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TCM (microbio) > Mechanisms of Microbial Pathogenesis > Flashcards

Mechanisms of Microbial Pathogenesis Flashcards

1
Q

Which are the endosomal located TLR?

A

TLR 3, 7, 8, 9

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2
Q

What does the PAMPs interact with initially on TLR?

A

PAMP interacts with the LRR (leucine-rich repeat regions) which will relay to the TIR domain to relay intracellular signaling.

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3
Q

Viruses will typically activate which TLR?

A
  • TLR 2, 4
  • TLR 9
  • TLR 3
  • TLR 7,8
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4
Q

Gram positive bacteria will activate which TLR?

A
  • DNA: TLR9
  • Lipopolysaccharides: TLR2
  • PG: TLR2
  • LTA: TLR 2
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5
Q

Gram-negative bacteria activate which TLR?

A
  • DNA: TLR 9
  • Porins: TLR2
  • PG: TLR2
  • LPS: TLR4
  • Flagellin: TLR5
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6
Q

Zymosan on fungi activate which receptors?

A

TLR 2

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7
Q

Mannan on fungi activate which receptors?

A

TLR 2,4

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8
Q

Beta-glycan on fungi activate which receptors?

A

TLR 2

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9
Q

Activation of the TLR leads to stimulation of what downstream products via which corresponding pathways?

A
  • TRIF pathway: to increase production of IFN and IFN inducible genes
  • MyD88 pathway: increases the production of inflammatory cytokines.
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10
Q

What are the 3 broad overview stages of Innate Immune system activation?

A
  1. Bacteria trigger macrophage to release cytokines/chemokines to direct inflammation.
  2. Vasodilation, permeability, and leukocytes/macrophages diapedesis.
  3. Inflammatory cells reach site and cause pain, temperature
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11
Q

What is the role of Commensal bacteria?

A
  • Commensal bacteria are introduced via vaginal birth passage.
  • Microbes still contain PAMPs but the host allows a certain level to maintain life.
  • This leads to colonization across the body.
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12
Q

What regulates the commensal bacteria from overgrowth?

A
  • Paneth cells detect the commensal bacteria.
  • Leads to activation of the MyD88 pathway, increasing components to remove the commensals and preventing them from overgrowing.
    • Lack of Paneth cells or MyD88 mutation
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13
Q

What is unique about opportunistic infections/pathogens?

A
  • These pathogens are most prevalent in immunocompromised individuals.
    • allows overgrowth and rapid replication.
    • thought to be facultative and obligate pathogens.
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14
Q

What are a few pathogens with opportunistic infectious activity?

A
  • Herpes
  • Bacterial pneumonia
  • Tuberculosis
  • Oral candidiasis
  • penumocystis pneumonia
  • cryptococcal meningitis.
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15
Q

Bacterial pathogens associated with persistent infections.

A
  • Mycobacterium tuberculosis
  • Treponema pallidum
  • Borrelia burgdorferi
  • E. coli
  • Enterococcus
  • Chlamydia
  • Mycoplasma
  • Psuedomonas aeruginosa
  • Helicobacter pylori
  • Staphylococcus, streptococcus, Brucells abortus
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16
Q

What is the pathology of latent/chronic infections?

A
  • Pathogen infects, and lays dormant within macrophages. Stress leads to increased inhibition of MHC II and allows re-emgergence.
    • downregulation of CIITA. transcription factor promoting MHCII expression.
    • allows the macrophage(infected) to avoid detention via Th4+ cells.
17
Q

What is the role of virulence factors?

A
  1. Help bacteria to invade the host.
  2. Help bacteria to casue disease.
  3. Help bacteria to evasde the host defenses.
18
Q

What is a list of common virulence factors?

A
  • Adherence factor
  • Invasion factor
  • Capsule
  • Endotoxin
  • Exotoxin
  • Siderophores.
19
Q

Adherence factor

A

Use of pili (fimbriae) to adhere to mucosal sites. Commonly found in GI bugs to assist against peristaltic motion.

20
Q

Invasion factors.

A
  • virulence factor
  • Membrane components taht allow bacterium to invade the host cells based on plasmids, or based on chromosomes.
21
Q

Endotoxins

A
  • Virulence factor common to Gram(-) bacteria.
    • Fever, blood pressure changes, inflammation, shock, toxic shock syndrome.
  • Lipopolysaccharide (lipid) based toxin.
22
Q

Capsules

A
  • Membrane protecting from phagocytosis/opsonization.
  • More difficult to detect and more likely to produce sepsis.
    • Common recurrent infections with splenectomy.
23
Q

Exotoxins

A
  • Protein based virulence factor of Gram (-)/(+) bacteria.
  • The most toxic type of poison of unit per weight.
    • clostridium, corynebacterium.
  • Induce more local and non-systemic effects.
24
Q

Siderophores

A
  • Competitive-Iron binding factors.
    • can compete for the host with hemoglobin, transferrin, lactoferrin availability.
25
Q

Describe the three types of processes that show where virulence factors are derived from.

A
  1. Virulence gene transfer:
    1. conjugation, transduction, transformation
  2. Viral Pass:
    1. bacteriophage introduces infectious genes into the host bacteria and promotes production of a toxin. Common in botulinism, diptheria.
  • virulence changes. can then lead to intestinal disease based on the changes.
26
Q

Which pathogens are associated with a purulent necrosis?

A
  • Klebsiella
  • Staphylococcus epidermidus/ aureus
  • Psuedomonas
  • Neutrophils enzymes lead to massive tissue destruction.
27
Q

Pathogens have to be able to sense their environmnent to detect survivability. What are the different categories of this?

A
  • Thermal dimorphism
  • Metabolism regulation
  • Neurotransmitter/auto-inducer detection
  • Intracellular replication.
28
Q

Thermal Dimorphism

A
  • 2 Phase pathogenic response. Allows pathogen to detect temperature and alter body type to adjust and thrive.
    • Blastomyces and histoplasmas.
  • Cold= mold/mycelle form
  • Heat+ yeast/proliferative form
29
Q

Perturbation of metabolism

A
  • Ability to detect meatbolite levels in a host. PPG synthase enzyme is able to detect level of FFA metabolism.
    • Seen in Legionarres’ Disease
30
Q

Neurotransmitter/autoinducer manipulation.

A
  • Sensors detecting Epi, Norepi levels.
  • Ability to activate virulence factors based on presence of these compounds.
  • Induces changes in gene expression to alter the host immune system defenses.
31
Q

Intracellular replication manipulation.

A
  • Methods are used to increase virulence, allowing bacteria to replicate within other immune cells.
  • Examples:
    • Brucella: able to replicate within a vacuole.
    • Toxoplasma gondi: encased in a network of lysosomes and host microtubules (inhibit ability of host defenses to reach, based on dense fibrous network).

TCM (microbio) (7 decks)

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