Ch 15 Mechanisms of Pathogenicity Flashcards
what is a microbes ID50?
number of microbes needed when presented to a population to infect 50% w the disease. (ID= infectious dose)
is a higher or lower ID50 better?
higher- more microbes needed to cause disease
what is a microbes LD50?
concentration of toxin needed to cause 50% of test population to die (LD= lethal dose)
3 portals of microbial entry and examples
- MM- resp. tract, GI tract, conjun., genitourinary tract
- skin- openings like sweat glands and hair follicles (acne)
- parenteral- damage due to cuts, insect bites, drying out of skin (cracking)
what is adherence of a microbe
latching on to particular receptors on cell surface of host via ligands/adhesins
examples of enzymes used by pathogens to escape host defenses
coagulase- clots blood creating a barrier from IS
kinase- blocks formation of clots, once a certain number of pathogens is reached, kinase used to launch attack
theraputic application of kinase
streptokinase used to break up blood clots that cause heart attacks
how antigenic variation is used to escape host defenses
ability of microbes to change its surface antigens, ecading antibodies
what are siderophores, how damage host cells?
protein secreted by some pathogens, have high affinity for iron, take iron (ex: from hemoglobin RBCs), pathogen will take-up iron for growth and reproduction
exo v endo toxins- gram neg or pos?
exo- pos
endo- neg
difference between endo and exo toxins (where they are)
endo- w/in outer membrane
exo- secreted by growing cell
what component of gram neg cell acts as endo toxin
lipid A
which usually has a lower LD, exo or endo toxins
exo (less needed to be deadly)
which causes fever, endo or exo toxins
endo toxins- lipid A released in macrophage-> produces cytokines->bloodstream-> hypothalamus-> make porstaglandin-> changes thermostat
why, if someone has a gram ned infection, we are not TOO aggressive w treatment
killing all at once releases endotoxins all at once-> bad fever
how A-B toxins work
- B component attaches to host cell receptor
- host cell invaginates A-B (receptor-mediated endocytosis)
- A part separates, disrutes cellular metabolism and prevents protein synthesis
why the A part of A-B toxin acts as an enzyme (what does that mean?)
repeated and continuous disruptive effect
how a virus can cause cancer?
insert into host genome leading to mutations and cancer.
can also decrease contact inhibition- stop knowing that, when they bump into each other, stop growing-> tumors
Bacterial enzyme associated w blackening of infected wounds, how does this aid in pathogenicity?
Hyalauronidase, helps microorganisms spread from initial site of infection (hydrolyzes hylaronic Acid)
How exotoxins are produced
Part of cells growth and metabolism
How exotoxins harm host
Inhibiting certain metabolic functions or destroying parts of host cell
A-B is a kinda of endo or exotoxins?
Exo
