Mechanisms of Action Flashcards
Corynebacterium diptheriae
AB subunit toxin that ADP ribosylates EF2 inactiving it and translation of human mRNA into proteins
B subunit binds to glycoprotein receptor on epithelial cells
Clostridium tetani
tetanospasmin encoded on non-transmissible plasmid
Produces AB subunit exotoxin
B subunit binds to gnagliosides on CNS neurons
A subunit is ZN dependent metalloprotease enters by enodocytosis.
Cleaves synatpobrevins inhibiting release of GABA and glycine
Vibrio Cholerae
Toxin ADP-ribosylates and inactivates G-protein leading to persistent activation of adenylate cyclase
hypersecretion of H2O, Cl- and blocked Na+ reabsorption
Penetrate mucus but not cells
Clostridium botulinum
AB subunit toxin
A is toxic Zn protease subunit
B is protective against acid
botox enters neurons and blocks release of Ach
inhibits muscle contraction causing flaccid paralysis
Staphylococcus aureus
Extracellular
Streptococcus pyogenes
Extracellular
avoids phagocytosis and opsonization by hyluronic acid capsule, Stretolysin O kills phagocytes
Streptolysin O and C5a peptidase inhibit chemotaxis
M proteins block phagocytosis by bidning Ig Complement factor H
Legionella pneumophila
Produces B-lactamase
Enters macrophages via coiling phagocytosis-requires DOT and ICM proteins
No oxidative burst or lysosome fusion
Replicates until macrophage acidifies and virulence factors produced
Lyse macrophage and spread producing proteases and phsopholipases contributing to lung damage
Mycobacterium tuberculosis
Bacteria is inhaled
Primary infection: Ghon complex moves to lymph node
Intracellular pathogen multiplies within macrophages
survive and multiply within macrophages spread throughout lymph or blood
Or latency
Chlamydia Trachomatis
Adherence to cell’s heparin sulfate, estrogen receptor complex
Invasion-actin rearrangements to from pedestal. requires live bacteria endocytosis (clathrin) pinocytosis or phagocytosis
EB domant until enters cell
EB to RB uses ATP in EB
RB multiplication pH drops
No Ab formation or lysosmal fusion
Vacuoles form inclusions
RB to EB type III secretion or endosome fuse with cell membrane and EBs exit
Neisseria gonorrhoeae
Attachment via pili, Opa LOS porins
LOS and PG trigger inflammatory response to epithelium and sloughing off of ciliated epithelial cells
Bacterial spread along mucosal surface or go to submucosa
Neisseria meningitidis
Attachment via pili adis colonization of nasopharynx
Opa, LOS and porins mediate contact
in CNS bacteria shed LPS and PG which trigger inflammatory response
Borrelia burgoferi
Outer surface proteins OspA: anchors to tick midgut OspC: targets salivary gland Osp E: inhibits complement DpbA: binds decorin in ECM
Salmonella
infects through M cells in mucosa of large intestine
triggers endocytosis by M cell via membrane ruffling
Bacteria ingested by macrophage in lamina propria surviving and multiplying in phagocyte
carried to lymph, spleen liver mutiply and are released into bloodstream
LPS in bloodstream leads to inflammation
move into gallbladder and back to intestine
Shigella
Pass through small intestine to large intestine
Trigger mechanism and membrane ruffling intestinal epithelial cells
Escapes phagosome into host cell cytoplasm
Polymerize actin tails
ETEC
Enterotoxigenic Not invasive Toxin mediated LT1 and LT2-Similar to cholera AB subunit Sta-binds GC increase cGMP hypersecretion of H2O Stb-increase in bicarbonate
