Microbiology: Ch3 Biology Of Infectious Agents

Front 1

genetics of prokaryotes

Back 1

haploid with extrachromosomal plasmids

Front 2

genetics of eukaryotes

Back 2

diploid + many chromosomes

Front 3

what is unique about protein transcription in prokaryotes

Back 3

translation and transcription can occur at the same time due to the lack of a nuclear membrane

Front 4

three demands made on microbes

Back 4

nutrition, occupancy and resistance

Front 5

two ways how bacteria adapt to nutrient availability

Back 5

efficiency and adaptability

Front 6

polysaccharide buildup that allows for bacterial growth

Back 6

biofilm

Front 7

when does urine become cloudy

Back 7

when bacteria get 1 million to 10 million per mililiter

Front 8

outer structures can amount to what percent of the dry weight of the cell

Back 8

20%

Front 9

where is the strongest antibody response to bacterial antigens directed

Back 9

surface antigens

Front 10

gram positive

Back 10

purple

Front 11

gram negative

Back 11

red

Front 12

what makes up the cell wall of a gram positive cell

Back 12

murein/peptidoglycan

Front 13

what is murein composed of

Back 13

glycan (sugar) cross-linked together via peptides

Front 14

rod

Back 14

bacilli

Front 15

spheres

Back 15

cocci

Front 16

helices

Back 16

spirilla

Front 17

how does murein protect against osmotic gradients

Back 17

allows to live in media of lesser osmotic pressure than cytoplasm, does not let it burst

Front 18

spheroplasts

Back 18

gram positive treated with lysozyme kept in a isoosmotic medium

Front 19

what cant pass through gram positive cell wall

Back 19

hydrophobic compounds, because of polar layer of charged murein

Front 20

why can gram positive bacteria withstand bile salts

Back 20

because they are hydrophobic compounds, naturally repelled by cell wall

Front 21

why are most inhibitors of DNA synthesis too toxic for clinical use

Back 21

they bind directly to the nucleic acid strains

Front 22

what is unique about metronidazole

Back 22

inert but can become selecticely modified to an active form by selective reduction of a nitro group, usually done by anaerobic bacteria

Front 23

how does metronidazole work

Back 23

partially reduced metronidazole is incorporated into the DNA of the bacteria rendering it useless

Front 24

what is metronidazole effective against

Back 24

anaerobic bacteria and amebas

Front 25

how does nalidixic acid work

Back 25

inhibits DNA gyrase and is bactericidal

Front 26

how do fluoroquinolones work

Back 26

interfere with DNA gyrase or topoisomerase and cause dsDNA breaks

Front 27

how do bacterial ribosomes differ from eukaryotic ones

Back 27

smaller subunits and smaller RNA molecules

Front 28

what rate is RNA made

Back 28

proportional to the number of RNA polymerase molecules

Front 29

when does rifampin work

Back 29

inhibits bacterial replication at the initiation step

Front 30

to which ribosomes does rifampin bind to

Back 30

free floating ribosomes in the cytosol, does not effect ribosomes already engaged in translation

Front 31

what is rifampin used to treat

Back 31

tuberculosis and leprosy, because it is non toxic to mamalian RNA polymerases

Front 32

what class of antibiotics is the most clinically useful

Back 32

those that inhibit protein synthesis

Front 33

which antibiotics bind at the tRNA binding site on the large ribosomal subunit

Back 33

amphenicol and macrolides (erythromycin)

Front 34

are the preceeding drugs reversible?

Back 34

yes, because once they detach from the subunit, they return to normal action

Front 35

which antibiotic is bactericidal

Back 35

aminoglycosides (class)

Front 36

which drugs are in the aminoglycoside class

Back 36

streptomycin, gentamycin and neomycin

Front 37

aminoglycosides bind to what subunit of the ribosome

Back 37

30s

Front 38

how do aminoglycosides work

Back 38

inhibit elogation of the peptide chains

Front 39

what is the method of cell death for aminoglycosides

Back 39

blocking of 30s causes build up of 70s particles, causes cell death

Front 40

how does linezolid work

Back 40

blocks the assembly of the initiation complex

Front 41

how does tetracycline work

Back 41

inhibits aminoacyl transfer RNA binding (tRNA)

Front 42

which antibiotics are cell wall inhibitors

Back 42

B lactams, glycopeptides, imadazoles, and echinocandins

Front 43

which antibiotics are inhibitors of membrane function

Back 43

lipopeptides and polyenes

Front 44

which antibiotics are folate antagonists

Back 44

sulfonamides and trimethoprims

Front 45

which antibiotics are protein synthesis inhibitors

Back 45

aminoglycosides, macrolides, ketolides, streptogramins and chloraphenicol

Front 46

which antibiotics are RNA synthesis inhibitors

Back 46

rifampin

Front 47

which antibiotics are DNA synthesis inhibitors

Back 47

metronidazole, fluoroquinolones and nalidixic acids

Front 48

memorize page 30

Back 48

racks on racks on racks