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BMS2052 MICRO > WEEK 2: MECHANISMS OF BACTERIAL PATHOGENESIS I & II > Flashcards

WEEK 2: MECHANISMS OF BACTERIAL PATHOGENESIS I & II Flashcards

1
Q

What % of bacteria are pathogenic?

A

Less than 5%

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2
Q

Can some types of bacteria have both pathogenic and non pathogenic strains?

A
  • YES

- e.g. E.coli and EPEC (enteropathogenic E.coli)

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3
Q

What is an opportunistic infection defined as and examples of when this can occur?

A
  • When there is a breakdown of the normal microbiota

- e.g. Antibiotic use, chemotherapy, burn trauma–> pseudomonas aeruginosa)

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4
Q

What are HAIs and some examples?

A
  • When the normal microbiota is transferred to (b/w) health COMPROMISED people
  • e.g. Surgical wound infection–> MRSA S.aureus (Mecithillin Resistant)
  • Bacterial pneumonia
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5
Q

What are 3 things that determine the nature and extent of damage between a pathogen and the host?

A
  1. Particular pathogen –> vibrio cholerae only infecting humans
  2. Particular Host –> Salmonella enterica (Typhoid in humans but nothing in mice)
  3. Host microbiota –> C. dificille
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6
Q

Why do pathogens cause disease in the context of commensal bacteria?

A
  • They express VIRULENCE DETERMINANTS not expressed by commensal organisms
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7
Q

What are 5 things that virulence factors mediate?

A
  • colonisation of de novo niches in body
  • Adhesion (ligands for host cell expressed proteins)
  • Invasion
  • Immune evasion mechanisms (capsules on bacteria)
  • tissue damage (toxins)
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8
Q

How do commensal bacteria become pathogens?

A
  • Bacterial virulence genes present on mobile genetic elements and ACQUIRED through horizontal gene transfer
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9
Q

What are the 3 main mechanisms that horizontal gene transfer occurs via to acquire mobile gene elements?

A
  • Plasmids (Conjugation)
  • Bacteriophages (Transduction)
  • Transposons (transformation)
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10
Q

What are pathogenicity islands a combination of?

A
  • Plasmids, bacteriophages, and transposons
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11
Q

What are 5 properties of virulence plasmids?

A
  • Circular, extrachromosomal
  • Self replicating
  • Found in Gram -ve and +ve bacteria
  • transmitted between bacteria by CONGUGATION
  • Encode VIRULENCE genes for invasion, toxins, drug resistance
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12
Q

What are 3 properties of bacteriohpages?

A
  • Bacterial viruses
  • Carry genes encoding toxins
  • Lysogenic (or can be lytic)
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13
Q

What are 3 examples of toxins that bacteriophages are involved with?

A
  • Diptheria
  • Cholera toxin A-5B
  • Shiga Toxin (Shigella)
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14
Q

What are transposons?

A
  • DNA segments capable of random integration

- Transferred on plasmids or bacteriophages

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15
Q

What are pathogenicity islands and some features?

A
  • Large areas of bacterial chromosome that are dedicated to virulence
  • Have a different G-C content to the host DNA (usually lower)
  • Discrete genetic units with defined boundaries (gained and lost ‘as a package’)
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16
Q

Are different PAIs present in different pathogens?

A
  • YES!

- These allow it to release different toxins

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17
Q

What do PAIs have systems for?

A
  • Allowing the bacteria to inject protein into host cell
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18
Q

When are virulence genes expressed?

A
  1. WHEN BACTERIA SENSE A SPECIFIC NICHE (Temperature, O2, lack of nutrients etc)
  2. IN RESPONSE TO POPULATION DENSITY
    - Quorum sensing (signalling through small organic molecules)
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19
Q

What is quorum sensing?

A
  • Tells the individual bacteria whether to turn genes on or off
  • Communication system that bacteria use
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20
Q

Which application is quorum sensing important in?

A
  • Biofilms
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21
Q

What were Koch’s postulates designed to establish?

A
  • Establish a causative relationship between microorganism and disease
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22
Q

What is Koch’s postulate 1? `

A
  • “The microbe must be present in every case of the disease (and absent from healthy hosts) “
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23
Q

What is Koch’s postulate 2?

A
  • “The microbe must be isolated from the diseased host and grown in pure culture”
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24
Q

What is Koch’s postulate 3?

A
  • ” The disease must (SHOULD ) be reproduced when the culture is introduced into the healthy (susceptible) host”
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25
Q

What is Koch’s postulate 4?

A
  • “The microbe must be recoverable from an experimentally infected host”
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26
Q

What is Koch’s 5th postulate that was developed later?

A
  • Effective therapeutic or preventive measure(s) should eliminate disease
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27
Q

Are Koch’s factors in use a lot now?-

A

NO!

- Not common use anymore because too many limitation

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28
Q

What is a demonstration of Koch’s postulates?

A
  • Helicobacter pylori isolation from Australians
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29
Q

What are the 5 limitations of Koch’s postulates?

A
  1. No host factors taken into account (carrier states or opportunistic infections)
  2. Emphasis on ability to culture the organism
  3. Organisms can lose virulence/pathogenicity during lab culture e.g. mycobacterium TB may lose lipids (i.e. virulence) in culture
  4. Disease may not require the organism to infect the host (e.g. toxins) BUT IS RARE–> botulinum -poorly processed food
  5. requires a suitable/susceptible animal model (e.g. Vibrio cholera only infects humans, not other animals)
30
Q

What are Koch’s UPDATED molecular postulates (1988)?(4)

A
  1. The ‘virulence’ gene is ALWAYS found in strains with a particular virulence phenotype
  2. The gene should be expressed in the host
  3. Mutation (inactivation) of that particular gene ABOLISHES (reduces) the virulence phenotype
  4. Reintroduction of the gene reconstitutes the virulence phenotype
31
Q

What are the 6 general steps that a pathogen must take to cause disease?

A
  1. Enter body
  2. Colonise the host
  3. Invade
  4. Evade HOST DEFENSES
  5. Multiply and disseminate
  6. Cause DAMAGE TO HOST
32
Q

Does colonisation = infection?

A
  • NOOOO!!!
33
Q

What is virulence determined by?

A
  • Adhesion
  • Penetration into cells
  • Antiphagocytic activity
  • Production of toxins
  • Interaction with the immune system
34
Q

What are genetic changes in bacteria due to?

A
  • Gain or loss of integrins
  • Pathogenicity islands
  • Transposons
  • Plasmids
35
Q

What is a virulence factor that H.pylori produces?

A
  • Urease
36
Q

What are three things that adhesion is mediated by?

A
  1. Pili and fimbriae
  2. Afimbrial adhesions
  3. Capsules
37
Q

What type of surface is the bacterial cell membrane in terms of adhesion mediated by capsules and why?

A
  • Sticky
  • To allow adhesion to each other like in biofilms
  • To allow adhesion to surfaces like teeth (plaque)
38
Q

Where can obligate intracellular pathogens multiply?

A
  • Inside the CELL
39
Q

What is bacterial invasion?

A

-Where bacteria invade cells that are not phagocytic

40
Q

What are the two forms of bacterial invasion?

A
  1. Into cells (INVASION) –> enteropathic E.coli

2. Through cells (TRANSCYTOSIS)

41
Q

What is bacterial invasion mediated by?

A
  • Bacterial INVASINS (virulence factors)
42
Q

What are the two TRIGGERS for bacterial invasion?

A
  • TRIGGER MECHANISM (bacterial trigger)

- ZIPPER MECHANISM ( cell surface receptor/ligand interactions)

43
Q

Which two things do both the zipper mechanism and the trigger mechanism result in from bacterial invasion?

A
  • Actin polymerisation and depolymerisation

- Pseudopod and membrane ruffle formation

44
Q

Which form of the bacterial triggers works from the outside in?

A
  • The zipper mechanism
45
Q

What is the example for the zipper mechanism for bacterial trigger to invasion?

A
  • Listeria Integrin A binds to + activates host cell E-cadherin
  • Yersinia OM invasin interacts with host cell Beta 1 integrins
  • Causes actin rearrangement in host cytoskeleton and internalisation
46
Q

Which form of the bacterial tirggers works from the inside out?

A
  • Trigger mechanism
47
Q

What is an example of the trigger mechanism for bacterial invasion?

A
  1. SALMONELLA spp and SHIGELLA sp
    T3SS–> Type 3 Secretion System –> changes Actin dynamics
    - Causes induction of membrane ruffling and closure after entry 1
  2. EPEC (enteropathic E.coli)
48
Q

What is the process of EPEC (enteropathic E.coli) using the trigger mechanism for invasion?

A
  • T3SS used for E.coli to ADHERE to + damage intestinal epithelial cells
  • T3SS INJECTS Tir
49
Q

What does Tir that T3SS injects in EPEC do bind and what does this cause?

A
  • Binds bacterial intimin

- Causes actin polymerisation and induction of pedestals

50
Q

How does having a capsule present allow a pathogen to avoid complement fixation?

A
  • It does not allow C3b to stick to surface (bind) because capsule is in way
    e. g. Haemophillus influenzae, Strep.phneuimoniae
51
Q

What are the three ways that a pathogen can avoid complement fixation?

A
  1. Having a capsule to prevent C3b from binding
  2. Secrete complement DEGRADING molecules which cleave complement –> S.puogenes –> C5a peptidase
  3. Bind Ig via Fc receptor –> NO ACTIVATION OF MAC –> Staphylococcal protein A
52
Q

What are the three broad ways that bacteria can evade phegocytes?

A
  • Avoid being recognised or or inhibit internalisation
  • Kill phagocyte/induce apoptosis (anti-phagocyte toxins)
  • Inhibition of phagolysosome (i.e. survive phagocytosis)
53
Q

What are 3 ways of avoiding being recognised or internalisation?

A
  1. Avoid Opsonisation (prevent C3b opsonisation or prevent Ig opsonisation)
  2. Form capsules to hide PAMPs (K.pnemoniae to hide LPS)
  3. Form biofilms
54
Q

What are the 4 ways that there can be inhibition of the lysosome?

A
  • Blocking fusion to lysosomes (Salmonella typhimurium. Mycobacterium)
  • Lyse phagosomal membrane –> escape into cytoplasm –> Shigella
  • block/be resistant to ACIDFICATION (Mycobacterium–> lives happily in phagosome)
  • Block assembly of NADPH oxidase
55
Q

Which part of the IgA molecule does the IgA protease cleave?

A
  • Hinge region
56
Q

What are the 5 ways bacteria can avoid eliciting or detection by Igs?

A
  1. Remain inside host cells
  2. Host mimicary
  3. Coat with host proteins
  4. Colonise sites with POOR access for Igs (or not accessed by APCs)
  5. Keep ahead of the immune system-antigenic variation
57
Q

What is the growth limiting micronutrient for bacteria?

A
  • IRON
58
Q

What is the main iron cheltor that pathogens use to obtain iron?

A
  • Siderophores
59
Q

What are 4 ways in which pathogens obtain iron despite being in a low iron environment?

A
  1. Secreting HIGH AFFINITY iron-chelators and having siderophore receptors to capture them
  2. Expressing high affintiy iron binding membrane proteins
  3. Expressing receptors for iron capture proteins like transferrin
  4. Expressing toxins like haemolysins to release host Fe
60
Q

In which two ways can INVASIVE bacteria cause damage to the host?

A
  • Extracellular enzymes that DAMAGE tissue

- Modulation of host immune responses

61
Q

What type of bacteria (invasive or non invasive) are bacterial toxins made?

A
  • NON INVASIVE
62
Q

What does DIRECT effect of bacterial toxins mean?

A
  • Secreted or cell associated bacterial toxins with a DIRECT cellular pathogenic consequence (action at the site of infection)
63
Q

What does INDIRECT effect of bacterial toxins mean?

A
  • Damage to the host caused by an EXAGGERATED IMMUNE RESPONSE - at a site or sites REMOTE to the toxin
64
Q

What is an example of a situation where the toxin is sufficient to produce the disease?-

A
  • Clostridium botulinum–> poorly preserved food
65
Q

Are exotoxins produced by BOTH gram positive and gram negative bacteria?

A
  • YES!
66
Q

In which 3 ways are Exotoxins characterised by?

A
  • They type of cell it damages (neurotoxin, cytotoxin)
  • The bacteria that produce them
  • Its pathogenic activity (enterotoxin–> enteric symptoms)
67
Q

What are the 3 types of protein exotoxins?

A
  • Membrane disrupting toxins (haemolysins)
  • A-B toxins
  • Super antigens (S.aureus toxic shock toxin)
68
Q

What are the two types of non protein heat stable exotoxins?

A
  • Glycopeptides

- Polyketides –> mycolactones –> cytotoxic and immunosuppressive

69
Q

What are the two types of membrane disrupting toxins>

A
  • Phospholipases

- Pore forming toxins

70
Q

What do subunit A and B do respectively inA-B exo toxins?

A
  • A has catalytic activity (potency) and B recognises membrane receptors and thus determines the cell specificity`
71
Q

What are the 4 types of A-B toxins?

A
  • Diptheria
  • Botulinum
  • Cholera toxin
  • Tetanus
72
Q

What do endo toxins do/what effect in general do they have on the body?-

A
  • Induce EXAGGERATED immune response –> LPS (Lipid A)

BMS2052 MICRO (10 decks)

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