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MICR 2420 > post lecture notes > Flashcards

post lecture notes Flashcards

1
Q

who was the god father of microbiology?

A

Anton van Leeuwenhoek

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2
Q

what were Anton van Leeuwenhoek’s first observations made on?

A

hand-crafted microscopes using plaques scraped from his teeth

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3
Q

what are animalcules?

A

what Anton van Leeuwenhoek called the first single celled organism

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4
Q

what are the 3 types of images we see on a microscope?

A

bright-field
phase contrast
dark-field

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5
Q

how does glow in the dark work?

A

absorbs 1 wave length, emits another

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6
Q

what’s the process of TEM sampling preparation?

A
  1. fixation
  2. staining
  3. dehydration
  4. polymerized
  5. sectioning
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7
Q

how does cry-term work?

A
  1. sample: apply to EM grid
  2. blot: remove liquid
  3. plunge freeze: liquid ethane
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8
Q

how does going from 2D to 3D work?

A
  1. specimen rotates in the beam
  2. combine and compute 3D transform
  3. reconstruct object in 3D
    (using electron microscope)
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9
Q

what does microscopy reveal?

A

the vast realm of organisms invisible to the unaided eye

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10
Q

what do fluorescent microscopes show?

A

how parts function within a living cell

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11
Q

what do electron microscopes show?

A

cell’s interior; how all the parts fit together

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12
Q

describe light microscopy

A

resolves images of individual bacteria by their absorption of light

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13
Q

what is brightfield microscopy?

A

specimen is a dark object against alight background

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14
Q

describe electron microscopy (EM)

A

uses beams of electrons to resolve details smaller than light microscope

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15
Q

describe scanning electron microscopy (SEM)

A

electron beam is scattered from the metal-coated surface of an object, generating an appearance of 3D depth

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16
Q

describe transmission electron microscopy (TEM)

A

the electron beam travels through the object where the electrons are absorbed by an electron-dense meal stain

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17
Q

what can H. pylori cause?

A

gastric cancer

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18
Q

true or false:

all H. pylori is bad?

A

false

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19
Q

what is a facultative anaerobe?

A

aerobic but can survive in anaerobic conditions

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20
Q

how many cells in the average bowel movement?

A

10 trillion

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21
Q

How do Cyanobacteria spp. inside rock photosynthesiz?

A

in quartz, translucent, some light can get through

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22
Q

can archaea’s have viruses?

A

yes, even more complex than bacteriophages

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23
Q

what are some barriers we have to manage our microbes

A

skin
mucous membranes
blood brain barrier

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24
Q

what is the immune system?

A

A complex system of organs, tissues, cells and cell products that work in concert to recognize and neutralize potentially pathogenic threats

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25
Q

what happens when human barriers are breached within the body

A

the immune system comes into play

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26
Q

what are the 2 arms of the immune system?

A

innate and adaptive

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27
Q

what does the innate immune system include?

A
  • Physical barriers

- Chemical and cellular responses (come into play if barriers are breached)

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28
Q

true or false:

Contact with an infectious agent guarantees that a person will get sick

A

false

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29
Q

what does a pathogen need to cause disease?

A
  • Breach host defenses
  • Survive innate defense mechanisms
  • Begin to multiply
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30
Q

why is the skin a good barrier?

A

Difficult to penetrate by microbes when intact (keratin)

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31
Q

why is the mucous membrane a good barrier?

A
  • 200-300 m2 in the average human!
  • Epithelial cells are tightly connected to support a strong barrier function
  • Selectively. permeable to allow absorption of nutrients
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32
Q

why are the lungs a good barrier?

A
  • Have a ‘mucociliatory escalator’
  • Microbes larger than ~100μm are trapped by hairs in the nose and by cilia lining the upper airways
  • Trigger sneezing, to forcefully remove foreign material, including microbes, from the respiratory tract
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33
Q

what are all physical barriers tightly connected to?

A

lymphoid tissues

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34
Q

which of the following is least likely to influence susceptibility to infection with a given food-borne disease:

a) infectious dose
b) virulence potential of the pathogen
c) previous appendectomy
d) host genetics
e) recent history of antibiotic use

A

c) previous appendectomy

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35
Q

how did the complement system get its name?

A
  • Complement is a set of proteins made by the liver

- Named in 1890s because they complement antibodies in the killing of bacteria

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36
Q

where do the complement proteins circulate?

A
  • in blood and enter tissues all over the body
  • Circulate as inactive forms and are proteolytically cleaved to make them active
  • complement activation
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37
Q

what is the name of the complement components/complexes?

A

C1-C9

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38
Q

how many soluble and membrane bound protein components of the complement system are there?

A

~30

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39
Q

what are the 3 complement activation pathways?

A
  • The classical pathway
  • The lectin pathway
  • The alternative pathway
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40
Q

where do all 3 complement pathways converge?

A

lytic pathways

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41
Q

what does protein shape determine?

A

what they can and cannot do

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42
Q

describe the gut concentration gradient of defensins

A
  • Higher in close proximity to the crypts of the epithelium
  • Secretion is from the crypts
  • Keeps out even the normal microbiota
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43
Q

What sort of cells are found within blood?

A
  • Red blood cells
  • White blood cells
  • Platelets
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44
Q

which kind of blood cells are part of the immune system?

A

white blood cells

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45
Q

what do white blood cells include?

A
  • polymorphonuclear leukocytes (PMNs, granulocytes or polys)
  • Monocytes & macrophages
  • Dendritic cells
  • Mast cells
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46
Q

how many blood cells does 1 literals of human blood contain?`

A

~6 billion

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47
Q

what does Myeloid bone marrow stem cells differentiate into?

A

phagocyte cells

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48
Q

what does phagocyte mean?

A

a cell that eats

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49
Q

wha are NETs

A

Neutrophil Extracellular Trap

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50
Q

what is NETosis?

A

An unusual form of cell death by the neutrophil

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51
Q

what do neutrophils do when they sense an invader?

A
  • spews a latticework of chromatin and antimicrobial compounds into the vicinity
  • Prevents spread of the pathogen
  • Allows rapid phagocytosis
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52
Q

what is inappropriate NETosis thought to underlie?

A

autoimmune disease called systemic lupus erythematosus (lupus)

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53
Q

what do monocytes differentiate into?

A

macrophages

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54
Q

where do monocytes circulate?

A

the blood stream

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55
Q

describe movement of monocytes?

A
  • attracted by chemical signals (cytokines) to sites where they are needed
  • As they travel through the blood vessels (extravasation) they differentiate into macrophage
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56
Q

true or false:

Monocytes are large structures that can ingest many microbes at one time

A

true

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57
Q

what do dendrocytes posses?

A

long protrusions that can squeeze through tight spaces to sample microbes

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58
Q

what do Cytokines, chemokines and interferons act as?

A
  • language of our immune system
  • Close-range acting ‘hormone’ system
  • particularly effective at signalling ‘danger
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59
Q

what are some cytokines important for?

A
  • anti-inflammatory signals after danger has passed

- Reset the homeostasis

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60
Q

what are Macrophages and dendrocyte also?

A

antigen presenting cells (APCs)

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61
Q

what do Macrophages and dendrocyte do when they ingest antigens?

A

process them and display them on their surfaces for T-cells

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62
Q

what is the link between innate and adaptive immune systems?

A

Macrophages and dendrocyte

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63
Q

what are Peyer’s patches?

A

Specialist sites within the small intestine

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64
Q

how do macrophages recognize microbial cells?

A
  • Have non-specific receptors on their surfaces

- But they also rely on circulating helper molecules

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65
Q

why are any pathogens encapsulated?

A

to help them evade the innate immune system

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66
Q

how are pathogens recognized by the immune system?

A
  • Cells of the innate immune system have specialized sets of receptors to recognize invariant and essential microbial factors that are unique to the microbe
  • These are referred to as Pattern Recognition Receptors (PRRs)
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67
Q

what do PPRs recognize?

A

MAMPs -Microbe Associated Molecular Patterns

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68
Q

what are Toll-like receptors?

A

transmembrane receptors on some immune cells that recognize viral and bacterial products

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69
Q

what are TLRs useful for sensing?

A

external MAMPs

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70
Q

what do NOD-like receptors do?

A
  • bind MAMPs and Activate cytokine production

- Form a complex called an inflammasome that triggers apoptosis

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71
Q

where are TLRs found?

A

outside the cell

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72
Q

where are NLDs found?

A

inside the cell

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73
Q

describe natural killer cells

A
  • Not phagocytic
  • A lymphocytic cell, distinct from T cells and B cells
  • Large and granular
  • Make up ~2% of lymphocytes in the body
  • Thought to be a halfway house between innate and acquired immunity
  • Don’t attack pathogens themselves, but instead attack host cells that have become overwhelmed by pathogens
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74
Q

true or false:

Most aspects of the innate immune response have a direct connection to the adaptive immune response

A

true

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75
Q

which branch of the immune system has memory?

A

adaptive immune system

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76
Q

what are the 2 types of immune memory?

A

humoral immunity

cell-mediated immunity

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77
Q

describe humoral immunity

A
  • Antibodies directly target microbial invaders (B-cell response)
  • Target infections in the body’s fluids (humors)
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78
Q

describe cell-mediated immunity

A
  • teams of T-cells (T-lymphocytes) work together to recognize antigens displayed on infected cells
  • Target infections in the body’s cells
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79
Q

true or false:

humoral and cell-mediated immunity are intertwined

A

true

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80
Q

true or false:

you are born with adaptive immunity

A

false:

develops as the need arises

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81
Q

what happens if the adaptive immune system is missing?

A

Usually a lethal mutation… SCID

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82
Q

how long does it take for the adaptive immunity to develop?

A

over ~3-4 day period following exposure to an invading microbe

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83
Q

what does the immune system recognize?

A

small pieces of a given antigen, called antigenic determinants or epitopes

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84
Q

what does phagocytosis produce?

A

many epitopes for the adaptive immune system

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85
Q

what does each B-cell recognize?

A

one specific epitope

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86
Q

what does the response to an infection involve?

A

thousands of different B-cells, each of which recognizes a particular epitope

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87
Q

what stimulate B-cells (B-lymphocytes) to differentiate into antibody producing cells?

A

Antigens (from ‘antibody generators’)

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88
Q

when does humoral response start?

A

when an antigen triggers the differentiation of B-cells into antibody-producing factorie

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89
Q

when does cell mediated response start?

A

when certain T-cells become activated by microbial antigens that are presented to them

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90
Q

what do activated T-cells do?

A
  • can directly kill an infected host cell

- Also produce cytokines that initiate a macrophage feeding frenzy at the site of infection

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91
Q

which lives longer: plasma cells or memory B cells?

A

memory B cells: decades vs. plasma cells 4-5 days

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92
Q

what can the adaptive immune system recognize?

A

immunogenicity

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93
Q

what is immunogenicity

A

The effectiveness by which an antigen elicits an immune response

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94
Q

where is an antigen placed?

A

on a major histocompatibility complex (MHC) protein

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95
Q

true or false:

Binding of antigen to MHC needs to be strongfor T-cell to recognize it properly

A

true

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96
Q

what do T-cell receptors bind?

A

antigen and MHC Together with accessory molecule

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97
Q

what do mature T-cells differentiate into?

A
  • T-helper (TH) cells/ CD4+ cells

- Cytotoxic T-cells (TC)/CD8+ cells

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98
Q

what do TH cells do?

A
  • Associate with MHC class II proteins on APCs
  • trained to memorize databanks of antigens and to alert B-cells if circulating antigen is detected
  • determine which cytokines will allow the immune system to be most useful for the host during infection
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99
Q

what do TC cells do?

A
  • associate with MHC Class I proteins on APCs

- trained to seek and destroy cells presenting noxious antigens on MHCI (indicating they may be infected)

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100
Q

where do B cells mature?

A

bone marrow

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101
Q

where do T cells mature?

A

Thymus

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102
Q

what are the 2 types of that TH cells differentiated into?

A

TH1 and TH2

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103
Q

what is TH1 most active against?

A

intracellular bacteria and protozoa

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104
Q

what is TH2 most active against?

A

helminthic infections

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105
Q

why do proteins generally make for the best types of antigens compared to carbohydrates, nucleic acids and lipids?

A

proteins have a greater differentiation of shape than carbohydrates, nucleic acids or lipids

106
Q

true or false:

As well as effector T-cells, some TH cells differentiate into memory TH cells

A

true

107
Q

what do regulatory T-cells do?

A

do not promote an immune response but help to restore homeostasis after infection

108
Q

what is the lack of Treg cells associated with?

A

chronic inflammation

109
Q

where do all T-cells pass through to get exposed to self antigens?

A

thymus

110
Q

how many T-cells survive the passing through the thymus?

A

2%

111
Q

How do we learn to live with the antigens of our own bodies/the foreign antigens of our microbiota?

A

antigen does is important

112
Q

why is antigen does important?

A
  • If antigen dose is over a threshold value, then B-and T-cells become over-stimulated
  • T-cells become non-functional
  • B-cells do not respond to subsequent antigen exposures to make antibodies
113
Q

what are vaccinations used for?

A

killed, attenuated or engineered antigen sources to induce an immune response without causing disease

114
Q

why is immunological specificity important in vaccinations?

A

An antibody made to one epitope will not bind to another epitope (unless that epitope is very similar)

115
Q

what is the key to immunological specificity?

A

Antibodies (immunoglobulins)

116
Q

what does the typical antibody look like?

A

antibody: 4 polypeptide chains
•2 large heavy chains
•2 smaller light chains
- Bound together by disulfide bonds

117
Q

what is anergy?

A

absence of the normal immune response to a particular antigen or allergen

118
Q

what are the 5 heavy chain types?

A

α, μ, γ, δ, ε

119
Q

what are the 2 light chain types?

A

κ, λ

120
Q

what does α =?

A

IgA

121
Q

what does μ =?

A

IgM

122
Q

what does γ =?

A

IgG

123
Q

what does δ =?

A

IgD

124
Q

what does ε =?

A

IgE

125
Q

what is an isotope?

A

define the various heavy chains of a species

126
Q

what is an allotype?

A

differences in the constant region shared by some but not all members of a species

127
Q

what is an idiotype?

A

differences in the hypervariable region within an individual

128
Q

describe IgG

A
  • Simplest, smallest and most abundant antibody in blood and tissue fluids
  • A monomer, with 4 classes (IgG1-4)
  • Each class varies in aa sequence and interchain cross-linking
129
Q

what are the jobs of IgG?

A
  • Binds and opsonizes microbes (allowing phagocytes to grab them more easily)
  • Binds and neutralizes viruses
  • Activates the classical complement pathway
130
Q

describe IgA

A
  • Major secreted antibody of mucosal surfaces
  • Most commonly found as a dimer, linked by disulfide bonds to the J (joining)-chain protein
  • Secretory piece is wrapped around both molecules during secretion
  • “secretory IgA” is found in tears, breast milk and on mucosal surface
131
Q

describe IgM

A
  • Can be found as monomers on the surface of B-cells
  • But is most commonly found as a pentamer held together by J-protein
  • First antibody isotype detected during the course of an infection
132
Q

describe IgD

A
  • Present in trace amounts in the blood
  • Exists in monomeric form on surface of B-cells
  • Plays a role in B-cell activation
  • Function not well understood
    •Does not bind complement
    •May play a role in allergy as well as activation of the immune response to respiratory pathogen
133
Q

describe IgE

A
  • Present in trace amounts in the blood
  • Found more prominently on the surfaces of mast cells and basophils
  • These cells are loaded with inflammatory mediators (held in granules)
  • When 2 mast cells or basophils are cross-linked by antigen via IgE, mast cells degranulate and act to quickly amplify the immune response
  • Unfortunate side-effect in some people: anaphylaxis
134
Q

what are the types of vaccines?

A
  • Live attenuated
  • Inactivated
  • Subunit
  • Toxoid
  • Conjugate
135
Q

why does some vaccines such as tetanus not benefit from heard immunity?

A

not passed foreperson to person, only from source

136
Q

true or false:
Normally, B cells that escape from the negative selection process cannot be activated because they require a cognate THcell

A

true

137
Q

why is it important to treat stream throat?

A
  • makes a protein called ‘M protein’
  • Parts of this protein very similar to a cardiac protein
  • The cardiac-like epitope may be encountered by an ‘escaped’ self-reacting B cell
  • The cognate T cell may recognize flanking non-self proteins and activate the B cell
  • The B cell responds –makes plasma cells that secrete antibodies to the cardiac protein
  • Damage to host cardiac tissue occurs
  • Rheumatic fever –can lead to scarring of heart valve
138
Q

what is the influenza virus?

A

a negative strand RNA virus

139
Q

what are the 3 types of influenza?

A
  • influenza A
  • influenza B
  • influenza C
140
Q

describe influenza A

A
  • one of the most common life-threatening viruses of the western world
    ~ 10% of the population of US and Canada are infected every year
    ~36000 deaths annually in the USA
  • Pregnant women and the elderly are most susceptible
141
Q

describe influenza B

A
  • Narrower host range than influenza A

- Can cause serious disease but mutates much more slowly

142
Q

describe influenza C

A
  • Narrower host range than influenza A

- Can cause serious disease but does not spread as easily

143
Q

what are the main influenza pandemics from history?

A
  • 1918: “Spanish ‘flu”
    •Infected 20% of the world’s population, originated from a bird-infecting strain
  • 1958: “Asian ‘flu”
  • 1968: “Hong Kong ‘flu”
  • 2009: fear that new H1N1 variant would cause the next pandemic
    •“swine ‘flu”
    •Turned out to be extremely infectious, but caused relatively mild disease
144
Q

what is the newest fear involving influenza?

A
  • H7N9 –causes very serious disease in a high proportion of infected people
  • However, as of yet, is not transmissible person-person (only bird-person)
  • Big fear –virus will mutate and become transmissible
  • A future strain may have the seriousness of H7N9 and the transmissibility of H1N1, and that would be very bad indeed
145
Q

describe the virion structure

A
  • No geometrical capsid
  • Instead a shell of matrix proteins (M1) that surround the 8 RNA chromosome fragments
  • Matrix is surrounded by a membrane envelope
  • Derived from the host cell during budding
  • Viral envelope proteins hemagglutinin(HA) and neuraminidase (NA) stud the surface of the virus
146
Q

how many negative sense RNA segments does the virion genome have?

A

8:

  • Each is coated with nucleocapsid proteins (NPs)
  • Each encodes 1 protein
  • 2 segments undergo splicing to encode 2 further proteins
147
Q

why does Each segment is packaged with an RNA-dependent RNA polymerase complex?

A
  • During viral assembly in an infected cell, segments are packaged precisely
    •They link to each other in order as they arrange themselves
    •Each segment lines up like a bundle of sticks
    •Tiny molecular extensions seem to connect these sticks
148
Q

how many virions can each host cell produce?

A

10,000

149
Q

what does the H part in influenza stand for?

A

hemagglutinin

150
Q

how many HA subtypes are there for influenza?

A

18

151
Q

what does the hemagglutinin form with an N-terminal fusion peptide?

A

a trimer complex

152
Q

describe what the H bit of influenza does

A

1) HA C-terminal domain recognizes and binds to host cell sialic acid receptor
2) Triggers uptake of virion by endocytosis
3) Endocytic vesicle acidifies and produces a conformational change that exposes the N-terminal fusion peptide
4) Fusion of host and viral membranes can now take place
5) Triggers release of the genome cargo into the host cytosol

153
Q

what is the natural reservoir for influenza A virus?

A

birds

154
Q

what determines if other animals are susceptible for influenza A virus?

A
  • the presence of a host cellular protease to cleave the hemagglutinin (HA) and initiate infection
  • nature of the cell-surface glycoproteins on host cells that bind the HA and allow endocytosis
155
Q

describe H7N9

A
  • The major contributor to this strain’s emergence is thought to be the mixing in close proximity of very large numbers of wild and domestic birds in food markets in China
  • does not easily spread from person to person, but it causes very high mortality in humans
  • approximately 1 out of 3 persons infected will die
156
Q

what is the pathway of the influenza virus once infected?

A

1) Viral segments travel to nucleus and enter nuclear pores
2) Attached viral RNA polymerase synthesizes (+) strand RNA (used as mRNA or as templates for generating progeny (-)RNA)
3) mRNA travels to cytoplasm for translation to viral proteins –these are processed by the ER/Golgi & sent to the host cell membrane

157
Q

what does the N bit of influenza do?

A
  • Envelope proteins and viral genome packages travel to cell membrane for packaging into new virions
  • Within the cell membrane, envelope proteins assemble around the genome and matrix proteins
  • Virion then buds out of the host cell
  • Neuraminidase cuts the virion loose from host glycoproteins to release it to the extracellular space
158
Q

how many neuraminidase ‘N’ variant are there?

A

11

159
Q

what is drifting regarding influenza?

A
  • The ability of influenza virus (A and B) to mutate and change slightly
  • Usually because of RNA replication errors in HA and NA genes
160
Q

what is shifting regarding influenza?

A
  • A big change in the structure of the ‘flu virus
  • Can be caused by jumping of the virus into a new species
  • Can be caused by reassortment of the genes from 2 different viruses mixing in a single host (usually a pig)
161
Q

what is a retrovirus?

A
  • a major class of RNA viruses
  • Reverse the normal order of synthesis to copy their RNA into a ds-DNA
  • Integrated into the host genome
162
Q

what group is HIV in?

A
  • lentivirus group of retroviruses
  • Cause infections that progress over many years (‘lenti’= slow)
  • Most famous is Acquired ImmunoDeficiency Syndrome (AIDS)
163
Q

who discovered HIV?

A

French virologist Luc Montagnier and American virologist Robert Gallo

164
Q

how long does it take to produce enough flu vaccine?

A

~6 months`

165
Q

what did HIV evolve from?

A

viruses infecting African monkeys

166
Q

when was the first case of AIDs in the USA reported?

A

1981

167
Q

how many people are newly infected with HIV every year?

A

1.7 million

168
Q

how many people globally were living with HIV by the end of 2018?

A

37.9 million

169
Q

why is there no cure for AIDs yet?

A
  • Retroviruses have a high mutation rate because of the high error rate of the reverse transcriptase enzyme
  • Even within a single patient, the virus evolves into many different ‘quasispecies
  • The replication of HIV is very complex
  • Large number of regulator proteins that allow the virus to hide effectively within host cells
170
Q

Structure and genome of HIV

A
  • envelope comes from host cell membrane
  • electron dense core
  • Unlike influenza, each RNA strand contains a complete ‘map’ of HIV genes
  • The 2 RNA genomes can have different mutations arising from distinct replication events, thus the HIV genome can be considered to be ‘diploid’
171
Q

what does gag code for?

A

capsid, matrix protein

172
Q

what does pol code for?

A

reverse transcriptase, integrase, protease

173
Q

what does env code for?

A

envelope protein

174
Q

what is the primary receptor for HIV?

A

CD4 surface protein on T-lymphocytes

175
Q

what is the HIV viral binding partner?

A
  • Envelope spike protein –gp120 –
  • (SU and TM regions)
  • SU binds, TM unfolds, extends fusion protein into host membrane
  • Host and viral membranes fuse
176
Q

what must retroviruses do in order to generate progeny virions?

A

integrate their genomes into the host cell genome

177
Q

describe the replicative cycle

A
  • RNA genome needs to serve as a template for DNA complement
  • Then RNA template needs to be replaced with DNA to give ds DNA for integration
  • Reverse transcriptase accomplishes all of this
178
Q

true or false:

HIV has an exceptionally large number of accessory proteins

A

true

179
Q

what do the large number of accessory proteins in HIV given?

A

the level of virus production and the duration of the quiescent phase

180
Q

when does AIDS develop?

A

when CD4+ T-cell counts are <300 per mm3

181
Q

what is the main symptom of AIDS?

A

susceptibility to infections that are unusual in the healthy population

182
Q

what might some potential anti-HIV drugs do?

A
  • Block attachment to host cell
  • Prevent fusion of viral and host membranes
  • Inhibit reverse transcriptase
  • Inhibit integrase
  • Inhibit HIV protease
183
Q

true or false:

HIV can survive outside the human body for long

A

false

184
Q

what is Shiga toxin?

A
  • Originally comes from a bacteriophage
  • One of the most potent bacterial toxins known
  • Acts to inhibit protein synthesis within target cells
  • A ribotoxin
  • Kidney cells are particularly sensitive to intoxication•2 subunits to this exotoxin: A and B (AB5)
185
Q

why does E.coliO157:H not cause disease in cattle?

A

receptor toxin is absent

186
Q

how does retrograding trafficking work?

A
  • Stxbinds to Gb3 receptors on host cells
  • Next is taken up by the host cell into an endosome
  • Next is trafficked to the Golgi
  • Then to the ER, where the active part of the toxin is separated from the binding part
  • The active subunit enters the cytosol and injures ribosomes, so that protein synthesis is halted
187
Q

describe V. cholerae

A
  • proteobacteria member, related to E.coli
  • Flagellated, highly motile bacterial cell (1 polar flagella), very short generation time
  • Lives in salt and fresh water, concentrates in shellfish and plankton
  • Over 150 identified serotypes based on O-antigen
188
Q

which 2 strands of V. cholerae are toxigenic?

A

O1 and O139

189
Q

how many world pandemics involving cholera have there been?

A

7

190
Q

what are the symptoms of cholera?

A
  • begin out of the blue with sudden onset of explosive, watery diarrhea
  • Painful abdominal cramping soon starts
  • Diarrhea continues
    ~ 20 litres of fluid may be lost per day
    •Rice-water stools
    •Te e m i n g w i t h b a c t e r I a
  • Without fluid/electrolyte replacement, death soon occurs
  • With treatment, disease is self-limiting
191
Q

what is cholera toxin?

A
  • A-B type toxin, AB5similar to Stx
    •1 A subunit (active)
    •5 B subunits (binding)
  • ADP-ribosylating toxin
  • Subunits are assembled in the periplasm and secreted via pseudopilins into the extracellular space
  • Mechanism analagous to a piston
  • Whole CTX (5xB subunits plus 1xA subunit) is secrete
192
Q

describe e. coli

A
  • Gram negative, facultative anaerobe

- Most strains are motile using flagella

193
Q

what phylum are e. Colin?

A

Proteobacteria

194
Q

what family are E. coli in?

A

Enterobacteriacea

195
Q

how many antigenic types of E. coli are there?

A

over 700

196
Q

what is EHEC?

A
  • Primarily a disease of the developed world
  • not a common infection, but very serious and sometimes fatal
  • Extremely low infectious dose
  • Zoonotic, mainly carried asymptomatically in ruminants (esp. cattle)
  • Can contaminate water supplies and vegetable crops
  • Virulence determinants: pedestal formation, and production of Shiga toxin
197
Q

what is a type 3 secretion systems?

A
  • Molecular syringe
  • Related to flagellar apparatus
  • For secretion of protein effectors directly into the host cell (as well as into the extracellular milieu
  • Used by several important pathogens including Salmonella enterica, Shigella, Yersinia
198
Q

what is secretion?

A

a highly organized complex of many proteins

199
Q

what is the T3SS or EHEC used for?

A

inject a very peculiar ‘effector’ into host cells (Translocated Intimin Receptor)

200
Q

what are effectors?

A

the mediators for communication between host and bacterium

201
Q

what is the e Gs alpha subunit (Gαs) protein involved in?

A

in hydrolyzing GTP to GDP + Pi

202
Q

what does the A1 subunit fragment catalyze?

A

ADP-ribosylation of the Gs alpha subunit (Gαs)

203
Q

what does longer activation than normal of (Gαs) lead to?

A
  • increased adenylate cyclase activity
    •Which leads to an increased intracellular concentration of cAMP
    •Which over-activates protein kinase A
    •Which phosphorylates the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel proteins
    •Which leads to ATP-driven efflux of chloride ions from the cell to the intestinal lumen
204
Q

what does accessory cholera toxin do?

A

fluid accumulation

205
Q

what does Zonnula occludens toxins do?

A

disturbed tight junction integrity

206
Q

what is the vaccine for cholera?

A
  • Dukoral is the best-known
  • Both killed, whole V. cholerae cells as well as recombinant CTX-B subunit
  • Given with a bicarbonate buffer
  • Stimulates both antibacterial and antitoxin antibodies
207
Q

how many subunits does the AB toxin have and what are they?

A

2 subunits –one for binding/internalization, one for toxic activity

208
Q

what famous AB toxins are there?

A
  • Bacillus anthracis toxins
  • Corynebacterium diphtheriae toxin
  • Some Clostridium perfringens toxins
  • Tetanus toxin
  • Botulinum toxin
209
Q

what used to be a major risk of death before vaccines and antibiotics?

A

tooth decay

210
Q

what is sterilization?

A

The process by which all living cells, spores and viruses are destroyed on an object

211
Q

what is disinfection

A

the killing or removal of disease-producing organisms from inanimate surfaces

212
Q

what is antisepsis?

A

Removing pathogens from the surface of living

213
Q

what is sanitation

A

Reduction of the microbial population to safe levels

214
Q

how is efficiency of an antimicrobial measured?

A

decimal reduction time (D-value)

- length of time it takes and agent of condition to kill 90% of the population

215
Q

what is the efficiency of an antimicrobial influenced by?

A

initial population size, concentration of antimicrobial agent, duration of exposure

216
Q

what are the physical agents that kill microbes?

A
  • high temperature and pressure
  • pasteurization
  • cold temperatures
  • filtration
  • irradiation
217
Q

what kind of heat is a more effective killing agent: dry or moist?

A

moist

218
Q

what does an autoclave do?

A

combines moist heat (steam) with high pressure to effectively kill even endospores

219
Q

who originally devised pasteurization?

A

Louis Pasteur

220
Q

what is pasteurization?

A

Involves heating a food to a specific temperature for a short time to kill Coxiellaburnetii

221
Q

true or false:

most pathogens grow poorly at temperatures <4-8C

A

true

222
Q

which food pathogen can grow in cold temperatures?

A

Listeria monocytogenes

223
Q

what do you do is your solution is sensitive to heat?

A

flitration

224
Q

what is irradiation?

A

Bombardment of food with high energy electromagnetic radiation

225
Q

what do commercial disinfectants do?

A

Cause damage to proteins, lipids and DNA

226
Q

tru or false:

copper ions are antimicrobial

A

true

227
Q

what binds to disinfectants, slowing penetration into the biofilm?

A

Extracellular matrix proteins and polysaccharides

228
Q

what is an antibiotic?

A

A compound that kills or inhibits the growth of microorganisms

229
Q

who helped with the discovery of antibiotics?

A
  • Duchesne, 1896
  • Fleming, 1928
  • Florey, Chain ~194
230
Q

true or false:

antibiotics are mainly natural products

A

true

231
Q

what are the main properties of antibiotics?

A
  • Selective toxicity

- Broad vs. Narrow spectrum

232
Q

what is bactericidal antibiotics?

A

Kills the target bacteria

233
Q

what is bacteriostatic antibiotics?

A

inhibits growth, immune system clears the infection

234
Q

what is minimum inhibitory concentration?

A

the lowest concentration of the antibiotic that will prevent the growth of the organism

235
Q

what are the classical targets of antibiotics?

A
  • Cell wall synthesis
  • Peptidoglycan
  • Cell membrane
  • Nucleic acid synthesis
  • DNA synthesis
  • RNA synthesis
  • Protein synthesis
  • Metabolism
236
Q

for the most part, what is penicillin more affective against: gram negative or gram positive?

A

gram positive

237
Q

what does gyrase do?

A

Gyrase functions to relieve the strain on the DNA as it is being unwound by helicase during replication

238
Q

what is resistance?

A

The ability of microorganisms to resist the effects of antimicrobial agents (one or more) that they were originally sensitive to

239
Q

why does resistance happen?

A

Antibiotics have been overused and misuse

240
Q

what is intrinsic resistance?

A

resistance of a bacterium to an antibiotic that is conferred by the normal physical attributes of the cell

241
Q

how can resistance occur?

A

DNA mutations
•Acquiring new genes through horizontal gene transfer
•Conjugation, transformation and transduction

242
Q

what are the 4 mechanisms of antibiotic resistance?

A
  1. alter the target
  2. destroy the antibiotic
  3. modify the antibiotic
  4. pump antibiotics out of the cell
243
Q

how does altering the target work?

A

modifying the target so it no longer binds to or is recognized by the antibiotic

244
Q

what is biocontrol?

A

A method of introducing an agent organism into a new ecosystem to naturally prey on and suppress target “pest” organisms

245
Q

what is an agent?

A

The newly introduced species -Predator

246
Q

what is a target?

A

The defined “pest,” whose population is suppressed by the agent -Prey

247
Q

true or false:

biocontrol eradicates a target species

A

false:

decreases, does not eradicate

248
Q

what is myxoma virus and how does it work?

A
  • Enveloped virions
    •Brick-shaped with a bio-concave core
    •Non-segmented, linear ds DNA genome
    •During lifecycle produces proteins that interfere with host immune system
249
Q

what is myxomatosis?

A
  • Lumps (myxomata) and puffiness appear around the head and genital area
  • Progresses to acute conjunctivitis
  • Loss of appetite, fever, listlessness
  • Death within 14 days, usually less than 48hr
250
Q

true or false:

The more specific the agent, the more controlled the intervention and fewer unintended consequences arise

A

true

251
Q

what are the 3 kinds of biological control?

A
  • Classical biological control
  • Conservation biological control
  • Augmentation biological control
252
Q

what is classical biological control?

A
  • Control of pests introduced from another region through importing specialized enemies of the pest from their native range
  • Aim: to establish a sustained population of the new enemies
253
Q

what is conservation biological control?

A
  • Manipulation of the environment to favor natural enemies of the pest
254
Q

what is argumentation biological control?

A
  • number of biological control agents is supplemented

- Commonly used when biocontrol agent cannot adapt and survive long-term in the new environment

255
Q

what is inoculation?

A

introduction of a small number of individuals of the biological control agent

256
Q

what is inundation?

A

introduction of vast numbers of individuals

257
Q

true or false:

Most pollutants can be broken down or detoxified by microbes under ideal conditions

A

true

258
Q

how do you get gut dysbiosis?

A

reduced microbiota diversity + poor lifestyle choices + poor diet

259
Q

what are probiotics?

A

live organisms that, when administered in adequate amounts, confer health benefits on the host

260
Q

what are prebiotics?

A
  • ‘Food’ for your gut microbes

•Typically non-digestible fibre compounds

261
Q

true or false:

fermented foods are full of probiotics

A

false

262
Q

what are the 3 main reasons fermentation is carried out?

A
  • Preservation
  • improvement of digestibility
  • Addition of nutrients and flavours

MICR 2420 (2 decks)

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