Pathogenesis Fundamentals Flashcards

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1
Q

In what ways can infectious disease be transmitted?

A

Respiratory, contact, faecal-oral, sexual, injection

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2
Q

What types of infectious agents are there?

A

Prions, viruses, bacteria, fungi, parasites

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3
Q

How do gram positive and gram negative cell walls differ?

A

Gram Positive

  • Thick peptidoglycan
  • Cell wall has teichoic acids o Lipid and protein inner membrane
  • Resistant to drying

Gram Negative

  • Thin peptidoglycan
  • Outer membrane with lipopolysaccharide
  • Porin proteins for transport (OM)
  • Periplasmic space
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4
Q

What are characteristics of viruses?

A

Replicate in host, ss or ds RNA or DNA, protein coat protects nucleic acid

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5
Q

What are the steps in viral replication?

A

• 1. Attachment

  1. Penetration
  2. Uncoating
  3. Early mRNA transcription
  4. Early protein translation
  5. Viral DNA replication
  6. Late mRNA transcription
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6
Q

How are opportunistic pathogens different to other pathogens?

A

They cause disease when defence mechanisms are compromised

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7
Q

How are virulent and avirulent organisms different?

A

• Virulent is most likely cause of disease, avirulent doesn’t cause disease in host with normal immune system

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8
Q

What are some features of normal microbiota?

A
  • Colonise host without causing disease
  • Specific and sustainable association with host
  • May become pathogenic if moved
  • Protect host against disease
  • Transient or permanent
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9
Q

What processes occur during infectious disease?

A

• Colonisation, penetration, replication, damage and disease, dissemination(maybe), immunity (maybe)

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10
Q

What processes are involved in the asymptomatic phase?The symptomatic phase?

A
  • Colonisation, penetration, replication
  • Symptomatic = Damage and disease, dissemination(maybe), immunity (maybe)
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11
Q

What are the two types of ligands used by bacteria to colonise/adhere hosts?

A

Fimbrial and non-fimbrial

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12
Q

What are the functions of pilli?

A

• Conjugation and adhesion

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13
Q

How does Uropathogenic E.coli colonise a host?

A
  • Attaches to receptors on bladder epithelia cells using type 1 pilli or P fimbriae
  • Bacteria internalise, allowed to replicate to high levels
  • Avoid being flushed out with urine
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14
Q

What do bacteria use to colonise a host using non-fimbrial adhesion?

A
  • Use molecules in call wall
  • Can use glycocalyx (polysaccharide capsule or slime layer)
  • Can adhere in a biofilm
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15
Q

What are differences between capsules and slime layers?

A
  • Capsules have strong adherence to cell envelope, help aid evasion of innate immune system (cover PAMPs)
  • Slime layers are loose, unorganised and easily removed
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16
Q

How can a pathogen penetrate epithelial cells?

A
  • Penetrate into cells
  • Penetrate between cells and into tissue
17
Q

What processes are used for penetration directly into cells?

A
  • Take advantage of Receptor Mediated endocytosis (RME)
  • Use invasion ligands
    • Bind receptor for cytoskeleton, directly induce penetration
    • Molecular interaction are adhesion causes penetration
18
Q

How do pathogens penetrate tissue and between cells?

A

• Penetration causes morphological change, change tight junctions, allow entry

19
Q

How can microorganism replicate within epithelial cells?

A

• Grow in endosome (RME) • Grow in cytoplasm

20
Q

What are the pros/cons of each method?

A
  • Endosome, less nutrients but better protection
  • Cytoplasm, more nutrient, but less protection
21
Q

Why is quorum sensing important?

A

• Signals can control expression of genes for replication, biofilm production, virulence factors

22
Q

What features of the host immune system must microorganisms avoid and how?

A
  • Physical barriers (surgery, trauma)
  • Complement (enzymes destroy C’)
  • Phagocytes (capsules, inhibit phagosome-lysosome function, escape phagolysosome, resist contents of lysosome, kill phagocyte)
  • Antibodies (enzyme destruction, coat in self-antigen) • APCs (down regulate MHC)
  • T cells (cytokines, CTL, impair T cells)
23
Q

In what ways can microorganisms damage cells?

A

• Exotoxins, endotoxins, immunopathology

24
Q

What are some features of exotoxins and endotoxins and how do they differ?

A

Exotoxins

  • G+ and G-
  • Secreted
  • Action depends on target molecule
  • Cytotoxic = cell death
  • Cytotonic = change cell function

Endotoxins

  • G-
  • Not secreted, part of cell wall
  • Lipopolysaccharides
    • Predominantly produced when G- cells die
    • Trigger alternate complement cascade
    • Trigger clotting cascade
    • Bind/activate macrophages and neutrophils
    • Activated macrophages release cytokines, enzymes etc.
25
Q

In what ways can dissemination occur?

A
  • By the organism (make enzymes that destroy cells or intercellular matrices)
  • By body systems (blood, neuronal)
26
Q

How can infection be avoided?

A
  • Maintain intact surfaces
  • Maintain innate immune system (keep good health)
  • Improve acquired immunity (vaccines)
  • Reduce virulence of organism (antitoxins)
  • Reduce number of organisms (aseptic technique, remove biofilms)
27
Q

What are the kinds of capsid symmetry and how are they different?

A

Icosahedral

  • Made of capsomers
  • Enveloped or non-enveloped viruses

Helical

  • Encloses genome in modified cell membrane envelope
  • Enveloped viruses
28
Q

How are +sense and –sense RNA different?

A

+ sense o Same as mRNA

  • Can produce polymerase when first entering cell
  • Can use genome as mRNA

– sense

  • Template for mRNA
  • Need to carry enzyme in virion
  • Use genome as template to make mRNA
29
Q

What is the most important thing that determines whether a virus can enter a cell?

A

• Receptors on host cells that match receptor binding proteins on the virus

30
Q

In what ways can a virus enter a cell?

A
  • Direct fusion with PM
  • Receptor mediated endocytosis followed by the virus fusing out of the endosome or the endosome lysing
31
Q

How do DNA and RNA viruses differ in the replication enzymes they use?

A

DNA viruses

  • Use host DdDp
  • Replicate in nucleus

RNA viruses

  • Must encode an RdRp (not present in host cell)
  • Retrovirus needs RdDp
32
Q

How do enveloped viruses exit a cell?

A
  • Particles are assembled at the PM during budding and the virus buds away from the cell
  • Virus may first bud into ER/Golgi then be transported
  • Envelope originates from host cell
33
Q

How do Non-enveloped viruses exit a cell?

A

• Build up in cell and released when cell lyses

34
Q

What are some defences against viral infection?

A

• Physical, cytokines, innate cells, adaptive immune system, adaptive immune cell products

35
Q

How can viruses evade host defences?

A

• Latency, mutation, production of specific immune blocking proteins

36
Q

What determines whether an infection is local or systematic?

A
  • Receptor availability
  • Host enzyme availability (replication)
  • Temperature
  • Ability to replicate in macrophages and lymphocytes
37
Q

What are the stages of viremia?

A
  • Small amounts of virus first enter blood from lymph nodes = primary viremia
  • Virus replicates in liver/spleen/blood vessel walls
  • Virus then release back into blood after replication = secondary viremia
38
Q

How does the Varicella-zoster virus (chickenpox) spread?

A
    1. URT infection
    1. Lymph node replication
    1. Primary viremia
    1. Replication in liver and spleen
    1. Secondary viremia
    1. Infection of skin and rash
    1. Virus can travel to sensory nerve to dorsal root ganglion and stay latent (shingles if travels back to skin)
39
Q

What are the outcomes of viral infection?

A
  • Fatal
  • Full recovery
  • Recovery but permanent damage
  • Persistent infection