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Prerequisites > Microbio Final > Flashcards

Microbio Final Flashcards

1
Q

how many microbes do we carry in our gut?

A

up to 2kg

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2
Q

tetrad

A

cubes of 4 and 8 squared

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3
Q

pallisade

A

side to side cells

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4
Q

what kind of cell fluctuates with how immunocompetent you are that day?

A

natural killer cells

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5
Q

what is the command center of level 3 defenses?

A

lymphatic system

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6
Q

where are B and T lymphocytes produced?

A

bone marrow

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7
Q

where do T cells mature?

A

thymus

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8
Q

where do B cells mature?

A

bone marrow

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9
Q

what are the lymphoid organs?

A

lymph nodes and spleen

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10
Q

what are the Mucosal Associated Lymphatic Tissues?

A
  • tonsils
  • adenoids
  • peyers patches
  • appendix
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11
Q

where are MHC-1 found?

A

all nucleated cells

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12
Q

what are MHC-1 used for?

A

ID of abnormal self cells

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13
Q

where are MHC-2 found

A

on antigen presenting cells

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14
Q

what are the antigen presenting cells?

A
  • macrophages
  • dendritic cells
  • B-lymphocytes
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15
Q

what are MHC-2 used for?

A

presenting the antigen to immune cells

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16
Q

when is cell mediated immunity initiated?

A

1-2 days

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17
Q

what kind of cell is activated during cell mediated immunity?

A

T cells

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18
Q

what are the two types of level 3 immunities?

A

cell mediated and humoral

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19
Q

when is humoral immunity initiated?

A

2-5 days

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20
Q

what kind of cell is activated during humoral?

A

B cells

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21
Q

APC with MHC-2 goes to lymph nodes and activates what ?

A

T helper 0 and T cytotoxic 0

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22
Q

how does the antigen on the MHC-2 activate the T cells?

A

T cell receptor protein matches with antigen on MHC-2

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23
Q

what does Th0 become?

A

Th1

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24
Q

what cell secretes cytokines?

A

Th1

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25
Q

what does Tc0 become?

A

TcC or T cytotoxic clones

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26
Q

what are the two main jobs of cytokines?

A
  • increasing phagocytosis
  • activating T cytotoxic cells
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27
Q

another name for T cytotoxic cells when activated…

A

Killer T cells

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28
Q

how do cytokines increase phagocytosis?

A
  1. more lysosomes
  2. other cells convert to phagocytic cells
  3. phagocytes become faster
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29
Q

how do cytokines activate Cytotoxic T cells

A

cause them to clone rapidly with info. about antigen

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30
Q

Two types of T cell clones are made. What are they?

A

T cytotoxic and T memory

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31
Q

which kind of T cell is the majority of clones made?

A

T cytotoxic

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32
Q

which kind of T cell is the minority of clones made?

A

T memory

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33
Q

although both kind of T cells are cloned, which one is activated and used immediately?

A

T cytotoxic

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34
Q

what is the only kind of T cell stays in the lymph node and does not leave to bloodstream and tissues?

A

T helper 1

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35
Q

why doesn’t Th1 leave the lymph node?

A

has to keep secreting cytokines to increase phagocytosis and activate T cytotoxic cells

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36
Q

how do T cytotoxic cells find infected or abnormal self cells?

A

chemotaxis

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37
Q

how do T cytotoxic cells destroy cells?

A

perforin + granzyme

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38
Q

what kind of pathogen does T cytotoxic cells work best to eliminate?

A
  • Infected self cells
  • cancerous self
  • yeast
  • protozoa
  • worms
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39
Q

when the threat is over which cells die from cell mediated immunity?

A

cloned T cytotoxic cells and T helper 1 cells

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40
Q

which cells live forever after cell mediated immunity?

A

T memory

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41
Q

in the second exposure (cell mediated), what happens?

A

T memory cells become T cytotoxic cells

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42
Q

is an APC needed in the second exposure?

A

no

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43
Q

how long does is take for T memory cells to become T cytotxic cells in the second exposure?

A

minutes

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44
Q

what are the two switches needed to activate B cells?

A

MHC-2 or B cell receptors in membrane

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45
Q

in humoral immunity, what happens after the APC enters the lymphoid organ?

A

Th0 becomes T helper 2

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46
Q

what does T helper 2 bind to?

A

MHC-2

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47
Q

What do the cloned B cells differentiate into?

A

plasma cells and B memory cells

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48
Q

what do plasma cells produce?

A

antibodies

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49
Q

when does antibody production begin?

A

5 days into infection

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50
Q

how many antibodies are produced from plasma cells?

A

2000/second

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51
Q

do plasma and B memory cells leave the lymph node?

A

no

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52
Q

when the threat is over after humoral immunity, which cells die?

A

plasma cells and T helper 2

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53
Q

when the threat is over after humoral immunity, which cells live forever?

A

B memory

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54
Q

in the second exposure (humoral), what happens?

A

B memory cells convert to plasma cells and secrete antibodies and do not need an APC

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55
Q

who calls antibodies gamma globulins?

A

blood scientitst

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56
Q

who calls antibodies immunoglobins?

A

immune scientists

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57
Q

what does Fab stand for?

A

Fractions which are Antigen Binding

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58
Q

what does Fc stand for?

A

Fraction which is Constant or Crystalizable

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59
Q

IgG

A
  • 80%
  • monomer
  • only one that crosses placenta and will stay with baby for up to 6 months
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60
Q

IgA

A
  • 10-15%
  • dimer
  • transported through glands for secretions
  • tears, saliva, mucus, milk
  • transmitted to baby through breastfeeding
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61
Q

IgM

A
  • 5-10%
  • pentamer
  • found in blood ONLY
  • grabs 10 antigens at a time
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62
Q

IgE

A
  • less than 1%
  • do not bind to antigens
  • monomers
  • allergic reactions
  • bind to mast cells, basophils, eosinophils
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63
Q

IgD

A
  • less than 0.5%
  • monomers
  • function as B cell receptors
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64
Q

B virgins make plasma cells and release these antibodies in this order… (first + subsequent exposure)

A

IgM first then IgG

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65
Q

how do B memory cells release antibodies in subsequent exposures?

A

IgG in large amounts and IgM at same time both earlier

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66
Q

anti viral drugs for attachment prossess

A

attachment antagonist

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67
Q

agglutination:

A

Fab binds to antigen causing clumping which increases phagocytosis

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68
Q

what type of pathogen does agglutination work best to eliminate

A
  • bacteria
  • larger viruses
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69
Q

opsonization

A

Fab binds to antigen and Fc binds to phagocyte surface and forces phagocytosis

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70
Q

what type of antigen does opsonization work best to eliminate?

A

bacteria only

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71
Q

Natural killer activation

A

Fab binds to antigen and Fc binds to NK cell and leads it to pathogen

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72
Q

what type of pathogen does Natural Killer Activation work best to eliminate?

A

eukaryotic abnormal self cells

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73
Q

complement activation

A

Fab binds to antigen Fc binds to loose complement proteins and causes inflammation, opsonization, and membrane attack complex

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74
Q

in humoral immunity what is the only molecule that leaves the lymphoid organ?

A

antibodies

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75
Q

inflammation works bets to eliminate which kind of pathogen?

A
  • bacteria
  • infected self cell, yeast, protozoa
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76
Q

opsonization works best to eliminate which kind of pathogen?

A

bacteria

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77
Q

membrane attack complex works best to eliminate which kind of pathogen?

A
  • bacteria
  • infected self, yeast, protozoa
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78
Q

neutralization

A

Fab binds to antigen and blocks binding ability of toxins, enzymes, adhesins, and viruses

79
Q

oxidation

A

Fab binds to antigen and H2O2 or O3 are made in the local area which is facilitated by Fc.

80
Q

oxidation works best to eliminate which kind of pathogen?

A

bacteria

81
Q

allergy producing antigens

A

allergens

82
Q

allergens trigger the production of what?

A

IgE antibodies

83
Q

IgE antibodies bind to which kind of cells?

A
  • mast cells
  • basophiles
  • eosinophiles
84
Q

what kind of granules are found beneath of the epithelium/endothelium?

A

histamines, leukotrienes, bradykinins, serotonin

85
Q

what is the name for a cell when it has hit the critical number of IgE?

A

fully loaded

86
Q

what is degranulation?

A

release of chemicals within vesiscles in cells

87
Q

what are the three effects of degranulation?

A
  1. general inflammation; capillaries dilate and become leaky which causes fluid to go to tissues
  2. smooth muscle contractions; constriction of airways, cramping and diarrea
  3. glandular secretion; mucus, tears, digestive enzymes, acid
88
Q

why do we have allergies?

A
  1. expel antigens from body
  2. “hygeine hypothesis”
89
Q

what are whole cell vaccines?

A

live but attenuated pathogen injected

90
Q

whole cell vaccines effectiveness and why

A

Highest: multiple antigens and reproduction - highest # of memory cells

91
Q

risk of whole cell vaccine:

A

could get the disease since its alive

92
Q

killed or inactivated vaccine:

A

pathogen has been killed but antigens still present

93
Q

killed or inactivated vaccine effectiveness and why:

A

highly effective: no reproduction but multiple antigens

94
Q

risk of killed or inactivated vaccine?

A

no risk of infection but strong immune response

95
Q

generalized transduction happens where?

A

lytic cycle only

95
Q

soluble subunit effectiveness and why:

A

lowest effectiveness: response to only antigens injected booster needed

95
Q

soluble antigens (subunits) vaccine:

A

antigens injected

96
Q

soluble subunit vaccine risk

A

lowest risk no danger of infection except to adjuvants

97
Q

how are recombinant vaccines created?

A

manipulating DNA

98
Q

bacterial conjugation donor

A

always F+

99
Q

bacterial conjugation recipient

A

always F-
can be same or dif species

100
Q

what does F+ cell do?

A

make sex pili

101
Q

F+ sends what to F- via cyto. bridge?

A

F+ copy

102
Q

recombinant attenuated vaccine effectiveness and why:

A

highly effective + safer: virulance factor deleted, reproducing w multiple antigens

103
Q

for hfr conjugation does the recipient become a donor?

A

no

104
Q

how do pathogens enter?

A

dose and portal of entry

105
Q

how are capsules used as weapons

A
  • neutralize antibiotics
  • avoid phagocytosis
  • block complement activation
  • delay immune response
106
Q

how are enzymes used as weapons

A

alter substrate in host tissue

107
Q

invasins

A

flagella along with invasin enzymes allow bacteria to push through cells of blood vessel walls

108
Q

what enzyme does spirochaetes use to make it more virulent?

A

invasins

109
Q

coagulase

A
  • clotting
  • prevents WBC from entering
  • localizing enzymes
  • helps form local infections
110
Q

streptokinase

A
  • breaksdown blood clots
  • allows speticemia
111
Q

hyalouronidase

A

dissolves hylauronic acid

112
Q

collagenase

A

breakdown collagen

113
Q

which two enzymes work together to get between and under cell layers?

A

collagenase and hylauronidase

114
Q

hylauronidase and collagenase spread through tissue not blood. what is that called?

A

systemic

115
Q

leucocidin

A
  • kills WBC
  • makes pus
116
Q

M protein

A
  • prevent phagocytosis by WBC
  • pseudopods cannot grab pathogens
117
Q

hemolysin

A
  • rupture RBC
  • releases Fe and proteins
  • decrease O2 and increase CO2 for microaerophiles
118
Q

protease

A
  • digest proteins
119
Q

lipase

A

-breaks down fats

120
Q

amylase

A
  • carbs
121
Q

how does liquifying tissues help pathogens?

A
  • they eat you
  • prevent circulation so theres no WBC
  • prevent drugs
122
Q

exotoxins

A

toxins that exit the bacterial cells

123
Q

how do exotoxins leave?

A
  • proteins
  • secreted from live cells
  • gram (-) and gram (+) can produce
  • antitoxins produce by immune system
124
Q

antitoxin

A

antibodies that destroy toxins only

125
Q

toxoid

A

denatured toxin used in a vaccin

126
Q

cytotoxin

A
  • directly kills cells
  • causes lesions
  • Ex. Anthrax
127
Q

neurotoxins

A

effects nerve system

128
Q

two types of neurotoxins

A
  • botulism
  • tetanus
129
Q

what type of paralysis is botulism

A

flaccid

130
Q

how does botulism toxic work?

A
  • binds to motor nerve endings
131
Q

botulism prevents release of what?

A

neurotransmitters - acetylcholine

132
Q

infant botulism is what?

A

it is a food infection NOT an intoxication

133
Q

what kind of paralysis is tetanus?

A

rigid

134
Q

how does tetanus work?

A
  • binds to nerve endings
  • releases neurotransmitter
135
Q

enterotoxin

A

effects digestive tract

136
Q

enterotoxin effects

A
  • fluid loss
  • increased peristalsis
137
Q

endotoxin

A

toxin released inside the cell

138
Q

where is lipid toxin found?

A

LPS layer

139
Q

what kind of cells are endotoxins found in?

A

gram (-) ONLY

140
Q

when are endotoxins released?

A

when cell dies

141
Q

systemic effect of endotoxins

A
  • shock
  • fever
  • inflammation
  • drop in BP
  • blood clots
142
Q

why are endotoxins lipids?

A

because they do not trigger an immune response

143
Q

if lipids do cause an immune response, what cannot be made in response to endotoxins?

A

antitoxins

144
Q

intra

A

same species

145
Q

inter

A

talk to other species

146
Q

evidence of viral infected cell abnormalities

A

cytopathic effects

147
Q

how do viral cytopathic effects show up

A

often as lesions and lack of function

148
Q

syncytium formation

A

cells merge into large mass

149
Q

multinucleated cells

A

cell has more than one nucleus but does NOT get bigger

150
Q

inclusion bodies

A

clumps of host cell organelles or viral products seen in host cell

151
Q

nucleomegaly

A

nucleus gets bigger but cell DOES NOT

152
Q

enlargement

A

cell gets bigger

153
Q

rounding

A

infected cell becomes round

154
Q

skin

A
  • normal flora
  • cornification
  • hair
  • salt
  • lysozyme
  • sloughing; flushing
155
Q

respiratory tract

A
  • lysozyme
  • flushing
  • cilliary escalator
156
Q

eyes

A
  • hair
  • salt
  • lysozyme
  • flushing
157
Q

mouth

A
  • normal flora
  • lysozyme
  • flushing
  • digestive enzymes
158
Q

urinary tract (male)

A
  • flushing
159
Q

female reproductive tract

A
  • normal flora (vagina only)
  • acid (vagina only)
  • lysozyme
  • cilliary escalator
160
Q

digestive tract

A
  • normal flora (intestines only)
  • acid (stomach only)
  • lysozyme
  • peristalsis; flushing
  • digestive enzymes
161
Q

what is phagocytosis?

A

engulfed material either digested or secreted

162
Q

where are neutrophiles found?

A

blood and tissues

163
Q

where are monocytes found?

A

blood only

164
Q

what cell is deprived from monocytes?

A

macrophages

165
Q

where are macrophages found

A

tissues only

166
Q

what are the three types of macrophages?

A
  • dendritic
  • kupffer
  • microglial
167
Q

where are dendritic cells found?

A

skin

168
Q

where are keupfer cells found?

A

liver

169
Q

where are microglial cells found?

A

brain

170
Q

first step of phagocytosis:

A
  1. WBC find bacteria via taxis
171
Q

what MUST phagocytic cells have?

A

lysosome pouch

172
Q

what is in the lysosome pouch?

A
  • lysosomes
  • acid
  • super oxide
  • digestive enzymes
173
Q

second step of phagocytosis:

A

pseudopods grab particle

174
Q

third step of phagocytosis:

A
  • phagocyte must digest particle material into the phagosome pouch
  • release alert signla via cytokines
175
Q

fourth step of phagocytosis

A
  • fusion phagosome + lysosome = phagolysosome
176
Q

fifth step of phagocytosis:

A
  • digest material
177
Q

sixth step of phagocytosis:

A
  • secrete undigested material vis exocytosis
178
Q

antigen

A

unique, recognizable molecules of pathogen saved

179
Q

what cells use MHC-2

A

APC:
- macrophages
- dendritic cells
- B- lymphocytes

180
Q

bacterial antigens:

A
  • membrane proteins
  • endo + exoenzymes
  • flagella
    -pilli
    digestive enzymes
  • capsules
181
Q

viral antigens:

A
  • capsomeres
  • peplomers or matrix proteins
  • enzymes
182
Q

fungal antigens

A
  • eukaryotic cells
  • protozoa and worms
  • cell surface proteins
  • enzymes
183
Q

your own cells that are not working normally

A

abnormal self cells

184
Q

neutralization toxins

A

cant bind to tissues

185
Q

neutralization enzymes

A

cant bind to substrate

186
Q

neutralization bacterial adhesions

A

cant bind to tissue/ surface

187
Q

neutralization viruses

A

cant bind to host cell

188
Q

dolor

A

pain

189
Q

rubor

A

red

190
Q

tumor

A

swelling

191
Q

calor

A

heat

Prerequisites (8 decks)

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