Week 11 Science and Scholarship: Pathogens Flashcards

1
Q

identify the different types of microorganisms

A

eukaryotes, prokaryotes and acellular organisms

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2
Q

examples of eukaryotes

A

protists and fungi

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3
Q

examples of prokaryotes

A

bacteria, mycobacteria, and mycoplasma

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4
Q

examples of acellular organisms

A

bacteriophages (non living and divide with bacteria) ; viruses

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5
Q

name the taxonomic ranks in descending order

A

domain, kingdom, phylom, class, order, family,genus, species

“Dear King Philip Came Over For Good Soup”

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6
Q

name the functions of bacteria on earth

A

Global ecosystems, saprophytes , economic biotechnology

nuisance and pathogens

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7
Q

how does bacteria contribute to global ecosystems

A

carbon, nitrogen, phosphorous and sulphur cycling

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8
Q

how are bacteria saprophytes

A

turnover over of organic material eg compost, recycling

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9
Q

how do bacteria contribute to economic biotechnology

A

production of ethanol, amino acids, food supplements and antibiotics

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10
Q

how are bacteria nuisances

A

spoilage of foods , biofilms

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11
Q

how are bacteria pathogens

A

contribute to infectious disease of plants and animals; bioterrorism

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12
Q

describe the chromosome in bacteria

A

single circular chromosomes in the cytoplasm

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13
Q

describe the plasmid in bacteria

A

circular, double stranded DNA
-range from 2-200kb
-can be 1-30 per cell

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14
Q

bacteria with larger genomes need ____ nutrients from environment

A

less

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15
Q

list the genetic variation methods in bacteria

A

point mutation
tranformation
conjugation
transduction

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16
Q

how do point mutations offer genetic variation in bacteria

A

insertion, deletion or substitution of DNA nucleotide bases offer variation

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17
Q

how does transformation offer genetic variation in bacteria

A

uptake of ‘free’ DNA, allowing acquisition of new genes and traits

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18
Q

how does conjugation offer genetic variation in bacteria

A

transfer of DNA by direct cell-cell contact using specialised pills, movement of genes between host and recipient

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19
Q

how does transduction offer genetic variation in bacteria

A

transfer of DNA by bacteriophage eg bacterial viruses allows for new genes and traits

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20
Q

name the functions of the bacterial plasma cell membrane

A

maintaining homeostasis
ATP generation
transportation

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21
Q

how does the plasma cell membrane of bacteria allow maintenance of homeostasis

A

maintains the gradients of NA + and K+

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22
Q

how does plasma cell membrane of bacteria allow for ATP generation

A

site of electron transport chain (aerobic respiration)

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23
Q

how plasma cell membrane of bacteria allow for transportation

A

imports nutrients, exports wastes, toxins and antibiotics

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24
Q

describe the structure of endospores

A

-complex, intracellular structures
-can be terminal, sub terminal or central
-stimulated by desiccation, radiation, chemical agents, enzymes etc

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25
Q

describe formation of endospores

A

-DNA is replicated
-cellular divison of cytoplasmic membrane
-prespore formation begins
-cortex formation
-spore coat formation begins
-maturation begins exosporium formation
-mother cell releases mature spore

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26
Q

name what bacterial cell walls are made of

A

peptidoglycan

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27
Q

cell walls can be either ___ or ___

A

gram positive or gram negative

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28
Q

name the shapes of bacterial cell walls

A

rods (bacilli) or spirals or spheres

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29
Q

describe rod (bacilli) bacterial cell wall

A

bacteria with rod like shape eg E.coli

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30
Q

describe spiral bacterial cell wall

A

bacteria with helical or spiral shape eg T.pallidium

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31
Q

describe sphere bacterial cell wall

A

bacteria with spherical or round shape eg S.pneumonia

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32
Q

what are gram positive bacterial cell walls

A

-bacteria that retain the crystal violet stain the gram staining method
-characterised by a thick peptidoglycan layer in cell wall

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33
Q

what are gram negative bacterial cell walls

A

-bacteria that do not retain the crystal violet stain in gram staining method
-characterised by thinner peptidoglycan layer in cell wall

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34
Q

purpose of gram staining

A

reveals bacteria shape and arrangement; some antibiotics are more effective against +gram bacteria

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35
Q

describe mycobacterial cell walls

A

-waxy hydrophobic cell wall: outer lipid layer, mycolic acids, arabinogalactan, peptidoglycan

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36
Q

name the structures external to bacterial cell walls

A

flagella
pili/fimbriae
capsule

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37
Q

structure of flagella

A

long whip like appendages on surface of bacteria

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38
Q

function of flagella

A

enable bacteria to move and navigate their environment

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39
Q

structure of fimbriae/ pili

A

short, hair like structures on surface of bacteria

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40
Q

function of fimbriae / pili

A

aid attachment to surface eg to host cells or other bacteria

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41
Q

structure of capsule

A

-protective layer of polysaccharides or proteins that surrounds cell wall of some bacteria

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42
Q

function of capsule

A

provides protection against the host’s immune system, enhancing ability to cause infection

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43
Q

Explain the differences between ‘commensals’ and ‘pathogens’

A

-commensals colonise all surfaces of host (mucosa of gut and lungs, skin) and provide metabolic benefits / protection eg folate production
-pathogens do not provide any advantage to the host, not part of normal microbiome, damages the host (direct or indirect) if evade immune repose

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44
Q

how can bacteria directly and indirectly damage host

A

indirect=bacteria could disturb metabolic balance, nutrient acquisition
direct=could secrete harmful toxins

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45
Q

Outline why commensal organisms are important

A

-help establish mutually beneficial relationships with their hosts
-help aid establishment of diverse ecosystems to provide essential services
-help maintain host health by preventing colonisation of harmful pathogens
-help provide evolutionary benefit to host, aiding adaption

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46
Q

Name the steps in pathogenic cycle

A

transmission
colonisation
proliferation
evasion

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47
Q

Describe transmission phase in pathogenic cycle

A

transmission from host or reservoir

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48
Q

describe colonisation phase in pathogenic cycle

A

colonisation motility, adhérence and invasion

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49
Q

describe proliferation phase in pathogenic cycle

A

proliferation within host, host provides nutrients for growth, may lead to host damage

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50
Q

describe evasion phase in pathogenic cycle

A

evasion of host immune response, circumvent hosts defence mechanisms

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51
Q

briefly what is meant by pathogenic cycle

A

action of pathogen once it enters body

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52
Q

name the routes of transmission

A

direct contact
indirect contact
aerosol
faecal-oral
self-inoculation
zoonotic

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53
Q

examples direct contact transmission

A

bites, open wounds, sexual contact

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54
Q

examples indirect contact transmission

A

via fomites; contact with contaminated objects

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55
Q

examples of aerosol transmission

A

respiratory aerosol transmission eg influenza

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56
Q

examples of faecal-oral transmission

A

faecal transmission eg E.coli,Hep A

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57
Q

examples of self-inoculation transmission

A

food poisoning

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58
Q

examples of zoonotic transmission

A

spread between animals and people eg bubonic plague

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59
Q

Describe the mechanism of virulence

A

the degree or intensity of pathogenicity, referring to the ability of a microorganism eg virus, bacterium or parasite to cause disease and the severity of the resulting illness

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60
Q

Describe the mechanism of pathogenesis

A

the process by which a disease develops and processes within a host organism, the interaction between the pathogen and the host’s immune response and physiological mechanisms

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61
Q

whats ID50

A

-infectious dose 50
-number of bacteria needed to infect 50% of individuals
-high ID50 indicates harmful impact at lower doses

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62
Q

what are the two categories of bacterial toxins

A

exotoxins and endotoxins

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63
Q

what are exotoxins

A

-proteins made and secreted during bacterial growth
-toxic at lower doses
-often categorised by site of activity

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64
Q

what are endotoxins

A

-are bacterial structural components that have toxic activity
-can cause endotoxic shock
-released on death of bacteria

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65
Q

outline two categories of exotoxins

A

cytolysins= disrupt membrane homeostasis and cause lysis leading to cell death
two-component=disrupt cellular processes only (A subunit =enzymatic and B subunit=bind to host cell)

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66
Q

name the outcomes of infection

A

clearance
asymptomatic carriage
symptomatic carriage

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67
Q

describe ‘clearance’ outcome of infection

A

no apparent disease, often no knowledge that exposure even occurred

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68
Q

describe ‘asymptomatic carriage’ outcome of infection

A

host may become a reservoir or ‘super spreader’

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69
Q

describe ‘symptomatic carriage’ outcome of infection

A

symptoms of highly variably severity, followed by clearance, carriage or death,
-may or may not have long term impacts

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70
Q

name disease patterns in terms of timing

A

acute, chronic and latent

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71
Q

whats acute disease pattern

A

develops and resolves rapidly eg GI infection

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72
Q

whats chronic disease pattern

A

develops slowly, persists for days/months/years eg TB

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73
Q

whats latent disease pattern

A

infection is initially asymptomatic, becoming symptomatic upon activation

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74
Q

name the disease patterns in terms of location

A

local or systemic

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75
Q

whats local disease pattern

A

confined to specific area (location and/or organ)

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76
Q

whats systemic disease pattern

A

affects most/all of body

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77
Q

contrast Acute vs chronic disease

A

A=sudden vs C=gradual
A=has cure usually vs C= no cure usually
A=short course vs C=long course
A=patient passive vs C=patient active
A=physician dominant vs C=team care w pt
A=likely to return to normal vs C=unlikely to return to normal
A=future uncertainty rare vs C=future uncertainty common

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78
Q

how do bacteria grow

A

via binary fission

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79
Q

what are the phases of bacteria growth

A

lag phase, exponential phase, stationary phase, death phase

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80
Q

Outline phases of bacterial growth

A

*lag=cells adapt to new conditions, enzymes and new metabolites accumulate
*exponential=maximum contact growth
*stationary=oxygen/nutrient demand can’t be met t/f plateau
*death=number of viable cells drop, death>growth

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81
Q

name the environmental factors affecting microbial growth

A

nutrient concentration
pH
osmolarity
temperature

(light, CO2, mechanical and sonic stress, moisture)

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82
Q

how does nutrient concentration effect microbial growth

A

bacterial colonisations require nutrients and oxygen to grow

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83
Q

how does pH effect microbial growth

A

optimal pH ranges depend across species of different bacteria

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84
Q

how does osmolarity effect microbial growth

A

some bacterial populations can proliferate in high/low salt concentration

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85
Q

how does temperature effect microbial growth

A

optimal temperature ranges depend across different species of bacteria

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86
Q

name the classes of bacteria

A

-obligate aerobe
-strict anaerobe
-facultative anaerobe
-aerotolerant anaerobe
-microaerophile

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87
Q

whats an obligate aerobe

A

-require oxygen as a terminal electron acceptor
-undergo oxidative phosphorylation to meet energy demands

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88
Q

whats a strict anaerobe

A

can’t survive in oxygen, converted to H2O2 and superoxide O2- which damages DNA and proteins (kills bacteria)

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89
Q

what is a facultative anaerobe

A

metabolise more efficiently with oxygen but can metabolise via fermentation when its absent

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90
Q

whats an aerotolerant anaerobe

A

do not use oxygen;however, are not harmed by its presence (indifferent to oxygen)

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91
Q

what are microaerophile

A

require specific oxygen concentration, less than atmospheric oxygen levels

92
Q

name the 4 mechanisms by which antibiotics work

A

-inhibit cell wall synthesis
-inhibit protein synthesis
-inhibit nucleic acid synthesis
-metabolic antagonism

93
Q

define bacteriostatic

A

antimicrobial substance that INHIBITS bacteria growth

94
Q

define bactericidal

A

antimicrobial substance that KILLS bacteria

95
Q

define chemotherapeutic agent

A

substance used to treat diseases, particularly cancer, by inhibiting or killing rapidly dividing cells

96
Q

define antibiotic

A

type of chemotherapeutic agent that specifically targets and kills bacterial growth (traits bacterial infection)

97
Q

briefly how does penicillin work

A

-binds to proteins involved in peptidoglycan assembly
-inhibits last step, prevents cross linkage of peptidoglycan strands
-lysis occurs (only works on growing bacteria)

98
Q

briefly how do bacetrial protein synthesis inhibitors work

A

-bind and inhibit to prokaryotic ribosome or inhibit a stage of protein synthesis

99
Q

briefly how do metabolic antagonists worm

A

-interfere with enzymes in folic acid synthesis
-pathogen dies b/c folic acid is a precursor to nucleic acid building blocks (purines and pyrimidines)

100
Q

briefly how do nucleic acid synthesis inhibitors work

A

-inhibit DNA replication, transcription or relevant enzymes)

101
Q

Define the mechanism of antibiotic resistance

A

-lots of germs and a few are drug resistant
-antibiotics kill illness causing bacteria as well as ‘good’ bacteria that protects body from infection
-the drug resistant bacteria can now grow and take over (b/c no good bacteria left)
-some bacteria give their drug resistant bacteria to others (via transduction, transformation and conjugation)

102
Q

what are gene cassettes

A

sets of resistance genes

103
Q

how can we prevent antibiotic resistance

A

-prescribe/ take antibiotics in higher concentrations (overpower resistance)
-prescribe/take antibiotics only when necessary
-consider alternative treatments such as bacteriophages to treat diseases
-prescribe/ take more antibiotics at same time (overpower resistance)

104
Q

what are the ‘processes’ for diagnostic schema

A

-design and bioinformatics
-experimental verification
-risk evaluation

105
Q

what are the ‘elements’ and ‘products’ for diagnostic schema

A

A=target organisms, genomic sequences, alignments primer selection and assay definition –> database of organism signatures
B=specimen types, specimen matrices, specimen preparation, PCR –>nucleic acid analysis (MS), experimental signature generation
C=nucleic acid analysis (MS), experimental signature generation–> reporting filters
D=medically actionable information (clinical) –> reporting filters

*database of organism signatures–> reporting filters–> organism identification

106
Q

list common procedures for detection and identification of bacteria

A

genetic tests
serologic tests
culturing
biochemical tests
microscopy
analytical test

107
Q

Outline how genetic tests are used for detection and identification of bacteria

A

analysing DNA or RNA to detect specific genetic markers of disease

108
Q

Outline how serological tests are used for detection and identification of bacteria

A

testing for antibodies in blood or body fluids

108
Q

Outline how biochemical tests are used for detection and identification of bacteria

A

performing tests to determine bacterial metabolic and enzymatic character

109
Q

Outline how culturing is used for detection and identification of bacteria

A

growing bacteria to identify growth hallmarks of certain bacteria

110
Q

Outline how microscopy is used for detection and identification of bacteria

A

using microscope to visualise bacteria directly, through staining or size analysis

111
Q

Outline how analysis is used for detection and identification of bacteria

A

characterising bacteria based on their unique chemical or molecular profiles

112
Q

what are the two ways culturing can be used

A

use selective agar plates (inhibit some bacteria) or differential agar plates (contain indicators to observe certain bacteria)

113
Q

Describe the importance of sensitivity and specificity for interpreting test results

A

-both are measures of accuracy of clinical diagnosis tests
-low sensitivity produces false negatives, can lead to misidentification of patients with a disease (some will continue to live with their condition, undiagnosed)
-low specificity produces false positives, can lead to unnecessary further testing, wasting various facets of individual and health care system

114
Q

name the key areas for appropriate lab stewardship

A

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

115
Q

appreciate the role of virus in ecosystem

A

-we are surrounded by viruses, regularly inhale them
-viral genomes in our genetic material (1.5%)
-can have positive impacts also
-we have a active virome (bacteriophages)
-viruses can have global impacts and can cause disease

116
Q

define term ‘virus’

A

infectious, obligate, intracellular parasites, comprising of genetic material (DNA or RNA), often surrounded by a protein coat and sometimes a membrane

117
Q

Describe structure of virus

A

-small (yet vary in size)
-can be enveloped or non enveloped
-do not grow or divide, instead replicate

118
Q

distinguish between enveloped and non enveloped virus

A

-enveloped virus possesses a lipid membrane derived from the host cell
-non enveloped virus lacks a lipid membrane, consists solely of a protein coat (capsid)

119
Q

name some common techniques used to study viral infections

A

cell culture
cytopathic effect
coral detection assay

120
Q

describe cell culture to study virus infections

A

the technique of growing and maintaining cells in a controlled environment to study viral replications and interactions with host

121
Q

describe cytopathic effect to study virus infections

A

observable changes in infected cells that results from viral replication, often leading to cell damage, death or morphological alterations

122
Q

describe visual detection assay to study virus infections

A

lab techniques used to identify and detect the presence of viral particles or components in samples, enabling diagnosis, monitoring and research on viral infections

123
Q

name the stages of viral lifecycle

A

1.viral entry
2.translation and genome replication
3.assembly

124
Q

describe viral entry stage of viral lifecycle

A

viruses encounter cells in a random manner, attach to specific cell surface receptor molecules, enters cell passively (with assistance eg passive endocytosis, un-coating etc) and transfers own genome into host

125
Q

describe translation and genome replication stage of viral lifecycle

A

viral mRNA is produced, viral genes are expressed, viral proteins are produced
-happens in nucleus or cytoplasm

126
Q

describe assembly stage of viral lifecycle

A

formation of enveloped or non enveloped viruses

127
Q

what specific viruses replicate in nucleus

A

most DNA viruses and influenza (RNA)

128
Q

what specific viruses replicate in the cytoplasm

A

most RNA viruses

129
Q

what specific viruses replicate in nucleus and cytoplasm

A

HIV, HBV (bi-phasic)

130
Q

what are the two types of RNA viruses

A

*positive sense (+) RNA
*negative sense (-) RNA

131
Q

whats positive sense (+) RNA

A

RNA is the same polarity as its mRNA

132
Q

whats negative sense (-) RNA

A

RNA is an opposing polarity to its mRNA

133
Q

What are the general rules for RNA virus replication

A

1.RNA-dependent RNA polymerase (RdRp) is the key entity that replicates viral RNA
2.RNA genome must be copied from end-end with no loss of sequence (5’ to 3’)

134
Q

Describe the replication of (+) strand RNA viruses

A

1.+RNA infects host cell, expresses viral genome; proteins including RdRp are produced and accumulate in cell
2.Once RdRp levels are sufficient, the replication complex is created, RdRp creates -RNA
3.-RNA acts as a template for synthesis of +RNA, this mRNA is utilised by hosts translational machinery

135
Q

Describe the replication of (-) Strand RNA viruses

A

1.-RNA infects host cell, it caries its own RNA Polymerase enzyme
2.RNA polymerase produces mRNA that codes for viral proteins
3.-RNA is transcribed into +RNA, which is transcribed back into -RNA, this process is viral replication

136
Q

Describe DNA virus replication

A

1.attachment and entry (via mediated endocytosis)
2.Host RNA polymerase transcribes immediate, early and late mRNA
-specific translated proteins replicated viral DNA genome
-capsids are assembled in nucleus and release virions

137
Q

define protein capsid

A

protective shell that enclosed DNA genome of virus

138
Q

define virion

A

complete infectious viral particle (DNA or RNA) enclosed in protein capsid

139
Q

name the types of viral transmission

A

direct
indirect
zoonotic
fomite
vector

140
Q

what is direct viral transmission

A

transmission between two hosts via physical contact

141
Q

whats indirect viral transmission

A

transmission between two hosts via indirect contact

142
Q

whats fomite viral transmission

A

transmission through contaminated inanimate objects

143
Q

what vector viral transmission

A

transmission between two hosts via a live vector eg mosquito

144
Q

whats zoonotic viral transmission

A

tranmission from a animal to a human eg zikavirus

145
Q

how can viruses enter the body

A

-mucosal surfaces eg airborne, oral or sexual
-penetration of skin eg blood borne, vector borne, cuts etc
-vertical transmission eg across placenta

146
Q

how do aerosol transmission of viruses occur

A

-via very small particles/droplets
-aerosol particles can be inhaled or deposited onto mucous membrane or environmental surfaces
-these viruses are usually enveloped
-eg influenza A and COVID 19

147
Q

how does faecal/oral tranmsiison of viruses occur

A

-enteric viruses often arise through ingestion of contaminated water or food
-replicate in intestinal tract, virus binds to cell receptor on GI tract
-eg Poliovirus, Hepatitis A

148
Q

how does sexual transmission of viruses occur

A

-virus is present in blood and body section
-occurs in unprotected sex
-virus infects cell at mucosal surfaces and spreads or stays local
-eg HIV or Hepatitis B

149
Q

how does blood-borne transmission of viruses occur

A

-‘viraemia’, virus circulation in blood
-can arise from virus replicating in target cells and being released into blood
-transmitted via exposure of infected blood
-eg Hepatitis B,C and HIV

150
Q

how does vector bone transmission of viruses occur

A

-viruses can infect and replicated inside a vector, t/f vector becomes infectious
-vector can transmit virus to host
-eg Dengue virus and zhikavirus

151
Q

name steps in viral pathogenesis

A

-tranmission
-viral replication
-proliferation
-host defence system

152
Q

what is meant by transmission

A

-movement from one host to another; virus enters host cell
-indirect (fomite,vector,aerosol) or direct (blood-borne, mucosal)

153
Q

what is viral proliferation

A

virus must proliferate and spread throughout the body, to affect multiple cells

154
Q

how does the host defence system effect viruses

A

the host defence system will kick in; this will either limit or prove ineffective against the virus

155
Q

what is a successful clearance of a viral infection called

A

transient infection

156
Q

whats an inability to clear infection called

A

persistent infection

157
Q

name the effect of viral infection on a cellular level

A

cytopathic effect
multinucleated giant cell
malignant transformation
inclusion bodies
no change

158
Q

whats a cytopathic effect (viral)

A

cell death; vital functions are taken over, cell bursts upon virus release

159
Q

whats a mutlinucleated giant cell (viral)

A

fusion of plasma membrane of adjacent cells

160
Q

whats a malignant transformation (viral)

A

unrestricted growth and division; cancerous character

161
Q

whats inclusion bodies (viral)

A

protein aggregates; localised areas in the cell where virus takes place

162
Q

what is no change outcome (viral infection)

A

viral genome incorporates into host genome and remains dormant

163
Q

whats a localised infection

A

localised to mucous membranes (eg cold) or areas of the skin (warts)

164
Q

whats systemic infection

A

infection of a specific area, followed by entry into circulatory system (lymphatic and/or blood) or NS (neurons)

165
Q

what can impact the effectiveness of the immune response against viruses

A

rate of viral replication, size of virus dose, route of infection, age of host, ability of virus to evade host immune response

166
Q

whats epidemiology

A

the scientific study of distribution, patterns and determinants of disease in a population

167
Q

what are epidemiologists

A

track outbreaks, understand dynamics of viral spread and develop strategies for prevention and control

168
Q

in the context of viruses what three key epidemiological factors must be considered

A

-viral factors; structure of virus
-transmission factors:route and type of transmission
-host factors: ecological changes, anthropogenic and environmental factors

169
Q

how has climate change impacted epidemiology of viruses

A

-water temperatures: can expand the habitats for vectors like mosquitoes
-extreme weather events and shifting ecosystems: disrupt human and animal interactions, facilitating zoonotic viruses

170
Q

what impact do emerging diseases have

A

-introduce viral threats into population, often with unpredictable spread
-overwhelm health care systems
-highlight importance of global surveillance and collaboration

171
Q

define epidemic

A

sudden increase in case spreading through large population

172
Q

define endemic

A

constantly present in a population; relatively low/no spread

173
Q

define pandemic

A

sudden increase in cases across several countries, continents or globally

174
Q

name the factors considered to control viral infections

A

interfere with transmission
establish protective immunity
establish effective treatment protocol

175
Q

what is meant by interfering with transmission to control viral infections

A

develop programs for public education/prevention, barriers, isolation, clean water/needle access

176
Q

what is meant by establishing protective immunity to control viral infections

A

develop vaccination programs for consenting, at risk individuals

177
Q

what is meant by establishing effective treatment protocol to control viral infections

A

using antiviral drugs to inhibit viral replication, use antibodies for passive immunisation

178
Q

name the principles for preventing disease outbreak

A

-hand hygiene; disinfection; sterilisation
-disposal of waste
-surveillance; contact tracing
-public health messaging

179
Q

what is involved in hand hygiene; disinfection and sterilisation

A

promoting a clean environment non conductive to viral transmission

180
Q

what is involved in disposal of waste

A

promoting a clean environment non conductive to viral transmission

181
Q

what is involved in surveillance; contact tracing

A

monitor individuals and viruses so that their spread can be limited

182
Q

what is involved in public health messaging

A

keep the public informed on current ‘best’ protocols/measures

183
Q

what cell type are fungi

A

eukaryotic

184
Q

when do we use ‘diagnostic test’ for diagnostic virology

A

depends on whether we are testing for current (virus particles and/or viral genome and proteins) or previous (serology/and or antibody response) infections

185
Q

what is the method of collection and test for GI tract infections

A

-faeces;vomit : test for viral particles, genomes,proteins

-blood: test for serum antibodies

186
Q

what is the method of collection and test for respiratory infections

A

nasal swab: test for viral particles, genomes,proteins
blood:serum antibodies

187
Q

what is the method of collection and test for blood-borne infections

A

blood:viral particles, genomes,proteins and serum antibodies
liver biopsy sample: viral particles, genomes,proteins and serum antibodies
heparinised: levels of CD4+ T cells (eg HIV)

188
Q

what is the method of collection and test for STD infections

A

vesicle fluid: viral paerticles genomes, proteins
blood: serum antibodies

189
Q

what are the key features transportation of specimens

A

viable virus is needed
-genome must be indicated
-appropriate temperature (either -80 or 4)
-viral collection kits = gold standard

190
Q

How do RAT tests work

A

-look for the presence of COVID 19 antigens
-samples taken via nasopharyngeal swab or saliva
-antigens bind to strips and gives a visual readout, indicated by ‘two lines’
-fast process, no experience needed (78% accuracy)

190
Q

Outline the diagnosis method for virus infection

A

1.grown virus in vitro in cell lines and identify, observe cells for cytopathic effects
2.look directly for virus using electron microscopy
3.detect virus proteins (antigens), detection relies upon availability of antigen specific ABS
4.detect genome (RNA or DNA) by RT-PCR or PCR
5.detect antibodies in serum or infected patients

191
Q
A
192
Q

term used to describe nutrition of fungi

A

heterotrophic (rely on external sources. to obtain their nutrition)

193
Q

fungi cell wall is made of

A

chitin

194
Q

name the motility of fungi

A

non motile

195
Q

how do fungi reproduce

A

mainly asexually, sometimes sexually

196
Q

whats medical mycology

A

branch of medical science that studies fungi capable of causing disease in humans and animals

197
Q

what do medical mycologists do

A

investigate the pathogenic mechanisms of fungi, their ecological niches and modes of transmission and develop antifungal medicines

198
Q

whats hyphae

A

branching, thread like filaments that make up the body of the fungus

199
Q

what are heptae

A

hyphae that contains cross walls or septa

200
Q

what are aseptae

A

hyphae that lack cross walls or septa

201
Q

what is mycelium

A

vegetative component of fungus, consist of an aggregated mass of hyphae

202
Q

whats a spore

A

reproductive structures produced by fungi, plants and other organisms

203
Q

what are yeast

A

fungi that are unicellular throughout their entire life cycle

204
Q

whats pseudomycelium

A

yeast cells clinging together

205
Q

name the types of fungal infections

A

superficial mycosis , cutaneous mycosis , subcutaneous mycosis , systemic mycosis

206
Q

whats superficial mycosis

A

localised to superficial skin layers, hair shafts and nails

207
Q

whats cutaneous mycosis

A

localised to dermis

208
Q

whats subcutaneous mycosis

A

localised to subcutaneous tissues

209
Q

whats systemic mycosis

A

affects multiple organs, including lungs, CNS and bones

210
Q

symptoms and treatment for superficial mycosis

A

symptoms=rash, itching and discolouration
treatment=topical or oral anitfungal meds

211
Q

symptoms and treatment of cutaneous mycosis

A

symptoms=lesions, inflammation and redness
treatment=topical or oral anitfungal meds

212
Q

symptoms and treatment of subcutaneous mycosis

A

symptoms=nodules and ulcers
treatment=antifungal medications, surgery

213
Q

symptoms and treatment of systemic mycosis

A

symptoms=respiratory symptoms and weight loss
treatment=antifungal meds

214
Q

what are the advantages for a parasite living in host

A

-host supplied food
-constant environment
-free from predation
-free transport

215
Q

what are the disadvantages for a parasite living in host

A

-may require remodelling of the environment
-needs to evade host immune response
-escape plan to find new hosts
-infection can kill host

216
Q

name two categories of intercellular parasites

A

facultative parasite and obligate parasite

217
Q

whats a facultative parasite

A

can reproduce outside of host cell eg salmonella

218
Q

whats an obligate parasite

A

cannot reproduce outside host cell eg viruses

219
Q

List the reasons underlying the rise of emerging viral infectious diseases in Australia

A

-increasing human population size
-aging global population
-high risk behaviours (drug use, unprotected sex)
-urbanisation
-fast-paced lifestyles
-more children in day care

220
Q

is there such thing as a ‘new’ virus

A

generally not, viruses have co-evolved with us for millennia, and simply become detected and/or transmitted to human population (from animals usually)

221
Q

why doesn’t hay fever cause feverish symptoms

A

there is no release of endogenous pyrogens

222
Q

Outline mechanism of fever/pyrexia

A

-infection/pathogen enters
-macrophages and neutrophils release endogenous pyrogens (IL-1,IL-6,TNF-alpha)
-these messengers travel to the hypothalamus (respiratory centre) via the bloodstream
-hypothalamus releases prostaglandins
-increases temperature set point in body
-this is achieved by vasoconstriction ,piloerection, shivering
-this provides a more hostile environment for the pathogen and increase metabolic rate (more WBC activity)

223
Q

Outline mechanism of a cough

A

-stimulation of mechanoreceptors in throat, upper respiratory tract or lungs)
-afferent impulses sent to medulla and pons via vagus nerve
-medulla and pons integrate the sensory input and generate a coordinated response, initiating the cough reflex
- Motor signals are sent from the medulla and pons to the muscles involved in coughing via efferent pathway
-effector:Deep inhalation is followed by compression and rapid expulsion of air, clearing irritants from the respiratory tract

224
Q
A