177
Q

Factors influencing the onset of a disease (microbe, host, outcomes

A

a. Microbes
- virulence, percentage of optimal infectious dose, correct portal of entry, virulence factor, how much attach you

b. host
- genetics, previous exposure, general health

178
Q

portal of entry

A

the route that a microbe takes to enter the tissues of the body to initiate an infection

179
Q

portal of entry is usually where

A

cutaneous or membranous body

–> usually the same anatomical regions that support normal flora

180
Q

Sources of infectious agent: exogenous

A

from outside the body

- ex. touching countertop and then eating chops and ingesting the microbe

181
Q

Sources of infectious agent: endogenous

A

opportunistic, within your body

ex. UTI

182
Q

The GI tract as portal

A

pathogens contained in food, drink or other ingested substances

  • pathogens can adapt to survive digestive enzymes and pH changes
  • usually food or fecal/oral
183
Q

The respiratory portal of entry

A

This is the portal of entry for the greatest number of pathogens; most enter here

184
Q

Urogenital portals of entry

A

STDs; enter skin or mucosa of penis, external genitalia, vagina, cervix and urethra
–> some can penetrate an unbroken surface

185
Q

Pathogens that infect during pregnancy

A

some microbes can cross the placenta (TRANSPLACENTAL INFECTION) –> congenital

186
Q

Pathogens that infect during birth

A

occur perinatally when child is contaminated by birth canal

  • eye infection of baby
  • syphilis
  • herpes

if it happens PASSED birth canal, it is NOT congenital

187
Q

ID50

A

how many organisms needed to infect 50% of the people exposed

188
Q

organisms with smaller ID50s have greater what

A

virulence

189
Q

virulence of a pathogen

A

degree of pathogenicity; how easily an organism causes disease

190
Q

What is next step for a pathogen becoming established in a host AFTER portal of entry

A

Adhesion

191
Q

The mechanisms for adhesion are what

A

virulence factors; those with more ability to adhere are more virulent

192
Q

What are some examples of adhesion factors

A

Fimbria –> main function is attachment; the bacteria’s fimbriae attach to host cell

Capsules and slime layer

Spikes (viral attachment proteins)

193
Q

Explain how microbial adherence to host cell requires specificity

A

some microbes require a chemical on host cell to adhere –> receptors aka chemicals on the host cell surface

194
Q

Adherence method: Three secretion system

A

Needle-like structure next to the flagellar basal body –> adheres to host cells –> injects proteins required for invasions –> proteins go into cell and tell cell to take up bacteria

195
Q

What is next step for a pathogen becoming established in a host AFTER portal of entry and adhesion

A

Surviving host defenses

196
Q

phagocytes

A

WBC that engulf and destroy pathogens

197
Q

Antiphagocytic factors

A

used by some pathogens to avoid phagocytes (no engulfment)

198
Q

Leukocidins

A

toxic to WBC

–> extracellular surface layer makes it hard for the phagocyte to engulf

199
Q

in order for microbes to survive in host organism they must scavenge what

A

nutrients

200
Q

iron overload increases what

A

susceptibility to infection

201
Q

Where are free iron levels low at in the body

A

body fluids

202
Q

Sideropheres

A

chelate iron and transport it into bacteria

–> bacteria make sideropheres which are iron stealers

203
Q

iron can be scavenged by siderophiles from where

A

directly from host iron-binding proteins (transferrin)

204
Q

What is next step for a pathogen becoming established in a host AFTER portal of entry adhesion and scavenging host defenses

A

causing disease

205
Q

How do virulence factors contribute to tissue damage

A

VF are simply adaptations a microbe uses to establish itself in a host and contribute to tissue damage

206
Q

3 ways microbes damage the host

A
  1. directly though action of enzymes (exoenzymes)
  2. directly through action of toxins (endotoxins and exotoxins)
  3. indirectly by inducing the host’s defense to respond excessively or inappropriately
207
Q

exoenzymes

A

Break down and inflict damage on tissues

- dissolve host defense barriers

208
Q

bacterial toxins

A

Specific chemical product that is poisonous to other organisms (kills the cells)

209
Q

Toxigenicity

A

the power to produce toxins

210
Q

tomemias

A

disease where toxin is spread by blood from site of infection

211
Q

intoxications

A

diseases caused by ingestion of toxins (botulism)

212
Q

endotoxin of GN is what

A

LPS (lipopolysaccaride)

213
Q

reminder: LPS is found where

A

outer membrane of GN bacteria

214
Q

What is the most toxic part of GN membrane

A

lipid A

215
Q

Exotoxins A-B subunit

A

Subunit A - enzymatic ACTIVITY

Subunit B - BINDing site

216
Q

Exotoxin: cytotoxins

A

act on our cells

217
Q

Exotoxin: leukocidins

A

WBC killer

218
Q

Exotoxin: neurotoxins

A

acts on nervous system

219
Q

left on on slide 40

A

of 78

Microbiology (6 decks)

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