H. influenzae B Virulence factor vaccine component

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

clostridium perfringens toxin

alpha toxin (exotoxin) lecithinase hydrolyzes lecithin in cell membranes --\> cell lysis --\> development of gas gangrene also causes hemolysis

Strep pyogenes (grp a strep) virulence factor toxin

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

S. aureus virulence factor toxin

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

M. tuberculosis what mechanism of survival does it use?

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_

bordatella pertussis toxin what factors wase pertussis invasion

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\ \

cryptococcus neoformans what stains are used what protects it from the immune system

stains ziehl neelson, mucicarmin, india ink \ \ liam neeson, carmin, and indiana Jones walk into the crypt of neo-man\ \ immune protection antiphagocytic polysacch capsule

enterococcus how can he grow? what stops him from growing?

-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)

strep pneumo virulence factor what else helps it resist the immune response

IgA protease breakdown IgA resistance to phagocytosis via its thick polysacch capsule

shigella dysenteriae toxin (--\> how does this manifest)

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)

corynebacterium toxin how will this manifest

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

listeria monocytogenes how you survive

form "rocket tails" actin polymeriation that allows intracelular movement and cell-to-cell spread across cell membranes --\> avoid Abs "tumbling mobility in broth"

bacillus anthracis toxin

\ \ 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

clostridium : how they survive toxins.. C. tetani C. botulinum C. perfringens

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

E. Coli - anatomy that helps it invade - toxin EHEC ETEC

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

neisseria how does it get into the body virulence factor toxin

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_

vibrio cholerae how does it get into the body toxin

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

endotoxin vs exotoxin who has it method of release chemistry components location of genes potency gen MOAs gen clin presentation antigenicity vaccines heat stablity

who has it ENDO: some G-, some G+ EXO: only G- bc its in the cell membrane outler later and only G- have an outer layer method of release ENDO: secreted into circulation EXO: when bacteria dies, its membrane breaks apart and the LPS/LPO is released into circulation chemistry components ENDO: a protein (thus can be inactivated) EXO: Lipopolysaccharide LPS (Lipid A core, O Ag at the terminal end) \ \ LPO in N. Meningitidis\ location of genes ENDO: plasmid or bacteriophage (for some- the bacteriophage will insert some extra DNA into the bac DNA so they need the bacteriophage to give them te ability to make exotoxin) EXO: bacterial chr potency ENDO: HIGH (cause ds at low concentrations) EXO: LOW (need high concentrations to cause shock gen MOAs ENDO: 6 gen mechanisms inhibit protein synthesis (4) inc fluid secretion in GI tract (3) inhibit phagocytosis (bordatella) inhbit NT release (2) lyse the cell membrane (2) super Ag (2) EXO: CD14 activation of Møs --\> inc IL-1+IL6, TNF-alpa, and inc NO synthesis activate complement C3a and C5s directly bind tissue factor --\> set off coagulation cascade gen clin presentation ENDO: not that sick, can be divided into categories of sx (dysentery, watery diarrhea, pharyngitis, toxic shock syndrome, NMSK block, skin changes) EXO: septic shock and meningococcemia (--\> shock) antigenicity ENDO: yes, induce high titers of Abs (anti-toxins) EXO: poor (no Abs form) vaccines ENDO: can be made from toxoid = inactivated bacterial toxin protein i.e. TDaP vaccine : tetanus toxoid + diptheria toxoid + acellular pertussis EXO: no vaccines heat stablity ENDO: mostly no (EXCEPT: staph superAg and ETEC ST) EXO: yes, it causes shock stable at 100 for up to an hour: febrile patients don't kill off the endo toxin itself even if the back dies

microbio "basics" Flashcards by Fatima Bilal

H. influenzae B

Virulence factor
vaccine component

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

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clostridium perfringens

toxin

alpha toxin (exotoxin)
- lecithinase hydrolyzes lecithin in cell membranes –> cell lysis –> development of gas gangrene
- also causes hemolysis

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Strep pyogenes (grp a strep)

virulence factor
toxin

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

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S. aureus

virulence factor
toxin

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

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M. tuberculosis

what mechanism of survival does it use?

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

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bordatella pertussis

toxin
what factors wase pertussis invasion

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**

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cryptococcus neoformans

what stains are used
what protects it from the immune system

stains
- ziehl neelson, mucicarmin, india ink
- **liam neeson, carmin, and indiana Jones walk into the crypt of neo-man**
immune protection
- antiphagocytic polysacch capsule

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enterococcus

how can he grow? what stops him from growing?

-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)

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strep pneumo

virulence factor
what else helps it resist the immune response

IgA protease
- breakdown IgA
resistance to phagocytosis via its thick polysacch capsule

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shigella dysenteriae

toxin (–> how does this manifest)

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)

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corynebacterium

toxin
how will this manifest

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

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listeria monocytogenes

how you survive

form “rocket tails”
- actin polymeriation that allows intracelular movement and cell-to-cell spread across cell membranes –> avoid Abs
- “tumbling mobility in broth”

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bacillus anthracis

toxin

** 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

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clostridium : how they survive

toxins..

C. tetani
C. botulinum
C. perfringens

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

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E. Coli

anatomy that helps it invade
toxin
EHEC
ETEC
*

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

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neisseria

how does it get into the body
virulence factor
toxin

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

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vibrio cholerae

how does it get into the body
toxin

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

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which organisms use Lipid A as a virulence factor- what does it cause

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

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what different virulence factors are used by different strains of E. Coli- link the different virulence factors to the different clinical presentations

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endotoxin vs exotoxin

who has it
method of release
chemistry components
location of genes
potency
gen MOAs
gen clin presentation
antigenicity
vaccines
heat stablity

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who has it
- ENDO: some G-, some G+
- EXO: only G- bc its in the cell membrane outler later and only G- have an outer layer
method of release
- ENDO: secreted into circulation
- EXO: when bacteria dies, its membrane breaks apart and the LPS/LPO is released into circulation
chemistry components
- ENDO: a protein (thus can be inactivated)
- EXO: Lipopolysaccharide LPS (Lipid A core, O Ag at the terminal end) **LPO in N. Meningitidis*
location of genes
- ENDO: plasmid or bacteriophage (for some- the bacteriophage will insert some extra DNA into the bac DNA so they need the bacteriophage to give them te ability to make exotoxin)
- EXO: bacterial chr
potency
- ENDO: HIGH (cause ds at low concentrations)
- EXO: LOW (need high concentrations to cause shock
gen MOAs
- ENDO: 6 gen mechanisms
  - inhibit protein synthesis (4)
  - inc fluid secretion in GI tract (3)
  - inhibit phagocytosis (bordatella)
  - inhbit NT release (2)
  - lyse the cell membrane (2)
  - super Ag (2)
- EXO:
  - CD14 activation of Møs –> inc IL-1+IL6, TNF-alpa, and inc NO synthesis
  - activate complement C3a and C5s
  - directly bind tissue factor –> set off coagulation cascade
gen clin presentation
- ENDO: not that sick, can be divided into categories of sx (dysentery, watery diarrhea, pharyngitis, toxic shock syndrome, NMSK block, skin changes)
- EXO: septic shock and meningococcemia (–> shock)
antigenicity
- ENDO: yes, induce high titers of Abs (anti-toxins)
- EXO: poor (no Abs form)
vaccines
- ENDO: can be made from toxoid = inactivated bacterial toxin protein
  - i.e. TDaP vaccine : tetanus toxoid + diptheria toxoid + acellular pertussis
- EXO: no vaccines
heat stablity
- ENDO: mostly no (EXCEPT: staph superAg and ETEC ST)
- EXO: yes, it causes shock
  - stable at 100 for up to an hour: febrile patients don’t kill off the endo toxin itself even if the back dies

who are the spore forming bacteria

what is the function of spores
how does this effect surgery

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= bacillus (the rocket) + clostridium (system= destination)

spores are released as a last ditch effort to keep the species alive : released by bacteria in very inhospitable environments (nutrients are limited)
- spores lack metabolic activity, and are highly resistant to heat and chemicals
need to autcoalve to kill spores on surgical equipment by steeming at 121C for 15 min to kill them off to avoid inection

Bacillus anthracis (anthrax)

bacillus cereus (food poisening)

C. botulinum (botulism)

C. difficile (pseudomembranous colitis)

C. perfringens (gas gangrene)

C. tetani (tetanus)

which bacteria need a bacteriophage to bring them the genes for exotoxin production

Study These Flashcards

corneybacterium diptheria ***the big, classic one***
Grp A strep (pyogenes)
EHEC
C. botulinism
V. cholerae

NAME THAT BUG

G(-) bacteria

exotoxin forming
Cocci
enteric bacilli
zoonotic bacilli
respiratory bacilli

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G(-) bacteria

exotoxin forming
- pseudomonas (exotoxin A)
- shigella (shiga toxin)
- EHEC (shiga like toxin)
- ETEC (shiga like toxin)
- Vibrio cholera (cholera toxin)
- bordetella pertussis (pertussis toxin)
Cocci
- Neisseria (meningitidis and gonnorrea)
enteric bacilli
- klebsiella
- enterobacters
- serratia
- salmonella (e + t)
- C. jejuni
- h. pylori
- proteus
zoonotic bacilli (“-ella)
- bartonella henslae
- brucella
- francisella
- pasteurella
respiratory bacilli
- H. influenzae
- legionella

which bugs do not gram stain well

(not G+ or G-)

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the legion of superheros in hiding

mycoplasma and ureaplasma (Marvel Universe)
- no cell wall
treponema (the space station) and leptospira
- too thin to be seen
mycobacteria
- cell wall has high lipid content
coxiella burnetti (the random brunette for love interest)
Gardnerella vaginalis (poison ivy)
Legionella (the Legion)
- intracellular
Rickettsia (black widow)
- intracellular
chlamydia (captain america)
- intracellular
bartonella (barton - hawkeye)
- intracellular
anaplasma (ant man)
- intracelluar
Ehrlichia (the Mummy chant)
- intracellular

who can be visualized using the giemsa stain

Ricky Try-ed to Please Gemma, but all she got was Bored and Chlamydia * rickettsia * trypanosomes * plasmodium * borrelia * chlamydia

who can be seen with the ziehl neeson stain

ziehl neeson = acid fast (liam neeson, the acid fast slinger who is very cryptic, sporadic, and has a card up his sleeve) * mycobacteria * nocardia * cryptosporidium (oocysts)

who can be seen with the india ink stain

cryptosporidium neoformans

who can be seen with a silver stain

the silver lining * of **Pneumocystis jiroveci**.. is that we figured out what AIDS was * of the trip was the helicopter ride (**H. pylori**) * of black panther's suit = **legionella** * of men is cock = **coccoidiodes**

who is seen w **chocolate agar**, what are the special media contents that this bug requires

H. influenzae -needs factors V (NAD+) and factor (hematin)

who is seen w **Thayer Martin**, what are the special media contents of this media that this bug requires

*_n_*eisseria : \*\*Thayer Martin acts like a *_V*_ery _*T*_ypical _*N*_eedy _*C_*hild \*\*\* he needs his own space so needs everyone else gone except him... - inhibition of G+ organisms with *_V_*ancomycin - inhibition of all other G- with *_T*_rimethoprim and _*C_*olistin - inhibition of fungi with *_N_*ystatin

who is seen w **bordet gengou agar** and **regan-lowe medium** , what are the special media contents that this bug requires

bordetella pertusses border gengou= potato extract regan-lower = charcol, blood, and abx

who is seen w **tellurite agar and Löffler medium**

cornybacterium diphtheriae

who is seen w **Lowenstein Jensen agar**, what are the special media contents that this bug requires

M. tuberculosis

who is seen w **Eaton agar**, what are the special media contents that this bug requires

M. pneumoniae -requires cholesterol \*\*pnEAmoniae??\*\*

who is seen w **MacConkey agar**, what are the special media contents that this bug requires

lactose fermenting enterics because they can ferment, they produce the acid, causing colonies to turn pink **G- bacilli, (+) lactase** * **E. Coli** * **Klebsiella** * **Enterobacter** (oppurtunistic infections in ppl on mechanical ventilation * **citrobacter** and **serratia** (both slow fermenters) *

who is seen w **eosin-methylene blue (EMB) agar**, what is special about the growth

E. Coli = colonies grow with green metallic sheen

who is seen w **charcoal yeast extract agar**, what are the special media contents that this bug requires

Legionella (black panther: charcaol suit with silver lining) - buffered with cystein and iron * buffered with his *sister* and *iron man*

who are the classic * aerobes * anaerobes * what propoery makes them anaerobic * what drugs cannot be used against anaerobes * facultative anaerobes (what does this mean)

* aerobes *"**N**agging **P**ests **M**ust **B**reathe"* * **n**ocardia * **p**seudomonas * **m**yco**b**acterium * anaerobes "**C**an't **B**reathe **Fr**esh **A**ir" * **C**lostridium * **B**acteriodes * **F**usobacterium * **A**ctinomyces israeli * \*\*don't have catalase and/or superoxide dismutase, generally soul smelling and produce gas in tissue: normal flora in the GI tract but pathogenic elsewhere\*\* * can't use Ami**no**glycosides (**no-o**) bc they require O2 to enter the cell * facultative anaerobes (what does this mean) * means they can use O2 to generate ATP but the can also use fermentation and other O2-independent pathways * strept, staph, and the enteric G- ( klebsiella, enterobacters, serratia, salmonella, yersinia, c. jejuni, h. pylor, poteus)

who are the **G+ bacilli** * aerobic * anaerobic

G+ bacilli **/rods** * aerobic * listeria * bacillus * corynebacterium * anaerobic * clostridium

Strep: * catalase + or -? aerobic or anaerobic? * who are alpha hemolytic? * bile soluble + optichin sensitive * NOT bile soluble or optochin sensitive * who are beta hemolytic? * bactitracin sensitive? * NOT bacitracin sensitive? * who are gamma hemolytic * grow in 6.5% NaCl * DONT grow in 6.5% NaCl

* catalase + or - ? * **cat (-)** : \*\*stripped your life of happiness\*\* * anaerobic/ facultative * **alpha hemolytic**: green, partial hemolysis * **bile** soluble + **optichin** sensitive * S. pneumo ^{**THE ALPHA- he did THAT**} * NOT bile soluble or optochin sensitive * *Strep Viridans* (green) = S. *mutans* or S. *mitis* * **beta hemolytic**: clear, complete hemolysis ^{there are two types of beta's : the sensitive pie bakers, the insensitive, reaching for the stars} * **bactitracin** sensitive? * Grp A= pyogenes * NOT bacitracin sensitive? * Grp B= galactiae * **gamma hemolytic**: no hemolysis, grows in bile * **grow in 6.5% NaCl** * enterococcus (E. faecium, faecalis) ^{(Emagine they are strep, but can't do hemolysis)} * DONT grow in 6.5% NaCl * S. bovis ^{strep "bozo"= no hemolysis, can't grow in NaCl} hemolytic : grows in blood --\> beta not hemolytic : grows in bile --\> gamma (radiaton) partial = some can grown in both, some only in blood --\> alpha (leader has to compromise)

staph * catalase + or -? aerobic or anaerobic? * who are coagulase (+) * who are coagulase (-), novobiocin (+) * who are coagulase (-), nobobiocin (-)

staph = anaerobic/facultative anaerobe, catalase (+) * coag (+) = S. aureus ^{**they stick together, cover everything**} * coag (-), novobiocin (+) = S. epidermidis ^{**plumber has the knowledge**} * coag (-), novobiocin (-) = S. saphrolyticis ^{**girl can't fix the sink**}

who are the G+ branching filaments * aerobic * anaerobic

G+, branching filament, aerobic = **nocardia** [weakly acid fast] G+, branching filament, anaerobic = **actinomyces** [not acid fast] * \*\*israeli soldier wears the gas mask\*\*

who are the G- dipplococci aerobic or anaerobc? maltose fermenting?

Neisseria + Moraxella = G-, aerobic, diplococci * maltose fermenting = **N. meningitidis** ^{brain only uses sugar} * non-maltose fermenting = **N. gonorrheae, Moraxella**

who are the G- coccobacilli

H. influenzae Bordetella pertussis pasteurella brucella francisella tularensis bartonella henslae

gram - bacilli * which are lactose fermenting * which are (-) lactase, oxidase (+) * lactase (-), oxidase (-). H₂S (+) * lactase (-), oxidase (-), H₂S (-)

* which are lactose fermenting * fast = E. coli, klebsiella, enterbacter * slow= serratia, citrobacter * which are (-) lactase, oxidase (+) * pseudomonas (rusty, green color) * lactase (-), oxidase (-). H₂S (+) * salmonella, proteus * lactase (-), oxidase (-), H₂S (-) * shigella, yersinia

who are the G-, comma shaped rods what makes each unique

G- comma shaped rodes * C. jejuni = grow in 42C (*hot camp fire*) * Vibrio cholerae = grow in alkaline media (*diarrhea is a base*) * H. pylori = produce urease

what is the "conjugate" vaccine and which bacterias is there one for

= a vaccine that convert T-independent Ags to T-dependent Ags (via conjugation w a protein) = H. flu b, neisseria meningitidis, and strep pnuemo (ENCAPSULATED bacteria that need their capsules to be conjugated)

the mecA gene is seen in what

MRSA (methicillin resistant Staph aureus)

microbio "basics" Flashcards

(48 cards)