Pathogenesis Flashcards

1
Q

Colonization vs. infection

A

Colonization - without harming the body

Infection - microbes damage tissues (directly via proliferation or actions of virulence factors or by stimulating the immune response)

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2
Q

Possible outcomes of infection

A
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3
Q

Horizontal transmission

Pathogen transmission

A
  1. Inhalation
  2. Ingestion
  3. Wound
  4. Sex
  5. Blood-to-blood
  6. hand/hand, hand/eye, hand/mouth, or mouth/mouth
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4
Q

Vertical transmission

Pathogen transmission

A

Pathogens passed from mother to fetus or infant - can occur in utero (antenatal/prenatal) or in the days/weeks immediately before, during, or after birth (perinatal), or after birth (postnatal)

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5
Q

Arhtropod vectors

A

mosquitoes, ticks, fleas, and mites

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6
Q

Quorum sensing

A

Mechanisms microbes use to assess the density of the local cell population allowing them to coordinate virulence factor production

Important to biofilm formation becuase it regulates polysaccharide matrix production

QSM compounds: usually acylated homoserine lactones, peptides, or alcohols

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7
Q

A/B subunit toxins

A

B - binds to host cell surface

A - enters host cell and performs the action of the toxin

B binds
A has activity

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8
Q

Intracellular Pathogen Cytopathic effects (CPE)

A
  1. Cell lysis
  2. Vacuolation
  3. Inclusion body formation
  4. Cell fusion
  5. Parasitophorous vacuole (PV)
  6. Transformation
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9
Q

Botulinim toxin action

A

A/B subunit toxin

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10
Q

Cholera toxin action

A

A/B subunit toxin

B - binds to ganglioside GM1 on intestinal epithelial cells

A - enters cell and activates adenylate cyclase - increases cellular cAMP - results in the secretion of electrolytes and water into the intestinal lumen

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11
Q

Cytolethal distending toxins

A

A/B subunit toxin

Cause host cell DNA damage - cause senescence in immune cells, but also increases the possibility of cancer-causing mutations

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12
Q

Pore forming toxins

A

Hemolysins are one type of bacterial pore forming toxins - leak or lyse RBCs

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13
Q

Superantigens

A

Cause non-specific activation of T cells and professional antigen presenting cells which results in systemic release of inflammatory cytokines

i.e. S. aureus secretes a superantigen - causes toxic shock syndrome

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14
Q

What immune cells target intracellular pathogens

A

Cytotoxic T cells, neutrophils and NK cells

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15
Q

Pro-inflammatory mediators

A

Type I interferons (IFN-alpha/beta) and inflammatory cytokines (IL-6, IL-1beta, and TNF-alpha)

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16
Q

Systemic Inflammatory response syndrome (SIRS)

A

Systemic circulation of DAMPs/PAMPs results in cytokine storm and other mediators - in which disseminated intravascular coagulation and severe hypotension can lead to shock, ischemic tissue damage, multiorgan failure, and death

17
Q

How do pathogen virulence factors transform host cells?

A
  1. Inactivate the host cellular growth suppressors p53 and Rb
  2. Increase activity of host cell growth activators (hormones and cytokines)
  3. Inhibit apoptosis - pathogens inhibit p53 and/or other apoptosis pathway factors - or by inducing mutations in host genes encoding these regulatory proteins
  4. Producing genotoxins that damage host cell DNA, cause incomplete host cell chromosome segregation, or induce host epigenetic changes
  5. Increasing host cell oxidative stress
18
Q

Candida albicans

Normal flora distribution

A

Mouth, colon, vagina

19
Q

Methods of dissemination

A
  1. Direct spread between cells or tissues using virulence factors
  2. Transversion across epithelial barriers at sites of mucosal associated lymphoid tissues (MALT)
  3. Hematogenous spread in the bloodstream and/or lymphatics is most common mechanism for systemic dissemination
  4. Neuronal - some virsues
20
Q

What age pop. is there the strongest immune response?

A

Young adults

i.e. chicken pox can be life-threating in a young adult

21
Q

Direct spread of Listeria monocytogenes

A

Expresses a virulence protein at one end of the bacterial cell to stimulate polymerization of host cell actin. These “actin comet tails” push the bacteria through the cytoplasm into neighboring cells or the surrounding tissue

22
Q

Multi-nucleated giant cells

A

This type of cytopathic effect is typically observbed in host cells infected with enveloped viruses - VAPs/viral fusion proteins are inserted into the host cell plasma membrane

23
Q

Syncitium

Common cytopathic effect

A

Fused cells (multinucleated giant cells)

24
Q

Syncitium

Common cytopathic effect

A

Fused cells (multinucleated giant cells)

25
Q

Mechanisms by which pathogens can promote cancer

A
26
Q

Immune Mediated Tissue Damage in Response to Pathogen

A
  1. CD8+ CTL and NK cell killing of infected cells
  2. Molecular mimicry and autoimmunity
  3. Immune complex deposition
  4. Inflammatory mediators
27
Q

Host cell mimicry in S. pyogenes infection

A

IgG/IgM mad against M proteins (streptococcal cell wall proteins) are able to cross react with cardiac tissue - cause rheumatic fever

Activates complement proteins C3a and C5a