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Microbiology Final > Handout 6 > Flashcards

Handout 6 Flashcards

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Biology 101 flashcards
1
Q

what is the most important mechanism of how bacteria become antibiotic resistant?

A

passing R plasmids
other mechanisms include biofilm formation, phage genes for resistance, mutation, enzymes to modify the bugs, and metabolic pathways changes

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2
Q

where were antibiotics first isolated from?

A

bacteria and fungi

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3
Q

why are semi synthetic antibiotics useful?

A

they help increase the spectrum and decrease the breakdown.

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4
Q

______ agents can be used internally to prevent infections. Example is antibiotics

A

chemotherapeutic agents

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5
Q

___ determines which drug will stop bacterial growth at the LOWEST concentration?

A

MIC

minimum inhibitory concentraiton

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6
Q

kirby baurer?

A

test drug susceptibility using agar diffusion

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7
Q

best guess ?

A

empirical- based on your evidence

what you would use as a dentist likely

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8
Q

antibiotic selected based on sensitivity

A

it’s the rational antibiotic therapy. Uses rational approach!

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9
Q

kill the microbe but doesn’t harm host?

A

selective toxicity

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10
Q

what inhibitor stops the peptidoglycan linkage by inhibiting transpeptidases?

A

beta lactam

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11
Q

what are the examples of Beta Lactam cell wall synthesis inhibitors?

A

-penicillins
-Cephalosporins
Beta-lactaMASE inhibitors (calvulanic acid)
-Carbapenems- imipendum, meropenem
Monobactams- AZtreonam, narrow spectrum and gram -. not widely used

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12
Q

what are the examples of the non beta lactic?

A

ISONiazid
Vancomyacin
bacitracin
Cycoserine

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13
Q

what part of the bacteria does the non beta lactic inhibit?

A

also cell wall synthesis like the beta lactam

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14
Q

what could you use if the bacteria have Beta-lactamase?

A

vancomycin

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15
Q

what attacks the cell wall of mycobacteria? two exmaples

A

you could use “isoniazid”
or cycloserine which is the second line against tuberculosis

*you could use nucleic acid synthesis “rifamycin”

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16
Q

what could you use on the skin that is effective against many gram positive organisms?

A

bacitracin
“Tracy” gram +
freckle skin

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17
Q

second line against mycobacterium tuberculosis (drug resistant) technically an oxazolidone because it inhibits protein synthesis?

A

cycloserine

**protein syntesis and ribo 30)

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18
Q

what are the 4 examples of non beta lactams?

A

Vancomyocin
bacitracin
cycloserine
isonazid

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19
Q

example of cell membrane that attacks lipopeptides?

A

daptomycin.
“DAP” the lipids with lip.
gram + only. drug resistant staph, strep, enterococci

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20
Q

what are the topical only that have a detergent action? for eye and skin infections?

A

POLYmycins!

Poly and her “topical drinks” the more she drinks the less she can “see” and her skin looks really cray

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21
Q

what are the nucleic acid sythensis inhibitors? they are narrow spectrum and inhibit DNA gyros/topioismerisa?

A

QUinolones!
“Quin goes to the club to look at some fine DNA”
he inhabits the gyrase action though and he is narrow minded.
nalidixic acid. “dix”

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22
Q

what are the broad spectrum modified quinines? ciproflaxin and damage growing bone?

A

At the club, QUIN modifies his game by giving FLOWES while he is “cipin” on his juice!
again for nucleic acid sytnehsis

23
Q

what is a hepatoticn used for mycobacterium tuberculosis?

A

rifamycin

“doc was into rif raf and had TB”

24
Q

what do ahminoglycosides inhibit?

A

translation.
they’re “mean” and bind to the ribosomes. They’re the “MYSIN”- mycin. HIS sin because he ismean and binds to ribosomes.
ototocic and nephrotoxic

25
Q

erythromycin is an example of what?

A

macrolides!

use when patient is penicillin allergic.

26
Q

what does erythromycin bind to?

A

the Pro Ribosomes.

targets gram positive

27
Q

what do we use DIFICID for?

A

MACROlides. works locally in GI for C DIFF

28
Q

what are the two macrocodes?

A

Erythromicin and Difiid.

ERR body is Different.

29
Q

example of a lincosamindes?

A 
#
lincoln and CLindamysin
"pseudomembranous colitis risk" presidents and "fake"
30
Q

what are broad spectrum and inhibit translation?

A

tetracycline. like a big broad cycle

31
Q

what can we use for MRSA???

A

GLycyclines. tigecycline. broad spectrum.
oxaxolidone. syvok and sivesxtor. resistant infecitons
streptogamins=== gram post baceria, MRSA, and VRE

32
Q

what do sulfonamides do?

A

metabolic inhibitors
stope FOLATE sytnehsis
when you smell suffer, you “foll” down

33
Q

what is the oral form of penicillin?

A

PEN V. cuz you give oral to the V

34
Q

what are some of the semisynthetic penicillins?

A

methicilin- narrow
Amp-= broad- also works on gram neg
Amoxicillin- prophylaxis of infective endocarditis

35
Q

what could you give patient for prophylaxis endocarditis?

A

amoxicillin

36
Q

what do we use polymyxin for?

A

externally for GRAM - infection (drinks cuz - and sad)
skin and eye infection.
neurotoxic, nephrotoxic, and not stable in the GI
“all related to POLY and her alcohol problem”

37
Q

what is reserved for serious anaerobic infection? translation inhibitor?

A

Clindamycin
president. inhbits the “translation” of important things.
anaerboic infeciton— no air

38
Q

what is the risk of Clindamycin?

A

risk is pesumembranous colts. it’s a C Diff superinfeciotn.

risk of the president is FAKE colitis”

39
Q

what are the risks of tetracycline use?

A

remember, it’s a broad spectrum translation inbhitior.

would risk superinfection, hepatotoxicity, and may effect bone growth with DEVELOPING teeth

40
Q

infection of hair follicles?

A

folliculitis

it’s a boil! eew

41
Q

deeper, sebaceous gland infection?

A

furuncle

42
Q

several furuncles merge?

A

carbuncle

43
Q

superficial skin infection?

A

impetigo

44
Q

how does cutaneous S. aureus differ from staph food poisoning?

A

food poising form ENTEROTOXIN/exotocin

cutenous S. aureus is a colonization of skin

45
Q

what are the exfoliative toxins of staph aureus?

A

ETA and ETB

46
Q

what are the antigens that stimulate the T cells nonspecifically in staph aureus?

A

superantigens! A/B etc.

47
Q

what are the 5 enzymes that staph aureus has?

A

-coagulase for clot formation
-catalase- H202 breakdown. all STAPH not STREP
-hyaluronidase- spreading in CT tissue
stayplokinse- fibrinolysin.- dissolve clots
penicillinase

48
Q

what is the enzyme that helps staph aureus spread in CT?

A

hyaluronidase

49
Q

what is the enzyme for staph aureus that raids in clot formation?

A

coagulase

50
Q

what is the enzyme is STAPH aureus that involves breakdown of H2o2?

A

catalase! not in STREP!

51
Q

what is staphylokinase?

A

fibrinolysin- dissolves clots

52
Q

what is the ID feature that causes scalded skin syndrome?

A

exfoliative toxin!

53
Q

difference between SSS and bullus impetigo?

A

both from staph.

bullus impetigo is local unlike SSS (it’s systemic_

Microbiology Final (20 decks)

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