exam 3 Flashcards

lines of defense, symbiosis

1
Q

what are the 3 lines of defense

A

(1)Exterior, (2)phagocytes and inflammation, and (3)adaptive immunity

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2
Q

What lines of defense are nonspecific

A

(1)exterior, (2)phagocytosis and inflammation

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3
Q

What lines of defense are specific

A

adaptive immunity

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4
Q

Eyes- tear ducts

A

contain lysozymes that hydrolyze peptioglycane

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5
Q

Nose

A

The most common way for bacteria to enter is by removing particles via cilla in the nasopharynx

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6
Q

Pharynx

A

Rich in microbes and containing microbial antagonism

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7
Q

Microbial Antagonism

A

residents’ microbiota that outcompetes transeit microbiota

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8
Q

Mucociliary Escalator

A

sticky mucus constantly being made and moving up the throat via cilia beating. hence the mini coughs we have

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9
Q

Smoker mucociliary escalator

A

Toxins from smoke inhibit the beating of cilia and, therefore, mucus doesn’t move up the throat, causing smokers to cough. NOTE: doesn’t inhibit the making of mucus

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10
Q

Lungs

A

Not axenic! Full of white blood cells that engulf and destroy foreign things!!

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11
Q

Stomach

A

has a high pH killing microbes,
some exceptions i.e acidophiles

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12
Q

Urine

A

peeing rid bacteria

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13
Q

skin

A

acts like a barrier, and shed 100 skin cells a day

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14
Q

Why is red blood stem not a true cell?

A

b.c doesn’t have a true nucleus

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15
Q

where do blood stems come from?

A

Bone marrow

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16
Q

3 types of phagocytes?

A

Neutrophil, Eosinophils, monocytes

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17
Q

Neutrophil

A

common blood cell, known as polymorphonuclear,

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18
Q

Eosinophils,

A

assoicated with allergies, worm infections

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19
Q

monocytes

A

referred as macrophage when in other tissue

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20
Q

subtype of cytokine

A

chemokine! and attract phagocytes

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21
Q

what are cytokine?

A

messenger molecules of the immune system

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22
Q

4 types of cytokine

A

interferon, prostaglandins, leukotrienes, histamine

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23
Q

Prostaglandins and leukotrienes both

A

stimulate vasular permeability

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24
Q

Histamines

A

promote vasodilation

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25
Q

vasodilation

A

when blood vessels widen, increasing blood flow and bringing more heat to trunk regions, i.e., arms, legs, etc. This causes rednesss and heat and increases vascular permeability.

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26
Q

Vascular permeability

A

vessels are “stretched” causes swelling and blood leaking into intracellular spaces of cells, increasing pressure and pain receptors

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27
Q

damage cells release

A

Cytokine, which then attracts phagocytes.

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28
Q

How do phagocytes work?

A

Phagocytes bind to the foreign thing, where phagocytes engulf it making phagosomes. In the inside of any phagocytes are lysosomes that fuse with the phagosome killing the bacteria(foreign substance). The final step is elimination, where through exocytosis dead bacteria are released.

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29
Q

Characteristics of interferon

A

non-specific, turns in antiviral genes hence a transcription factor.

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30
Q

How does interferon work?

A

When a virus enters a cell, the interferon gene is activated. The gene is transcribed and translated to produce interferon molecules, which are then released. These interferons signal neighboring cells to activate their own interferon genes, leading to the production of antiviral proteins. These proteins help block viral replication, protecting the surrounding cells from infection * think of alarm system

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31
Q

arteries

A

blood moves away from heart

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32
Q

veins

A

blood towards the heart

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33
Q

payer’s patches

A

a small cluster of lymphatic tissue in the intestine, and it is rich in microbe, and conducts surveillance of the GI tract.

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34
Q

lymphs nodes….

A

help mature white blood cells, filter the blood from pathogens and waste, and are located all over the body to protect from pathogens

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35
Q

lymphocytes

A

type of leukocyte that fight against pathogens

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36
Q

lymphatic system

A

composed of lymphatic vessels that conduct the flow of lymph.

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37
Q

Antigen

A

any foreign molecule that causes an immune responds

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38
Q

an antigen can have many…

A

epitope, *antigen and epitope is interchangeable term

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39
Q

antibody

A

proteins that bind to antigens and facilitate their removal

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40
Q

3 functions of phagocytes

A

1.) phagocytosis
2.) cytokine release
3.) antigen presentation

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41
Q

MCH1 is found in

A

all nucleated cells (phagocytes included!!)

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42
Q

MCH2 displays

A

is for all displayed non-self epitope

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43
Q

Why does MCH1 display non-self?

A

displays virus to show the immune system when there is a intracellular pathogen

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44
Q

Helper Cells other names

A

Th cells, CD4 cells,

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45
Q

Cytotoxic T-cells other name

A

TcCells, T8 cells, CD8 T cells, T8 lymphocytes

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46
Q

what is the specific function of CD4

A

is to bind to MCH2 receptors to simulate a humoral immunity and fight extracellular pathogens

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47
Q

The function of MCH1 is to..

A

is to display intracellular pathogens on nucleated cells and phagocyte

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48
Q

The CD4+ binds to

A

MCH2

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49
Q

CD8 binds to

A

MCH1

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50
Q

Cytotoxic cells are simulated by recognizing and binding to

A

MCH1

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51
Q

What are the pros of plasma cells being shorted lived?

A

since they are short lived they are produced antibodies faster, and therefore work faster

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52
Q

What are the cons of plasma cells being shorted lived?

A

There are rapid clearance and i.s doesn’t remember past infections aka ni immunity

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53
Q

what are the pro of long-lived memory B cells

A

they help build immunity aka they remember past infections!

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54
Q

what are the cons of long-lived memory B cells

A

they divide slower and hence take a long time to start working ther first time around

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55
Q

Where are perforin and granzymes found

A

found in cytotoxic/TcCells

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56
Q

BCR

A

are antibodies. We call them BCR when they are attached, and antibodies detached

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57
Q

How many regions of Fab/variable region are there

A

2 regions

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58
Q

Fc region is

A

the constant region doesn’t change. It interacts with the immune system

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59
Q

Neutralization

A

physically blocks foreign things

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60
Q

Agglutination of bacteria

A

clumping of bacteria

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61
Q

Precipitation of dissolved antigens

A

clumping of antigen molecules

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62
Q

activation of complement activation

A

antibodies attract proteins to make pores, aka form the MAC, which makes many pores leading to apoptosis/cell lysis

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63
Q

Opsonization

A

antibody-enhanced phagocytes. This works because phagocytes can detect Fc constant

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64
Q

Since antibodies can make every possible epitope, what is the downside of this?

A

It starts attacking your proteins!! not fun

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65
Q

what does RAG do?

A

mix and matches the antibodies gene to make a variety of antibodies

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66
Q

how does antibodies know what is self and non self

A

There are autoantigens that recognize host proteins. They bind to the B-cell. If there is a match, it rids the antibody, if it doesn’t make the antibody, it is free to do its job!

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67
Q

B cells start as..what type of antibody?

A

IgM when are still attached

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68
Q

What is the role of lymph nodes?

A

help mature white blood cells
help filter the blood from pathogen and waster
located all over the body to protect from pathogens

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69
Q

Mucosa Associated Lymphoid Tissue (MALT)

A

Similar functions to lymph nodes but for mucosal and monitor exterior foreign cells.

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70
Q

Most to least common antibodies

A

IgG, IgM, IgA, IgE (Go Make A Egg)

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71
Q

what antibody is found in secretions?

A

IgA

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72
Q

What antibody can cross the placenta?

A

IgG

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73
Q

What antibody is associated with allergies

A

IgE

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74
Q

Which antibody dimerizes

75
Q

Which antibody has pentamers

76
Q

Which antibody provides passive immunity to babies via break milk

77
Q

Adaptive Immunity

A

Mount your own immune responds to pathogen and vaccines

78
Q

Adaptive Immunity examples

A

vaccines that trick your body to create immune response

79
Q

Passively acquired

A

receive pre-formed antibodies from other.

80
Q

examples of passively acquired

A

In babies, when they are breastfed, they receive antibodies from their mother(IgA)
or
IgG that crosses the placenta and gives babies maternal immunity.

81
Q

What is Live “Attenuated” vaccine

A

When the pathogen is alive, but its ability to cause disease is impaired

82
Q

What is Live “Attenuated” vaccine Pros and Cons

A

Pros: Don’t need a booster, large immune response (more robust).

Cons: Not easy to transport, risk of reverting!, not cheap!

83
Q

What is the killed vaccine

A

The pathogen is killed, but it retains its full normal shape. It’s important to keep shape because every epitope is intact.

84
Q

What are the killed vaccine Pros and Cons

A

Pros: easy to use, cheap
Cons: requires a booster as a 2nd line of defense, can clear it out, so the 3rd line of defense never kicks in:(

85
Q

What is a Subunit Vaccine

A

individual antigens from the pathogen is used

86
Q

What are the Subunit Vaccine Pros and Cons

A

Pros: can’t be reverted, easy to transport
Cons: not as robust, needs a booster

87
Q

What is the Nucleic acid Vaccine

A

DNA or RNA encodes a pathogenic antigen is used, the patient cells produce the antigen by transcribing and translating ex. COVID vaccine

88
Q

commensalism

A

An association between two organisms in which one benefits and the other derives neither benefit nor harm.

89
Q

parasitism

A

one benefit, the other is hurt

90
Q

Mutualism

A

both benefit

91
Q

correlations

A

when 2 things are present together, but that doesn’t mean there is a relationship!

92
Q

Necessity

A

Is the symbiont necessary for development? Can the host survives without it

93
Q

Sufficiency

A

If, when the symbiont is removed from the host organisms, development stops, and when the symbiont is reintroduced into the host, does development continue where it left off?

94
Q

Describe the relationship between the Hawaiian bobtail squid and V. fishceri

A

V. fisheri live in the squid’s light organ and provide light to limit shadow production.

95
Q

What role does Quorum Sensing play in the interaction between V. fischeri and Euprymma scolopes

A

V. fishceri can sense when bacterial density is dense enough to fluoresce

96
Q

How does V.fishceri avoid the Hawaiian bobtail squid immune system

A

V fishceri is gram-negative, which means it can survive in the squid’ mucus and V.fisheri is immune to the squids phagocytes

97
Q

What type of virulence factors are more likely to help V. Fishceri survive in bobtail fish

A

Antiphagocytosis factors that prevent digestion by phagocytosis

98
Q

We know what V. fischeri gains from its association with bobtail squid. What does bobtail squid have to gain from this association, and what type of association is this?

A

V. Fischer facilitates the physical development of bobtail squid/mutualism, and can avoid predation

99
Q

Virulence

A

ability to cause disease

100
Q

Koch Postulates

A

a set of criteria used to establish a causal relationship between a specific microorganism and a disease

101
Q

1 step in koch’s Postulates

A

A suspected germ has to be present in every case of disease.

102
Q

3 step in koch’s Postulates

A

The cultured germ must cause the disease when it is inoculated into a healthy experimental host.

103
Q

2 step in koch’s Postulates

A

The suspected germ should be isolated and grown in pure culture.

104
Q

4 step in Koch’s Postulates

A

The same germ must be re-isolated from the disease experimental host

105
Q

In step 2 of Koch postulates remember that…

A

We must be able to culture the said disease, and a virus can’t be cultured, so it only works on bacteria and fungi.

106
Q

Miasma

A

bad/poisoned air

107
Q

What bacteria don’t follow the typical “the number of pathogenic bacteria in a patient is greatest during the most severe disease stage.

A

Bordetella pertussis, as they are most severe in the prodromal period.

108
Q

Are B.Theta fecal coliforms?

A

No, because they are anaerobes

109
Q

Can bacteria influence mammalian development?

110
Q

What bacteria are most common in the gut of mice?

111
Q

What do fold in the epithelial do?

A

They increase surface are therefore able to absorb more nutrients. More dense=better at absorbing minerals

112
Q

Where do the nutrients go after?

A

the cardiovascular system

113
Q

Epithelial cells in the fold are..

A

constantly shedding because more prone to infections

114
Q

Stem cells in the fold

A

making new epithelial because it is constantly shedding.

115
Q

Paneth cells

A

increase the vasculature of the intestine (aka expanding the number of blood vessels) and inhibits the growth of bacteria in the intestine.

116
Q

When B. Theta interacts with Paneth cells what do they make?

A

Proteins called Ang4 (angiogenin)

117
Q

Angiogenin is in the family

A

Angiogenesis

118
Q

what does Ang4 do?

A

make blood vessels and are antimicrobial.

119
Q

Why is Ang4 being antimicrobial important?

A

Kills other microbes except for B. Theta because B. Theta activates its produced!!

120
Q

3 types of evidence- correlation

A

B. Theta happens to be in the small intestine and
there is a produce of Ang4 which makes more blood vessels

121
Q

3 types of evidence- Necessity

A

If we remove B. Theta to see what happens when not present.
Germ free= little amount of blood vessels
Germ present= rich in blood vessels

122
Q

3 types of evidence- Sufficiency

A

B. Theta later added and sufficient to restore normal development

123
Q

What does the Mouse again, and what does the B.Theta gain?

A

B. Theta gains easy access to food and space
Mouse gains better nutrient absorption

124
Q

The thymus, the spleen, and peyer patches are part of the

A

lymph system

125
Q

Describe three mechanisms that help squid establish the symbiosis with V. Fishceri

A
  • They beat their ciliated appendages on the light organ to attract bacteria
  • They secrete a selective mucus for gram-negative bacteria
  • The squid’s hemocytes do not recognize V. Ficheri
126
Q

What are two ways V. Fischeri escape squids immune system

A
  • V. fischeri are resistant to squid acid and oxidase enzymes that kill bacteria
  • V. fischeri are not recognized by squid hemocytes that destory other bacteria.
127
Q

fomite

A

inanimate object that spread disease

128
Q

What are the 5 phases in intensity of sign of symptoms in order!

A

Incubations, prodromal, Illness, Decline, Covalescence

129
Q

What is the incubations period

A

no sings or symptoms

129
Q

what is the prodromal period

A

vague general symptoms, like itchy throat

130
Q

what is the illness stage

A

most severe symptoms and signs

131
Q

what is the Decline stage

A

decline signs and symptoms

132
Q

what is the convalescene

A

no signs or symptoms

133
Q

what bacteria does not follow this trend of signs and symptoms and why?

A

Bordetella pertussis doesn’t follow the graph; it peaks in the prodromal period, therefore doesn’t display severe symptoms

134
Q

Direct contact

A

hand shakes, kissing, sex, bites

135
Q

Indirect contact

A

drinking glass, toothbrushes, toys, punctures

136
Q

droplet transmission

A

droplets from sneezing w/in 1 feet

137
Q

Airborne

A

dust particles

138
Q

waterborne

A

steams, swimming pools

139
Q

foodborne

A

poultry, seafood, meat

140
Q

mechanical vector transmission

A

on insect bodies flies, roaches

141
Q

biological vector transmission

A

lice, mites, mosquitoes, ticks

142
Q

Acute disease

A

disease in which symptoms develop rapidly that runs its course quickly

143
Q

chronic disease

A

disease with mild symptoms that develop slowly and last long time

144
Q

latent disease

A

within incubations period, they appear for a long time after infection

145
Q

asymptomatic disease

A

disease w/out symptoms

146
Q

communicable disease

A

disease transmitted from one host to another

147
Q

contagious disease

A

communicable disease that is easily spread

148
Q

noncommunicable disease

A

disease arising from outside of host or from opportunistic infections

149
Q

local infections

A

Infections confined to a small region of the body

150
Q

systemic infection

A

widespread infections in many systems of the body, travels from the lymph system

151
Q

focal infections

A

infections that serve as a source of pathogens for infections at other sites in the body

152
Q

primary infections

A

initial infection with a given patient

153
Q

secondary infections

A

infections that follow primary infections, often by opportunistic pathogens

154
Q

what do exotoxins

A

Bacteria secrete exotoxins like cytotoxins that kill the cell

155
Q

Endotoxins

A

Dead gram-negative bacteria release exotoxins i.e lipid A that cause fever, inflammation, diarrhea, shock, and blood

156
Q

DIC

A

disseminated intravascular coagulation

157
Q

Hyaluronidase and collagenase

A

These are exoenzymes, not toxins! Bacteria release hyaluronidase which destroys polysaccharide b/n epithelial cells and collagenase, which invade deeper allowing bacteria penetrate deeper destroy collagen

158
Q

Coagulase and Kinase

A

Bacteria produce Coagulase to form a blood clot. The clot is considered ectopic. The bacteria hide in the clot until the immune response is over, and grows. Bacteria later produces a kinase to break from clot

159
Q

Phagocytosis block by capsule

A

A capsule around bacteria prevents phagocytes from binding to it, this is b/c bacteria starts producing human proteins tricking phagocytes

160
Q

Incomplete phagocytosis

A

Bacteria after being engulfed (phagosomes) can’t be lysed via lysosome, so it just hides in phagocytes and grow due to the capsule surrounding the bacteria, ir bacteria release cytotoxins to kill phagocytes

161
Q

membrane ruffling

A

Negative gram bacteria inject proteins via the type three secretions system

162
Q

how does type 3 system

A

Bacteria inject effector proteins that manipulate the actin cytoskeleton to form an ectopic pseudopod shape to engulf bacteria. Once inside bacteria produce more effector proteins to return shape back to normal and bacteria goes deeper.

163
Q

Why do bacteria do type three secretions?

A

To avoid the immune response, if bacteria produce proteins on the outside, it alerts the immune system that something is wrong and kills the bacteria.

164
Q

What structure latches onto the human plasma membrane in type 3 secretion

A

translocom

165
Q

what is one role of Paneth cells

A

They secrete Ang 4 upon contact with B. theta

166
Q

Biofilm

A

extracellular matrix of organic molecules secreted by bacteria onto a surface

167
Q

planktonic

A

free swimming

168
Q

sessile

A

surface associated

169
Q

chemotaxis

A

movement towards an attractant or away from a repellant

170
Q

A bacteria basal body moving clockwise cw

171
Q

A bacteria basal body moving counter-clockwise ccw

172
Q

True or False bacteria can switch cw and ccw contantly and can’t control this?

173
Q

what can bacteria control in terms of chemotaxis

A

They can control the speed or lower the tumbling

174
Q

what kind of bonds are present in antibodies

A

disulfide bonds

175
Q

IgG distribution and functions?

A

blood, lymph and fx is complement activations (MAC), opsonization is able to cross the placenta

176
Q

IgA distribution and functions?

A

secretions and fx is opsonization

176
Q

IgM distribution and functions?

A

lymph, blood, and BCR, 1st antibody made

177
Q

IgE distribution and functions?

A

Blood and lymph and fx is allergic reactions and parasites

178
Q

what is MAC

A

Membrane attack complex