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Bacteriology Flashcards

1
Q

Why are two-component systems important for bacteria?

A

They are essential for monitoring changes in the environment and responding to them

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2
Q

Which two components constitute a two-component system?

A
  1. Sensor kinase
  2. Response regulator
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3
Q

Where are sensor kinases in two-component systems often located?

A

Cytoplasmic membrane

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4
Q

What is the function of the sensor kinase in two-component systems?

A

Detection of environmental signal, after which it autophosphorylates

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5
Q

Where are response regulators in two-component systems often located?

A

Cytoplasm

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6
Q

What is the function of response regulators in two-component systems?

A

DNA binding protein -> regulates gene transcription

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7
Q

True or false: a response regulator always has the same effect on the genes it regulates

A

False; response regulators can be inhibitory for one gene, whilst activating another

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8
Q

What are bacterial processes (partially) regulated by two-component systems? (5)

A
  1. Bacterial mobility
  2. Spore formation
  3. Regulation of metabolism
  4. Quorum sensing
  5. Stringent response
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9
Q

True or false: all bacteria are able of movement

A

False; some bacteria are immmobile

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10
Q

How will a bacterium move
1. When no attractant is present
2. When attractant is present
3. When repellent is present

A
  1. No attractant = random movement
  2. Attractant = targeted movement
  3. Repellent = targeted movement away
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11
Q

What drives (targeted) bacterial movement?

A

Presence of attractans/repellents

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12
Q

By which process can bacteria mostly find directionality?

A

Chemotaxis

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13
Q

In which way do chemotactic two-component system differ from others?

A

Don’t influence gene transcription, but rather modify existing proteins

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14
Q

What is the main protein that is modified when a chemotactic two-component system is activated?

A

Flagellin

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15
Q

Which forms of attraction can be identified in bacteria? (5)

A
  1. Chemotaxis
  2. Phototaxis
  3. Aerotaxis
  4. Osmotaxis
  5. Hydrotaxis
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16
Q

What are bacterial spores?

A

Survival structures to endure unfavourable growth conditions

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17
Q

Why are bacterial spores resistant to many environmental influences?

A

Dormant stage -> metabolic processes cannot be disrupted

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18
Q

To which factors are spores resistant? (3)

A
  1. Heat
  2. Harsh chemicals
  3. Radiation
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19
Q

How is spore formation in bacteria triggered?

A

Two-component systems detect unfavourable conditions and activate spore-forming genes

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20
Q

What is an additional advantage of spore formation to bacteria (in addition to survival)?

A

Easily dispersed via wind, water or (animal) guts

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21
Q

True or false: all bacteria are capable of spore formation

A

False; only ~20 genera of Gram+ bacteria are able to do so

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22
Q

How many genes are involved (approximately) in spore formation in bacteria?

A

~200

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23
Q

How does the presence of maltose start transcription of maltose-related genes?

A

Maltose activates maltose activator protein, which activates RNA polymerase on the mal promotor

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24
Q

What is catabolite repression?

A

A global control system in bacteria that controls the use of carbon sources if more than one is present

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25
Q

What are global control systems in bacteria?

A

System that regulates expression of many different genes simultaneously

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26
Q

Which carbon source do bacteria favour?

A

Glucose

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27
Q

What happens to bacteria in the presence of glucose?

A

‘Glucose-effect’ -> repression of lactose & maltose operons

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28
Q

Which system controls transcription in catabolite repression?

A

cAMP activates cAMP receptor protein (CRP), which blocks transcription maltose/lactose related genes

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29
Q

What is diauxic growth in bacteria?

A

Two exponential growth phases if two energy sources are available. Source one is used up first, after which the second source is used.

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30
Q

Why is there a delay between two growth phases in diauxic growth in bacteria?

A

Time necessary to transcribe genes needed to be able to consume another energy source

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31
Q

What is quorum sensing in bacteria?

A

A system by which bacteria assess population density

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32
Q

Why do bacteria use quorum sensing?

A

To ensure that a sufficient population density is reached before initiating certain responses

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33
Q

E. coli uses quorum sensing. Which toxin is upregulated when a quorum is reached?

A

O157:H17 shiga toxin

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34
Q

Which processes are activated in E. coli when a quorum is reached? (3)

A
  1. Bacterial motility
  2. Toxin production
  3. Production of lesion-forming proteins
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35
Q

E. coli uses human hormones as part of its quorum sensing. Which hormones, and why?

A

Adrenaline/noradrenaline & AHL AI-3

Presence of human hormones notifies the bacterium that it is located intracellularly

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36
Q

In which two ways can S. aureus use autoinducing peptide (AIP) in its quorum sensing?

A
  1. To gauge bacterial population density
  2. To gauge whether it is located intracellularly (intracellularly, concentration builds up)
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37
Q

Which processes are activated by AIP in S. aureus? (2)

A
  1. Damage to host cells
  2. Alteration of the host immune system
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38
Q

Why can quorum sensing disruptors be used as drugs?

A

Bacteria often express virulence genes when a quorum is reached -> this can be prevented by quorum sensing disruptors

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39
Q

What is a stringent response in bacteria?

A

Stress response that modifies bacterial metabolism based on surroundings

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40
Q

What is an example of a stringent response in E. coli?

A

Voiding of E. coli reduces nutrients -> initiates production of ppGpp

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41
Q

What is an example of a stringent response in Caulobacter?

A

Carbon/ammonia starvation triggers production of ppGpp -> increases motile cell formation, which may reach niches with more nutrients

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42
Q

What is an example of a stringent response in mycobacteria?

A

Hypoxic & phostphate-limited environment of the lung produces a population of dormant persisting cells, that are also resistant to antibiotics

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43
Q

What kind of response is the heat shock response in bacteria?

A

Global control network

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44
Q

True or false: the heat shock response is unique to bacteria

A

False; this response is widespread in all domains of life

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45
Q

What is the effect of the activation of the heat shock response?

A

Production of heat shock proteins, which counteract damage of denatured proteins and help cells recover from temperature stress

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46
Q

Which exposures induce a heat shock response? (3)

A
  1. Heat
  2. Ethanol
  3. UV-radiation
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47
Q

What is the main controller of heat shock responses in bacteria?

A

RpoH

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48
Q

What is the phosphate/pho regulon?

A

Global response network responding to evironmental phosphate concentrations

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49
Q

What is the RpoS regulon in bacteria?

A

Global response network that initiates a bacterial stress response

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50
Q

What is the role of RpoS in the RpoS regulon?

A

Master controller, controlling 400+ genes

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51
Q

Genes involved in which processes are activated by the RpoS regulon in bacteria? (4)

A
  1. Nutrient limitation
  2. Resistance to DNA damage
  3. Biofilm formation
  4. Responses to osmotic, oxidative & acidic stress
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52
Q

What kind of bacterium is S. pneumoniae?

A

Gram+ microaerophilic diplococcoid bacterium

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53
Q

In how many % of children & adults is S. pneumoniae present asymptomatically?

A

Children: 27-65%
Adults: <10%

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54
Q

How does S. pneumoniae spread?

A

Shedding of mucus

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55
Q

Which areas of the body can S. pneumoniae invade?

A
  1. Lungs -> pneumonia
  2. Bloodstream -> bacteriaemia/meningitis
  3. Local invasion -> otitis media
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56
Q

How does S. pneumoniae reach the bloodstream?

A

Often times after invasion of the lungs

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57
Q

Why does S. pneumoniae have a so-called U-shaped curve?

A

Incidence is highest in young children & elderly

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58
Q

In which population does S. pneumoniae mainly cause mortality?

A

Elderly

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59
Q

Is the epidemiology of S. pneumoniae the same in the whole world?

A

Unknown; limited data from developing countries, epidemiology could be different

60
Q

What is a common co-infection that often occurs with S. pneumoniae?

61
Q

Why does the epidemiology of influenza influence the epidemiology of S. pneumoniae?

A

Influenza infection predisposes for S. pneumoniae -> increased incidence of S. pneumoniae in case of high incidence of influenza

62
Q

Why does influenza predispose to S. pneumoniae infection? (4)

A
  1. Epithelial cell damage
  2. Decreased mucociliary velocity
  3. Reduced CCL2 expression
  4. Reduced macrophage functionality
63
Q

From which sources can S. pneumoniae be diagnosed? (4)

A
  1. URT
  2. Blood
  3. Sputum
  4. CSF
64
Q

What are characteristics of S. pneumoniae cultures? (5)

A
  1. Alpha-hemolytic
  2. Shiny colonies
  3. Autolytic changes -> depressed centra of bacterial colonies
  4. Optochin susceptible
  5. Bile solubility test
65
Q

How does bile solubility differentiate S. pneumoniae from other streptococci?

A

S. pneumoniae are bile soluble, whilst other streptococci are not

66
Q

Which other modalities (in addition to culture) can be used to diagnose S. pneumoniae? (2)

A
  1. PCR
  2. MALDI-TOF
67
Q

What does the Griffith experiment show? What can be concluded from that?

A

Bacterial transformation
Shows:
1. Bacteria can transfer DNA
2. Capsules are an important virulence factor
3. Pneumococci are adept at picking up genetic material from their surrounding

68
Q

How many serotypes of pneumococcal capsules have been identified?

69
Q

Why is the bacterial capsule a virulence factor for S. pneumoniae? (2)

A
  1. Resistance to phagocytosis
  2. Hides surface structures that lead to pathogen recognition
70
Q

Which two pathways are involved in the synthesis of capsules? Which serotypes are produced by each pathways?

A
  1. Synthase pathway -> serotypes 3 & 37
  2. Wzx/Wzy-dependent pathway -> all other serotypes
71
Q

How are capsule serotypes 3 & 37 bound to S. pneumoniae bacteria?

A

Capsule is bound to membrane

72
Q

How are all capsule types (not 3 & 37) bound to S. pneumoniae bacteria?

A

Bound to peptidoglycan

73
Q

True or false: bacterial capsules are genetically determined and cannot be influenced by surroundings

A

False; bacteria can adapt their capsule properties & thickness depending on surroundings

74
Q

Which two parts can be identified in the genome of S. pneumoniae?

A
  1. Core genome = conserved part
  2. Accesory genome
75
Q

Which two techniques are there to determine genetic variation in bacteria? (2)

A
  1. Multi locus sequence typing
  2. Whole genome sequencing
76
Q

How can S. pneumoniae obtain accesory genes?

A

Horizontal gene transfer

77
Q

What does ‘competence’ in bacteria mean?

A

Able to transfer genetic information based on environmental signals

78
Q

Which environmental factors induce horizontal gene transfer in bacteria?

A
  1. High cell density
  2. Stress
79
Q

Which characteristics of the URT favour natural transformation of S. pneumoniae? (2)

A
  1. Lower temperature
  2. Nutritionally challenging
80
Q

What is the regular treatment of S. pneumoniae?

A

Penicillin

81
Q

Pneumococci often contain a lot of ABC-transporters in their membrane. What are they, and what is their function?

A

ABC-transporter = ATP-binding casette transporters

Essential for niche adaptation through nutrient transport

82
Q

What is pneumolysin?

A

Toxin produced by pneumococci

83
Q

Which toxin do pneumococci produce?

A

Pneumolysin

84
Q

What is the effect of pneumolysin?

A

Makes a pore in the cell membrane -> damages epithelium

85
Q

What is the immunologically beneficial effect of pneumolysin?

A

Induces immune response, leading to faster clearance and decreased transmission of pneumococci

86
Q

In which age group are pneumococcal colonization rates highest?

87
Q

Which two different stages can be identified in the establishment of colonization by pneumococci? What happens during each of these stages?

A
  1. Adherence -> expression of adherence factors & reduction of capsule thickness
  2. Persistence -> increased capsule thickness
88
Q

Production of pneumolysin leads to [higher/lower] shedding of pneumococci

89
Q

Capsule type [does/doesn’t] influence pneumococcal shedding

A

Capsule type does influence pneumococcal shedding

90
Q

What is the effect of IgG on pneumococci?

A

Agglutination of bacteria, decreasing shedding

91
Q

What is the effect of IgA on pneumococci?

A

Cleaved by pneumococcal IgA protease -> does not affect pneumococci

92
Q

What is the effect of viral co-infection on pneumococcal shedding? (2)

A
  1. Increased bacterial load
  2. Mucus production
93
Q

Why is invasive disease unfavourable for pneumococci?

A

Dead-end road -> no effective transmission

94
Q

What are the three main reasons why S. pneumoniae is a prevalent cause of disease? (3)

A
  1. High carriage rates
  2. Genetic adaptability
  3. Ability to shift from commensal to pathogenic within its host
95
Q

What type of vaccines were the first pneumococcal vaccines?

A

Whole cell vaccines

96
Q

Which two types of pneumoccoccal vaccines are currently used?

A
  1. Polysaccharide vaccines
  2. Conjugate vaccines
97
Q

What is the main polysaccharide vaccine against S. pneumoniae?

98
Q

What do pneumococcal polysaccharide vaccines contain?

A

Polysaccharides of 23 most prominent serotypes

99
Q

What is the downside of using polysaccharides in vaccines?

A

They are sugar structures -> cannot be presented to T-cells in MHCII, leading to a less effective immune response

100
Q

In which population are pneumococcal polysaccharide vaccines mostly used?

101
Q

Why are polysaccharide vaccines not effective in children <2 years?

A

B-cells are immature -> incapable of mounting immune response to these vaccines

102
Q

What do pneumococcal conjugate vaccines contain?

A

10/13/23 purified capsular polysaccharides, conjugated to carrier proteins that activate an immune response

103
Q

Which carrier proteins are used in pneumococcal conjugate vaccines? (3)

A
  1. Diphteria toxoid
  2. Tetanus toxoid
  3. H. influenzae protein 3
104
Q

What is PPV23?

A

A 23-valent pneumococcal conjugate vaccine

105
Q

Which adjuvant does PPV23 contain? What is its effect?

A

Aluminium phosphate -> activates Th2-response -> increased antibody responses by B-cell stimulation

106
Q

How can polysaccharide-only vaccines still induce an immune response?

A

T-cell independent B-cell activation by crosslinking of BCR

107
Q

What are the disadvantages of the T-cell independent activation of B-cells by polysaccharide-only vaccines? (3)

A
  1. Weak/no induction of memory B-cells
  2. Only IgM production -> not a very strong response
  3. No somatic hypermutation -> no affinity maturation
108
Q

How do conjugate vaccines induce an immune response? (3)

A
  1. B-cells get stimulated by polysaccharides and internalize them
  2. Conjugated carrier proteins are broken down and presented in MHCII by B-cells, activating Th-cells
  3. Th-cells provide B-cell stimulation
109
Q

What is the beneficial effect of the presence of T-cell help in conjugate vaccines? (3)

A
  1. Memory formation
  2. Class switch recombination
  3. Somatic hypermutation
110
Q

What is a ‘correlate of protection’?

A

Threshold of antibody that is considered sufficient for protection

111
Q

What is the main mechanism of protection against pneumococci after vaccination?

A

Osonophagocytosis

112
Q

What are important limitations of current pneumococcal vaccines? (3)

A
  1. Protection against a limited number of serotypes
  2. Designed based on prevalence in US/EU
  3. Expensive and complex to develop/manufacture
113
Q

Current pneumococcal vaccines cover the serotypes responsible for the highest morbidity. Why is it still disadvantageous that they don’t cover all serotypes?

A

Vaccine serotypes are replaced by serotypes not covered by the vaccine

114
Q

Why is it a disadvantage of current pneumococcal vaccines that they are designed based on prevalence in EU/US?

A

Suboptimal constitution to protect against prominent serotypes in other parts of the world

115
Q

What are important requirements of new pneumococcal vaccines? (4)

A
  1. Broadly protective, no serotype dependency
  2. Afforable
  3. Targeted at infants & elderly
  4. Reduces carriage and not only transmission
116
Q

What are the two routes of administration of pneumococcal vaccines?

A
  1. Parenteral
  2. Mucosal
117
Q

Which two types of mucosal vaccines can be used against pneumococci?

A
  1. Intranasal
  2. Oral
118
Q

What are the advantages of using mucosal vaccines against pneumococci?

A

Activates MALT, leading to local and systemic immunity

119
Q

Which are the two main immunological systems protecting against pneumococci?

A
  1. Antibodies
  2. Th17 immunity
120
Q

What are the functions of antibodies in the defence against S. pneumoniae? (3) Which types
of antibodies are involved?

A
  1. Opsonophagocytosis: IgG, IgA, complement
  2. Blocking interaction with epithelium: IgA
  3. Agglutination: IgG
121
Q

How does IgG from the circulation reach pneumococci in mucosal surfaces?

A

Transcytosis by FcRs

122
Q

Why are Th17-cells involved in defence against pneumococci?

A

Th17-cells are involved in defence against extracellular pathogens

123
Q

What is the main effector mechanism of Th17-cells in pneumococcal infection?

A

Production of IL-17A

124
Q

What is the effect of IL-17 secreted by Th17-cells in pneumococcal infection? (3)

A
  1. Production of AMPs
  2. Recruitment of neutrophils
  3. Production of IgA
125
Q

What are the advantages of using outer membrane vesicles in pneumococcal vaccines? (2)

A
  1. DCs recognize both the antigen and the structure they are presented in -> vesicles induce a stronger response than loose antigens
  2. OMVs contain PAMPs and can display surface antigens -> act as a combination of antigen & adjuvant
126
Q

What are outer membrane vesicles?

A

Bacterial extracellular vesicles

127
Q

What is the difficulty of using OMVs in pneumococcal vaccines? How can this be overcome?

A

OMVs induce a strong immune response due to high immunogenicity of LPS -> causes severe side effects

Can be overcome by detoxification of LPS

128
Q

Which pneumococcal antigens are currently being investigated for use in pneumococcal vaccines? Why are they advantageous over polysaccharides?

A

Pneumocccal protein antigens -> more conserved than polysaccharides

129
Q

How are pneumococcal protein antigens discovered?

A

Bacteria are cultured under conditions similar to the URT, causing them to express proteins that can be targeted

130
Q

How many % of nosocomial infections is caused by S. aureus?

131
Q

How many % of bacteriaemia is caused by S. aureus?

132
Q

What are possible virulence factors of S. aureus? (4)

A
  1. Panton-Valentin leucocidin (PVL)
  2. TSST
  3. Exfoliative toxins
  4. Enterotoxins
133
Q

What is the danger of enterotoxins?

A

Can act as superantigens, causing toxic shock syndrome

134
Q

Which two main antibiotic-resistant forms of S. aureus can be identified?

A
  1. MRSA = methyicillin-resistant S. aureus
  2. VRSA = vancomycin-resistant S. aureus
135
Q

True or false: MRSA only occurs in hospitals

A

False; there is now community-acquired MRSA

136
Q

True or false: VRSA only occurs in hospitals

137
Q

True or false: nasal carriers of S. aureus also have a higher carriage rate on the rest of their body

138
Q

What is the age distribution pattern of nasal S. aureus colonization?

A

Very young children = high colonization, colonization rates decline as children age, but increase between 10-30 years old, and again decrease after 40 years of age

139
Q

Which part of the nose is mostly colonized by S. aureus?

A

Vestibulum nasi -> border between skin and nose

140
Q

How many % of people is S. aureus persistent/intermittent/non-carrier?

A

Persistent: 15-20%
Intermittent: 30-45%
Non-carriers: 40-50%

141
Q

True or false: persistent S. aureus carriers often carry multiple strains

A

False; 98% of permanent nasal carriers only carry 1 strain

142
Q

What are host factors that influence S. aureus colonization? (4)

A
  1. Fasting glucose levels -> higher = higher colonization
  2. Smoking -> decreases carriage rate
  3. Ethnicity -> differences between groups
  4. Intranasal production of AMPs
143
Q

Which pathogen factors influence S. aureus colonization? (3)

A
  1. Local immunosuppression by S. aureus
  2. SpA levels -> positively correlated with carriage duration
  3. Clumping factor B
144
Q

What is SpA?

A

Staphylococcal protein A; associated with carriage of S. aureus

145
Q

How can bacterial interference influence S. aureus colonization?

A

Competition with other bacterial species can reduce S. aureus carriage

146
Q

With which bacterial species does S. aureus often compete in the nose? (2)

A
  1. S. pneumoniae
  2. S. epidermidis

I&I WC1 (20 decks)

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