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Principles in Infectious Diseases > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

What are the three domains of life?

A

Eukaryota, Bacteria and Archaea

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2
Q

What are the key differences between Prokaryotes and Eukaryotes?

A
  1. Size, prokaryotes are 0.2-2.0µm in diameter, Eukaryotes are 10-100µm in diameter.
  2. Prokaryotes don’t have a nucleus, Eukaryotes do
  3. Prokaryotes don’t have organelles, Eukaryotes do, e.g. Golgi, mitochondria, endoplasmic reticulum
  4. Prokaryotes have a cell wall, Eukaryotes do not
  5. Prokaryotes have smaller ribosomes (70s) than Eukaryotes (80s)
  6. Prokaryotic DNA is single circular chromosomes - no histones whereas Eukaryotes have multiple linear chromosomes with histones.
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3
Q

How does bacteria grow/multiply

A

By binary fission. It’s the equivalent of the cell cycle in Eukaryotes. Bacteria has a large circle of DNA + smaller circles of DNA called plasmids. When the bacteria wants to divide, the DNA is all replicated. The large circles of DNA migrate to opposite sides of the cell. The plasmids are then distributed evenly between the two sides. Then the cytoplasm and the bacteria divides creating two separate cells.

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4
Q

How often does bacteria divide?

A

Once every 20 minutes

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5
Q

What is artificial media?

A

A mixture of different compounds to help bacteria grow. This can be liquid (i.e. nutrient broth)

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6
Q

What are the stages of bacteria growth when counting the number of viable cells?

A
  1. Lag phase, the initial period just after the time starts
  2. Log phase, where the bacteria is growing exponentially (graph has a positive slope)
  3. Stationary phase, where the bacteria stops dividing (graph is flat)
  4. Death phase, where the bacteria begins to die (graph has a negative slope)
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7
Q

What do bacteria need to grow?

A
  • The correct temperature
  • The correct pH
  • Carbon source
  • Potassium, magnesium, calcium and cofactors
  • Oxygen
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8
Q

What are the correct temperatures for bacteria (depending on temp type)?

A
  1. Thermophiles - optimal growth is 50-60 degrees celsius or below
  2. Mesophiles (the mid range) have an optimal growth temperature of 25-40 degrees celsius
  3. Psychrophiles - cold - optimal growth 15 degrees celsius or below
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9
Q

What is the correct pH depending on the type of bacteria?

A
  • Most bacteria need a neutral pH of 6.5-7.5
    1. Acidophiles require an acidic pH, less than pH 5.4
    2. Neutrophiles pH 5.4 to 8.5
    3. Alkaliphiles pH 7-12 or higher
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10
Q

Why must bacteria have a carbon source to grow?

A
  • Carbon makes up 50% of the dry weight of the cell
  • Helps with breakdown of lipids, proteins and carbohydrates
  • For CO2 fixation
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11
Q

Does bacteria need oxygen for growth?

A
  • Obligate aerobes require oxygen
  • Facultative anaerobes only use oxygen if it is present
  • Obligate anaerobes do not require oxygen
  • Microaerophilic require very little oxygen
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12
Q

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

A
  • Gram positive bacteria have a wall structure on the outside of the cell with the membrane on the inside
  • Gram negative bacteria have a wall structure sandwiched between two membranes
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13
Q

What are the three main functions of the cell envelope?

A
  • For defence
  • For strength
  • For biofilms
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14
Q

What colour is the Gram stain on Gram positive and negative bacteria?

A
  • Gram positive is stained purple
  • Gram negative is stained pink
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15
Q

What are the bacterial shapes as seen by microscopy?

A
  • Shape: rods, cocci
  • Arrangement: chains, single, groups
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16
Q

The bacterial cell wall is made out of peptidoglycan. What is the function of peptidoglycan?

A
  • It stabilises the cytoplasmic membrane, enabling it to withstand high internal osmotic pressures
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17
Q

What is a bacteria capsule?

A

A polysaccharide layer outside of the cell. Its function is to allow adherence to host tissues, form biofilm, immune evasion, helps with antimicrobial resistance.

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18
Q

What are the three common bacterial cell surface structures?

A
  • Fimbriae
  • Pili
  • Flagella
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19
Q

What is the function of fimbriae?

A

Cell adhesion

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20
Q

What is the function of pili?

A
  • Genetic exchange
  • Adhesion
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21
Q

What is the function of flagella?

A
  • Motility
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22
Q

What does infectivity mean?

A
  • The ability to produce disease in a host organism
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23
Q

What does pathogenicity mean?

A
  • The ability to produce disease in a host organism
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24
Q

What is an opportunistic pathogen?

A

A microbe that typically infects a host that is immunocompromised in some way, either by a weakened immune system or breach to the body’s natural defences, such as a wound

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25
Q

What is virulence?

A

The measurement of pathogenicity is called virulence, with highly virulent pathogens being most likely to cause disease in a host

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26
Q

What does the host-pathogen interaction describe?

A

How pathogens sustain themselves and cause disease within hosts or host populations.

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27
Q

What are the 3 levels of thinking for host-pathogen interactions

A
  1. Population level
  2. Individual level
  3. Cellular and molecular level
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28
Q

What are the outcomes after pathogen exposure?

A
  • Clearance
    or
  • Colonisation
    • disease
      or
    • no disease
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29
Q

What are the key variables that influence the outcome of exposure to a pathogen?

A
  • The ability of the pathogen to colonise and cause host damage
  • Immune status of the host
  • Constant variables and dynamic relationship
  • Exposure to a pathogen does not ensure that disease will occur, since a host might be able to fight off the infection before disease signs/symptoms develop
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30
Q

What is commensal bacteria and what are the benefits?

A

Bacteria that resides on the surface of the body or mucosa without causing harm, e.g. gut microbacteria.

Benefits:
- Protection against pathogens
- Production of nutrient

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31
Q

What are the host-pathogen interactions when the commensals turn bad?

A

Host commensal causes infection which then causes symptomatic disease.

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32
Q

Opportunism is common among bacterial pathogens. What do we know about staphylococcus epidermidis?

A
  • Usually non-pathogenic
  • Can enter body, e.g. during surgery
  • Usually rapidly killed by defences of the innate immune system
  • But can colonise immunologically compromised sites, e.g. the plastic surface of a heart valve.
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33
Q

What are some common bacterial pathogens in human and veterinary medicine?

A
  • Shigella
  • Campylobacter
  • Helicobacter
  • Salmonella
  • Escherichia
  • Staphylococcus
  • Streptococcus
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34
Q

What do we know about shigella, campylobacter, helicobacter, salmonella, escherichia

A
  • Gram Negative
  • Can be zoonotic
  • Diarrhoeal diseases
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35
Q

What do we know about staphylococcus and streptococcus?

A
  • Gram positive
  • Can be zoonotic
  • Skin and throat infections
  • E.g. mastitis in dairy cattle
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36
Q

What are some key abilities of bacterial pathogens?

A
  • Transmit between hosts
  • Colonise hosts
  • Cause host damage
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37
Q

How can pathogens gain access to new hosts (disease transmission)?

A
  • Direct contact
    • Skin-skin e.g. staphylococcus aureus infections
    • Sexual intercourse - neisseria gonorrhoea
  • Indirect contact
    • Aerosol e.g. mycobacterium tuberculosis
    • Inanimate objects e.g. water, food, blood, fomites (e.g. toys) e.g. salmonella enterica, vibrio cholerae
    • Vectors e.g. ticks, fleas, e.g. borellia burgdorferi
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38
Q

How is bacteria recognised by the host innate immune system?

A
  • Cell-to-cell interaction
  • Pathogen-associated molecular patterns (PAMPs)
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39
Q

How does the CLR in the host innate immune recognise bacteria?

A
  • Transmembrane proteins localised at the plasma membrane
  • Recognise glycans from the wall of some bacteria
  • Activate kinase sky and CARD9/MALT1/Bcl-10 adapter complex
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40
Q

How does the NLR in the host innate immune recognise bacteria?

A
  • Cytoplasmic sensors
  • Multiple subfamilies
    NLPs recognise bacterial, viral, parasitic and fungal PAMPs
    AIM2 detects viral and bacterial DNA
  • Form multiprotein signalling complexes known as inflammasomes
  • Activates caspase-1-mediated processing and activation of pro-interleukins IL-1ß and IL-18
    NOD1 and NOD2 recognise bacterial peptidoglycan
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41
Q

How does the TLR in the host innate immune recognise bacteria?

A
  • Transmembrane proteins localised either at the plasma membrane or in endosomes
  • Broad range of specificities recognising proteins, nucleic acids, glycans etc
  • Activate MAP kinase, NFxB and IRF pathways

Example:
TLR4 recognises lipopolysaccharide (LPS), a component of the gram-bacteria cell wall

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42
Q

How does the RLR in the host innate immune recognise bacteria?

A
  • Cytoplasmic sensors of viral RNA
  • Signal via the mitochondrial adaptor protein MAVS
  • Trigger antiviral responses including the production of type I interferon

Examples: RIG-I and MDAS

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43
Q

What are the routes of entry for bacteria?

A
  • Sites of vulnerability:
    • Respiratory tract
    • Intestinal tract
    • Urogenital tract
    • Conjunctive
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44
Q

What are the physical removal strategies?

A
  • Coughing and sneezing
  • Vomiting and diarrhoea
  • Urination
  • Tear production
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45
Q

What are the attributes in effective host colonisation?

A
  • Adhere to host cells and resist physical removal
  • Invade host cells
  • Compete for iron and other nutrients
  • Evade the immune system
  • Virulence factors
46
Q

What do we know about fimbriae and pili in gram-negative pathogens?

A
  • Found in virtually all Gram-negative bacteria but not in many gram-positive bacteria
  • Made up of a protein called Pilin
  • Bind to sugar (e.g. mannose) receptors on the surface of eukaryotic cells
  • E.g. pathogenic Escherichia coli
  • Can colonise gut and urinary tract - diarrhoea and UTI
  • Adhere to host cells and resist physical removal
47
Q

What are the functions of fimbriae and pili?

A

To promote attachment and resistance to physical removal

48
Q

What is the function of adhesins?

A

To enable attachment and resistance to physical removal

49
Q

What do we know about adhesions and gram-positive bacteria?

A

They bind to specific receptors to allow intimate attachment.
- E.g. streptococcus pyogenes
Protein F binds to fibronectin
Lipoteichoic acid binds to fibronectin on epithelial cells
M-protein also functions as an adhesin
Adhere to host cells and resist physical removal

50
Q

What do we know about motility helping colonisation at mucosal surfaces?

A

Motility helps colonisation.
- Gram-negative pathogen
- Colonises gut, stomach ulcers and cancer
- Flagella help move bacteria through the mucus and attach to gut epithelial cell
- Urease produced in bacterial cytosol produces ammonia from urea
- Ammonia passes into periplasmic space - buffer against acidic pH of the gut
- Resist physical removal

51
Q

What is the process of bacterial invasion of host cells?

A
  • Invasins, molecules that activate the host cells cytoskeleton, promote cell entry by phagocytosis.
  • They facilitate the growth and spread of the pathogen
  • Once the bacteria is within host cells it is provided with a ready supply of nutrients and protected from complement, antibodies and other body defence molecules.
52
Q

What is the process of bacterial invasion of epithelial cells?

A
  • Bacterial secretion systems co-opt the functions of the host cell (gram-positive and gram-negative)
  • Type 3 secretion is the most common (gram-negative)
  • Injectosome
  • Effector molecules interfere with cytoskeleton
  • Encourage phagocytosis
  • Eventual cell to cell spread
  • E.g. Escherichia coli, Shigella dysenteriae
53
Q

How does the bacteria grow and survive in the host?

A

The host is a source of nutrients for the growth of bacteria
- Carbon
- Nitrogen
- Iron
Bacteria have the ability to compete for iron and other nutrients

54
Q

What is bacterial theft of host iron?

A

Where bacteria have the ability to compete for iron and other nutrients

55
Q

What do we know about iron in the host cell?

A
  • Insoluble
  • Carried in the host in complexes with glycoproteins
  • Transferrin, serum
  • Haemoglobin, red blood cells
  • Lactoferrin, tears, sweat, saliva, mucus
56
Q

What are phagocytes and what do they do?

A

Macrophages, neutrophils and dendritic cells. They are key cells of the innate immune system.

Engulf and breakdown bacteria and enzymes for nutrient starvation

57
Q

Bacteria can evade phagocytosis. How?

A

Staphylococcus aureus can produce the enzyme coagulase.

This changes fibrinogen to fibrin which causes clotting.

Fibrin then coats the surface of the bacteria which allows evasion of phagocytosis as phagocytes cannot recognise receptors on the bacteria.

Coagulase activity is almost solely found in pathogenic strains and almost never found in non-pathogenic strains of S.aureus

58
Q

What does lysozyme in tears do and how does bacteria defend against it?

A
  • Lysozyme can cleave the bonds in peptidoglycan
  • So gram positive cells are particularly vulnerable as the peptidoglycan is on the outside of the bacteria unlike gram negative where it is sandwiched between two membranes
  • N-deacetylation has been shown to protect bacteria from lysozyme
59
Q

How can bacteria interfere with the function of antibodies?

A

Some bacteria can change the epitope on the outside of the cell to prevent binding to the antibody

Staphylococcus aureus can produce protein A which make the antibodies bind in the wrong orientation

60
Q

What do we know about bacterial toxins?

A
  • They were the first virulence factors to be identified and studied in detail
  • Many toxins are released or excreted (relatively easy to isolate, purify and characterise)
  • Toxins often have very specific modes of action and clearly defined targets in mammalian cells
61
Q

What are the functions and benefits of bacterial toxins?

A
  • Can release iron or carbon sources
  • Can be subtle, dampening the immune response through modulation of the signalling pathways for cytokine production

Benefits:
Kill neutrophils and macrophages
Protect bacteria from the phagocytic cells that might clear them

62
Q

What is an endotoxin?

A

Component of the cell wall e.g. lipids

63
Q

What is an exotoxin?

A

Secreted proteins and peptides

64
Q

What do we know about clostridium botulinum (botox)?

A

Produces a toxin called botulism

65
Q

What is botulism?

A

A food-borne disease that causes spores in food (hard to see the benefit to bacterial growth for a pathogen that doesn’t colonise the host)

It can cause paralysis and even respiratory collapse

66
Q

What are the benefits to clostridium botulinum in environmental habitat?

A

May play roles in the physiology of the bacteria and their viruses, possibly regulation of cellular or phage functions or cell-cell signalling

The impact in the human body is merely an accidental side effect of their action

67
Q

What is the interaction of LPS with host macrophages in modulating cytokine production?

A

Binding of LPS on gram-negative bacteria to the PRR results in the activation of a signalling pathway

This causes the transcription factor NF-kB to enter the nucleus

This initiates the transcription and eventual secretion of the cytokines IL-8, IL-1 and TNF-alpha

68
Q

What are Type I toxins?

A

Toxins that do not enter the host cell, e.g. superantigens (e.g. S.aureus)

69
Q

What are type II toxins?

A

Toxins that disrupt eukaryotic cell membranes e.g. phospholipases

70
Q

What are type III toxins?

A

A-B toxins
They are single-chain peptides with multiple domains, such as the botulinum NTs
Multi-subunit complexes, such as cholera toxin and anthrax toxin

They act intracellularly
The B-region binds to the eukaryotic cell by recognising a receptor
The A portion enters the cytoplasm

71
Q

What are superantigens and what do they do?

A

Superantigens (sAG) bypass normal antigen presentation by binding to class II major histocompatibility complex molecules on antigen-presenting cells and to non-specific regions of the T-cell antigen receptor

They activate T cells at orders of magnitude above antigen-specific activation, resulting in massive cytokine release.

The usual level or T-cell activation is 1 in 10,000 cells activated but via sAGs it is 1 in 5

Excess IL-2 TNF-alpha causes tissue damage

This induces nausea, vomiting, malaise and fever.

72
Q

What are some examples of superantigens (Type I)?

A
  • Gram +ve cocci
  • Staphylococcus aureus
  • Staphylococci enterotoxins
  • Enterotoxin producing staphylococci (food poisoning)
  • Livestock common reservoir
73
Q

What does staphylococci enterotoxin B do?

A

Induces massive cytokine production. This leads to sepsis and shock.

74
Q

What are pore-forming toxins (type II) and what do they do?

A

Membrane disrupting toxins form channels in the membrane. Osmotic pressure of the host cell cytoplasm then results in cell lysis

Pore-forming toxins tend to be highly helical in their water-soluble state and form pores in membranes using helices

They interact with a cell surface receptor. Membrane insertion is often facilitated by acidic pH, leading to a conformational change in the protein’s tertiary structure to an insertion-competent state, followed by membrane penetration

75
Q

What are some examples of pore-forming toxins?

A
  • Staphylococcus aureus
  • Streptococcus pneumoniae
  • Escherichia coli
  • Mycobacterium tuberculosis
  • Streptococcus pyogenes
  • Streptolysin O and S
  • Clostridial alpha-toxin zinc-dependent phospholipase
76
Q

What are some examples of bacteria that produce A-B toxins?

A
  • Cholera enterotoxin
  • Diphtheria toxin
  • Shiga toxin
  • Tetanus toxin
77
Q

What are some beneficial uses of bacterial toxins?

A
  • Healthcare
  • Agriculture
  • Cosmetic (like botox)
78
Q

What can A-B toxins do?

A
  • Ribosylation of G proteins stimulates adenylate cyclase and increases cAMP in cells of the GI tract, causing secretion of water and electrolytes (cholera enterotoxin)
  • Ribosylation of elongation factor 2 leads to inhibition of protein synthesis in susceptible cells (Diphtheria toxin)
  • Enzymatically cleave rRNA resulting in inhibition of protein synthesis in susceptible cells (shiga toxin)
  • Zn++ dependent protease that inhibits neurotransmission at inhibitory synapses resulting in spastic paralysis (tetanus toxin)
79
Q

What are some key differences between prokaryotic and eukaryotic genetics?

A
  • Prokaryotes have a single circular genome whereas eukaryotes have multiple linear chromosomes.
  • Prokaryotes are haploid while eukaryotes are diploid
  • Prokaryotes have extra-chromosomal plasmids while eukaryotes do not
  • Prokaryote genetics are in the cytoplasm, eukaryote are in the membrane-bound nucleus
  • Prokaryotes have coupled transcription and translation (translation begins while the mRNA is still being synthesised) while eukaryotes are separate
80
Q

How do bacteria pass on genetic information?

A
  1. Horizontal gene transfer, bacteria to bacteria
  2. Vertical gene transfer (during binary fission)
81
Q

Why is there genetic variation in bacterial populations?

A
  • To respond to new selective pressures
  • To survive adverse environmental conditions
  • To exploit new environments that it encounters
82
Q

What are some genetic changes passed on through VGT?

A
  • Spontaneous mutations
  • Single-nucleotide polymorphisms (SNPs) eg. CAT to CGT
  • Mutation rates are low, slow, driven by replication rate
  • Can select out mutants, like M.tuberculosis, point mutation is rpoB gene
83
Q

What are the three processes of horizontal gene transfer?

A
  1. Conjugation
  2. Transduction
  3. Transformation
84
Q

What is conjugation?

A

The transfer of plasmids via pili

85
Q

What is transduction?

A

The transfer of DNA via bacteriophage (virus)

86
Q

What is transformation?

A

The uptake of DNA from the environment

87
Q

What are bacterial plasmids and their properties?

A

Small circular molecules that are extra-chromosomal pieces of DNA

  • They are self-replicating
  • They can be present in multiple copies (copy number)
  • They can have genes required for virulence, antibiotic resistance, some toxins and genes that promote adherence to host cells
88
Q

What is the process of conjugation?

A
  1. The donor cell’s pilus seeks out the recipient
  2. The pilus then attaches to the recipient cell
  3. The F plasmid of the donor cell is replicated and transferred to the recipient cell
  4. The pilus detaches, leaving a pilus on the old donor cell and one on the new donor cell which now contains an identical F plasmid that can be passed on to the next recipient
89
Q

What are the phage lifecycles?

A
  1. Phage infects bacterium
  2. Phage DNA circularises

Next, the phage can either undergo lysogeny or lysis.

Lysogeny:
1. Phage DNA integrates
2. Bacterium grows as lysogen
3. Phage DNA excises
4. New phage particles are produced and lyse bacterium
5. Lysis and release of phage

Lysis:
1. The phage DNA replicates
2. New phage particles are produced and lyse bacterium
3. Lysis and release of phage

90
Q

How do transductants form?

A
  1. Donor strain infected with phage
  2. Bacterial DNA partially degraded
  3. Rarely a phage head takes up bacterial DNA
  4. Transducing particle containing only bacterial DNA infects recipient strain
  5. Creates a recombinant recipient, the transductant
91
Q

Transduction can result in Pathogenicity islands (PAIs), what are PAIs?

A
  • Large pieces of DNA (10Kb to 100Kb)
  • They encode one or more virulence factors
  • They are present in the genomes of pathogenic strains but absent from the genomes of non-pathogenic members
  • Encode genes involved in virulence e.g. toxins
  • Acquisition of a PAI is a rapid evolutionary change, non-pathogen to a pathogen in a single step.
92
Q

What is transformation, how does it occur?

A
  • Uptake of naked DNA from the environment
  • Can occur naturally or be induced artificially
  • Important for molecular biology
  • The conditions must be favourable and bacterial cells must be competent
93
Q

What is the importance of horizontal gene transfer for bacterial pathogens?

A
  • The gene pool available for bacterial pathogens is much larger than originally thought, pangenome
  • Allows for rapid emergence of bacterial pathogens
  • Allows for a single species to colonise diverse niches and cause a range of disease
  • Diversity allows escape from antibiotic treatments or vaccination strategies
94
Q

What are some sites of pathogenic E.coli colonisation?

A
  1. Brain, neonatal meningitis E.coli (NMEC)
  2. Bloodstream, Uropathogenic E.coli (UPEC), neonatal meningitis E.coli (NMEC)
  3. Large bowel, Enterohaemorrhagic E.coli (EHEC), Enteroinvasive E.coli (EIEC), Enteroaggegrative E.coli (EAEC)
  4. Kidney, Uropathogenic E.coli (UPEC)
  5. Small bowel, Enteropathogenic E.coli (EPEC), Enterotoxigenic E.coli (ETEC), Diffusely adherent E.coli (DAEC), Enteroaggegrative E.coli (EAEC)
  6. Bladder, Uropathogenic E.coli (UPEC)
95
Q

What are some examples of the importance of horizontal gene transfer?

A

Virulence factors
- Plasmid encoded heat-liable enterotoxin of enterotoxigenic E.coli
- PAI encoding haemolysin, pili and cytotoxins
- Phage encoded dtxR gene from C.diptheriae

Transfer of antibiotic resistance in Gram-negative bacteria
- Beta-lactamases plasmid encoded
- Chromosomal encoded beta-lactamases

96
Q

What are promotor regions?

A

Non-coding regions in DNA required for gene transcription

96
Q

What is 5’UTR and what does it do?

A

5’UTR, or the 5’ untranslated region, is the region of a messenger RNA (mRNA) that is directly upstream from the initiation codon

The 5’UTR sequence has a critical role in the recruitment of ribosomes to mRNA as well as in many processes related to the mechanisms regulating translation

97
Q

What do promoters contain?

A

Conserved sequences that are recognised by RNA polymerase

98
Q

What is RNA polymerase holoenzyme and what does it do?

A

Consists of a core enzyme and a sigma factor
The RNA polymerase binds to gene promoters

99
Q

What is a sigma factor?

A

A protein that is needed for the initiation of transcription in bacteria.

It is a bacterial transcription initiation factor that enables specific binding of RNA polymerase to gene promoters.

100
Q

What are transcriptional repressors?

A

Regulatory proteins that have negative control on the promoter region, shutting down gene transcription

101
Q

What are transcriptional activators?

A

Regulatory proteins that have positive control on the promoter region, triggering gene transcription.

102
Q

Where do transcription factors bind?

A

To motifs within the DNA called operators, found on the 5’ end of the promoters

103
Q

How many genes can a single regulator regulate?

A

Several genes!

104
Q

What are virulence factors?

A
  • Factors required for host colonisation and damage
  • More than one virulence factor involved in pathogenesis
  • Often co-ordinately regulated
105
Q

What do environmental cues do to virulence factors? What are some examples of these environmental cues?

A

Environmental cues signal the entry into host tissues and induce the expression of virulence factors

These cues are:
- low iron
- temperature
- stress
- pH
- oxygen tension

106
Q

Describe the induction of toxins in low iron environment in Corynebacterium diphtheriae:

A
  • Corynebacterium diphtheriae is a gram-positive, rod-shaped aerobic bacteria
  • It is airborne and highly infectious
  • Has a range of severity, more severe associated with toxin production encoded by the top gene
  • Causes sore throat, fever, cough, and enlarged lymph nodes.
  • However there is a successful vaccination programme
107
Q

When is diphtheria toxin produced?

A

During the stationary phase and in iron-limiting conditions.

The Tox protein, encoded by tox gene, produces the A-B diphtheria toxin

108
Q

What are DtxR-like proteins in other pathogens?

A

As diphtheria toxin was discovered first, all of the similar proteins (toxins) in other bacteria species are called diphtheria toxin-like (DtxR-like) proteins.

Each species has its own name for it and they each have their own metal ion-related regulation of the genes.

E.g. Streptococcus mutans, SloR, Mn2+/Fe2+
Streptococcus pyogenes, MtsR, Mn2+/Fe2+
Staphylococcus aureus, MntR, Mn2+
Staphylococcus epidermidis, SirR, Fe2+
Mycobacterium tuberculosis, IdeR, Fe2+
Listeria monocytogenes, MntR, unknown
Clostridium botulinum, unnamed, unknown

109
Q

How many cells per ml of media at the end of exponential bacteria growth?

A

Around 100,000,000 cells per ml of media

110
Q

What is the chemical language of bacteria at high cell density?

A

Cell-to-cell communication
Chemical signals, small molecules or peptides, can be referred to as AIs (auto inducers)

111
Q

What is bacterial quorum sensing, at a low vs high cell density?

A

At a low cell density, the bacteria may be sending out AIs (signalling molecules) but not to a degree where it affects anything. This is an example of individual behaviours.

At a high cell density, the bacteria would be sending out many AIs (signalling molecules) which are at a high concentration and will begin to interact with the cells. This is an example of group behaviours.

Principles in Infectious Diseases (3 decks)

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