Bacterial Pathogenesis Flashcards

1
Q

how do pathogens evade our bodily restriction of them

A

they adhere/invade host tissues, secrete toxins/effectors, steal nutrients from host, subvert, evade and counteract immune defenses

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2
Q

what do primary pathogens do / what do opportunisitc pathogens do

A

cause disease in healthy hosts - will get sick every time (example Shigella flexneri) / cause disease only in compromised hosts or following entry into unprotected sites (example lysteria)

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3
Q

how did Koch identify his postulates

A

you can isolate a bacteria from a diseased organism, regrow that bacteria in medium, reintroduce the bacteria into an organism, and be able to isolate the same bacteria again

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4
Q

what are molecular koch’s postulates

A
  1. the phenotype under study should be found in pathogenic strains of a species 2. inactivation of virulence genes should be associated with a decrease in pathogenesis 3. replacement of inactivated gene should restore pathogenicity
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5
Q

what are virulence factors

A

what pathogens use to meet requirements of infection cycle - include toxins, attachement proteins, capsules, and other devices

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6
Q

where are most virulence genes in bacterial pathogens found / where do pathogenicity islands appear

A

some reside on plasmids or in phage genomes - often clustered into pathogenicity islands that encode virulence functions / appear to have been horizontally transmitted via conjugation or transduction (moved between bacterial species)

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7
Q

what is a pathogenicity island / what are they usually linked and associated to

A

a region of the genome that has a distinct nucleotide ratio (GC/AT ratio) - indicates horizontal gene transfer / linked to a tRNA gene and associated with genes homologous to phage/plasmid genes

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8
Q

what is a microbial factor that promotes attachment called

A

an adhesin - a specific virulence factor required for attachment or adhesion

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9
Q

what do adhesins bind to

A

pili and nonpilus proteins

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10
Q

how do bacteria avoid our chemical defenses in mucosal colonization

A

they modify their peptidoglycan structure to prevent breakdown from lysozyme - they change the charge of their membrane to repel the positively charged defensins (antimicrobial peptides) - they ahve specific receptors that harvest essential molecules (iron)

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11
Q

how does Neisseria gonorrhoeae avoid adaptive immunity

A

they have proteases that cut the antibodies we have - it also mutates its type IV pillus often to avoid antibody attachment (immobilization)

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12
Q

how do cells invade host tissues

A

enter through damaged skin, damaged epithelium or epithelial cell invasion

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13
Q

how do Salmonella and Shigella force uptake into epithelial cells

A

they use a Type III secretion system by using needles to inject proteins in a cell

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14
Q

what is M cell transcytosis

A

when a bacteria uses getting phagocitzed by a macrohage to get across the epithelial layer - some can replicate in the macrophage

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15
Q

what does SEC stand for

A

Subvert , Evade , Counteract

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16
Q

what does subvert entail

A

the deployment of effectors/toxins to block signaling pathways or to remove key immune cells that aid in bacterial clearance

17
Q

what are toxins and effectors / how are toxins deployed / how are effectors deployed

A

proteins produced and secreted by pathogens to disable immune defenses and attain nutrients / secreted into the extracellular space / injected into host cells using specialized secretion apparatuses

18
Q

how does S. aureus get toxin into a host cell

A

create a pore in the host cell with a receptor that is only found on immune cells - this puts the bacteria at an advantage

19
Q

how does Diptheria toxin get induced

A

during iron starvation so that the iron gets released from our dead cells to fuel the pathogen

20
Q

how does the EPEC - Enteropathogenic E. coli cause food borne diarrheal disease

A

it injects its toxin into the cell of the epithilium - this toxin rearanges its cytoskeleton and allows it to get nutrients from the dead cells

21
Q

what does Evade entail / what does this for a pathogenic cell

A

mask MAMPs to avoid immune detection / capsules block our immune cell proteins from binding to outer things on the cell

22
Q

what does counteract entail / how does staphylococcus aureus do this

A

shields used to render host defenses useless against the pathogen - counterattacks the anitbody response evolved / binds the antibodies backward by binding to its Fc region which makes the immune system not see the bacteria is infected

23
Q

what is Yersinia pestis / what features does it have

A

the bacteria that causes the plague / a gram negative rod, facultative anaerobe, primary pathogen, facultative intracellular pathogen, plasmid encoded virulence factors and has a T3SS

24
Q

how does yersinia pestis avoid our immune system

A

it completely changes its structure of lipid A core in the LPS that we usually use as a MAMP to induce inflammation through the PRR TLR4 - make it undetectable by TLR4

25
Q

what does the Type III needle protein bind to / what do the effectors do

A

the formyl peptide (fMet) on the phagocytes and injects them with effectors / they block cytokine production and disrupt actin polymerization required for phagocytosis

26
Q

when the TLRs and NLRs are turned off what happens to inflammation / why does yersinia cause swollen lymph nodes

A

there is none because the immune response would not be working / because the macrophages are killed in the lymphoid tissue and the yersinia is released all of the bacteria build up and cause swelling