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BDS2 PMI > PMI02-2007/8 > Flashcards

PMI02-2007/8 Flashcards

1
Q

What is pathogenicity?

A

Ability of a microbe to cause disease, discrete (yes/no)

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2
Q

What is virulence?

A

Degree of pathogenicity of an organism, continuous (spectrum)

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3
Q

What are virulent bacteria?

A

Bacteria that usually cause disease when they infect a host

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4
Q

What is a virulence factor/gene?

A

Bacterial component/gene only involved in pathogenesis

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5
Q

What is a housekeeping gene?

A

Gene involved in all aspects of a bacterium’s life

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6
Q

List Koch’s Postulates.

A
  1. Pathogen occurs in every case of the disease and distribution corresponds to that of lesions observed
  2. Pathogen does not occur in healthy subjects
  3. After isolated and repeated growth in pure culture, pathogen can induce disease in susceptible animals
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7
Q

Why do Koch’s Postulates not apply to HIV?

A

Cannot be grown in pure culture (virus)

Poor animal models

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8
Q

Why do Koch’s Postulates not apply to Helicobacter pylori?

A

Present in healthy people

Poor animal models

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9
Q

Why do Koch’s Postulates not apply to Streptococcus mutans?

A

Present in healthy people

Not the sole cause of dental caries

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10
Q

Why do Koch’s Postulates not apply to Chlamydia?

A

Bacterium cannot be grown in pure culture

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11
Q

Why do Koch’s Postulates not apply to Diphtheria?

A

Bacterial distribution does not match lesions (systemic disease but organism only found in throat)

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12
Q

Why do Koch’s Postulates not apply to Mycobacterium tuberculosis?

A

Found in healthy (asymptomatic) people (1/3 of pop)

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13
Q

List the Molecular Koch’s Postulates.

A
  1. Disease phenotype should be associated significantly more often with the pathogenic organism than with a non-pathogenic strain
  2. Specific inactivation of the gene(s) associated with the suspected virulence trait should lead to a measurable decrease in virulence
  3. Restoration of full pathogenicity should accompany replacement of the mutated gene with the wild-type original
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14
Q

What are virulence genes often encoded on and why is this beneficial for microbes?

A

Mobile genetic elements

Can be swapped between micro-organisms

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15
Q

Give an example of a mobile genetic element.

A

Plasmid

Transposon

(Bacteriophage)

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16
Q

What is the main benefit of virulence genes for a microbe?

A

Improves competitive fitness advantage in host

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17
Q

What are pathogenicity islands?

A

20-50 genes with low G/C ratio found in genome

Often flanked by mobile elements so can be swapped in their entirety

Encode toxin gene systems and other virulence factors

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18
Q

What virulence genes are often found in plasmids?

A

Adhesins

Antibiotic resistance

Toxins

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19
Q

Why do bacteria adhere to surfaces?

A

Prevent rapid clearance/protection

Gain a source of nutrients

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20
Q

What three factors are usually required for a bacterium to cause infection?

A

Transmission

Adherence

Invasiveness (sometimes)

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21
Q

How could a microbe be transmitted?

A

Inhalation

Ingestion

Inoculation (needles, skin contact, insects)

Fomite route

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22
Q

What is fomite transmission?

A

Breathing/coughing/sneezing out droplets onto a surface and someone else touching that surface

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23
Q

What cellular structures can be used by bacteria to adhere to a surface?

A

Flagellae

Fimbriae

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24
Q

What are found within flagellae and fimbriae which aid adhesion?

A

Specialised surface proteins involved in:

  • direct attachment
  • signalling to eukaryotic cell to trigger further adhesion or ingestion
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25
Q

What qualities of a microbe can adhesion affect?

A

Virulence

Tissue tropism (what it can infect)

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26
Q

Is adhesion always linked to virulence? Why?

A

No

Long-term commensals need to adhere to surfaces too

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27
Q

What does adhesion of a bacterial to a cell/surface cause?

A

Change in gene expression within bacteria

Induction of eukaryotic intracellular signalling = changes in gene expression and production of compounds (eg antimicrobial markers, adhesion proteins)

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28
Q

What is colonisation?

A

Presence of micro-organisms without accompanying disease

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29
Q

What is infection?

A

Presence of micro-organisms resulting in disease

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30
Q

Describe the changes from contamination to infection.

A

Initial contamination is just the beginning of colonisation, bacteria not always bound

Become resident micro-organisms on adhesion = colonisation; can stay here or progress further

Division and invasion into deeper tissue = critical colonisation

Gross changes in tissue and host = infection

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31
Q

How can bacteria obtain nutrients from a host?

A

Soluble waste products or host cell not taking up some nutrients

Released from host cells through damage

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32
Q

What are the two options for a pathogenic bacterium to survive in a host?

A

Evade immune system

Oppose immune function

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33
Q

What is superoxide dysmutase used for?

A

By microbes to prevent phagocytosis/damage by oxygen radicals

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34
Q

What is the benefit of being invasive for a microbe?

A

Penetrate mucosal layers and establish at systemic sites

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35
Q

What is septicaemia?

A

When a bacterial infection enters the bloodstream

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36
Q

What factors can aid the invasiveness of an organism?

A

Secretion of bacterial enzymes

Anti-phagocytic factors

Toxins that control host cell uptake mechanisms

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37
Q

Give an example of a bacterial enzyme that can aid the invasiveness of an organism.

A

Strep. pyogenes = collagenases

Staph. aureus = proteases

Haemophilus leucocidins = coagulases

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38
Q

Give some examples of anti-phagocytic factors that aid the invasiveness of an organism.

A

Capsule to prevent phagocytosis (Strep. pneumoniae)

M proteins by Group A Streptococci prevent antibodies binding

Fc binding proteins to prevent effector functions

Leukotoxins to kill macrophages

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39
Q

Give an example of an obligate intracellular organism.

A

Some bacteria:

  • Chlamydia trachomatis
  • Rickettsia prowazekii
  • Mycobacterium leprae

All viruses

40
Q

Give an example of a facultative intracellular bacteria.

A

Salmonella

Mycobacterium tuberculosis

Legionella

Listeria

41
Q

What is a facultative intracellular bacteria?

A

Bacterium that can survive within or outside of a cell

Often have intracellular phases of transcytosis

42
Q

What cell invasion mechanisms do intracellular bacteria have?

A

Phagocytosis and escape of phagosome

Inducing macropinocytosis or endocytosis by:

  • interaction of invasins with host receptors to control actin
  • injection of bacterial proteins into cell
  • complex interactions between toxins and proteins
43
Q

What organism causes typhus?

A

Rickettsia prowazekii

44
Q

What does Mycobacterium leprae cause?

A

Leprosy

45
Q

Describe the possible life of a dimorphic intracellular bacterium.

A

Starts as infectious and metabolically inert elementary body

Reorganises itself within phagosome to form a non-infectious and metabolically active reticulate body

Multiplies and leaves cell to repeat

46
Q

Describe Rickettsiae bacteria.

A

Gram-negative bacilli

Arthropod-borne

Replicates in cytosol of host endothelial cells after escaping phagosome

Uses host’s actin to escape cell

47
Q

What common features of obligate intracellular bacteria?

A

Long generation time as not facing as many environmental pressures

Small size and small genome (can use host mechanisms)

Require exogenous energy supply

May infect non-phagocytic cells

Protected from lysosomal degradation

Use own expression and replication mechanism so not completely dependent on host

No environmental reservoir (acquired from other hosts)

Cannot be grown by standard bacterial culture techniques so difficult to study

48
Q

What are the advantages of intracellular invasion for a bacterium?

A

Immune evasion

Easily carried around body

Obtain nutrients from host

Smaller genome (500-1000 genes vs 1500-6000) - “reductive evolution”

49
Q

What is reductive evolution?

A

Intracellular bacteria lose genes for metabolic pathways as they can rely on host mechanisms

Not wasting resources

Adaptation to a defined ecological niche

50
Q

Describe pyogenic inflammation.

A

Acute fever/increased body temperature

Recognition of pathogen by innate immune system causes:

  • release of large amounts of cytokines
  • neutrophil and macrophage recruitment
  • opsonisation and bacterial killing

Massive reactions may lead to shock

51
Q

What organisms may cause pyogenic inflammation?

A

Streptococcus pyogenes

Streptococcus pneumoniae

Staphylococcus aureus

52
Q

Name an organism that causes granulomatous inflammation.

A

Mycobacterium tuberculosis

53
Q

What is a cytokine storm?

A

Overactivation of a healthy immune system leading to massive production of cytokines

Surge in pro-inflammatory cytokines followed by surge in anti-inflammatory cytokines

Usually multiple surges; leads to tissue damage, multiple organ failure, shock and death

54
Q

What are the main cytokine participants in a cytokine storm?

A

TNF-α

IL-6

IL-1

55
Q

In what conditions are cytokine storms mainly seen?

A

Sepsis and septic shock

Viral pneumonias

56
Q

What group of microbes use molecular mimicry to induce a harmful antibody response?

A

Group A β-haemolytic streptococci

57
Q

What are superantigens?

A

Antigens that inappropriately, excessively activate the immune response leading to shock

58
Q

What is endotoxin?

A

Membrane structure/toxin associated with Gram-negative organisms, a type of PAMP

LPS

Heat-stable and poorly antigenic but triggers a strong innate immune response leading to shock and fever

59
Q

What is an exotoxin?

A

Pore-forming or surface-acting or intracellular toxin

60
Q

Describe the structure of endotoxin.

A

Lipid A core with 3 polysaccharide regions

Polysaccharide region split into inner and outer cores

O antigen, a repeating motif of polysaccharides, may protrude from the outer core

61
Q

What is smooth LPS?

A

LPS/endotoxin with a long O antigen

Gives shiny colonies

62
Q

What is semi-rough LPS?

A

LPS/endotoxin with a very short O antigen

Gives slightly matte colonies

63
Q

What is rough LPS?

A

Damaged LPS/endotoxin with no O antigen

Sometimes increases toxicity

64
Q

How does LPS trigger strong innate immune responses?

A

Lipid A (of LPS) complexes with LPS Binding Protein (LBP)

Macrophage surface complex (TLR4, CD14 and MD2) recognises LBP

Triggers signalling in macrophage = cytokine storm, iNOS activation (vasodilation) and inflammation

65
Q

What is endotoxinaemia?

A

Presence of LPS/endotoxin in blood

66
Q

What are the possible different actions that membrane-acting exotoxins can have?

A

Enzymatic (digestion of membrane constituents)

Pore formation

Detergent-like action

Perturb signalling

67
Q

What is the enzymatic membrane-acting toxin?

A

Phospholipase used by C.perfringens, Listeria, C.albicans

68
Q

What size are the pores formed through action of membrane-acting exotoxins and which enzymes may be involved?

A

Small or large pores = 7-30 subunits

E.coli = α-haemolysin

S.pyogenes = streptolysin O

S.pneumoniae = pneumolysin

69
Q

Describe the pore formation action by membrane-acting toxins.

A

Toxins associate with a particular receptor in the membrane (may be protein or cholesterol)

Causes polymerisation of subunits (toxin + receptor)

Undergo conformational change after polymerisation to protrude through membrane

70
Q

How can a membrane-acting toxin have a detergent-like action?

A

Hydrophobic protein toxin associates with hydrophobic tails of membrane = disruption

71
Q

Which types of membrane-acting toxins perturb signalling?

A

Stable toxin

Specific proteases

Superantigens

72
Q

What is a stable toxin?

A

Small, cysteine-rich peptide produced by Enterotoxigenic E.coli (ETEC)

Heat-stable

Binds to extracellular domain of guanylyl cyclase C as it is similar to the natural ligand guanylin

Leads to inappropriate activation of intracellular domain to produce cGMP from GTP

Leads to efflux of Cl- and prevents Na+ influx => osmotic diarrhoea as water is drawn out of cells

73
Q

How can membrane-acting toxins act as superantigens?

A

Associate with MHC class II on APCs and cross-link it to a vβ region of a TCR of a non-specific T cell

Causes non-specific activation of T cells (polyclonal activation)

74
Q

Give an example of a membrane-acting toxin that can act as a superantigen.

A

TSST-1 from S.aureus (leads to toxic shock syndrome)

75
Q

What do intracellular toxins do?

A

Bind cell surface, cross membrane and have enzymatic activity in the cell (may be injected in directly)

76
Q

What are the different parts of an AB toxin?

A

A fragment is active

B fragment is involved with binding

77
Q

Give an example of a neurotoxin.

A

Botulinum toxin

Tetanospasmin

78
Q

What do neurotoxins do?

A

Attack signalling between nerve cells or vesicle docking in synapse

Associated with zinc proteases

79
Q

What does tetanospasmin do?

A

Prevents postsynaptic inhibitory molecules from binding so signal never turns off

80
Q

What does botulinum toxin do?

A

Prevents release of excitatory transmitter so no signal is generated

Attacks syntaxin, synaptobrevin, SNAP-25

81
Q

What are the symptoms of tetanus?

A

Restlessness

Headaches

Irritability

Muscle spasms, eg lockjaw

82
Q

What are the symptoms of botulism?

A

Muscle weakness

Excess sweating

Dry mouth

Parkinson’s type symptoms

83
Q

Describe the diphtheria toxin.

A

AB toxin - additional T region as part of B region involved in endosome insertion/toxin translocation

T region = series of α-helices with negatively charged loops between

Acidic conditions in endosomes = H+ associate with negative loops which allows the α-helices to closely associate with the membrane and escape endosome

Blocks EF-2 involved in peptide extension (translation) by adding ADP ribose (from NAD) => ADP-ribosylase enzyme

84
Q

How is diphtheria treated/managed?

A

Vaccine

Antitoxin

Antibiotics

Rest

85
Q

What are the symptoms of diphtheria?

A

Inflamed throat

Fever

Diphtheric membrane in throat

86
Q

Give examples of ADP-ribosylating enzymes and what they do.

A

Diphtheria toxin and P.aeruginosa ETA = modifies EF-2

Cholera and pertussis toxins, E.coli labile toxin = modify signalling proteins

87
Q

Name some non-toxin diseases and their causative agents.

A

Plague = Yersinia pestis

Typhoid = Salmonella typhoid

Shigellosis = Shigella flexneri

88
Q

How do non-toxin diseases cause damage?

A

Use secretion systems to inject toxins directly into cells

89
Q

What did the type III secretion system evolve from?

A

Flagellae

90
Q

What did the type IV secretion system evolve from?

A

Pili

91
Q

What did the type VI secretion system evolve from?

A

Bacteriophages

92
Q

Describe the type III secretion system.

A

Resting state = coiled, compressed protein complex spanning the membrane bilayer

Contact with eukaryotic cell causes decompression and protrusion of system into cell to allow toxin secretion into it

93
Q

Name a genus that uses type III secretion systems.

A

Yersinia

94
Q

Describe how the type VI secretion system arose.

A

Viral DNA injected into bacteria

Bacteriophage incorporated into inner membrane and genome

Over time, these mutate and can be used by the target organism to inject their own toxins into a host

95
Q

Give an example of an organism that uses type VI secretion systems.

A

Vibrio cholera

96
Q

Why are toxins so potent?

A

Target key cellular components (membrane, protein synthesis, signalling)

Usually enzymatic action so can be used repeatedly

BDS2 PMI (21 decks)

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