microbio "basics" Flashcards
1
Q
H. influenzae B
- Virulence factor
- vaccine component
A
- IgA protease- cleaves IgA
- **vaccine= anti PRP**
- capsule made of PRP = stop complement mediated phagocytosis capsule made of PRP
- (polyribosyltibitol phosphate) –> binds factor H in body which will prevent C3b depo onto host cell
2
Q
clostridium perfringens
- toxin
A
- alpha toxin (exotoxin)
- lecithinase hydrolyzes lecithin in cell membranes –> cell lysis –> development of gas gangrene
- also causes hemolysis
3
Q
Strep pyogenes (grp a strep)
- virulence factor
- toxin
A
- V FACTOR
- M protein (in bac cell wall)binds factor H tp prevent opsonization and destruction via the alternative complement pathway
- molecular mimicy of the M protein is what causes either rheumatic heart ds or glomerulnephritis
- TOXINs
- streptolysin O
- lyse cell membranes (along w streptolysin S will make S. pyogenes beta hemolytic
- ASO Ab are against streptolysin O
- erythrogenic exotoxin A+C =
- SUPERANTIGEN –> cause toxic shock-like syndrome
- streptolysin O
4
Q
S. aureus
- virulence factor
- toxin
A
- virulence
- Protein A= in the cell wall, prevent opsonization by binding Fc region of Igs (turn upside down= can’t bind complement)
- exotoxin
- superantigen toxic shock syndrome toxin (TSST-1)= cross link MHCII –> activate so many T cells –> over production of IL-1, Il-2, IFN-y, TNF-alpa –> toxic shock syndrome
5
Q
M. tuberculosis
- what mechanism of survival does it use?
A
trehalose dimycolate + cord factor
- cell wall component ,
- protect from Møs and instead stimulate granuloma formation
- after a few weeks of latent Mø infection, the Møs start expressing MHCII which will recruit CD4 and lead to granuloma formation)
- (CD4 cells will release IFN-y and better able phagocytosis against the TB)
- aka prevention of phagosome-lysosome fusion
6
Q
bordatella pertussis
- toxin
- what factors wase pertussis invasion
A
- exotoxin= pertussis toxin
- inhibit phagocytic ability via disabling Gi –> inc cAMP in Nø –> unable to do oxidative burst
- also inhibit Møs
- ***sketchy= a disableed G.I. Joe**
- adhesins
- pertactin= allows adhesion to ciliated upper respiratory epithelium
- **military tactics**
7
Q
cryptococcus neoformans
- what stains are used
- what protects it from the immune system
A
- stains
- ziehl neelson, mucicarmin, india ink
- **liam neeson, carmin, and indiana Jones walk into the crypt of neo-man**
- immune protection
- antiphagocytic polysacch capsule
8
Q
enterococcus
- how can he grow? what stops him from growing?
A
- -gamma hemolysis (no do hemolysis)
- PYR + can grow in bile
- can grow in 6.5% NaCl- (will not appear on a urine nitrite bc cannot turn nitrate into nitrite)
9
Q
strep pneumo
- virulence factor
- what else helps it resist the immune response
A
- IgA protease
- breakdown IgA
- resistance to phagocytosis via its thick polysacch capsule
10
Q
shigella dysenteriae
- toxin (–> how does this manifest)
A
- shiga (exo)toxin= inhibit host protein synthesis
- bloody diarrhea = dysentery
- also will enahnce cytokine release and cause HUS (hemoyltic uremic syndrome = acute renal failure with hemolytic anemia)
11
Q
corynebacterium
- toxin
- how will this manifest
A
- diptheria (exo)toxin=
- inactivate elongation factor 2 (EF-2) by adding ADP-ribose to it
- prevent protein elongation
- manifestation=
- sore throat (pharyngitis) + pseudomembrane on the back of the throat (dyptheria)
- lymphadenopathy = BULL NECK
12
Q
listeria monocytogenes
- how you survive
A
- form “rocket tails”
- actin polymeriation that allows intracelular movement and cell-to-cell spread across cell membranes –> avoid Abs
- “tumbling mobility in broth”
13
Q
bacillus anthracis
- toxin
A
** vikings around the cAMP fire, on water (bc edema) **
- edema toxin
- exotoxin that mimics cAMP in the GI tract –> inc Cle excretion –> inc fluid secretion –> watery diarrhea
- cutaneous anthrax= black eschar lesions on skin w characteristic edematous borders
- GI ulcers will also have the edema borders
- can also cause a necrotizing pneumonia with inc edema and
- forms spores that are resistant to high temperatures, chemical disinfectants, irradiation, and desiccation
- the only bacterium with a polypeptide capsule that keeps it safe
- medusa head appearance of colonies = halo of projections coming from the bac
14
Q
clostridium : how they survive
toxins..
- C. tetani
- C. botulinum
- C. perfringens
A
- survivie
- forms spores that are resistant to high temperatures, chemical disinfectants, irradiation, and desiccation
- toxins
- C. tetani : tetanospasmin
- (the Joker): protease cleaves SNARE protein –> cannot bring pres-synaptic vescicle full of NTs to the membrane for fusion and dispersment into synapse
- inhibit GABA and glycine in renshaw cells of SC–> constant M activation –> rigid Ms ( spastic paralysis, risus sardonicus = the grin, lockjaw “trisumus” )
- C. botulinum
- botulnium exotoxin; protease cleaves SNARE protein –> cannot bring pres-synaptic vescicle full of NTs to the membrane for fusion and dispersment into synapse
- inhibit the release of Ach = no activation of post-synaptic membrane = FLACCID paralysis (“floppy baby”)
- C perfringens = alpha toxin
- exotoxin that will lyse the membrane via lecithinase =–> myonecrosis –> dec BF to the area = less O2 in env (necessary bc is an anaerobe) = gas gangrene and hemolysis = “double zone” of hemolysis on blood agar
- C. tetani : tetanospasmin
15
Q
E. Coli
- anatomy that helps it invade
- toxin
- EHEC
- ETEC
*
A
- anatomy to get it: fimbriae/pilli for attaching to target cells K1 capsular Ag
- in strains that cause neonatal meningitis
- exotoxin
- EHEC : H for hemorrhagic diarrhea
- EHEC O157:H7 -Shiga-like toxin aka “verotoxin”: inhibit protein synthesis
- bind directly to 60S ribosome in bacteria and remove a very specfic adenosine –> inactive teh ribosome –> x protein synthesis
- bloody diarrhea (dysentery ) and will often cause HUS (acute renal failure with hemolytic anemia)
- ETEC: T for Temperature
- cause watery diarrhea via increased fluid secretion in the GI tract
- Heat Labile Toxin (LT) = does not survive hot temps
- increase cAMP in the GI tract –> Cl- + fluid secretion
- **labile in the air**
- Heat Stabile Toxin (ST)= survive hot temps aka fever
- inc cGMP –> block reabsorption of Cl- via NaCl transporter –> inc Cl- in the lumen and fluid secretion
- EHEC : H for hemorrhagic diarrhea
16
Q
neisseria
- how does it get into the body
- virulence factor
- toxin
A
- fimbriae/ pilli for attaching to target cells
- virulence= IgA protease (breakdown IgA to evade immune response)
- endotoxin LSP for N. gonorrhea BUT LPO for N. meningitidis
17
Q
vibrio cholerae
- how does it get into the body
- toxin
A
- fimbriae/ pilli for attaching to target cells
- toxin
- exotoxin= cholera toxin : cause fluid secretion via permaneny activation of Gs –> inc cAMP –> watery diarrhea
- = rice water diarrhea
- v serious: can cause death from dehydration and electrolyte abnormalities
18
Q
which organisms use Lipid A as a virulence factor- what does it cause
A
Lipid A is the core of the endotoxin (O Ag is the end) found on select G(-) bacteria
- LPS= endotoxin = cause shock via 3 MOA
- bind CD14 on Møs –> inc IL-6 + IL-1 (fever) , TNF-alpha (fever and hypotension) + N.O synthesis (hypotension)
- actviates complement via incr _C3a (_histamine release) and C5a (nø chemotaxis)
- directly binds tissue factor –> coagulation cascade actvation –> DIC
lipid A unit in lipopolysaccharides is found in enteric bacteria it causes activation of macrophages –> widespread release of IL-1 and TNF-alph –> SEPTIC SHOCK
19
Q
what different virulence factors are used by different strains of E. Coli- link the different virulence factors to the different clinical presentations
A
39
Q
who are the G+ bacilli
- aerobic
- anaerobic
A
G+ bacilli /rods
- aerobic
- listeria
- bacillus
- corynebacterium
- anaerobic
- clostridium
