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32 Cards in this Set

  • Front
  • Back
define colonization.
organism adheres to cell surface or ECM
define infection
bacteria colonize and grow, there may be no disease (symptomatic vs. asymptomatic). Disease is when they cause damage to the host
what are frank pathogens?
non normal flora found in the niche of normal flora
what sites in the body are usually sterile?
blood, internal organs, bones, CNS, CSF, and lymph
define latency.
chronic infection with org w/o any signs or symptoms
define opportunist.
org that does not normally cause disease in healthy host but can when host is immunocompromised or if it infects sterile site
what are the importances of normal flora?
they protect from pathogens (competition for space and nutrients and producing substances to inhibit other orgs), help in maturation of immune system (exposes to many antigens thus making natural Ab's), stimulate development of tissues (Peyer's patches), aid in metabolism (digestion, synthesis, and removal of by products), and mosulate response to epithelial cell injury
What are some adverse effects of normal flora?
some are opportunistic and autoimmunity from some natural antibodies
define tropism
an organism remains confined to one location or tissue
what are the 6 vehicles of transmission?
fingers, food, feces, fetones, flies, and fornication
define specialized facultative intracellular parasites and generalized facultative intracellular parasites.
specialized: can grow wi nonphagocytic cells but are killed by macs. generalized: can grow in normal macs but usually killed by activated macs
howdo bacteria adhese to epithelial cell surfaces?
via noncovalent bonds
how do bacteria control the expression of virulence factors?
via transcriptional regulation mechanisms in response to environmental (host) signals. This response is due to spatial (where the bac is in the body) or temporal (how long the bac has been there) stimuli
disease to host can primarily be due to what?
bacterium (toxin, etc) or host's response to pathogen
what are the characteristics of endotoxins?
cannot be inactivated into toxoid; are heat, protease, and autoclave resistant; produced by gram neg bacteria; toxic in only high amounts; made of carbs and lipid (LPS); released from live bacteria via blebs as well as dead bac's; initiates septic shock cascade; poorly neutralized by antibodies despite antigenicity but recognized by TLR.
what are the characteristics of exotoxins?
can be inactivated to toxoids; are protease, heat and autoclave sensitive; found in both gram + and gram -; is toxic in very small amounts; usually made of proteins (enzymes); actively secreted from live bacteria; exhibit cell tropism (type of cell damage depends on toxin's mode of action); neutralised by antibodies.
what are the adverse effects of LPS on the host?
increase vasc. permeability, hypotension, shock, DIC thrombosis; hypoglycemia; fever; decreased iron
what is the classic structure of exotoxins?
A-B toxins in which A is the activity subunit (enzyme) and B is the binding subunit.
What is a common mechanism of A-B exotoxins that neutralizes the target protein?
ADP ribosyltransferase activity using NAD+ as a substrate
a bacteria that can completely destroy blood cells is called what? partially destroy?
beta hemolysins. alpha hemolysins
what do infectious bacteria do to the extracellular matrix?
bind it and destrpy it to aid in spread
how can we tell if a bac has a pathogenecity island?
the chromosome will be larger than usual with a different G:C content. The pathogenicity island itself will also be flanked by direct repeats, is usually associated with tRNA genes, is instable, and has mobility genes.
what is special about the type III secretion mechanism of certain virulent bacs?
they inject proteins directly into the target cell thus these proteins evade the hosts immune response.
what are the two ways in which pathogenic bacs get iron?
siderophore mediate uptake (bacs release siderophore protein that "steals" iron from iron containg host proteins and then the siderophore goes back to its receptor on the bacteria) or non - siderophore mediated via iron protein receptors on the bac itself.
describe phase and antigenic variation as well as why some bacs perform these processes.
phase: on/off switching of a gene's expression thus resulting in the presence or absence of an antigen. antigenic: org produces distinct proteins with similar functions but are antigenically distinct. These are performed to evade the immune system specefically to overcome the Ab response.
how do staph aureus and strep pyogenes overcome antibodies?
they bind the Fc portion of the Ab not the antigen binding site thus inactivating the Ab.
how do some bacs specefically evade IgA Ab's?
IgA protease
how do capsules help evade the immune system?
they are anti-phagocytic
how can some bacs cause a massive non specefic immune response with lots of T cells?
by superantigen exotoxins
how can some bacs overcome compliment?
C5a peptiase and serum resistance
how can some bacs overcome macs?
capsule, inhibit respiratory burst, inhbit phagolysosome fusion
what aspects of the immune system can some bacs overcome?
antibody response, complement, macs, and T cells