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MSc Sommer 2021 > Pathogenicity of Organisms > Flashcards

Pathogenicity of Organisms Flashcards

1
Q

What are characteristics of pathogenic bacteria?

A

x

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2
Q

Describe the typical process of infection.

A

x

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3
Q

What are mobile genetic elements?

A

X

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4
Q

In which processes are mobile genetic elements involved?

A

x

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5
Q

What is the mode of action of the Cholera toxin?

A

x

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6
Q

How do novel pathogens develop, and why can they affect humans?

A

x

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7
Q

What was Louis Pasteur’s swan neck flask experiment?

What was the hypothesis?

What was the outcome?

A

spontaneous generation

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8
Q

Which are Koch’s postulates in teh germ theory of diseases?

A

x

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9
Q

Why is the determination of the complete genome seq of a pathogen important?

A

x

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10
Q

What can be learned from the genome sequence (of a pathogen)?

A

x

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11
Q

Which factors favor the appearance and spread of infectious diseases?

A

x

global spread

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12
Q

Name 5 organs/systems and typical pathogens infecting each.

A
  1. x
  2. x
  3. x
  4. x
  5. x
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13
Q

Which bacteria can be involved in a low-infectious dose infection?

A

just for fun

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14
Q

What is the size of a typical bacterium such as E. coli

A

good to know

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15
Q

Which infections do not fulfill Koch’s postulates?

A

which postulates?

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16
Q

What are insertion elements / IS?

A

x

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17
Q

What are possible reasons for the recent increase in the incidence of B pertussis infections?

A

x

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18
Q

Which are the major antigens used in modern acellular vaccines against whooping cough?

A

x

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19
Q

Why is whooping cough frequently not diagnosed early enough for antibiotics therapy?

A

Because the early phase shows only non-specific sx

what are the phases and symptoms

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20
Q

Describe the major properties of the adenylate cyclase toxin of B pertussis.

A

x

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21
Q

Describe the chemical composition of the tracheal cytotoxin of B pertussis and its presumed role in virulence.

A

x

22
Q

Which cell type is the major target for adhesion and colonization by B pertussis?

A

?

23
Q

Briefly describe how expression of most virulence genes is regulated in B pertussis.

A

x

24
Q

Which groups of genes can be classified according to their BvgAS mediated expression pattern?

Provide examples for each group.

A

*

25
Q

Compare briefly some important genomic properties of the classical Bordetellae.

A
26
Q

Denominate 3 Bordetella species pathogenic for animals and which animals are infected by them.

A
  1. B. pertussis
    • humans
  2. B. parapertussis
    • humans
    • pigs??
  3. B. bronchiseptica
    • cows
    • pigs
    • don’t remember
27
Q

What group does H. pylori belong to and what is one other member of this group?

A
  • Epsilonproteobacterium
  • look it up
28
Q

Physical characteristics of H. pylori:

A
  • gram-negative
  • spiral shaped
  • etc
29
Q

Name several H. pylori virulence and colonization factors and their mechanisms.

A
  1. Urease enzyme
    1. buffers acidic pH of the human stomach
  2. Cag pathogenicity island
    1. with T4SS and CagA effector - what do they do?
  3. Multifunctional VacA toxin
    1. what does it do?
  4. Motility is crucial for colonization
  5. High genetic diversity among strains contributes to host adaptation
30
Q

Colonization/infection features of H. pylori (not sx).

A
  • human specific
  • mainly extracellular
  • thrives in stomach mucus layer
  • colonizes human stomach
31
Q

What is the prevalence of H. pylori?

A

Widespread, worldwide, about 50% of the world’s population

32
Q

What disease(s) is/are caused by H. pylori?

A
  • gastritis
  • ulcers
  • gastric cancer - class I carcinogen
33
Q

Why is H. pylori so versatile in adapting to its human host?

A
  • high genetic diversity among strains
  • different people harbor different strains
  • the same person may harbor different strains within varying areas of the stomach
34
Q

How is C. jejuni spread/contracted?

A

food-borne, etc

zoonotic pathogen - commensal in chicken vs pathogen in humans

35
Q

What mediates virulence and causes disease in C. jejuni?

A

x

36
Q

What are some challenges in treating C. jejuni?

A

increasing abx resistance

gaps in knowledge about basic aspects of molecular biology and pathogenicity

37
Q

How closely is C. jejuni related to other enteropathogens such as Salmonella, Shigella, Vibro, Listeria?

A

only distantly related

has disting virulence mechanisms

38
Q

Name 4 antifungal drug classes and their targets.

A
  • Cell wall synthesis - Echinochandins
  • Membrane functions – Polyene drugs
  • Ergesterol biosynthesis – Azoles
  • RNA and DNA synthesis - Flucytosine
39
Q

What is the mechanism of action of Flucytosine (5FC)?

A
  1. 5FC is taken up by the cell via cytosine permease
  2. it is deaminated, then phosphorylated to become 5FUMP
  3. then incorporated into RNA which is toxic to the cells
  4. 5FUMP also converts to 5dUMP and irreversibly inhibits DNA synthesis
40
Q

What is the Amphotericin B mechanism of action?

A

drug class: polyene

binds to ergosterol

  • Sequesters ergosterol in fungal membranes and impairs membrane function
  • Forms pores in membranes, causing cellular leakage
41
Q

How do fungi become resistant to Polyenes?

A
  • Alterations in sterol biosynthesis – decreased ergosterol content
42
Q

What is Echinocandins mechanism of action?

A
  • Inhibit β-1,3-glucan synthase which synthesizes the major cell wall component β-1,3 glucan from UDP-glucose
43
Q

How do fungi become resistant to Echinocandins?

A
  • They acquire mutations in B-1,3-glucan synthase that abolish drug binding
44
Q

What is Azoles mechanism of action?

A
  • Inhibit ergosterol biosynthesis by targeting Sterol 14α-demethylase which converts lanosterol to ergosterol
  • -> ergosterol depletion, toxic lanosterol accumulation
  • -> inhibits growth
45
Q

How do fungi become resistant to Azoles?

A
  • Mutations in target enzyme -> reduced drug binding
  • Overexpression of ERG11 gene -> increases amount of enzyme
  • Overexpression of genes for efflux pumps -> reduces intracellular drug concentration
46
Q

How do fungi become resistant to Flucytosine?

A
  • mutations in cytosine permease to prevent transport into cell
  • inhibition of intracellular conversion of 5FUMP
47
Q

What is the significance of the opaque form of C. albicans?

A

It is the sexual form of C. albicans.

It is not an invasive form.

Neutrophils ignore it for the most part.

It is homozygous for either MTLa or MTLα.

48
Q

Name several clinically important pathogenic fungi.

A
  • Dermatophytes - cutaneous mycoses
    • Trichophyton, Epidermophyton, Microsporum
  • Dimorphic fungi - systemic mycoses
    • Blastomyces
    • Histoplasma capsulatum
    • Coccidioides immitus
    • Paracoccidioides
  • Opportunistic fungi
    • A. fumigatus
    • C. neoformans/gattii
    • C. albicans, auris, tropicalis, glabratta, parapsilosis
49
Q

Name several virulence traits of Candida

A
  • adherence to host tissues
  • biofilm formation
  • iron uptake mechanisms
  • hyphal growth
  • white-opaque phenotypic switching
50
Q

Describe Candida reductive iron uptake.

A
  • reductive iron uptake – reduces Fe3+ to soluble Fe2+ by iron reductase
  • reoxidation by a multicopper ferroxidase, internalization by a high-affinity Fe3+ permease
52
Q

Describe Candida adherance and biofilm virulence mechanisms.

A
  • adherence to host tissues mediated by lectin-like adhesins or protein-protein interactions or transglutaminase-mediated covalent linkages with host proteins
  • biofilm formation – via adhesins, causes resistance and are source of disseminated infections
  • hyphal growth -> invasion of tissues, host cell damage by toxins, escape from macrophages, biofilm formation
53
Q

How do genomic alterations facilitate the evolution of better adapted variants in the pathogenic yeast Candida albicans?

A
  • Overexpression of mutated homozygous alleles
    • Mrr1 tr. factor controls expression of MDR1 gene - efflux pump
    • Tac1 tr. factor for CDR1/CDR2 gene – efflux pump
    • Upc2 tr. factor for ERG11 – drug target enzyme
  • Gain of function mutations, loss of chromosomes, and genomic rearrangements
  • The MTL is on same arm of Chr5 with TAC1 and ERG11; loss of homozygocity for TAC1 or ERG11 may also result in homozygous MTLa or MTLα, -> switching to mating-competent opaque state.

MSc Sommer 2021 (3 decks)

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