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BOD > Structure > Flashcards

Structure Flashcards

1
Q

What are Koch’s postulates?

A
  1. Bacterium is present in every case of the disease
  2. Bacterium must be isolated from the disease and grown in pure culture
  3. Specific disease must be reproduced from the pure culture in healthy susceptible host
  4. Bacterium must again be recovered
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2
Q

What is ‘endemic’?

A

Disease that occurs regularly at low or moderate frequency

Eg. dental caries

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3
Q

What is ‘epidemic’?

A

Sudden appearance of disease, or increase above endemic level

Eg. diphtheria

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4
Q

What is ‘pandemic’?

A

Global epidemic

Eg. cholera

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5
Q

How is bacteria spread by direct contact?

A
  1. Sexual contact
  2. Respiratory tract
  3. Contamination from own flora
  4. Contact with skin
  5. Transplacental
  6. Parturition
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6
Q

How is syphilis spread?

A
  1. Sexual contact

2. Transplacental

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7
Q

How is bacteria spread by indirect contact?

A
  1. Inanimate objects
  2. Food
  3. Water
  4. Animals
  5. Soil
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8
Q

What is a point source outbreak?

A

Outbreak arising from a single origin

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9
Q

What is a continuous source outbreak?

A

When the source is not eliminated, spread continues

Especially in poor environments

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10
Q

What is a propagated outbreak?

A

Host-to-host transmission results in ever greater numbers of infections

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11
Q

What is a biofilm?

A

Complex multicellular community of bacteria

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12
Q

What bacteria is an obligate parasite?

A

Chlamydia

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13
Q

What is the difference between bacterial and mammalian cell flagellae?

A

Bacteria - rotates

Mammalian - waves

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14
Q

How is bacterial mRNA?

A

Polycistronic - colinear genes

Unstable

No 5’ cap or 3’ polyA tail

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15
Q

How are bacterial cells regulated?

A

Initiation of transcription rather than post-transcriptional modification

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16
Q

What are the four general types of pathogenic bacteria?

A
  1. Cocci
  2. Rods
  3. Curved rods
  4. Spiral
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17
Q

What are endospores?

A

Dormant bacteria that survive in the environment/soil

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18
Q

Give four examples of bacteria that form endospores

A
  1. Tetanus (C. tetani)
  2. Gas gangrene/food poisoning (C. perfringens)
  3. Botulism (C. botulinum)
  4. Anthrax (Bacillus antracis)
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19
Q

What is the difference between Gram-positive and Gram-negative bacteria?

A

Gram-positive have thicker peptidoglycan cell wall that retains the stain

Gram-negative have extra outer lipopolysaccharide membrane that does not retain the stain

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20
Q

Which bacteria do not Gram-stain?

A
  1. Mycobacteria (TB) - acid fast due to waxy lipid coat
  2. Chlamydia - no cell wall
  3. Mycoplasma - no cell wall
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21
Q

What is the cell wall made of?

A

Peptidoglycan

Huge macromolecule of alternating sugar molecules N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM)

These are cross-linked by short oligopeptides

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22
Q

How thick is the Gram-positive peptidoglycan wall?

A

150-500 angstroms

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23
Q

What is the role of the plasma membrane?

A
  1. Osmotic barrier
  2. Site of signal recognition
  3. Transport of nutrients
  4. Respiration
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24
Q

What is the periplasm?

A

Located between the two membranes in Gram-negative bacteria

Contains hydrolytic enzymes and components of transport

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25
Q

What is the outer membrane of Gram-negative bacteria made of?

A

Lipopolysaccharide (LPS)

Contains porins for to import/export materials

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26
Q

What is the O-antigen on LPS?

A

Highly variable

Generates different antigens and therefore different serotypes

Important defence against host attack

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27
Q

What is lipid A in LPS?

A

Endotoxin

Released from dying bacteria

Major PAMP that triggers wide-ranging immune response

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28
Q

What is the bacterial capsule?

A

Prevents drying

Protects from host defences

Made of polysaccharide

Eg. Haemophilus influenzae
Eg. Streptococcus pneumoniae

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29
Q

How do proteins cross the inner bacterial membrane?

A

N-terminal secretion signal

Standard secretion (sec) pathway

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30
Q

Give two examples of facultative anaerobes

A
  1. Salmonella

2. Staphylococcus

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31
Q

Give two examples of strict anaerobes

A
  1. Clostridium

2. Bacteroides

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32
Q

How do strict anaerobes gain energy?

A

Fermentation

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33
Q

Give two examples of bacteria with flagellae

A
  1. H. pylori

2. Vibrio cholera

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34
Q

How does a motile bacterium change direction?

A

Switch direction of rotation of flagellum to clockwise

Causes tumbling

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35
Q

What is an operon?

A

Contiguous genes with common promoter

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36
Q

How does the bacterium sense its environment?

A

Histidine-aspartate phosphorelay (HAP) signalling pathway

Signal transduction system

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37
Q

What is a regulon?

A

Network of operons

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38
Q

What is quorum sensing?

A

Detection of a high population density

Secrete small signal molecule and sense its concentration

Switch on virulence genes only at this point

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39
Q

What is the K antigen?

A

Capsular polysaccharide

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40
Q

How do bacteria cause DNA rearrangements?

A

Random capture and insertion of DNA elements called insertion sequences

Few hundred base pairs long

Enter DNA by own recombination system

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41
Q

What are transposons?

A

Larger bits of DNA

Pick up useful genes

Eg. resistance/virulence genes

Can be picked up by main genome or plasmids

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42
Q

What is a pathogenicity island?

A

Genes required for infection and survival in the host are grouped together in the bacterial genome

Evolved by integration of transposons, plasmids and bacteriophage, and transformed DNA

Have higher GC content than surrounding DNA

Facilitates virulence gene coregulation

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43
Q

What does Salmonella SP-1 do?

A

Gene determining entry into non-phagocytic cells

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44
Q

What does Salmonella Sp-2 do?

A

Gene determining survival in macrophages

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45
Q

Give three ways that bacteria acquire DNA

A
  1. Transduction
  2. Transformation
  3. Conjugation
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46
Q

What is transduction?

A

Transfer of DNA to bacteria from bacterial viruses, eg. bacteriophage

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47
Q

What is transformation?

A

Uptake of DNA from dead/lysed bacteria

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48
Q

What is conjugation?

A

Direct transfer requiring contact between two bacteria

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49
Q

How does the skin protect against bacteria?

A
  1. Dry, acidic, cool, high salt so limits growth

2. Sloughing cells removes bacteria

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50
Q

How do the mucous membranes protect against bacteria?

A
  1. Mucin layer traps bacteria
  2. Cilia waft up mucus out of respiratory tract to be swallowed
  3. Tight junctions limits paracellular invasion
  4. Lysozyme in tears splits peptidoglycan
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51
Q

How does the body reduce iron available to bacteria?

A

Sequestration by lactoferrin and transferrin

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52
Q

How does resident microflora protect against infection?

A

Inhibits colonisation by occupancy and competition for space and nutrients, too high levels of waste,

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53
Q

Which complement pathway is activated by bacteria?

A

Alternative

54
Q

How do bacteria attach to host cells?

A

Cell surface adhesins bind to carbohydrate and glycolipid receptors on host membrane or extracellular matrix

55
Q

How are adhesin proteins assembled?

A

On the tips of long rigid pili

Eg. P-pilus adhesin of UPEC binding to kidney receptor

56
Q

What do common (type 1) pili bind to?

A

Bladder cells

57
Q

What do Pap (P-pili) bind to?

A

Kidney receptors

58
Q

How does UPEC persist in bladder cells?

A
  1. Superficial epithelial cells undergo exfoliation during infection
  2. UPEC invades underlying immature epithelial cells
  3. Persist in quiescent reservoirs and can resurge to cause reinfection
59
Q

What are pedestals?

A

EHEC and EPEC use specialised needles to inject proteins into host cell

Including specialised Tir receptor

Binding of bacterial surface intimin to Tir subverts host cell signal transduction and leads to actin polymerisation, forming a pedestal

Bacterium is very tightly adherent to pedestal

60
Q

Give three bacteria that form biofilms

A
  1. Streptococcus mutans - forms plaque on teeth leading to caries
  2. Staphylococci - colonise catheters
  3. Pseudomonas aeruginosa - colonise contact lenses leading to conjunctivitis
61
Q

Where do P. aeruginosa biofilms form?

A
  1. Contact lenses

2. Lungs of people with cystic fibrosis

62
Q

What do P. aeruginosa form in the lungs of people with cystic fibrosis?

A

Biofilm

Copious production of alginate polysaccharide slime

Protects bacteria in biofilm from host defences and antimicrobials

63
Q

What are the two mechanisms by which bacteria enter host cells?

A
  1. Zipper mechanism

2. Trigger mechanism

64
Q

What is the zipper mechanism?

A

Receptor mediated endocytosis

Bacterial invasins mimic eukaryotic ligands

Eg. triggered by Listeria

65
Q

What is the trigger mechanism?

A

Subversion by bacterial effector proteins

Delivered directly into cell by needles

Eg. Salmonella

66
Q

How does Listeria spread?

A

Escapes from entry vacuole into cytosol

Intracellular movement and replication leads to intercellular spread

Forms a comet tail by actin polymerisation

67
Q

How does Salmonella spread?

A

Stays in entry vacuole and replicates

Survives in macrophages

Spread locally and throughout body by host defence system

68
Q

Give two diseases caused by Chlamydia

A
  1. Trachoma

2. Non-gonococcal urethritis

69
Q

What is trachoma?

A

Most common cause of infectious blindness in developing world

70
Q

What is non-gonococcal urethritis?

A

STI

Often asymptomatic - many silent carriers

Can cause acute prostatitis, pelvic inflammatory disease and infertility

71
Q

How big is the Chlamydia genome?

A

Approx 900 genes

72
Q

What are the two stages of Chlamydia development?

A
  1. Infectious elementary body (EB)

2. Reticulate body

73
Q

What does the infectious elementary body of Chlamydia do?

A

Low metabolic activity and cannot replicate

  1. Attaches to host membrane and induces uptake in endosome
  2. Chlamydia effector Tarp injected by needle rearranges host actin cytoskeleton
  3. Differentiates into RB in endosome
74
Q

What does the reticulate body of Chlamydia do?

A

Metabolically active and replicates

  1. Produces both RBs and EBs
75
Q

What causes damage in Chlamydia infection?

A

Host cell lysis

Inflammation triggered by chlamydial LPS

76
Q

What enzymes break down connective tissue?

A
  1. Collagenase

2. Hyaluronidase

77
Q

What does staphylokinase do?

A

Breaks down blood clots

78
Q

What does coagulase do?

A

Induces fibrin clot formation

79
Q

What does DNAse do?

A

Breaks down DNA in pus

80
Q

What does pyogenic mean?

A

Pus-making

Eg. Streptococci and Staphylococci

81
Q

What are siderophores?

A

Iron-binding proteins secreted by pathogens to bind iron and reimport it into the bacterial cell

82
Q

What is pyoverdin?

A

Siderophore

Secreted by P. aeruginosa

Green fluorescent

83
Q

How do bacteria protect themselves from stomach acid?

A
  1. Pump H+ out of their cells

2. Secrete urease to produce NH3 to neutralise pH

84
Q

How do bacteria prevent uptake by macrophages?

A
  1. Paralyse macrophage by subverting its functions
  2. Inhibit chemotaxis
  3. Resist phagocytosis by shielding with antiphagocytic capsules
  4. Kill macrophages with secreted cytolysins
85
Q

How do bacteria paralyse macrophages?

A

Disrupt intracellular trafficking and signal transduction by injecting anti-phagocytic proteins via needle

86
Q

What is YopT?

A

Yersinia (plague) effector

Protease that targets small GTPases to disrupt cytoskeleton

Paralyses macrophages

87
Q

What is YopP?

A

Yersinia effector

Acetyl transferase that inhibits signalling to initiate apoptosis

Paralyses macrophages

88
Q

How do bacteria inhibit chemotaxis?

A

Cleave complement C5a with C5a peptidase

89
Q

How do capsules help avoid phagocytosis?

A
  1. Non-immunogenic polysaccharide - sialic acid

2. Lack affinity for complement factor B - C3b not formed

90
Q

What are cytolysins?

A

Pore-forming toxins

Disrupt cell functions

Cause apoptosis

Destroy cell membrane integrity - enzymatic destruction of membrane phospholipids

91
Q

What produces cytolysins?

A
  1. Gram positive Strep. pyogenes (streptolysin O and S)
  2. Pneumococcus (pneumolysin)
  3. Pertussis
92
Q

How do bacteria survive inside the macrophage?

A

Interfere with phagosome maturation

Inhibit phagosome-lysosome fusion

Resist oxidative burst

93
Q

How does Legionella survive?

A

Multiplies in alveolar macrophages

Prevents oxidative burst by modifying host phagosome with bacterial proteins that block lysosome fusion

Stimulates cytokine release and intense inflammatory response

94
Q

How does Legionella survive in air conditioning?

A

Facultative intracellular parasite of amoebae

95
Q

How do bacteria resist complement?

A

LPS O-antigen and capsule hinder access to bacterial cell wall, preventing formation of membrane attack complex

96
Q

How do bacteria evade recognition by antibodies?

A
  1. Mimic host
  2. Shut off or change expression of surface antigens by phase variation
  3. Antigenic variation
97
Q

How do bacteria inactivate antibodies?

A
  1. Secretory IgA is cleaved by specific proteases of mucosal pathogens
  2. Bind Fc region of antibody to prevent opsonisation
98
Q

Give four bacteria that cleave secretory IgA

A
  1. Streptococcus pneumoniae
  2. Haemophilus influenzae
  3. Neisseria gonorrhoea
  4. Neisseria meningitidis
99
Q

What are the two groups of bacterial exotoxins?

A
  1. Cytolysins

2. Intracellular enzymatic toxins

100
Q

Give an example of a cytolysin

A
  1. Phospholipase - C. perfringens α-toxin
  2. Pneumolysin
  3. Haemolysin
  4. Helicobacter VacA
101
Q

What is the advantage of cytolysins?

A
  1. Disable immune cells
  2. Assist tissue damage
  3. Bacterial spread
102
Q

What do cytolysins do at low concentrations?

A

Subvert the host cell signal transduction

Cause release of leukotrienes and histamine

Trigger apoptosis

103
Q

What do enzymatic intracellular toxins do?

A

Poison host cells by specific catalytic activity

104
Q

What is the structure of enzymatic intracellular toxins?

A

Intracellularly active (A) component

Receptor binding (B) component

Can be single polypeptides cleaved to active fragments or multimeric

105
Q

Give examples of single polypeptide enzymatic intracellular toxins

A
  1. Diphtheria toxin
  2. Tetanus toxin
  3. Botulinum toxin
106
Q

Give examples of multimeric polypeptide enzymatic intracellular toxins

A
  1. Anthrax
  2. Pertussis
  3. Cholera
107
Q

How do intracellular toxins enter cells?

A
  1. Receptor-mediated endocytosis

2. Retrograde transport

108
Q

What do ADP-ribosylating enzymes do?

A

ADP-ribosylate regulators of adenylyl cyclase

Leads to disturbance of cAMP levels, signalling and ion balance

109
Q

Give three examples of ADP-ribosylating enzymes

A
  1. Cholera toxin
  2. Pertussis toxin
  3. E. coli enterotoxin (labile toxin LT)
110
Q

What does diphtheria toxin do?

A

ADP-ribosylates elongation factor 2

Blocks protein synthesis

111
Q

What does pertussis toxin do?

A
  1. ADP-ribosylates regulators of adenylate cyclase

2. Produces its own adenylate cyclase, which mimics host AC

112
Q

What does anthrax toxin do?

A

Produces adenylate cyclase, mimicking host AC

Disturbs cAMP levels

113
Q

What does Shiga toxin do?

A

Glycosidase that depurinates 28S rRNA

Blocks protein synthesis

114
Q

What does C. difficile toxin do?

A

Glucosylates small GTPases involved in signal transduction

Disrupts actin cytoskeleton and tight junctions

115
Q

What do cytolethal distending toxins do?

A

Cleave DNA

116
Q

What is cytotoxic necrotising factor?

A

Deamidase that targets host cell GTPases

Disrupts cell signalling to reorganise acting cytoskeleton

117
Q

Give two examples of neurotoxin

A
  1. Tetanus toxin

2. Botulinum toxin

118
Q

On which nerves does tetanus toxin act?

A

Inhibitory interneurons

Blocks transmitter release

119
Q

On which nerves does botulinum toxin act?

A

Peripheral nerves

A chain cleaves synaptobrevin

Blocks ACh release

120
Q

What paralysis does tetanus cause?

A

Spastic paralysis

Uncontrollable muscle contraction

121
Q

What paralysis does botulism cause?

A

Flaccid paralysis

122
Q

What are the advantages of enzymatic toxins?

A
  1. Aid colonisation
  2. Aid transmission
  3. Aid dissemination by killing host and providing anaerobic environment for growth (tetanus and botulism)
123
Q

What are superantigens?

A

Bind outside normal antigen binding pocket on TCR

Bridge weakly interacting MHC II and TCR

Activates useless T cells

Can cause cytokine storm

124
Q

What is toxic shock syndrome?

A

Toxic shock syndrome toxin produced by S. aureus growing in highly absorbent tampons

Causes shock, multi-organ failure, cytokine storm

125
Q

How does LPS cause acute inflammation?

A
  1. Released from dead bacteria
  2. Bound by LPS-binding protein
  3. Delivered to macrophage receptors (CD13 and TLR4)
  4. Triggers activation of cytokine genes
126
Q

What causes septicaemia?

A

Lipid A endotoxin overload as large numbers of bacteria die

Triggers strong innate immune response

127
Q

What bacterial components trigger acute inflammation?

A
  1. LPS
  2. Lipid A
  3. Peptidoglycan
  4. Flagellin
128
Q

What causes meningitis?

A
  1. Bacteraemia
  2. Endothelial cell damage
  3. Bacteria crosses blood brain barrier
  4. Inflammation of meninges caused by lipid A
129
Q

What bacteria can cause meningitis?

A
  1. Neisseria meningitidis
  2. Haemophilus influenzae type B
  3. Streptococcus pneumoniae
  4. E. coli (neonatal meningitis)
130
Q

What is streptococcal glomerulonephritis?

A

Type III hypersensitivity reaction following lodging of immune complexes in the kidney

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