bacteria and toxins Flashcards
influenza
2 antigens: hemagglutinin (promotes viral entry), neuraminidase (promotes progeny virion release)
clostridium perfringens
alpha-toxin/ lecithinase: phospholipase that degrades phospholipids–> degrades tissue and cell membranes–> death of these tissues
clostridium botulinum
botulinum toxin: preformed, heat labile toxin that inhibits ACh release at NMJ (also via cleaving snare)
bacillus cereus
cereulide: preformed toxin
mycobacteria
cord factor: inhibits macrophage maturation, damages mitochondria, and induces the release of TNF-alpha
sulfatides: surfae glycolipids that inhibit phagolysosomal fusion
corynebacterium diphtheriae
diphtheria exotoxin: encoded by beta-prophages (specialized transduction/ lysogenation), protein synthesis via ADP- ribosylation of EF-2
bacillus anthracis
edema/ anthrax toxin: mimics adenylate cyclase enzyme (–> increases cAMP)
chlamydiae
Elementary body: small/dense, enters cell via endocytosis and transforms into reticulate body
reticulate body: replicates in cell by fission then reorganizes into elementary bodies
strep pneumo
encapsulated bacteria, IgA protease
salmonella (NOT typhi)
endotoxin
shigella
endotoxin
shiga toxin (enterotoxin)
invasion in the key to pathogenicity (toxin not necessary to still have disease)
salmonella typhi
endotoxin
Vi capsule: protects from opsonization
pseudomonas aeruginosa
endotoxin (fever, shock)
exotoxin A: inactivates EF-2
mucoid polysaccharide capsule may contribute to chronic pneumonia in CF pts (via biofilm formation)
vibrio cholerae
enterotoxin: permanently activates Gs, increases cAMP–> NaCl efflux–> water loss
staph epidermidis
glycocalyces
ETEC
Heat labile enterotoxin: overactivates adenylate cyclase (increases cAMP)–> increased chloride secretion and water efflux in gut
heat stable enterotoxin: overactivates guanylate cyclase (increases cGMP)–> decreased resorption of NaCl and water in the gut
note: no inflammation or infvasion
neisseria gonorrheae
IgA protease
pili
neisseria meningitidis
IgA protease
polysaccharide capsule
LPS/LOS endotoxin: severity of disease correlates with blood concentration of LOS
pili: attach to respiratory mucosa (help gain access to blood stream)
H flu
IgA protease: allows for colonization of the respiratory mucosa
HiB: antiphagocytic polysaccharide capsule
EIEC
microbe invades the intestinal mucosa and causes necrosis and inflammation
EPEC
no toxin; adheres to apical surface, flattens villi, prevents absorption
listeria monocytogenes
only gram positive organism to produce endotoxin
form actin “rocket tails” that allow for intracellular movement and cell-to-cell spread across cell membranes (avoiding antibody)
staph aureus
Protein A
group A strep (strep pyogenes)
Protein M= major virulence factor (inhibits phagocytosis and complement activation)
streptolysin O= toxin
EHEC
shiga-like toxin: inactivates 60s ribsosome by removing adenine from rRNA; enhances cytokine release
parainfluenza
surface F (Fusion) protein which causes respiratory epithelial cells to fuse and form multinucleated cells
RSV
surface F (Fusion) protein which causes respiratory epithelial cells to fuse and form multinucleated cells
measles (Rubeola) virus
surface F (Fusion) protein which causes respiratory epithelial cells to fuse and form multinucleated cells
mumps virus
surface F (Fusion) protein which causes respiratory epithelial cells to fuse and form multinucleated cells
clostridium tetani
tetanospasmin/tetanus toxin: exotoxin causing tetanus; protease that cleaves SNARE (set of proteins required for NT release via vesicular fusion)–> prevents release of inhibitory (GABA, glycine) neurotransmitters from Renshaw cells in the spinal cord
clostridium difficile
toxin A (enterotoxin): binds brush border of the gut (–> diarrhea)
toxin B (cytotoxin): causes actin depolymerizatin–> cytoskeletal disruption–> necrosis
rotavirus
villous destruction with atrophy leads to decreased absorption on Na+ and loss of K+
