Pathogens Flashcards

1
Q

What are the classifications of microbes

A

Eukaryotes (organelles)
Prokaryotes (no organelles)
Acellular organisms (non living)

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2
Q

Why are microbes important

A

They make up global ecosystems
They are saphrophytes
They are used in economic biotechnology
They can be nuisances
They can be pathogenic

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3
Q

Describe the bacterial genome

A

Located in the cytoplasm
Comprises the single circular chromosome and plasmid
Dictates metabolic and biosynthetic capacity

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4
Q

Bacteria with _____ genomes tend to have ____ fastidious growth requirements

A

Larger, less

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5
Q

What are the 3 types of mutations and what could they lead to

A

Point, insertions, deletions&raquo_space; gain or loss of function

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6
Q

What are the 3 methods of DNA exchange

A

Transformation - uptake of free DNA

Conjugation - transfer of DNA by direct cell to cell contact

Transduction - transfer by bacteriophage

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7
Q

Describe the plasma membrane

A

Semi permeable Lipid bilayer - maintains homeostasis
Site of ATP generation
Range of transport proteins

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8
Q

What are endospores

A

Complex intra-cellular structure formed during replication of certain bacteria when growth conditions are poor

Resistant to temp, desiccation, radiation, chemical agents, enzymes etc.

Visualised by -ve staining

Cause deep tissue infections

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9
Q

Describe the chemical component cell wall is made of

A

Made of peptidoglycan
Polymer of NAM and NAG
Protects against osmotic pressure
Crosslinks can be inhibited by beta-lactam antibiotics

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10
Q

Describe the structure of gram positive cell walls

A

Thick peptidoglycan layer - molecules diffuse through interbridge gaps

Embedded in teichoic acids - attachment

Simple systems to secrete proteins

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11
Q

Describe the structure of gram negative cell walls

A

Thin peptidoglycan layer

Outer, non energised membrane - porins = transfer of molecules across / lipopolysaccharides = attachment

Molecules diffuse through peptidoglycan

Tightly regulated mvmt across PM

Many varied complex systems to secrete proteins

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12
Q

What is the clinical relevance of gram staining

A

Reveals bacterial shape and arrangement

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13
Q

What is different abt the cell wall of mycobacterial species

A

It has outer lipid layer, mycolic acids, arabinogalactan, and peptidoglycan

Detected using acid fast staining

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14
Q

What is flagella

A

External structure of bacteria

Complex structure required for bacterial chemotaxis (mechanism for bacteria to move towards nutrients or away from toxins)

Number and arrangement varies

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15
Q

What are fimbriae/pili

A

External structure

Hair like protein chains

Virulence factor - involved in attachment (to other cells or surfaces)

Mechanism for DNA transfer (conjugation) - connects bacteria and then retracts which allows for transfer of antibiotic resistance genes

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16
Q

What is the capsule

A

External structure

Polysaccharide layer beyond the cell wall

Found in both gram +ve and gram -ve

Protection from desiccation and phagocytosis

Adhesion to cells/surfaces

Can be visualised through a negative capsule stain which stains in the inside but not the capsule creating a halo effect or through transmission electron microscopy which is where the negative capsule binds to positive gold particles

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17
Q

what are commensal bacteria

A

colonise all surfaces of host

several benefits > metabolic / protection against pathogens by competing for colonisation sites

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18
Q

how are some pathogens also commensal

A

they are commensal but become opportunistic (pathogenic) in response to immunological insult such as tissue damage > provide access to deeper tissues to access more nutrients

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19
Q

what are primary pathogens

A

provide no advantage to host

not part of normal microbiome

damage the host

egg E.coli > secrete toxin

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20
Q

what are pathogens

A

disease causing agents

damage can be indirect (ie disturbs metabolic balance or nutrient acquisition) or directly (ie toxins)

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21
Q

structural and non structural features contribute to…

A

mechanism of disease (pathogenesis) and capacity to cause disease (virulence)

these allow for competition to establish infection and damage the host and cause symptoms

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22
Q

outline the pathogenic cycle

A

transmission > colonisation > proliferation > evasion > repeat

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23
Q

what are some transmission routes

A

direct contact e.g bites or wounds

indirect contact via fomites (contact w contaminated objects) > important route for Nosocomial infections

airborne

faecal-oral

food borne

zoonotic

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24
Q

what is ID50

A

infectious dose - number of bacteria needed to infect 50% of individuals

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25
Q

what is inoculum size

A

amount of pathogens an individual is actually exposed to

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26
Q

what is the relevance of extracellular enzymes released by bacteria

A

role in pathogenesis

e.g beta haemopysin is a secreted phospholipase which ha a distinct phenotype on blood agar

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27
Q

what are exotoxins

A

proteins made and secreted during bacterial growth

toxic at low doses

categorised by site of activity

two groupings = cytolysins (cause lysis) and two-component toxins (disrupt cellular processes)

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28
Q

what are endotoxins

A

bacterial structural components that have toxic activity

released on death of bacteria (meaning sometimes taking antibiotics can actually make it worse)

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29
Q

what are some host factors that affect outcome of infection

A

age, immune status, prior exposure, diet

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30
Q

what are outcomes of infection

A

clearance

asymptomatic carriage

symptomatic carriage

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31
Q

what factors are related to disease patterns

A

timing (acute, chronic, latent)

location (local, systemic)

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32
Q

what is an example of a bacterial pathogenesis

A

L.monoctyogenes - gram postive, motile

> food borne zoonosis
incubation ~3 weeks
secretes several toxins

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33
Q

by which process do bacteria grow

A

binary fission

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34
Q

what are the four phases of bacterial growth

A

lag phase
exponential phase
stationary phase
death phase

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35
Q

what happens in the lag phase of growth

A

adapt to new conditions, enzymes and new metabolites accumulate

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36
Q

what happens in the exponential phase of growth

A

maximum constant growth rate

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37
Q

what happens in the stationary phase of growth

A

oxygen and nutrient demands cannot be met > death rate = growth rate

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38
Q

what happens in the death phase of growth

A

death rate > growth rate

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39
Q

what factors affect bacterial growth

A

nutrient availability, O2 availability, pH, temperature, osmolarity

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40
Q

what are the oxygen requirements of obligate aerobes

A

require o2

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41
Q

what are the oxygen requirements of strict anaerobes

A

cannot survive in o2

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42
Q

what are the oxygen requirements of facultative anaerobes

A

more efficient with o2 but can still metabolise via fermentation when absent

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43
Q

what are the oxygen requirements of aerotolerant anaerobes

A

unaffected by presence of o2

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44
Q

what are the oxygen requirements of microaerophiles

A

require a specific o2 concentration

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45
Q

what are chemotherapeutic agents

A

chemical agents used to treat disease
kill or inhibit growth of pathogenic microbes

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46
Q

what are the primary mechanisms/classes of actions

A

inhibitors of cell wall synthesis
protein synthesis inhibitors
metabolic antagonists
nucleic acid synthesis inhibtion

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47
Q

what does bacteriostatic mean

A

inhibits growth

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48
Q

what does bactericidal mean

A

kills the bacteria

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49
Q

describe inhibitors of cell wall synthesis

A

e.g penicillins

binds to proteins involved in peptidoglycan assembly

inhibition of last step in bacterial cell wall synthesis

prevents crosslinkage of peptidoglycan strands > lysis

acts on GROWING bacteria

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50
Q

describe protein synthesis inhibitors

A

e.g aminoglycosides

either bind specifically to prokaryotic ribosome and interfere w function or inhibits stage of protein synthesis

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51
Q

describe metabolic antagonists

A

e.g sulfanomides

interfere w enzymes involved in folic acid synthesis (unable to construct basic building blocks for nucleic acids)

selectively toxic for bacteria

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52
Q

describe nucleic acid synthesis inhibition

A

e.g quinolones

block DNA replication
block transcription

not as selectively toxic

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53
Q

where can antibiotic resistance genes be found

A

bacterial chromosomes
plasmids
transposons (mobile genetic elements)
interns (gene capture system)

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54
Q

through what mechanisms can antibiotic resistance genes be spread

A

through transformation, conjugation, transduction (rare)

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55
Q

how do antibiotic resistance genes spread

A

acquisition of resistance genes from mobile genetic elements such as plasmids, transposons etc

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56
Q

what are resistance plasmids

A

can carry multiple antibiotic resistance genes
usually transferred to other cells by conjugation or transformation
carry transposons that encode antibiotic resistance

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57
Q

what are composite transposons

A

contain genes for antibiotic resistance

within a cell - rapidly move b/w chromosome and plasmids

b/w cells - can move thru a bacterial popn

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58
Q

what are gene cassettes

A

sets of resistance genes
can be part of transposons, interns, or located on bacterial chromosome

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59
Q

what are integrons

A

gene capture system > capture an expression of genes and gene cassettes

mechanism for accumulating antibiotic resistance genes in bacteria

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60
Q

what can be done to prevent antibiotic resistance

A

give antibiotics in high concentrations

give two antibiotics at once

don’t give antibiotics unless necessary

possible future solutions - dev of new antibiotics and use of alternative therapies e.g bacteriophages

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61
Q

describe the diagnostic schema

A

symptomatic patient > signs and symptoms > presumptive clinical diagnosis > specimen collection > select tests > results and interpretation > definitive diagnosis > treatment options > if patient is now asymptomatic then successful, if not, then reevaluate signs and symptoms

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62
Q

what is an example of a genetic test in detection and identification of bacteria

A

real time PCR

> amplified targets fluorescently tagged > relative fluorescent units plotted in real time hence no need for gel electrophoresis

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63
Q

what is an example of a serologic test in the detection and identification of bacteria

A

rapid immunoassay (RIA)

> relies on monoclonal antibodies (mAbs)

  • capillary flow moves antigen > specific interaction b/w mAb and antigen > binding at test line results in colour change > control mAbs confirms RIA validity

indicative rather than definitive

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64
Q

why are multiple tests used in the process of detecting and identifying

A

to account for variability in sensitivity and specificity

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65
Q

what is an example of culturing in detection and identification of bacteria

A

agar plates
> selective = allows for growth of selected groups of bacteria
> differential = allows growth of a number of types of bacteria w defined characteristics

utilise agar medium elevate to specific bacteria

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66
Q

what is an example of a biochemical test in detection and identification of bacteria

A

catalyse assay
> h2o2 is a by-product of metabolism > breaks down to o2

if o2 gas generated then catalase positive

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67
Q

what are different types of microscopy in detection and identification of bacteria

A

gram stain
acid fast stain
spore stain

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68
Q

describe gram stain in detection and identification of bacteria

A

gram -ve = transparent after alcohol decolourising

gram +ve = purple

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69
Q

describe acid fast stain in detection and ID of bacteria

A

non acid fast = transparent after alcohol decolourising and then blue after counterstain

acid fast = pink

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70
Q

what is an example of an analytic method in detection and ID of bacteria

A

mass spectrometry = peaks release to specific molecules, pattern to specific bacteria

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71
Q

what are advantages of mass spec

A

rapid
high throughput
relatively high sensitivity and specificity

72
Q

what are disadvantages of mass spec

A

in some cases requires sample culture
requires access to database of sample spectra

73
Q

what are the focusses of lab stewardship

A

appropriate test selection
secure yet accessible data management
correct interpretation of test results
sustainable financial resourcing

74
Q

what are the goals of lab stewardship

A

appropriate utilisation of clinical lab services
improve quality of patient care
reduce costs to patients, hospitals and health systems

75
Q

what is a virus

A

infectious, obligate intracellular parasite comprising of genetic material, often surrounded by a protein coat or sometimes a membrane

they replicate, not grow or divide

they must make mRNA that can be translated into proteins

76
Q

describe the enveloped structure of a virus

A

they pickup part of the cell membrane as they move out, hence they have a host lipid bilayer

have genetic material surrounded by capsid

77
Q

describe the non enveloped structure of a virus

A

no cellular envelope ie no host lipid bilayer

spontaneous assembly of capsid structure

very stable

78
Q

do viruses carry enzymes?

A

yes, some do

they are present if they are required prior to mRNA production

79
Q

what is the function of viral enzymes

A

make new genomes or mRNA

80
Q

what is the best cell type for viral propagation in cell cultures

A

primary cell lines

81
Q

how do you know that a virus is replicating in a cell

A

causes a cytopathic effect (CPE) ie cell death

or there is syncytia formation (cell fusion)

82
Q

what can CPE be used for

A

tell us how many viral infections there are in a sample

83
Q

how do we study viruses if they do not cause CPE

A

use imminofluorescence microscopy to detect viral proteins

use genetically engineered genomes to detect viral proteins in real time

RT PCR to detect viral genetic material

84
Q

why are in vitro viral replication methods important

A

assists in development of new antiviral strategies

85
Q

why are animal models important in viral replication

A

gives better understanding of the pathogenesis of viruses

86
Q

what are the main steps of viral replication

A
  1. viral entry
  2. translation and genome replication
  3. assembly and release
87
Q

outline the first step of viral replication

A

viral entry

viruses randomly adhere to cell surfaces
if the cell surface has a specific receptor, then the virus can bind to it, allowing for the virus to enter the cell (active process as it is too large to diffuse across the PM) and transfer its genome to the inside of the cell

88
Q

outline the second step of viral replication

A

translation and genome replication

the genome is replicated in the nucleus (DNA viruses) or in the cytoplasm (RNA viruses)
the replicated genetic material (mRNA) can then undergo translation to produce viral proteins

89
Q

outline the third step of viral replication

A

assembly and release

the viral genetic material is then covered by a protein shell (non envelope happens spontaneous and envelope acquires a host lipid bilayer)
then the virus with the protein coat can be released from the host cell ready to infect another cell

90
Q

why do positive sense viruses not need to carry their own RNA polymerase enzyme

A

postive strands have the same polarity as mRNA, meaning that can actually function as mRNA and be translated into viral proteins directly

91
Q

why do negative sense viruses need to carry their own RNA polymerase enzyme

A

negative strands cannot functions as mRNA, meaning they first need to be converted into mRNA in order to be translated into viral proteins. to do this, the RNA needs to be converted into mRNA, but the host cell does not have an enzyme that is capable of converting RNA to RNA so the virus has to carry its own RNA dependent RNA polymerase

92
Q

outline the replication of positive strand RNA viruses

A
  1. positive strand translation results in poly protein and production of RdRp
  2. RdRp used to make complementary negative strand RNA using the positive strand
  3. more positive strands are made which is the ultimate goal
93
Q

outline the replication of negative strand RNA viruses

A
  1. negative strand uses RNA polymerase to convert to mRNA
  2. mRNA translated to produce viral proteins
  3. replicase proteins move back into the nucleus for more genome replication
  4. viral genetic material packaged into proteins > released
94
Q

example of positive strand RNA virus

A

hepatitis C

95
Q

example of negative strand RNA virus

A

influenza

96
Q

example of DNA virus

A

hepatitis B

97
Q

describe the coding capacity of DNA viruses

A

dependent on genome size

smaller genomes need more host proteins as they do not encode the entire replication system, hence they have a restricted coding capacity

larger genomes encode all the proteins required for DNA synthesis, so they can replicate more easily

98
Q

what is viral transmission

A

mvmt of a virus from one host to another

99
Q

what is direct transmission

A

direct body contact w tissues or fluids of an infected individual > physical transfer of viruses

100
Q

what is indirect transmission

A

without close contact

fomite transmission = contact w contaminated inanimate objects

vector mediated transmission = insects feeding on infected host > transmit to new host when feeding

101
Q

what is zoonotic viral transmission

A

transfer of virus from animals to humans either by direct body contact for indirect transmission

e.g monkeys = HIV; dogs = rabies

102
Q

what are two main ways viruses can enter our body

A

mucosal surfaces
skin

103
Q

how can a virus enter through mucosal surfaces and describe them

A

respiratory - small particles from breathing, coughing or sneezing > inhaled and deposited onto mucous membranes > replicate in resp tract (e.g influenza)

enteric - contaminated food or water due to faeces, urine or saliva > replicated in intestinal tract (e.g poliovirus)

sexual transmission - blood and body secretions by unprotected sexual contact (e.g Hep B, HIV)

104
Q

how can a virus enter through skin and describe them

A

blood borne infections - exposure to infected blood > replicates and released into bloodstream (e.g Hep B, HIV)

vector borne diseases - bloodsucking insects ingest virus from infected host > replicate > pass on to new host (e.g zikavirus)

cuts, scratches w contaminated fomite

105
Q

what are the four steps in pathogenesis of virus infection

A
  1. transmission
  2. viral replication
  3. spread within body
  4. host defence systems
106
Q

what are the effects of virus infection at a cellular level

A

cytopathic effect
multinucleate giant cell formation
malignant transformation
inclusion bodies
no change (dormant)

107
Q

describe spread within the body during pathogenesis of a virus

A

localised infections - stays in area of infection

systemic infection - infection of a specific area then entry into circulatory or nervous system

108
Q

what determines the effectiveness of immune response to virus

A

rate of virus replication and presentation of antigens

size of infecting virus dose

route of infection

age of host

ability of virus to evade immune response

109
Q

what are the two outcomes of a viral infection

A

transient virus infection
persisting viral infection

110
Q

describe transient viral infection

A

successful clearance of infected cells
memory response developed

111
Q

describe persistent virus infection

A

infected cells are not cleared
viral replication continues > ongoing disease and death

112
Q

what are the four classifications of viral infections

A

transient localised
transient systemic
chronic localised
chronic systemic

113
Q

what is an example of a transient localised viral infection

A

influenza

114
Q

what is an example of a transient systemic viral infection

A

measles

115
Q

what is an example of a chronic localised viral infection

A

Hep C

116
Q

what is an example of a chronic systemic viral infection

A

HIV

117
Q

what are the different types of viral infections

A

respiratory
GIT
liver
NS
skin

118
Q

what are some common symptoms of a viral infection

A

high fever
tiredness
headache
sore throat
coughing
runny nose
diarrhoea
nausea

119
Q

what are the 3 key cytokines involved in viral infection

A

type 1 interferon (IFN) - produced by virally infected cells and DC’s

IL1 - produced by infected cells and cells of innate immune system

TNF - produced by macrophages and NK cells

120
Q

describe the innate response to virus

A
  1. infection involves PAMPs (pathogen associated molecular patterns) and DAMPs (damage associated molecular patterns)
  2. detection of infection by pattern recognition receptors (PRRs)
  3. production of cytokines/chemokines
  4. killing of virally infected cells by NK cells
121
Q

what are the 3 things that triggers innate immune response to virus

A

presence of foreign genetic materials in host cell

release of viral genetic material into extracellular space

accessibility of viruses to phagocytes

122
Q

what are PAMPs

A

broadly shared molecules among pathogens

123
Q

what are DAMPs

A

components of hosts cell that are released during cell damage

124
Q

what do PRRs mediate

A

release of inflammatory cytokines
initiation of antigen specific adaptive immunity

125
Q

what are the two types of PRRs

A

cytosolic receptors
toll like receptors

126
Q

how do CRs distinguish pathogenic RNA and DNA in the cytoplasm

A
  1. mammalian mRNA has a methyl cap whereas viral RNA do not
  2. presence of dsRNA in cytoplasm
  3. presence of dsDNA in cytoplasm
127
Q

what are two ways CRs can detect a viral infection

A

RNA sensors
DNA sensors

128
Q

what are two ways TLRs can detect a viral infection

A

cell surface - recognition of extracellular pathogens

endoscopes - through phagocytosis - TLR3, 7, 8, 9

129
Q

how do TLRs distinguish between pathogenic genetic material and our own

A

bind to microbial nucleic acid that are different from mammalian nucleic acid

e.g TLR 3 recognises double stranded RNA which is rare in mammalian cells

130
Q

what does TLR3 detect

A

dsRNA

131
Q

what does TLR7 detect

A

ssRNA

132
Q

what does TLR9 detect

A

DNA

133
Q

what is the outcome of detection of virus infection by TLRs and CRs

A

expression of IFN - 1

134
Q

what are the functions of IFN 1

A

direct antiviral effect and immunoregulatory role

135
Q

what are the outcomes of IFN 1

A

cellular resistance to viral infection

inhibition of viral replication

impediment of viral dissemination

136
Q

what are the factors that promote the emergence and spread of viruses

A

virus factors
virus transmission
host factors

137
Q

what things do we need to think about when considering virus factors in the emergence and spread

A

which virus > structure, subtypes

hosts

cellular receptors and target tissues

mutations > antigenic drift/shift

138
Q

what is primary transmission

A

animals to humans

either through direct or indirect contact

common for emerging viruses

139
Q

what is secondary transmission

A

human to human

140
Q

what things to we need to think about when considering host factors in viral emergence and spread

A

environment related factors > season and climate conditions/presence of animals/ecological changes/environmental changes

human related factors > living standards/living conditions/life style/demographicchanges in human behaviour

141
Q

what are the 3 elements to controlling a virus infection

A

ID the disease causing agent
understand the epidemiology
develop control strategies

142
Q

what are the 3 steps involved in developing control strategies

A

interfere virus transmission > public education, prevention measures, surveillance system, vector control

establish protective immunity > vaccination

establish effective treatment > antivirals, antibodies

143
Q

what is the importance of vaccination

A

induce protective immunity to protect the individual (prime immune response > rapid secondary response) and protect the community (herd immunity)

144
Q

what things make a vaccine ideal

A

protective
long term
safety
stable
easily administered
single or few doses
cheap

145
Q

what is involved in a neutralising antibody response

A

form noninfectious aggregates that cannot enter cells

blocking virion attachment to cells

blocking endocytosis

blocking uncoating

146
Q

what factors determine which samples are taken

A

clinical presentation
risk factors
test type

147
Q

what factors determine what tests we do

A

testing for current vs previous infections

148
Q

what samples would you collect for enteric virus infections

A

faeces/vomit
blood sample

149
Q

what samples would you collect for respiratory virus infections

A

respiratory sample (nasal swab)
blood sample

150
Q

what samples would you collect for blood borne virus infections

A

blood sample/heparinised blood sample
liver biopsy

151
Q

what samples would you collect for sexually transmitted virus infections

A

vesicle fluid
blood sample

152
Q

how should specimens be transported to ensure the virus is not inactivated

A

cold but not frozen ie around 4 degrees Celsius

153
Q

what are the diagnostic methods for virus infection

A

grow in vitro in cell lines and ID

look directly for virus using electron microscopy

detection of viral antigens

detect genome by PCR/RT PCR

detect antibodies in serum of infected patients

154
Q

what are the basic characteristics of fungus

A

eukaryotes
heterotrophs
cell wall composed of chitin
unicellular (yeast) or multicellular (hyphae)
non motile
decomposers, parasites, symbiotes
typically asexual reproduction
haploid or dikaryotic

155
Q

what is a hyphae

A

multicellular fungi

156
Q

what is a mass of hyphae called

A

mycelium ie mould

157
Q

how do mycelium/moulds reproduce

A

produce spores

158
Q

what are unicellular fungi called

A

yeasts

159
Q

how do yeasts reproduce

A

budding

160
Q

what are the two classifications of hyphae

A

septate and aseptate

161
Q

septate vs aseptate

A

septate = many separate cells whereas aseptate = undivided mass of cytoplasm

162
Q

superficial infections

A

infection of dead skin and hair > no living tissue invaded > no immune response

163
Q

cutaneous infections

A

infection of skin, nails, mucosa > minimal invasion of living tissue > immune response

164
Q

subcutaneous infections

A

infection of skin, muscle, fascia, lymphatic system > immune response

often due to traumatic injury

often caused by zygomycete fungi

165
Q

systemic mycoses

A

invasive disseminated infections > multi organ

often acquired by inhalation or hospital environment

high mortality rates

166
Q

what defences exist against fungal infection

A

physiological barriers e.g human body temp

non specific host defences e.g mechanical barriers and skin surface secretions

nonspecific immune response

acquired immune response

167
Q

opportunistic vs primary pathogens

A

opportunistic lack virulence so they take advantage of impaired immune system
whereas
primary are highly virulent so they can establish an infection even with an intact immune system

168
Q

what is a parasite

A

organism that resides on or within another living organism to find the environment and nutrients it requires for growth and reproduction

169
Q

benefits of being an intracellular parasite

A

host supplies the food
constant environment
free transport?
new niche?
free from predation?

170
Q

disadvantages of being an intracellular parasite

A

may require remodelling of the environment
host immune response
infection can kill the host

171
Q

what are the two types of intracellular parasites

A

facultative (can reproduce outside of the host cell)

obligate (cannot reproduce outside of the host cell)

172
Q

what is the main source of emerging viruses

A

zoonosis

173
Q

what factors lead to emerging viral diseases

A

human demographics and behaviour

climate and weather

international travel and commerce

174
Q

SARS-Cov-1

A

2002

illness begins w prodrome of fever

only infectious if symptomatic

175
Q

MERS-Cov

A

2012

spread from camels

not very transmissible between humans

still exists today

176
Q

SARS-Cov-2

A

2019

easily transmissible between humans

infectious even if asymptomatic