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Summer exams > AID > Flashcards

AID Flashcards

1
Q

Microbiology

A

=study of organisms too small to see with naked eye

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2
Q

archaea

A

Archaea is a domain of single-celled organisms. These microorganisms lack cell nuclei and are therefore prokaryotes.

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3
Q

protozoa

A

one-celled animals found worldwide in most habitat

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4
Q

whittlers five kingdom tree is wrong because it is

A

outdated

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5
Q

the three domains

A

monera = archaea and bacteria
-crown taxa = very little diversity
-protista is eukaryotes and microbial world s much more diverse

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6
Q

what are microbes

A

-small bacteria 1-6 micrometers in size
-largest bacteria visible to eye

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7
Q

eukaryote microbes

A

-fungi

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8
Q

significance of microbes to global biomass

A

-estimate of total microbial cells on earth is 4-6 x 10^30
-microbial carbon equals that of all plants
-microbial N and P is >10X that of plant biomass

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9
Q

bacteria and archaea

A

-major portion of biomass on earth
-microbial carbon equals that of all plants

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10
Q

why are there so many bacteria

A

-rapid growth rate = many changes at speciation
-lateral gene transfer

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11
Q

phototroph

A

energy from light

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12
Q

chemotroph

A

energy from chemical bonds

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13
Q

ganotroph

A

organic compounds as e donors

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14
Q

lithograph

A

inorganic compounds as e donors

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15
Q

autotrophs

A

CO2 as carbon source for example plants

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16
Q

heterotrophs

A

organic carbon as carbon source HUMANS

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17
Q

photolithoautotroph

A

light energy, water as e donor, fix carbon dioxide

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18
Q

more complex media

A

some microbes have to be grown inside eukaryotic cells or in an animal

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19
Q

growth of bacteria

A

-by binary fission or budding
-cells double in size then split into two
-exponential growth

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20
Q

why can bacteria not grow forvever

A

bacterial growth curve

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21
Q

measurement of growth

A

-cell number
-optical density
-fresh/dry weight
-protein
-DNA

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22
Q

ways to identify microorganisms

A

-microscopy and staining
-growth on selective media
-testing substrate spectrum supporting growth
-testing enzyme activities

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23
Q

selective media

A

= allows growth of only some types of organisms used to culture presumed pathpogens

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24
Q

differential media

A

= allows the identification of organisms based on growth and appearance on that medium often based on colour differences used to determine if potentially pathogenic

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25
Q

testing of enzyme activities

A

-ApiZym a common test system mainly optimised towards pathogens
-culture of organism resususpended in buffer
-test wells are inoculated
-resulting colour in test strip is compared against a database

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26
Q

Darwins’ warm little pond hypothesis

A

-life started in warm water body (primordial soup) with nutrients to live
-evidence that organic molecules can form spontaneously
-unlikely to be true due to hostile conditions on surface (high UV)

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27
Q

subsurface origin hypothesis

A

-earth has water 4.6 bill years ago
-planet surface was still volcanic so hydrothermal vents at ocean floor suggested around was more stable conditions
-

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28
Q

origins of cellular life

A

-from prebiotic chem to cellular life
-in hydrothermal vents
-lots of compounds necessary for life

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29
Q

origins of cellular life simple compounds became

A

more complex (long chain fatty acids to form lipids
-self replicating RNA by making nucleic acids

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30
Q

landmarks in biological evolution early life dependent on H2 and CO2

A

-bacteria making acetate = simple organic compound using organisms to make energy
-archaea can turn acetate back into methane and carbon (a carbon cycle)
-life is starting to settle as there are microbes growing and volcanic activity is decreasing

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31
Q

phylogenetic methods

A

-ribozyme = ribosome is the best known example of surviving ribozyme
-before molecular biology didn’t know archaea existed
-allows us to determine how related organisms are to each other
-contradicted whittlers tree of life

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32
Q

why are ribosomes useful to study

A

all orgnanisms have them (universal)

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33
Q

3 domains of life

A

-phylogenetic tree of life as defined by ribosomal RNA sequencing

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34
Q

evolution of eukaryotes

A

-the separation of archaea and eukaryotes is mitochondria = an archaea with bacteria stuck inside and created an organelle with other abilities

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35
Q

fossils suggest eukaryotes rose around

A

2.5 billion years ago

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36
Q

endosymbiont theory

A

-mitochondria incorporation of aerobic chemo-organotrophic bacteria into host cell
-chloriplasts : incorporation of phototrophic cyanobacteria into a eukaryotic cell

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37
Q

hydrogen hypothesis

A

-association of an archaea host using H2 as energy source with an aerobic bacterium that produced hydrogen as a waste product
-bacterial cell was producing hydrogen as waste and lots of archaea use hydrogen as energy source so they stuck together becoming endosymbiotic

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38
Q

cyanobacteria and plastids

A

-blue treen algae
-plastids were originally cyanobacteria

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39
Q

actinobacteria

A

= high GC content they vary in morphology and metabolisms and are heterotrophs

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40
Q

what is systematics

A

-study of the diversity of organisms and their relationships
-links phylogeny with taxonomy
-bacterial taxonomy traditionally focused on phenotypic comparisons
-recently molecular analyses allow taxonomy to reflect evolutionary relationship between organisms

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41
Q

no unified species concept

A

-higher organisms species - interbreed and produce viable offspring
-problematic in microbiology due to asexual reproduction, lateral gene transfer and phenotypic genotypic plasticity of microorganisms

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42
Q

polyphasic bacterial taxonomy

A

-phenotypic analysis = morphological, metabolic, physiological and chemical characteristics
-genotypic = comparative at the gene and genome level
-phylogenetic = framework of evolutionary relationships

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43
Q

issue with phenotypic analysis

A

-observable traits can be altered by one single muation

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44
Q

morphological is studied with

A

gram staining

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45
Q

gram staining procedure

A

-stain to help visualise
-spread culture in thin film over slide
-dry
-pass through flame to fix
-flood slide with stain and rinse dry
-place drop of oil on slide examine with 100 x objective
-add iodine for 3 minutes

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46
Q

phenotype- biochemical tests

A

-decomposition of simple carbs
-acid from glucose in anaerobic conditions

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47
Q

phenotype - biochemical tests

A

-enzymes that decompose large molecules are tested in agar plates
-DNA hydrolysis (DNase)

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48
Q

identifying bacteria cultural characteristics

A

-colony based characters

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49
Q

relationship to temperature

A

_____phile

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50
Q

psychrophiles

A

-low temperatures (<15°C)
-permentaly cold temps
-adapted to deal with low temps
-adapted with PROTEIN STRUCTURE and MEMBRANE FLUDITY

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51
Q

hyperthermophile

A

-very high temps (>80°C)
-believe last common ancestor was hermothermophic

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52
Q

genotyping analyses

A

-pre-sequencing approaches to bacterial identification
-DNA hybridisation genome wide comparison of sequence similarity useful for discrimination of strains of a species
-fatty acid profiling

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53
Q

sequencing trumps all

A

-ability to sequence DNA (late 1980s)
-PCR and Sanger sequencing

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54
Q

why study the cell surface

A

-where microbes and immune system interact

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55
Q

outer layers of bacterial cells outside to in

A

diagram on lecture 4 copy down

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56
Q

capsules

A

-polysaccharide component of outside cell wall
-usually loose network of polymer fibres extending outwards from the wall
-tight matrix

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57
Q

role of capsules

A

-not required for growth or repoduction
-carbon store
-protection against desiccation
-capture nutrients attachment to biofilms

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58
Q

s-layer

A

-paracrystalline outer wall layer composed of protein
-regularly structured external to cell wall
-may protect against ion and ph fluctuations

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59
Q

peptidoglycan or murein

A

-alternating residues of NAG and NAM
-arranged in dimers which are cross linked by amino acid side chains
-a mesh-like polymer that retain the gram stain in gram +ve cells

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60
Q

D-amino acids

A

-non-protein
-protect against degradation
-makes peptidoglycan resistant to proteases

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61
Q

PG synthesis cross links

A

-chains of linked peptidoglycan subunits joined by cross-links between the peptides
-often carboxyl group of terminal D-alanine connected to amino group of diamond pimelic acid (DAPA) causes strong bond
-Sacs are strong enough to retain shape when isolated yet are porous(small molecules can get through), elastic and stretchable

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62
Q

overall structure of gram +ve cell wall

A

-all of the outer layer of gram + bacteria thicker than -

and up to 90% of cell wall up to 25 sheets of peptidoglycan

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63
Q

peptidoglycan and the gram -ve cell wall

A

-little PG in gram negative bacteria typically 10% of total cell wall
-between inner and outer membrane

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64
Q

lysozyme

A

-antibacterial enzyme
-degrades the beta 1,4 glycosidic bond in PG backbone
-loss of PG makes cells sensitive to changes in osmotic pressure

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65
Q

penicillin inhibits PG synthesis

A

-linker peptide initially has two D- Ala
-halting cell wall synthesis

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66
Q

overall structure of gram + ve cell wall

A

-teocoic aci found only in these cells
-role is unclear may make membrane negatively charged

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67
Q

membrane basics

A

-hydrophillic phosphate heads face outwards
-channel proteins have hydrophobic proteins

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68
Q

sterols/hopanoids

A

-hopanoids in bacteria and sterols in eukaryotes
-rigid planar molecules while fatty acids are flexible
-stabalise membrane structure

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69
Q

OM linked to cell in two ways

A

-brauns lipoprotein = most abundant protein in OM covalently linked to peptidoglycan and embedded in OM by hydrophobic end
-adhesion sites = where two membranes adhere
allows transport of substances

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70
Q

how do archaea membranes show they are different domains to eukaryotes and prokaryotes

A

they are different

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71
Q

major lipids of the archaea

A

-single headed like phospholipids and make bi-layer and biphytanyl is double headed ether lipids make a mono layer to stabilise membrane at extreme temp/ph

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72
Q

lipopolysaccharide (LPS)

A

-large complex molecules containing lipid and carbohydrate
-lipid A
-core polysaccharide
-O side chain

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73
Q

structure of LPS of Gram - ve :component 1: lipid A

A

-two glucosamine residues linked to fatty acids and phosphate
-lipid A is integrated into the outer membrane

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74
Q

structure of LPS of Gram - ve : component 2 core polysaccharide

A

-also referred to as R antigen or R polysaccharide side chains of NAG
-highly structural can in itself induce immune response

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75
Q

structure of LPS of Gram - ve : o side chain

A

variable region responsible for antigenic make-up of bacteria
-different O serotypes linked to disease
-species specific attachment to specific receptors
-extends outwards from the cell
-lipid A and core polysaccharide are straight and O side chain is flexible and bent
-rough or smooth depends on side chain length

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76
Q

functions of LPS

A

-lipid A stablises outer membrane structure
-core polysaccharide charged
-charged hydrophilic external layer reduces permeability of hydrophobic substances
-protects against host defences

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77
Q

endotoxin

A

-many pathogens produce endotoxins
-released during cell division or by lysis of bacterial cells
-can act to prime immune system against pathogen

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78
Q

assaying for LPS limulus amaebocyte lysate - LAL test

A

-amaebocytes are the blood cells of limulus polymephus
-contains a clotting factor that is released if coming into contact with bacterial endotoxin
-natural immune mechanism that contains bacterial infection

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79
Q

important properties of endotoxins

A

-heat stable
-toxic in nanogram amounts
-interacts with immune system cells = trigger release of cytokines in cascade and
can REESULT IN
-inflammmation fever

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80
Q

OM as permeability barrier

A

-OM is more permeable than inner membrane
-due to presence of porins
-allow small molecules in

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81
Q

prin superfamily

A

-homotrimeric transmembrane proteins
-highly conserved structure
0form water filled channels in OM

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82
Q

porin selectivity

A

-most are non-specific that allow passage of small meolcules

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83
Q

porin qualties

A

-high thermal stability
-resistant to protease and detergent degradation
-essential for survival of gram - ve bacteria

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84
Q

porins have common beta strand structure

A

-unusal structure with 16 antiparalelle Beta barrel

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85
Q

cross section of porin monomer

A

-hourglass
-hydrophobic band that sits in membrane
-charges inside pore define size of solute hat can transverse channel

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86
Q

periplasmic space

A

-compounds diffuse through porins into periplasm
-gel like consistency due to abundant proteins
-removal of cell walls without lysing the cells allows study of the proteins and enzymes present in this space

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87
Q

enzyme activity in periplasm

A

-nutrient acquisition
-hydrolytic enzymes such as alkaline phosphatase
-energy conservation = ET protein

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88
Q

protein export into periplasm

A

-sec pathway = exports nascent polypeptide through cytoplasmic membrane using a translocase
-foliding of protein occurs after translocation
-proteins have an N-terminal signal peptide
TAT pathway
-exports fully folded enzymes across cytoplasmic membrane
-proteins have a twin arginine in N terminal region

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89
Q

transport across cytoplasmic membrane

A

-the three classes of membrane transporting systems
-particularyly happens to glucose

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90
Q

types of transport events

A

several well-characterised simple transporters of E.coli

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91
Q

what are flagella

A

-long thin extracellular helical structures made of protein subunits that aid in motility
-flagella are connected to a motor that spins them clock or anti clockwise allowing bacteria to swim
-motor is a nano-technoligical marvel

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92
Q

structure if the flagellum

A

-complex outer ring structures anchored into the membrane
-flagellum shaft is easily removed by vigorous shaking
-different antigenic properties of shaft tip of shaft and hook

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93
Q

the motor

A

driven due to transfer of protons through the ring structure

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94
Q

structure of the flagellum filament

A

-filament made of single protein
-base is different to the shaft and is known as the hook
-single protein connecting the shaft to the motor
-moves like a rotary motor

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95
Q

flagella synthesis

A

-MS and C rings in cytoplasmic membrane
-motor proteins
-P and L ring hook and cap
-flow of flagellin through hook , growth of filament

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96
Q

how does the motor work

A

-rotary motion provided by the basal structure
-powered by proton motive force
-mutational analysis suggests dependence on an Asp residue in MotB

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97
Q

flagella are different in gram +ves

A

-in gram +ve no L and P rings
-anchor in the membrane layer is more complex
-mot proteins surround inner ring and movement of these relative to each other provides the force

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98
Q

types of flagella

A

-monotrichous = single tail
amphitricious = tail on either side
lophotrikhous = multiple on either side (can spin)
peritrichous = multiple on both sides but face one direction

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99
Q

motilitlity alternates betwen

A

-run and tumble
-Run = motor routes anti-clockwise, flagella filaments form bundle and propel cell
-tumble = quick reversal of motor to clockwise rotation produces twisting force that transforms flagella into a right handed-helix

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100
Q

aerotaxis

A

usually movement towards oxygen

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101
Q

motaxis

A

movement towards nutrients or away from toxins

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102
Q

magnetotaxis

A

movement along lines of magnetism

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103
Q

phototaxis

A

movement towards light

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104
Q

chemicals that are attractants will

A

have high concentrations of cells/organisms

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105
Q

chemotaxis biased random walk
METHYL-ACCEPTING CHEMOTAXIS PROTEINS(MCP)

A

bacteria sense changes in nutrient concentration in environment
-they may have a set of transmembrane proteins METHYL-ACCEPTING CHEMOTAXIS PROTEINS(MCP) which interact with cytoplasmic proteins
-che proteins which interact with rings of motor regulating direction in which it turns

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106
Q

chemotaxis signal recognition

MCP also called

A

transducer

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107
Q

MCP interacts with sensor kinase CheA which can autophosphorylate it can be an attractant and repellent

A

-attractant decrease in CheA
-repellent increase in CheA

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108
Q

fimbriae are

A

bacterial adhesions

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109
Q

fimbriae/pili role in adhesion

A

-loose association
-adhesion role for pili fimbriae
-invasion into or through submucosal epithelial cells

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110
Q

type 1 fimbriae

A

-well characterised fibril system widespread in bacteria like e coli
-important virulence factor
-thin

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111
Q

Virulence

A

is described as an ability of an organism to infect the host and cause a disease

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112
Q

p-pili

A

also known as PAP: pyelonephritis- associated-pill
-its a UTI
-can be fatal
-similar structure to type I fimbriae

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113
Q

type IV pili

A

-widely distributed in gram negatives
-some in gram positives
-typically longer than fimbriae and only a few per cell
-thin flexible fibres
-involved in HOST CELL ADHESION and TWITCHING

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114
Q

species specificity of pathogens

A

-many pathogens are species specific
-specificity of e coli pathogens is determined by LPS and fijmbraie

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115
Q

CFA colonising factor antigen

A

fijmbraie are present on E coli pathogenic to humans

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116
Q

sex pilus

A

-the e coli f plus
-identified in 1960s
-required for gene transfer
-bacteria observed in light microscopy obviously tethered by an invisible thread

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117
Q

conjugation steps

A

-attachemnt of F+ donor and F- recipient
-retraction
-exchange
-transformation of both F+ cells

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118
Q

bacterial endospores

A

-dormant stage in bacterial life cycle
-called endospores because they form inside bacterial cell
-very different from fungal exospores
-survival stage = extremely resistant to heat, desiccation and radiation
-some viable for 100,000 years

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119
Q

spore stain malachite green

A

-white in gram stained cells
-internal spores pink
-ecternal are red and blue

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120
Q

sporulation

A

-complex series cellular differentiation events
-several stages each controlled by different genes
-more than 200 genes involved
-process takes around 8h to complete

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121
Q

structure and resistance of endopsores

A

-many new layers outermost layer is exosporium- thin layer of proteins
-not essential for survival but maybe for dispersal
-there is a metabolically inactive core with genome cytoplasm and ribosomes
-can be resistant up to 150 °C

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122
Q

germination of gram +

A

-uptake of water and amino acids triggers germination
-rapid in 30 minutes
-loss of refractive nature as re-hydrates at same rate as loss of resistance
-cell is released and begins to grow in normal way

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123
Q

areas of body not sterlie

A

urinary tract abd lungs

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124
Q

gut has lots of

A

bacteria but as yo go through there Is less due to PH

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125
Q

the human microbiome

A

-concept suggested by Joshua lederberg
-“microbiome = the ecological community of commensal, symbiotic and pathogenic microorganisms that literally share our body space

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126
Q

human microbiome

A

-production of vitamins by bacteria
-implicated in a range of conditions like colon cancer

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127
Q

virulence factors

A

determined by many factors that aid in adhesion and antiphagocytic activity and production of toxic s

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128
Q

genetic elements encoding virulence factors

A

-virulence may be plasmid or phage encoded
-in chromosome they may occur clustered in so- called pathogenicity islands
-some genetic elements are the result of horizontal gene transfer
-other genetic elements can aid in horizontal gene transfer from one strain to another

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129
Q

MRSA and VRSA

A

emerging pathogen as little antibiotic treatments left

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130
Q

vaccination history

A

evidence of variolation in china over 1,000 years ago
-Edward jenner 1796 invents vaccination with cowpox

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131
Q

haemophilus influenzae

A

-gram negative coccobacillus
-non-encapsulated strains carried asymptomatically in urinary tract
-major cause of bacterial meningitis

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132
Q

what is the immune system

A

network of different organs and cells to protect body from pathogens

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133
Q

gram +

A

n bacteriology, gram-positive bacteria are bacteria that give a positive result in the Gram stain test

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134
Q

tetanus and bacteria

A

-gram positive spore forming anaerobic bacterium
-spores extremely hardy restate to heat and most widely distributed in matured soils
-tetanospasmin is too small to induce an immune response

135
Q

sleeping sickness and our immune systems

A

-afircan trpanosomiasis caused by a protozoan carried by tsetse flies
-they acquire a dense layer of glycoproteins that continually change allowing the parasite to dodge an attack from the hosts immune system

136
Q

adaptive immune response memory

A

-re exposure to pathogens is common: the immune response must have a memory
-adaptive response
-7-10 days is the primary
-secondary takes 4-6 to peak

137
Q

blood brain barrier response

A

(BBB) separates circulating fluid and brain extracellular fluid
-tight junctions around brain and capillaries
-brain uses innate immune response only

138
Q

innate immune system - mucus layers

A

-skin and other epithelial surface lining respiratory tracts
-made from secreted MUCINS and other glycoproteins
-it is slippery

139
Q

mucus layers contain defencins

A

-small (12-50 amino acids in length)
-positively charged which have hydrophobic or amphipathic helical domains

140
Q

mucus layers and defensins

A

-defensins have wide-antimicrobial activity and can kill or inactivate

141
Q

how do defensins work

A

-their hydrophobic domains or ampiphatic helices may enter the core of the lipid membrane of the pathogen and destabilise it leading to cell lysis
-following membrane disruption the positive charges may interact with negatively charged nucleic acids in the pathogen

142
Q

pathogen associate molecular patterns(PAMPs)

A

-pathogens do occasionally breach the epithelial barriers
-how does the immune system recognise them as non-self
-innate recognises molecules that are common to pathogen and absent in host

143
Q

toll receptors

A

-a drosophila trans-membrane protein with a large extracellular domain with repeating motifs that are versatile for a variety of proteins
-binding sends a signal to nucleases leading to DEFENSINS

144
Q

neutrophils

A

-most common granulocyte
-they phagocytose and destroy microorganisms like bacteria
-recruited to infections by macrophages, peptide fragments and PAMPs

145
Q

eosinophils help to

A

-destroy parasites
-modulate allergic inflammatory responses

146
Q

granules

A

dense membrane bound lysosomal derivatives
-fuse with phagosome membrane and release their contents to digest pathogen walls

147
Q

neutrophils are the sucide squad because

A

they will even use their own DNA to accomplish their task

148
Q

some pathogens can survive the killing frenzy due to

A

addition of silica acid avoids complement attack

149
Q

inflammation aids the killing frenzy

A

-blood vessels dilate leading to local swelling and the accumulation of components

150
Q

interferons

A

-viruses invade cells and host cell ribosomes make viral proteins. Also host cell lipids are used to make new viruses

151
Q

innate immune system relies on

A

-recognition of CpG motifs in viral DNA by TLR9 which are usually on membrane
-recognition of viral dsRNA that is an intermediate in the life cycle of many viruses

152
Q

dsRNA induces interferon (IFN) production

A

-induce changes in the infected cell= autrocrine action
-changes induced in neighbouring = Paracrine

153
Q

adaptive immune system

A

destroy invading organisms and any toxins that they produce
-adaptive immune system can raise immune responses against pathogens that have never been encountered before by the host organism
-highly specific
-long lasting protection

154
Q

adaptive responses are performed by lymphocytes

A

lymphocytes develop in central locations marrow and thymus
-then migrate

155
Q

experiment 1950s lumphocytes

A

-used mice and rats to mount adaptive immune response
-antigen + radiation = no adaptive

156
Q

dendritic cells link innate and adaptive

A

-they display a wide range of tLRs
-DC are activated by binding of pathogen to any of these receptors

157
Q

T cells develop in

A

thymus from thymocytes

158
Q

3 classes of t cell

A

-cytotoxic
-helper
-lymphoid organ

159
Q

how do cytotoxic T cells work

A

-secrets performs which form a channel in the target cell wall then secrete proteases leading to apoptosis

160
Q

T cells and B cells have common progenitors

A

both derived from common lyphoid progenitor cells

161
Q

unlike T cells b cells recognise their antigens as soluble proteins STEPS

A

1)soluble antigens in blood or lymph
2)BCR recognises self antigen therefore no action taken
3)BCR recognises no antigen
4)BCR recognises non-self antigen activation mitosis and clonal expansion of specific b cells

162
Q

antibody basic structure

A

-tetrameric with four polypeptide chains - 2 identical heavy chains and two identical light chains
-held by COVALENT and DISULPHIDE bonds

163
Q

the structure of an antibody allows

A

-one antigenic determinant = one antibody tetramer (green) can bind two identical antigens
-two identical antigenic determinants = can cross link

164
Q

ability to cross link antigens

A

-coupled with a flexible hinge region that allows spatial geometric of antigen binding (easier for phagocytosis to occur)

165
Q

collective name for antibodies

A

immunoglobin

166
Q

antibody structure domain level

A

-ig domains the n terminal domains of both chains are called variable (v) domains
-and the remaining are constant (c) domains

167
Q

class switching

A

-pre b cells in the bone marrow express igM membrane bound
-during maturation they express igM and IgD membrane bound in lymphoid tissue
-mature b cells can switch from igM to other ig classes
-this requires the same Vh domain and different heavy chains

168
Q

clonal selection

A

individual clones are selected by antigen based on how well the antigen and the receptor fit together
-teh result is pathogen specific lymphocytes are selected from pools of b and t cells

169
Q

local expansion

A

-selected clones undergo mitosis, proliferate and differentiate into effector cells

170
Q

clonal deletion

A

those lymphocytes that react inappropriately with self antigens are destroyed

171
Q

affinity maturation

A

antibodies over time made by b cells improve in affinity and become more specific due to point mutations in the v domains long after the coding sequences have been assembled from the segmented genes

172
Q

generation of extra diversity and improved specificity

A

-affinity maturation occurs in the lymph nodes and some b cells proliferate in the LYPHOID FOLLICLES and form germinal centres
-they are confined to the gene segments that encode V domains
-referred to as SOMATIC HYPERMUTATION

173
Q

18th century Edward jenner

A

-milkmaid who had cowpox was now immune to small pox which was used to successfully vaccinate 8 year old James Phipps

174
Q

iwanowski 1892 aim

A

demonstrated extracts from infected tobacco plants could transmit disease to other tobacco plants

175
Q

iwanowski 1892 chamberlain filter

A

-developed porcelain filter to remove bacteria from drinking water
-pasteur found that rabies agent passed through it and thought it was small bacterium

176
Q

iwanowski 1892 identifying virus

A

-filtering extracts with ceramic filters fine enough to remove bacteria did not prevent transmission

177
Q

beijernick 1898

A

confirmed same findings and showed that filtrate contained a new form of infectious agents
-demonstrated that the agent multiplied only in cells (living)
-he called it contagium vivum fluid (soluble living germ)
-used the term filtrable agent to describe it

178
Q

virus

A

smallest infectious agents (20-300 nm)
-genetic element
-with protein coat(capsid)
-cannot replicate independently of living (host) cell

179
Q

virus properties

A

-contain DNA or RNA
-different replication strategy do not divide by binary fission
-obligate intracellular parasites
-small
-simple

180
Q

viral replication vs bacterial

A

-assembly of pre-formed components into many new viral particles
-viral components produced (eclipse phase)
-component assembles to final viral particle

181
Q

why study viruses TECHNOLOGY

A

CRISPR best example of gene editing process that is normally used by bacteria to edit the genomes of invading viruses destroying them so scientists can use it to study functions of genes and again in treatmemt

182
Q

bacteriophages

A

a virus which parasitizes a bacterium by infecting it and reproducing inside it. Bacteriophages are much used in genetic research.
- a polyhedral head, a short collar and a helical tail

183
Q

virion vs virus

A

Viruses are nucleoproteins. They are non-cellular structures with infectious genetic material. Virions are capsid-encapsulated viruses with DNA or RNA molecules. It has both nucleic acid as well as protein layers.

184
Q

information encoded in viral genome

A

-nucleic acid
-structual proteins = capsid proteins
-non structural = DNA/RNA polymerase
-pathogenisis

185
Q

what genes are NOT encoded in viral genome

A

-no genes encoding the complete protein synthesis (tRNA)
-no genes for cell wall production
-no centro/telomeres

186
Q

capsid

A

-protein shell that surrounds viral genome
-composed of a number of protein molecules

187
Q

capsomere

A

-subunit of capsid
-smallest morphological unit visible with an electron microscope

188
Q

symmetry in building viral particles

A

-most viral particles are either ROD or ROUND
-viral genomes are small and encode a limited number of proteins
-round viruses : identical protein subunits are arranged in icosahandral symmetry
-rod in helical symmetry

189
Q

viral particles are metastable

A

-protects viral genome (stable)
-facilitates delivery of viral genome into the host cell, must dissociate on infection

190
Q

how is metastability achieved STABLE

A

-stable structure
-achived by symmetrical arrangement of many identical viral protein subunits provide maximal contact
-each subunit has identical bonding contacts with its neighbours and this repeated interaction at the subunit interfaces natural provides symmetric arrangement

191
Q

how is metastability achieved UNSTABLE

A

-this contact is not covalent (not usually permentantly bounded together)
-can be dissociated or taken apart once the virus attacks to the host cell to release the genome

192
Q

self assembly into VLPs

A

-some capsid proteins self-assemble into virus like particles (VLPs)
-like the HPV vaccine

193
Q

subunit

A

single folded polypeptide chain

194
Q

structural subunit

A

-unit from which the capsid is built one or more subunit

195
Q

icosahedron

A

-20 faces each an equilateral triangle
-30 edges-each an interface between 2 faces
-12 vertices - each a point where 5 faces meet

196
Q

icosahedron permits the greatest number of

A

UNITS
to be packed in a regular stable figure
-easiest way to make stable structure from smallest number of proteins

197
Q

simple icosahedral capsids

A

-made of 60 identical protein subunits
-interactions of all molecules with their neighbours is identical

198
Q

helical symmetry

A

-rod shaped viruses
-length of virus determined by length of nucleic acid
-width of virus determined by size and packaging of protein subunits

199
Q

bacteriophages

A

-the tail is attached at one of the 12 vertices of the capsid
-the tail is a complex rod uses helical symmetry in many places and TAILS ARE CONTRACTILE

200
Q

presence of envelope confers instability of

A

virus

201
Q

classification of viruses based on diseases AND DISADVANTAGES

A

-examples based on hepatitis respiratory

-focuses on some viruses and ignores others
-a single virus may cause more than one disease
-viruses infect more than one host

202
Q

classification of viruses classification based on host

A

-some have restricted host range
-others infect a small number of hosts
-some based on nature of host cell

203
Q

classification of viruses based on morphology and nucleic acid

A

-type of DNA or RNA
-single or double stranded
-linear circular
-icosahedral helical or complex capsid

204
Q

virus classification doesn’t have three cases which are

A

-kingdoms phyla and classes

205
Q

ossification based on taxonomy viruses

A

-order
-family
-subfamily
-genus
-species member

206
Q

characteristics for ICTV

A

-host range
-morphological features
-nature/genome of nucleic acid
-additional features may allow subdivisions
-phylogentic trees can be determined with nucleotide sequencing

207
Q

Baltimore classification of viruses

A

-all viruses must make their own mRNA THEREFORE THIS CAN BE READ

208
Q

David Baltimore noble laureate genomes and strategies of replication most important featuresfor classification and proposed six different major categories

A

-if u know genome structure u can determine mRNA made from genome

209
Q

viroids

A

-novel agents of disease In plants
-contains a single circular ssRNA molecule as infectious materials
-no protein
-viroid genomes range in size from 220 to 400nt
-up to 70% of nucleotides in the genome RNA are base-paired
-appear as rod shaped or dumb bell shaped

210
Q

prions

A

-agents of a number of diseases characterised by slow progressive neurological degeneration that are fatal
-diseases are associated a spongy appearance of the brain
-replicate slowly within hosts (NOT VIRUSES)
-no nucleic acid

211
Q

Baltimore classification and different strategies viruses use to replicate are

A

related

212
Q

viral replication major steps

A

1)attachment
2)penetration
3)uncoating
4)biosynthesis
5)assembly
6)release

213
Q

recognition

A

viruses can recognise specific structures on the host cell called cellular receptors through their VAPs

214
Q

attachment

A

-binding or attachment of the virus to the target cells through and interaction between these VAPs and specific cellular receptors
-this interaction is very specific and it determines the host cell and the species range

215
Q

viral tropism

A

=the specificity of a virus to a specific host

216
Q

entry

A

entry of the virus into the cytoplasm
-possibly through fusion with plasma membrane

217
Q

enveloped viruses fusion via endosemos at

A

low pH

218
Q

entry through no enveloped

A

endocytosis

-the hole in the membrane is caused due to release of capsids with nucleic acids
-or through entering membrane

219
Q

uncoating

A

-removal of the capsid
-delivery of the NA into cytoplasm or nucleus = DNA must be delivered into teh nucleus except poxviruses RNA must be delivered into the cytoplasm expect HIV and influenza

220
Q

synthesis of viral proteins and NA

A

-proteins and NA synthesis mRNA is translated into proteins and NA is replicated

221
Q

assembly and release

A

-packaging of NA and proteins into the viral capsid

could assemble
-helical capsids
-icosahedral capsids
-complex capsids

222
Q

release

A

new visions exist the cells (not everyone infectious)

223
Q

viral RNA genomes

A

-replication of NA viruses is via RNA-dependent RNA polymerase (RdRp) replicase
-cells have no RNA-dependent RNA polymerase
-RNA virus genomes encode
-RdRp produce RNA genomes and mRNA from RNA templates

224
Q

cultivation of viruses

A

-in vivo (animal) or in vitro (cell culture)

225
Q

cultivation of viruses in eggs

A

-inoculate membrane/amniotic/yolk sac/allantoic

226
Q

Henrietta lacks (HL)

A

HeLa cell line
-cervical carcinoma
-first continued tissue culture cell line

227
Q

city pathic effects (CPEs) of viral infections

A

distinct observable cell abnormalities /changes in the cells due to viral infection

228
Q

hemadsorption

A

cells infected with certain viruses acquire the ability to bind to and absorb red blood cells

229
Q

cell culture disadvantages

A

-relatively slow
-low sensitivity
-successful culture depends on the viability of the virus
-cell cultures are very susceptible to contamination
-cell culture is not applicable to a number of viruses

230
Q

purpose of virus titration

A

-research for studying viruses and their effects
-therapeutic

231
Q

Quantification of Viruses

A

-Measuring the number of viral particles
-Measuring the number of infectious viral particles

232
Q

electron microscopy

A

-measuring number of viral particles
-time consuming
-expensive
-requires skilled personnel

233
Q

ELISA test and immunoflurescense

A

-measures number of viral particles/proteins
-Any Ag in the sample (serum) will bind to Ab
2o Ab binds Fc region, This has a conjugated chromogen which cleaves a substrate when added leading to a proportional colour change.

234
Q

PCR

A

-measures number of viral nucleic acids copies

235
Q

plaque assay

A

-cytopathic viruses can be quantified by the plaque assay
-virus is added to monolayer of cultured cells
-agar is added on top to prevent diffusion
-should be diluted due to large numbers!!!

236
Q

how do u calculate PFU

A

If we plated 250 µl of diluted virus per plate:

(75) = PFUs for 250 µl of the 10-6 virus dilution = 75PFU/250 µl
75 * 106 = PFUs for 250 µl of the stock virus (undiluted)= 7.5x107 PFU/250 µl

Therefore, the PFU / ml is: 75 * 106 x 4 = 3 x 108 PFU/ml
237
Q

haemagglutination (HA) assay

A

-some viruses (influenza) can bind to RBC (haemagglutinatin
-they cross link the erthrocytes
-Thus, we can use red blood cells to in this case detect the presence of influenza virus in such samples in an assay called direct hemagglutination assays(HA)

238
Q

portals of entry

A

-conjunctiva
-respiratory tract
-gastrointestinal tract
-skin
-genital tract
-congenital tract

239
Q

respiratory tract

A

-middle sized droplets are inhaled as small dry and large fall out

240
Q

gastrointestinal tract

A

-spread is favoured by poor sanitation and poor personal hygiene
-very high titres of viruses in faecal material

241
Q

the eye

A

-infection of the cornea can occur due herpesviruses , and herpes simplex virus (HSV) infection of the cornea is the most common infectious cause of corneal blindness in the United States.

242
Q

genital tract

A

Viruses that infect via genital tract have to overcome local barriers to infection, such as mucus and the low pH of the vagina.

243
Q

the skin

A

Trauma or inoculation:
Medical procedures
Sharing needles (IDUs)
HBC,
HBV

244
Q

vertical transmission

A

-in utero (pregnancy)
perinatal transmission (during birth)

245
Q

dissemination of viruses

A

can be localised or systemic (when the virus infects initial site of entry and replicate locally then spread to other site within the body)

246
Q

portals of exit

A

-localised infection (virus is shed from the primary site of infection )
-skin = only few viruses are shed from skin in an infectious form can be shed from the oral mucosa or from salivary glands

247
Q

pathogensis

A

the ability of the virus to cause disease

248
Q

virulence

A

-quantitave or relative measure of the pathogenesis of the infecting virus :
-virus A is more virulent than virus B
-virulent vs avirulent

249
Q

viral pathogenesis

A

Virulence can be quantitated:
Virus titre
Mean time to death
Mean time to appearance of disease
Measurement of fever, weight loss
Measurement of pathological lesions (poliovirus)
Reduction in CD4 T cell (HIV)
Case fatality ratio/ hospitalization rate…

250
Q

mechanism of viral injury and disease

A

-direct cytoxcity of the virus
-virus induced immunopathogensis
-virus induced immune suppression
-virus induced transformation

251
Q

direct virus killing (cytotoxic viruses)

A

-dmage to the host may be a consequence of virus replication
-poliovirus kills neurones paralysis of muscles innervated by those neurons
-ebola virus damages vascular endothelial cells causing hemorrhage

252
Q

virus induced immunopathogenesis

A

-tissue injury may reflect host defence mechanism that include apoptosis or immune responses that target virus-infected cells

253
Q

virus-induced immune suppression

A

-Some viruses can specifically target and infect cells of the immune system causing immunodeficiency. The most prominent of these is HIV infection, which is known to cause AIDS

254
Q

HIV

A

One family: Retroviruses
Two human pathogens:
Human Immune deficiency virus (HIV)
Human T-Lymphotropic Virus (HTLV)
HIV

255
Q

Pathogenesis and Clinical Course of HIV and AIDS SUMMARY

A

acute
chronic
AIDS

256
Q

Acute phase

A

-characterised by infection of activated CD4 T cells in mucosal lymphoid tissues and the death of many infected cells
-modest reduction in CD4 T cell counts but at the number of blood CD4 T cells often returns to normal as individuals may continue to make them

257
Q

Chronic phase

A

-virus spreads throughout body to infect helper T cells
-may last for years
-virus is contained in lymphoid tissues
-patients asymptomatic or minor infections

258
Q

AIDS phase

A

-lymph nodes and teh spleen are sites of continuous HIV replication
-cell destruction and the number of circulating CD4 T cells steadily declines
-Eventually, the continuous cycle of virus infection, T cell death, and new infection leads to loss of CD4+T cells:
AIDS stage =CD4+T cell< 200 cells/mm3

259
Q

cytopathic effects of viral infection

A

The production of viral proteins including gb41 , and gp120 in the plasma membrane and budding of viral particles Increase plasma membrane permeability:
Influx of lethal amounts of calcium, which induces apoptosis,
Osmotic lysis of the cell caused by the influx of water.

260
Q

viral virulence genes

A

Gene/genes products that affect viral replication
Gene encoding toxins
Genes encoding modulators of the immune response
Gene/gens products that enable the virus to spread in the host

261
Q

viral toxin proteins

A

the co-transporter is important for fluid balance and the inhibition of the transporter causes fluid to leak out of cell
it also stimulates intracellular Ca that also increases removal of the fluid from the call.

It turns out that administration of this protein to animal it will cause diarrhea in the absence of the virus

Why would the virus do this , well this is a good way of spreading the infection similar to vomiting.

262
Q

Vaccination concept two points

A

-infection often leads to life-long immunity
-virulence of different strains of a pathogen may vary

263
Q

vaccine defintion

A

A vaccine is a biological product that can be used to safely induce an immune response that confers protection against infection and/or disease on subsequent exposure to a pathogen.

264
Q

Live attenuated vaccine

A

Live /attenuated vaccines: contains the whole virus that has been weakened or attenuated to produce an immune response similar to that seen during natural infection.

265
Q

killed/inactivated vaccine

A

Killed/Inactivated viral vaccines: contain whole virus which has been killed or have been altered, so that they cannot replicate

266
Q

subunit vaccine

A

Subunit viral vaccines: Do not contain the whole virus at all, they contain one or more specific component/ unit/antigens usually from the surface of the virus.

267
Q

nucleic acids/genetic vaccines

A

Nucleic Acid-Based Vaccines: Do not provide the viral protein/ antigen. Instead they provide the genetic instructions/ genes that encode for that specific viral antigen to host cells. These genes are then expressed by the host cells to produce the viral antigen, which stimulates an immune response against it.

268
Q

antiviral

A

Vaccines can prevent viral diseases

They have limited or no therapeutic effect if someone already infected
( rabies?)
Antivirals can stop infection once it has started

269
Q

Why do we have limited number of antiviral drugs

A

many compounds that interfere with virus growth cause adverse effects in the host
-Some medically important viruses can’t be propagated, have no animal models, or are dangerous
-Many acute viral infections are short-lived
-An antiviral drug (compound) must be potent- completely inhibit viral replication

270
Q

Why Hydroxychloroquine failed?

A

Licensed drug ( for Malaria)
HCQ known to inhibit replication of multiple viruses by inhibiting endosomal acidification
Found to inhibits SARS-CoV-2 replication in cell culture
Given emergency approval by FDA (EUA in US)
But then failed
EUA was withdrawn

SIDE EFFECTS OF CARDIAC ARTHYMIASS DRUGS MECHANISM NOT UNDERSTOOD

271
Q

Anti-HIV Drugs:

A

Control viral replication prolonging survival,
Anti-HIV drugs inhibit viral replication at many different phases of the HIV replicative cycle.

272
Q

parasites micro and macro

A

-microparasites = small difficult to count and multiply in their host (viruses, bacteria protozoa)
-macroparasites = large can be counted and multiply external to host (worms, ticks and flees)

273
Q

transmission routes one to one

A

-direct = body surface to body surface (sex)
-indirect = deposited onto object or surface and survives long enough to transfer to another person who touches object
-droplet = contact but transmission is through air

274
Q

transmission routes non-contact

A

-airbourne = via airborne particles
-vehicle = single contaminated source spreads the infection to multiple hosts
-vector Bourne = transmission by insect or animal

275
Q

disability adjusted life year DALYs

A

the number of healthy years of life lost due to premature death and disability

years lived with disability + Years of life lost

276
Q

plague was a ______ born disease

A

vector (fleas)

277
Q

incidence

A

number of new cases

278
Q

macroparasites

A

-Chronic recurring infections (little/no immunity)
-High morbidity, low mortality
-Endemic in nature = regularly occurring within an area or communit
-Continual reinfection (limited post-recovery immunity)
-Age-related exposure, burden, pathology

279
Q

what is an epidemic

A

-an increase in incidence of disease in excess of that expected

280
Q

R_0

A

= the basic case reproductive number (not a rate)
-the average number of new cases arising from one infectious case introduced into a population of wholly susceptible individuals

281
Q

an epidemic occurs when the number of secondary cases is

A

> 1

282
Q

how to estimate R0 for a pathogen

A

R0 = p x c x d
p=probability that contact results in transmission
c = the frequency of host contacts between infectious and susceptible individuals
therefore p x c is the effective contact rate
d= average amount of time host is infectious

283
Q

effective R (Re) is the

A

restrained growth rate
R0 is defined for a “virgin” population with all individuals susceptible

“Effective” R (Re) is the true reproductive rate:
R0 x fraction of susceptible individuals (S)

284
Q

why does Re decrease in value

A

Effective R (Re) decreases in value as the fraction of susceptible (S) declines
Re = R0S

285
Q

why do epidemics end

A

-pool of susceptible individuals is depleted
-Re declines to < 1
-Re cannot return to >1 until new susceptible are generated

286
Q

how do epidemics continue

A

Susceptibles (S–increases)
-born
-migrate into a population
No immunity (SI model)

Pathogen mutates (e.g. antigenic drift) and can re-infect/or continually infect individuals
Immunity wanes

287
Q

recurrent epidemics in small populations

A

-slow regeneration (birth) of susceptible due to small population size
-successive epidemics follow reintroduced measles virus by visitors when Re > 1

288
Q

epidemic fade-out

A

-the elimination of the infectious agent due to chance
-in small populations rather than large
-generatio(birth) of threshold susceptible is slow
-numbers of infected is low

289
Q

incubation period =

A

the period between infection and clinical onset of the disease

290
Q

latent period

A

= the time from infection to infectiousness

291
Q

point epidemic

A

-single common exposure and incubation period
-does not spread by host-to-host transmission

292
Q

continuous common source epidemic

A

-prolonged exposure to source over time
-cases do not all occur within the span of a single incubation period
-curve decay may be sharp or gradual

293
Q

Snow’s grand experiment 1853-54

A

found that water company and cholera was linked once the pump handle was removed cholera cases went down showing cholera was water Bourne as well

294
Q

when is an epidemic not a epidemic

A

-successive epidemic waves await replenishment of susceptibles
-host-parasite relationships may eventually dampen down to a stable equlibrium (endemic) state

295
Q

endemic equlibrium

A

-stability is the incidence of infection (constant)
-persistence of the parasite in the host population
-each infection produces 1 secondary infection on average
effective R = 1

296
Q

Re > 1 means

A

epidemic and

Re = S x R0

297
Q

endemicity

A

-not overly common in the developed world
-in the less developed world more severe diseases are endemic

298
Q

why are endemic disease common in animal populations?

A

-wild no one is treating
-managed - it can be advantageous

299
Q

fraction of susceptible (S) in the population at equlibrium is

A

S = 1/R0

300
Q

Determinants of Persistence

A

depends on
-Critical community size (CCS)
-rate of contact (mixing) for transmission
-duration of infectious period
-survival of host

301
Q

Critical Community Size (CCS) =

A

The minimum host population size required for the pathogen to persist
-particular concern for microparasites as macro can survive outside host and aggregate

302
Q

Duration of infectious period

A

-increasing infectious period but maintaining R0
-likely low host mortality
-eliminates cycles improves persistence
-increases prevalence

303
Q

how migration effects epidemics

A

Population migration can trigger disease outbreaks (epidemics)

Reservoir hosts (not vulnerable species) can reintroduce parasites/disease to susceptible populations (vulnerable species)

The pathogen is endemic in the reservoir. They are a reservoir because while they have the infection, they are not diseased.

304
Q

reservoir host =

A

referring to population or species

305
Q

carrier =

A

referring to an individual

306
Q

Basic Reproduction Number R0 for macroparasites

A

-avergae number of female offspring that survive to maturity

307
Q

Measurements of macroparasite infections

A

-Infection intensity/mean burden per host is directly related to R0 (e.g. accumulation of environmental infective Ascaris larvae)
-prevalence = determined by the mean worm burden and degree of parasite aggregation

308
Q

What is the aim of the intervention?

A

Control = Maintains the parasite population to an acceptable level
Elimination = Zero incidence in a defined geographical area (local eradication).
Eradication = Zero incidence worldwide
Extinction = Infectious agent no longer exists in nature or in lab.

309
Q

preventing transmission

A

-mass vaccination
-tracing or isolation

310
Q

the logic interventions Re

A

Re = s x c x p x D
Re = S x R0

S = susceptible proportion
D = duration infection
c = contact rate
P = probability of transmission ( c x p = effective contact)

311
Q

how many should be vaccinated?
Pc is the minimum proportion of individuals you need to vaccinate

A

-R0 < 1
S = 1/R0
S = 1 - Pc
Pc = immune proportion
Therefore
Pc = 1 - 1/ R0

312
Q

why To achieve herd immunity, active is immunisation required.

A

-a pathogen that generates total herd immunity would go extinct which opposes evolution

313
Q

vaccination coverage depends on demography

A

-A/L is the proportion of lifetime before infection
-A/L is the proportion of the population not infected (or previously infected)

R0 = 1 + L/A
this is a simple way to estimate R0 from available disease data

314
Q

control without eradication

A

eliminated locally not eradicated

315
Q

infectiveness curtailment: surveillance tracing and isolation

A

-surveilance for infected
-trace contacts
-isolate/vaccinate contacts

Tracing focuses on potential secondary/ tertiary cases

316
Q

isolation by ring CULLING

A

culling the farms with the highest probability of becoming infected.

317
Q

Anthroponotic

A

human-arthropod-human

(malaria)

318
Q

zoonotic

A

animal-arthropod-human

(sandflies)

319
Q

vector control

A

vectorial capacity = the average number of potentially infective bites that will be delivered by all the vectors feeding upon a single host in 1 day” hence, has units “per day”

R0 = C x d
where d = the duration of host infectiousness (in days)

320
Q

examples of vector control

A

-human bait traps
-non-human bait traps
-urban breeding site source reduction

321
Q

why is climate change related to vector borne diseases

A

-Host environment is relatively robust for parasite
-Environmental parasite stages sensitive to climate
-Vector sensitive to climate thus affecting parasite/pathogen
e.g. seasonality in vector abundance, breeding sites
-Parasite development is often climate dependent

322
Q

The link between Climate and disease

A

can climate be used to predict vectorial capacity
(el nino and la nina)

323
Q

is El Niño responsible for periodic epidemic cycles

A

-El Nino of the Southern Oscillation (ENSO)
-El Niño surface pressure: high (warm) over W. Pacific (Peru and Ecuador); low over SE Pacific.
Inverse cold phase: La Niña
-Strong determinant of inter-annual variation in sea-level pressure across the Pacific Ocean

324
Q

el nino years

A

“El Niño years” cycle 2-7 years, persisting for 12-18 months

“El Niño years” Cause weather changes around the world.

325
Q

is El Niño ENSO forecasting universal

A

not for Brazil and ecudar no evidence why its not universal though

326
Q

summary of el nino and climate

A

-Climate plays an important part in vector-borne disease dynamics.

-As an extreme climate ‘event’, El Nino offers evidence of that.

-Climate is not fully a predictor of disease

327
Q

potential biological influences on BTV transmission

A

-temperature = warm/hot periods in autumn/summer increases transmission potential which INDUCES COMPENTANCE OF TRADITIONALLY NON-VECTORIAL EUROPEAN MIDGES

328
Q

Co-morbidity

A

occurs when a person has more than one disease or condition at the same time

329
Q

covid was linked to co-morbidity

A

Increased risk of death with co-morbidities is known/quantified
Of the 33,841 deaths that occurred in March and April 2020 involving COVID-19 in England and Wales, 30,577 (90.4%) had a co-morbidity (ONS).

330
Q

multiple studies of covid suggested the R0 value was

A

between 2 and 4

331
Q

what is waning immunity

A

-A reduction in the host’s immune response OR
A specificity of immune response that does not respond to a mutated/different strain

332
Q

What can/will a vaccine do?

A

Prevent disease – lowering morbidity and mortality in those vaccinated
Prevent infection transmission - protecting those vaccinated, AND indirectly protecting those not vaccinated due to reduced transmission
Prevention of disease means that infection can still circulate.

333
Q

problem with identifying microorganisms

A

limited morphological diversity most microbes looks similar down a microscope

Summer exams (6 decks)

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