Bacterial Pathogenesis Flashcards
how do pathogens evade our bodily restriction of them
they adhere/invade host tissues, secrete toxins/effectors, steal nutrients from host, subvert, evade and counteract immune defenses
what do primary pathogens do / what do opportunisitc pathogens do
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)
how did Koch identify his postulates
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
what are molecular koch’s postulates
- 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
what are virulence factors
what pathogens use to meet requirements of infection cycle - include toxins, attachement proteins, capsules, and other devices
where are most virulence genes in bacterial pathogens found / where do pathogenicity islands appear
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)
what is a pathogenicity island / what are they usually linked and associated to
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
what is a microbial factor that promotes attachment called
an adhesin - a specific virulence factor required for attachment or adhesion
what do adhesins bind to
pili and nonpilus proteins
how do bacteria avoid our chemical defenses in mucosal colonization
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)
how does Neisseria gonorrhoeae avoid adaptive immunity
they have proteases that cut the antibodies we have - it also mutates its type IV pillus often to avoid antibody attachment (immobilization)
how do cells invade host tissues
enter through damaged skin, damaged epithelium or epithelial cell invasion
how do Salmonella and Shigella force uptake into epithelial cells
they use a Type III secretion system by using needles to inject proteins in a cell
what is M cell transcytosis
when a bacteria uses getting phagocitzed by a macrohage to get across the epithelial layer - some can replicate in the macrophage
what does SEC stand for
Subvert , Evade , Counteract
what does subvert entail
the deployment of effectors/toxins to block signaling pathways or to remove key immune cells that aid in bacterial clearance
what are toxins and effectors / how are toxins deployed / how are effectors deployed
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
how does S. aureus get toxin into a host cell
create a pore in the host cell with a receptor that is only found on immune cells - this puts the bacteria at an advantage
how does Diptheria toxin get induced
during iron starvation so that the iron gets released from our dead cells to fuel the pathogen
how does the EPEC - Enteropathogenic E. coli cause food borne diarrheal disease
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
what does Evade entail / what does this for a pathogenic cell
mask MAMPs to avoid immune detection / capsules block our immune cell proteins from binding to outer things on the cell
what does counteract entail / how does staphylococcus aureus do this
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
what is Yersinia pestis / what features does it have
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
how does yersinia pestis avoid our immune system
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
what does the Type III needle protein bind to / what do the effectors do
the formyl peptide (fMet) on the phagocytes and injects them with effectors / they block cytokine production and disrupt actin polymerization required for phagocytosis
when the TLRs and NLRs are turned off what happens to inflammation / why does yersinia cause swollen lymph nodes
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
