Micro Intro

Front 1

acid fast microorganisms stain what color with the acid fast stain?

Back 1

red

Front 2

Color of gram positive cells

Back 2

purple

Front 3

murein/peptidoglycan peptide crosslinks form between what sugars?

Back 3

N-acetylmuramic acid

Front 4

between what amino acids does transpeptidation occur

Back 4

D-alanine to D-alanine

Front 5

where do the peptide chains form in gram neg. organisms?

Back 5

diaminopimelic acid and D-alanine

Front 6

what are the 3 components of LPS

Back 6

Lipid A, Core, and O antigen

Front 7

What organisms have LPS?

Back 7

gram negative bacteria

Front 8

What is the probable function of the O antigen?

Back 8

it is hydrophillic ( imparts resistance to hydrophobic compounds such as bile salts and antibiotics)

Front 9

What transport mechanism uses the proton movie force (symport)

Back 9

active transport

Front 10

how do gram neg. bacteria allow for entry of small esential hydrophilic molecules

Back 10

porins

Front 11

what are siderophores?

Back 11

chelating compounds that bind iron

Front 12

where does oxidative metabolism take place in bacterial cell?

Back 12

the cytoplasmic membraine

Front 13

MOA of β-lactams

Back 13

Interfere with cell wall cross-linking through interaction with penicillin-binding proteins (transpeptidases); *auto*lysis

Front 14

list the β-lactams

Back 14

Penicillins, cephalosporins, carbapenems, monobactams

Front 15

MOA of bactracin

Back 15

inhibits the generation of a membraine lipid carrier required for the transfer of murein monomeric units from the cytoplasm to the growing chain

Front 16

MOA of Glycopeptides

Back 16

binds to D-ala-D-ala terminal amino acids on disaccharide subunits blocking their addition to the growing chain of disaccharides (murein)

Front 17

list Glycopeptides

Back 17

vancomycin

Front 18

MOA of Imidazoles

Back 18

Blocks synthesis of ergosterol required for fungal cell wall integrity

Front 19

list Imidazoles

Back 19

fluconazole, itraconazole, voriconazole, posaconazole
-conazole

Front 20

MOA of Echinocandins

Back 20

Blocks β-glucan synthesis, a major constituent of fungal cell walls

Front 21

list echinocandins

Back 21

caspofungin, mycofungin
-fungin

Front 22

MOA of lipopeptides

Back 22

Forms channels in cell membranes of Gram-positive bacteria resulting in K+ leakage and metabolic death

Front 23

list lipopeptides

Back 23

daptomycin

Front 24

MOA of polyene

Back 24

Bind to sterols in eukaryotic cell membranes, leading to membrane leakiness and, at high levels, lysis

Front 25

MOA of Sulfonamids

Back 25

Competitive inhibitor of dihydropteroate synthesis; blocks synthesis of tetrahydrofolate and cell-linked metabolic pathways (folate antagonist)

Front 26

list sulfonamids

Back 26

sulfamethoxazole, sulfadiazine
sulfa--

Front 27

MOA of trimethoprim

Back 27

Inhibition of bacterial dihydrofolate reductase

Front 28

MOA of aminoglycosides

Back 28

Bind to 30S subunit of bacterial ribosome; cause translational misreading and inhibit elongation of protein chain; kill by blocking initiation of protein synthesis

Front 29

list aminoglycosides

Back 29

gentamicin, tobramycin, streptomycin, amikacin, neomycin

Hint 29

Aminoglycosides Tackle Susceptible Gram Negatives

Front 30

MOA of macrolides

Back 30

Bind to ribosome 50S subunit; inhibit protein synthesis at chain elongation step

Front 31

list macrolides

Back 31

erythromycin, azithromycin, clarithromycin
--thromycin

Front 32

MOA of chloramphenecol

Back 32

same as macrolides (binds to 50s subunit)

Front 33

MOA of Rifampin

Back 33

Binds to bacterial RNA polymerase and blocks transcription (synthesis of RNA) at initiation step

Front 34

MOA of Metronidazole and nitrofurans

Back 34

anearobic bacteria and protozoa partially reduce to unstable nitro groups which are incorporated into DNA and lead to strand breakage

Front 35

MOA of fluoroquinolones

Back 35

Interfere with DNA replication by inhibiting the action of DNA gyrase and/or topoisomerase IV

Front 36

list fluoroquinolones

Back 36

ciprofloxacin, levofloxacin, gatifloxacin, moxifloxacin, gemifloxacin
-floxacin

Front 37

MOA of linezolid

Back 37

blocks the formation of the initiation complex---inhibits protein synthesis (usually at 50s)

Front 38

MOA of tetracycline

Back 38

inhibits tRNA binding to ribosome (30s)

Front 39

MOA of nalidixic acid

Back 39

inhibits DNA gyrase (topoisomerase II)

Front 40

protein synthesis inhibitors are generally _____ except aminoglycosides which are ____

Back 40

bacteriostatic, bactericidal

Front 41

what surface protein can bateria change to avoid immune recognition

Back 41

pillin

Front 42

purpose of DNA gyrase

Back 42

supercoiling of bacterial DNA

Front 43

purpose of topoisomerase I

Back 43

relaxes supercoils by making single-strand breaks in the DNA

Front 44

what is phase variation

Back 44

change in flagellar proteins

Front 45

what is the electron aceptor and product of lactic acid fermentation

Back 45

pyruvate-> lactate

Front 46

what is the electron aceptor and product of ethanol fermentation

Back 46

acetyl CoA-> ethanol

Front 47

how does attenuation work?

Back 47

Atenuation sequences occur on DNA with segments A, B, C, and D if the ribosome stalls allowing a stem-loop structure to form between B and C then transcription will be able to continue, but if the ribosome continues quickly from A to B allowing a stem-loop structure to form between C and D then the ribosome will be kicked off the DNA and transcription is terminated

Front 48

what is an induceable enzyme?

Back 48

the transcription of the enzyme is controlled by an operon sequence and a repressor protein

Front 49

what does an inducer do?

Back 49

causes a confirmational change in the repressor protein causing it to detach from the operon and transcription can continue

Front 50

aminoglycosides work better on areobes or anaerobes?

Back 50

aerobes because it is not taken up under anaerobic conditions

Front 51

nitrofurantoin is only useful in what type of infection

Back 51

urinary tract

Front 52

mechanism of resistance to b-lactams

Back 52

Hydrolysis of β-lactam ring by β-lactamase

Front 53

mechanism of resistance to methicillin and penicillins

Back 53

Change in penicillin-binding protein (transpeptidase); not on a plasmid

Front 54

mechanism of resistance to tetracycline

Back 54

Efflux pump pushes drug out of cell

Front 55

mechanism of resistance to aminoglycosides

Back 55

Enzymatic modification of DRUG by plasmid encoded enzyme; drug has reduced affinity for ribosome, and transport into cell is reduced

Front 56

mechanism of resistance to sulfonamides

Back 56

Sulfanilamide-resistant dihydropteroate synthase

Front 57

mechanism of resistance to trimethoprim

Back 57

Trimethoprim-resistant dihydrofolate reductase

Front 58

mechanism of resistance to erythromycin /macrolides

Back 58

Enzymatic modification (methylation by methylase) of 23S ribosomal RNA

Front 59

mechanism of resistance to chloramphenicol

Back 59

Acetylation of hydroxyl groups of chloramphenicol transacetylase; interference with transport into cell

Front 60

mechanism of resistance to oxazolidinones

Back 60

Point mutations in 23S ribosomal RNA; not on a plasmid

Front 61

mechanism of resistance to quinolones (fluoroquinolones and naladixic acid)

Back 61

Mutations in genes encoding DNA gyrase and topoisomerase IV and/or eflux pumps; not on a plasmid

Front 62

mechanism of resistance to vancomycin

Back 62

change in binding site (from D-ala-D-ala terminal amino acids to D-ala-D-lactate

Front 63

mechanism of tolerance to b-lactams

Back 63

lack of autolysin

Front 64

gram neg. adhesions and their ligand

Back 64

pili(fimbriae) to glycolpids, surface protein (invasin) to integrins, capsules

Front 65

gram + adhesions and their ligands

Back 65

surface protein to fibronectin, capsules

Front 66

list 6 ways that bacteria avoid complement activation

Back 66

1.Coat with capsule (e.g., staphylococci) 2.Coat with IgA antibodies 3.Coat with Sialic acid on LPS 4.Apply appropriate inhibitor of activation to surface: bind factor H ; bind decay-accelerating factors ; mimic component C4bp
5.Cover up target of membrane attack complex (e.g., E. coli, salmonellae) 6.Inactivate complement chemotaxin C5a; activate surface of plasminogen to plasmin which cleaves C3b

Front 67

how do bacteria inhibit phagocyte recruitment and function?

Back 67

increase cAMP preventing mobilization or produce C5a peptidase which inactivates the chematactic product of the complement cascade

Front 68

how do some bacteria kill neutrophils and macrophages?

Back 68

leukocidin exotoxins

Front 69

how does protein A reduce opsinization?

Back 69

binds IgG at the Fc portion so that phagocytic cells can't use the antibodies to get a grip

Front 70

name 4 ways in which bacteria survive phagocytosis

Back 70

1. inhibition of phagosome fusion with lysosome 2. escape into the cytoplasm (e.g. listeriolysin forms pores in the phagosome) 4.inherant resistance to lysosomal enzymes 5.inhibit lysosomal oxidative killing (e.g catalase breaks down H2O2)

Front 71

how do superantigens work?

Back 71

bind to Vb domain on TCR which makes the TCR more likely to bind to the MHC despite a lack of TCR-MHC antigen compatability

Front 72

how do trypanosomes evade antigen recognition in sleeping sickness?

Back 72

Trypanosomes are covered with a thick protein coat called variable surface glycoprotein, which undergoes periodic antigenic changes during the infection

Front 73

what causes relapsing feaver?

Back 73

borreliae undergo antigenic variation of their major surface antigen

Front 74

what is the difference between antigenic shift and antigenic drift

Back 74

minor changes in virus antigens which occur every 2-3 years is drift; majoir antigenic changes which take place ~10yrs is antigenic shift

Front 75

what viral proteins change in antigenic variation

Back 75

hemeagglutinin and neuraminidase

Front 76

what is the function of staphlokinase?

Back 76

it cleaves host plasminogen into plasmin which then degrades both IgG and the complement protein C3b

Front 77

what are the A-B toxins?

Back 77

shiga, diptheria, cholera, and tetanus

Front 78

what does diptheria toxin do?

Back 78

ADP ribosylates elongation factor 2

Front 79

describe the MOA of heat-labile enterotoxin of Escherichia coli, and pertussis toxin ?

Back 79

ADP ribosylates a G protein that stimulates adnylate cyclase, increading CAMP

Front 80

what toxins cleave intracellular proteins responsible for the fusion of intracellular vesicles with the plasma membrane?

Back 80

Botulinum and tetanus toxins

Front 81

what type of toxins modulate actin?

Back 81

type III cytotoxins

Front 82

what are the pattern recognition receptors?

Back 82

endotoxin from Gram-negative bacteria, lipoteichoic acid from Gram-positive bacteria, lipoglycans from the mycobacteria, and mannans from yeast

Front 83

by what pathway does exotoxin activate complement?

Back 83

alternative pathway

Front 84

What is the Waterhouse-Friderich syndrome?

Back 84

adreanal insufficiency resulting from DIC

Front 85

how does endotoxicity result in DIC?

Back 85

Endotoxin contributes to coagulation of blood in three ways: clotting factor XII (the so-called Hageman factor) is activated to set off the intrinsic clotting cascade; platelets release the contents of their granules, which are involved in clotting; and neutrophils release proteins known to stabilize fibrin clots.

Front 86

what is the order of release of sepsis mediators?

Back 86

C5a, then tumor necrosis factor α (TNF-α) triggers the release of interleukin 1 (IL-1) and IL-6 (IL-6 does not cause shock)

Front 87

name some membrane damaging toxins and their MOA

Back 87

lipase (eg. Lecithinase), hemolysins

Front 88

what type of toxin is Staph aureus's a-toxin?

Back 88

a homoggenous pore former

Front 89

what type of toxin is streptolysin O?

Back 89

heterogenous pore former