Chemotherapy and Antibiotic Resistnace - Kozel Flashcards
1
Q
T/F: Antibiotics are naturally produced chemicals
A
true
2
Q
Is the ideal antimicrobial bacteriocidal or bacteriostatic?
A
bacteriocidal
3
Q
T/F: resistance can be caused by enzymatic inactiavation of the abx or simply a failure to convert it to its active form
A
true
4
Q
T/F: overproduction of an abx target can cause resistance
A
true
5
Q
(Pharmacokinetics/dynamics) describes the interaction between concentration and antimicrobial effect
A
dynamics
6
Q
Concentration vs. time in tissue and other body fluids determines (blank)
A
pharmacologic or toxic effect
7
Q
Concentration vs. time at site of infection determines (blank)
A
antimicrobial effect
8
Q
What are the pharmacokinectic issues that prevent an abx from reaching the bacteria?
A
absorption from the site of administration
transfer from plasma to site of infection
elimination from plasma
elimination from the site of infection
9
Q
What is the difference between bacteriostatic and bacteriocidal?
A
cidal= KILL the bacteria static= inhibit growth but does not kill
10
Q
What are some examples of bacteriocidals?
A
beta lactams, vancomycin, fluoroquinolones, metronidazole, aminoglycosides
11
Q
What are some examples of bacteriostatics?
A
tetracyclines, clindamycin, macrolides, sulfonamides
12
Q
What type of abx relies on the host to kill the microbe?
A
bacteriostatics
13
Q
A combination of antibiotics produces a 2-log10 increase in action relative to each agent alone is known as (blank)
A
syngergy
14
Q
A synergistic relationship between penicillina nd gentamycin is used to treat (blank)
A
viridans streptococcal meningitis
15
Q
What is the post-abx effect
A
suppresion of growth following exposure to abx
16
Q
Hows does the post-abx effect work?
A
slows growth that the sub- minimum inhibitory concentration (MIC) and alters morphology
17
Q
What effects does post-abx leukocyte enhancement have?
A
increases susceptibility to phagocytosis and phagocytic killing
18
Q
Time > MIC is what type of killing?
A
time-dependent killing
19
Q
Describe the persistent effects of time-dependent killing?
A
minimal to moderate
20
Q
The AUC/MIC ratio shows us the (blank)
A
total exposure of microbe to antimicrobial agent
21
Q
Describe the persistent effects of AUC/MIC?
A
prolonged persistent effects
22
Q
Cmax/MIC ratio shows what type of killing?
A
concentration-dependent killing
23
Q
Describe the persistent effects of Cmax/MIC type killing?
A
prolonged persistent effects
24
Q
Absorption, distribution, and elimination are part of pharmaco(blank)
A
kinetics
25
What two ratios are predictors of outcome for concentration dependent mechanisms?
AUC/MIC and Cmax/MIC
26
IN plain english, what does it mean if something is concentration dependent when it kills?
higher drug concentrations have a higher rate and extent of bacteriocidal activity
27
What are some examples of concentration dependent abx?
aminoglycosides, fluoroquinolones, metronidazole
28
What type of killing is relatively slow
TIME dependent killing
29
In time dependent killing, (blank) occurs at low multiples of the MIC
saturation of killing
30
What are some examples of time dependent abx?
B-lactams and vancomycin
31
T/F: bacteriostatic agents have minimal post-abx effect
false; prolonged effect
32
What ratio predicts the outcome of bacteriostatic agents?
AUC/MIC
33
What are the natural penicillins?
B-lactams
34
What other categories of drugs fall under B-lactams besides penicillin?
cephalosporins, carbapenems, Beta lactamase inhibitors
35
The spectrum of the natural penicillins includes (blank)
ONLY GRAM POSITIVE
36
T/F: natural penicillins provide the starting material for semisynthetic penicillins
true
37
```
Carboxypeptidases
Endopeptidases
Transglycosylases
Transpeptidases
Are all examples of (blank) binding proteins
```
penicillin binding proteins
38
what is the function of the penicillin binding proteins?
construct the pentapeptide-pentaglycine bridges that cross-link peptidoglycan
39
Describe the MOA of penicillin?
Penicllin binds to penicillin binding proteins. PDG cross-linking blocked; cell lysis due to autolytic enzymes that destroy the cell wall
40
T/F: beta lactamase is carried by a plasmid
ture
41
T/F: beta lactamase is carried by a transposable chromosome gene
true
42
Gram (blank) have an intrinsic ability to block the access of penicillin to PBPs
gram negative
43
An altered (blank) protein in N. gonorrheoeae creates penicillin resistance
porin
44
Newly resistant strains of S. pneumoniae have what changes to their abx binding site?
reduction in number or affinity to the PBP
45
S. pneumoniae, N. gonorrheoeae, and MRSA are all examples of what type of abx resistance?
alteration in abx binding site
46
Penicillinase resistant penicillins work by (blank)
introducing a bulky R group near the site of hydrolysis
47
What are two examples of penicillinase resistant PCN?
methicillin and nafcillin
48
What is the trade off when using a PCNase resistant PCN?
they are 1/10th as potent as penicillin G
49
Where is lipoteichoic acid found in the gram pos wall?
in the PDG layer above the PM
50
Where is lipid A and O polysacc found in the gram neg wall?
OUTER layer of the OUTER membrane
51
Where is PDG found in gram neg?
in between the two membranes
52
Where are porins found in the gram neg wall?
outer layer of the outer membrane
53
What does O polysacc attach to in the gram neg wall?
Lipid A
54
The outer membrane of gram neg resists penetration of (hyrophobic/philic) molecules
hydrophobic
55
How do you enchance the penetration of PCN thru outer membrane porins?`
add a hydrophilic charged group
56
T/F: broad spectrum PCNs like ampicillin and carbenicillin have the same sensitivity to PCNases as natural PCN
true
57
T/F: PCN forms a covalent irreversible bond with PBPs
true
58
How do PBPs prep the PDG for crosslinking?
they remove the D-alanine precursor from PDG
59
Where in the bacteria do you find PBPs?
membrane bound and in the cytosol
60
How do PBPs aid in abx resistance?
overproduction of PBPs and formation of PBPs that have low affinity for PCN; b-lactamase production as well
61
Which PBP is responsible for causing MRSA ?
PBP 2A
62
Generally speaking, are PCNs cleared rapidly or slowly from the kidneys?
rapid secretion
63
Are PCNs generally distributed to most tissues?
yes
64
Do PCNs penetrate the blood brain barrier?
no
65
How do you maximize drug exposure for PCN that use time-dependent killing?
optimize your dosing strategy; lower doses more frequently; keep the dose above the MIC
66
Opening of the b-lactam ring allows for binding to host proteins causing the (blank) reaction and creating an allergic reaction
hapten
67
Disturbances of GI flora is most prominent with what abx?
ampicillin
68
An allergic reaction can occur with reactivity to the (blank) ring within PCN
thiazolidine ring
69
T/F: cephalosporins have high immunological cross reactivity with PCN
false
70
cephalosporins are resistant to what enzyme?
b-lactamases
71
Describe the characterization of the spectrum of cephalosporins from gen's 1-4?
1. narrrow
2. expanded
3. Broad
4. Extended
MRSA-active
72
What generation of cephalosporin includes gram neg activity that will kill Pseudomonas?
3rd gen
73
High affinity for (blank) allows for MRSA-active cephalosporin
PBP 2A'
74
Which penicillins are acid labile?
PCN G, methicillin
75
which PCNs are acid stable?
PCN V; most semi-synthetic PCNs
76
Differences between acid labile or stable PCNs creates a large variation in (blank)
oral absorption
77
T/F: cephalosporins generally have good tissue distribution
false; distribution and metabolism varies widely from one to the other
78
T/F: cephaolosporins are capable of CNS penetratioN
TRUE
79
How are cephalosporins excreted? In what patients do you need to alter the dosage?
Renal excretion; pt's with renal insufficiency
80
What is the most common side effect of cephalosporins?
diarrhea and nausea (GI symptoms)
81
(blank)-infections are possible with broad spectrum cephalosporins
superinfections
82
What are the three mechanisms by which N. gonorrheoeae is resistant to cephalosporins?
altered PBP2A
overexpression of efflux pump
mutation in porin reduces uptake
83
Carbapenems, imipenem, and muropenem have what structure?
B-lactam
84
the modified alpha ring in carbapenems eliminates (blank)
sulfur
85
What is the spectrum of carbapenems?
HIGH AFFINITY for essential PBPs of gram pos and neg
86
Carbapenems can penetrate the gram neg outer membrane via a specific (blank)
OMP (outer membrane protein)
87
Are carbapenems effective against MRSA?
NOPE
88
The hydroxyethyl at C-6 in carbapenem makes it highly resistant to (blank)
beta lactamase
89
T/F: carbapenems are only used when the specific microbe is known
false; used in empirical therapy
90
What is the preferred route of administration of carbapenem? why?
pareneterally; poor absorption after oral ingestion
91
Carbapenem is rapidly hydrolyzed by (blank) in the renal tubule
peptidase
92
What is the peptidase inhibitor that blocks renal degradation of imipenem?
Cilastatin
93
What are the side effects of carbapenems?
generally well tolerated; can cause allergic reactions
94
NDM-1 plasmid encoding extended spectrum beta lacatamase confers resistance to which abxs?
imipenems, all B-lactams, aminoglycosides, tetracyclines, and fluoroquinolones
95
T/F: NDM-1 plasmid is found in common enteric bacilli
true
96
In what setting do you typically see NDM-1 cause problems?
Pts getting elective surgery in SE asia
97
What are two common b lacatamase inhibitors?
clavulanic acid and sulbactam
98
Why do we use b lactamase inhibitors?
used with b lactams with little direct antibacterial action to improve their power
99
what is the MOA of b lactamase inhibitors?
SUICIDE INHIBITION; clavulanate will bind to the b-lactamase IRREVERSIBLY (suicide) to prevent it from functioning; forms an acyle enzyme intermediate that is hydrolyzed VERY slowly
100
B-lactamase inhibitors are used in conjuction with (blank)ase sensitive b-lactams
PCNase
101
What humongous class of abx inhibits cell wall synthesis?
b-lactams
102
what drug is used against M. tuberculosis that inhibits cell wall synthesis
cycloserine
103
What class of abx is vancomycin?
glycopeptide
104
Where does vancomycin bind on the cell wall?
terminal D-ala-D-ala
105
What function does vancomycin block?
transpeptidation
106
Is vancoymycin bactericidal or bacteriostatic?
bacteriocidal
107
Vancomycin resistance is (blank) mediated
plasma mediated
108
What are two bugs that are vancomycin resistant?
enterococcus spp. and S. aureus
109
How do VRE and VRSA avoid vancomycin?
they substitute lactate for alanine
110
VISA avoids vancomycin how?
multiple free ala-ala to act as decoys for vancomycin
111
What is the spectrum of vancomycin and glycopeptide abx?
gram pos ONLY
112
T/F: vancomycin is a firstline drug
false; drug of LAST RESORT
113
What is the usual route of administration of glycopeptide abx?
IV
114
What bug is vancomycin especially useful for?
C. diff
115
What is the mode of excretion of vancomycin? what kind of pts should you alter dose for?
renal; renal insufficiency
116
vancomycin is (blank)-toxic at high doses
ototoxic, nephrotoxic
117
Red Man syndrome is associated with what abx?
vancomycin; rapid IgE mediated mast cell degranulation causing red rash
118
Is VRSA or VISA the most common form of resistant S. aureus?
VISA
119
Is polymyxin useful againt gram pos or gram neg bacteria? why?
gram neg; fatty acid tail penetrates the phospholipid bilyater
120
What is the MOA of polymyxin?
leakage of metabolites and disruption of membrane function
121
Is polymyxin bacteriocidal or static?
cidal
122
The toxicity of polymyxin limits its use to (blank)
topical applications
123
highly resistant strains of Pseudomonas, Klebsiella, and Acinetobacter warrant of use of parenteral (blank)
polymyxin
124
Why is polymyxin given in parenterally?
not absorbed after oral administration
125
Polymyxin shows dose-related (blank)toxicity
nephrotoxicity
126
What abx should be used when an enteric carries that fucking god-awful NDM b lactamase plasmid?
Poly-fuckin-myxins
127
P. aeruginosa, A. baumanii, and enterobacteriacaeae that are resistant to all b-lactams, fluoroquinolones, and aminoglycosides should be treated with (blank)
polymyxins
128
What is the MOA of quinolones?
inhibits DNA synth via inhibition of DNA gyrase
129
are quinolones cidal or static?
cidal
130
How can a bug have resistance to quinolones?
mutation to DNA gyrase
131
what is the spectrum of quinolones?
gram neg and pos
132
what are the clinical uses of quinolones?
UTIs and other bacterial infections
133
do quinolones have good oral absorption?
yes
134
What is the method of clearance of quinolones?
renal
135
What is the most common cause of C. diff colitis?
Ciproflaxin!
136
What are the three classes of side effects with quinolones?
GI, CNS, and achilles tendon damage
137
what is the trade name of metronidazole?
flagyl
138
what is the MOA of metronidazole?
PRODRUG reduced to active form by electron transport protein
139
(aerobic/anaerobic) bacteria are able to convert metronizadole prodrug to active form
anaerobic via electron transport, strangely
140
T/F: some protozoa have a mechanism that makes them susceptible to metronizadole?
true
141
What does metronizadole do once it is converted to its active form?
produces cytotoxic compounds that DAMAGE DNA
142
What is the spectrum of mentronidazole
obligate anaerobes and many protozoa
143
Does metronidazole work in facultative anerobes or obligate aerobes?
nope
144
is metronidazole cidal or static?
cidal
145
What drug is given as a prophylaxis in colorectal surgery?
metronidazole
146
Trichomonas vaginalis is commonly treated with (blank)
flagyl
147
T/F: flagyl has roughly similar blood levels following oral and IV administration
true
148
What is the most common side effect of flagyl?
GI upset; mutagenic effects UNPROVEN, but possible
149
What is the mechanism of Rifampin?
binds to DNA-dependent RNA pol, blocks CHAIN INITIATION and RNA transription
150
T/F: Rifampin is active on eukaryotic polymerases
false; only on bacterial!
151
T/f: Rifampin is cidal or static depending on the concentration of the BACTERIUM
TRUE
152
How do bugs become resistant to Rifampin?
single step mutation in the beta subunit of RNA Pol; very rapid mutation
153
what are the clinical uses of Rifampin?
Tx of TB, leprosy, prophylaxis of N. meningitidis
154
What is the normal route of administration of Rifampin?
oral
155
Describe the distribution of Rifampin?
good throughout the body, limited CNS penetration
156
what is method of elimination of Rifampin?
30% urine and 60-70% feces!
157
What drug causes ORANGE DISCOLORATION of tears, sweat, and urine?
Rifampin
158
What are the most common side effects of Rifampin?
GI
159
Rifampin is (blank)toxic
hepatotoxic
160
Rifampin upregulates CYP450 and therefore decreases hormone and drug (blank)
half lives; need to check to see if there is a potential med interaction!
161
Is streptomycin cidal or static?
cidal
162
what is the MOA of streptomycin?
irreversibly binds to 30S unit
depletes ribosome pool
misreads the message
premature release from the ribosome
163
Aminoglycosides like streptomycin are syngergistic with (blank), that facilitate their uptake by gram pos bacteria
cell wall-active antimicrobials
164
What is the method that a bacteria becomes resistant to streptomycin?
Plasmid mediated enzymatic alteration: acetylation, phosphorylation, adenylation (most common) or reduced uptake or intrinsic resistance
165
Do aerobes or anaerobes have intrinsic resistance to aminoglycosides?
anaerobes
166
what is the spectrum of streptomycin?
BROAD spectrum: gram pos and neg, and TB
167
Streptomycin is a (first/second)line drug in TB Tx
second line
168
what other terrible diseases do you use streptomycin to treat?
tularemia, plague; more toxic than newer agents
169
Gentamycin, tobramycin, and amikacin are used in empiric therapy of (blank)
suspected aerobic, gram NEG bacteria
170
Once starting pt on empiric gentamycin and you get cultures back, do you continue therapy or switch abx?
switch abx
171
What is needed to make aminoglycosides more effective against gram pos bacteria?
combo therapy with cell wall active agents
172
T/F: aminoglycosides are minimally absorbed from the GI tract
true; must give IM or IV
173
what is the clearance mechanism of aminoglycosides?
renal
174
What pharmacodynamic ratio is a predictor of efficacy?
Cmax/MIC; CONCENTRATION DEPENDENT EFFECT
175
What type of toxicity is most common with aminoglycosides? 2nd most common? Any other side effects?
1. Nephrotoxicity 5-25%
2. ototoxicity --IRREVERSIBLE 2-10%
3. neuromuscular blockade: rare
176
To what ribosomal subunit does tetracycline bind?
30s
177
Where on the 30s does tetracycline bind?
A-site, blocks binding of aminoacyl tRNA
178
is tetracycline binding reversible?
yes!
179
is tetracycline bacteriostatic or cidal?
STATIC
180
What is the most common mechanism for tetracycline resistance? Next most common?
Active efflux pump; ribosomal protection: cytoplasmic proteins bind to the ribosome to protect it
181
What is the spectrum of tetracylcine?
VERY BROAD; gram pos and neg, many anaerobes, spirochetes, mycoplasma, rickettsiae and chlamydia
182
(blank) is firstline Tx in chlamydia, rickettsia, and spirochetes,
tetracycline
183
What factors make tetracycline a second line choice?
toxicity, resistance, and availability of alternatives
184
What factors play into oral absorption of tetracyline?
varies from person to person and amongst various types, also impaired by MILK and divalent/trivalent cations
185
What are the two methods that tetracycline is excreted?
kidney and bile
186
T/F: tetracycline can cause superinfection
true
187
T/F: tetracyline may stain teeth and bones in early years
true
188
what are the side effects of tetracyline?
photosensitivity, GI problems, nephrotoxicity, bone/tooth staining, superinfection
189
Is chloramphenicol used in the US?
nope
190
What is the more common name for lincosamides?
clindamycin
191
to what ribosomal unit does clindamycin bind?
50s
192
what is the MOA of clindamycin?
blocks peptidyl transferase
193
is clindamycin static or cidal?
static
194
Describe the mechanism of resistance to clindamycin
plasmid mediated methylation of ribosome reducing abx binding
195
what is the spectrum of clindamycin?
Aerobic GRAM POSITIVE COCCI
| ANAEROBES
196
Is clindamycin effective against gram negative?
nope
197
what is the clinical use for clindamycin?
anaerobic infections, alternative to PCN if allergy, MRSA is susceptible!
198
How do you deliver clindamycin?
Oral and pareneteral
199
how is clindamycin excreted?
urinary and fecal
200
The (blank) of clindamycin increases with renal failure
half life
201
Pseudomembranous colitis is associated with what bug?
C. diff; intrinsically resistant to clindamycin
202
What is the most common side effect of clindamycin?
GI disturbances
203
what part of the ribosome does linezolid bind to?
50s unit
204
what is the MOA of linezolid?
prevents formation of the 70s complex; unusual mechanism makes it SUPER EFFECTIVE! against resistant bacteria
205
is linezolid static or cidal?
static
206
what is the spectrum of linezolid?
most clinically important gram pos; limited with gram neg
207
What drugs do you use linezolid for?
MRA, multi-drug resistant strep pneumoniae, VRE, and as a reserve abx for difficult bacteria
208
What are the ways to give linezolid?
IV or orally
209
What is the bioavailability of linezolid?
FUCKING OUTSTANDING
210
how is linezolid excreted?
broken down in vivo and excreted in urine
211
Long term use of linezolid results in (blank)
myelosuppresion
212
What is the most common side effect of linezolid?
GI upset
213
Linezolid is a weak nonspecific inhibitor of monoamine oxidase and should therefore not be given with (blank)
SSRIs!!
214
What are the common macrolides?
erythromycin, azithromycin, and clarithromycin
215
where do the macrolides bind and what is there MOA?
to the 50s; blocks peptidyl transferase and translocation
216
are macrolides static or cidal?
static
217
T/F: macrolides also have a plasmid mediated resistance method
treu
218
what does the macrolide resistance plasmid carry?
gene for methylation of ribosome
219
Macrolides have cross resistance with (blank)
lincomycin/clindamycin
220
Besides being generally broad, define the spectrum of macrolides?
most active against aerobic, gram pos
221
What is the clinical use of macrolides?
firstline for mycoplasma and Legionella, alternative for PCN if allergic
222
(blank) inactivates macrolides, therefore oral dosing is givien as enteric-caoted or more-stable salts or esters
gastric acid
223
Which macrolide is acid stable?
azithromycin
224
What are the only areas where macrolides are not well distributed?
brain and CSF
225
what is the primary mode of excretion of macrolides?
BILIARY WTF
226
What are the side effects of macrolides? (think of mode of excretion)
hepatotoxicity
stimulates GI motility--i.e. GI upset
INHIBITOR OF CYP450; SIG. DRUG INTERACTIONS
CARDIAC ARRHYTHMIAS
227
sulfonamides and trimethoprim both function in what pathway?
folic acid metabolism
228
suflonamides block the synthesis of (blank)
dihydrofolic acid
229
Trimethoprim blocks the synthesis of (blank)
T for Tetrahydrofolic acid
230
THF is used in the synthesis of (blank)
DNA and RNA
231
while sulfonamides block the synth of DHF, they are analogs to (blank)
PABA
232
By what mechanism do sulfonamides block DHF synth?
competitive inhibitor
233
are sulfonamides cidal or static?
static
234
Plasmid resistance of sulfonamides mediates production of (blank) enzyme with decreased affinity for the drug
dihydropteroate synthetase
235
Gram pos, gram neg, chlamydia, and NOCARDIA are in the spectrum of (blank)
sulfonamides
236
T/F: you can use sulfonamides for UTIs
true
237
T/F: sulfonamides have good GI absorption
true
238
T/F: sulfonamides are excreted in feces
false; urine
239
What is the common side effect to sulfonamides?
hypersensitivity reactions -- rash and hivez
240
Confluent dermatological necrosis is an emergency that is part of the (blank) syndrome in response to sulfonamides
Stevens-Johnson syndrome; shows with the confluent epidermal necrosis and immune reaction
241
Hemolytic anemia, agranulocytosis, aplastic anemia, and other hematopoietic disorders are rare side effects associated with (blank)
sulfonamides
242
T/F: trimethoprim is synergistic with sulfonamides
true
243
cotrimoxazole (Bactrim and Septra) is a combo of what?
trimethoprim and sulfamethoxazole
244
what is the drug of choice for Pneumocystis jirovecii??
trimethoprim
245
what is a firstline for MRSA?
sulfamethoxazole/trimethoprim
246
Impaired folate usage is a side effect of sulfa/trimeth?
trimeth
247
What is the MOA of Isoniazid?
PRODRUG that is activated in the bacteria; inhibits synthesis of mycolic acids
248
What is the very limited spectrum of Isoniazid?
only effective agains MYCOBACTERIA
249
T/F: Resistance against Isoniazid is very common
true
250
What is the mechanism of resistance against Isoniazid?
deletion of gene encoding the activating enzyme that takes it from prodrug to active drug
251
What is the use of isoniazid?
TB tx
252
What are the methods of administration of Isoniazid?
orally and IM
253
Isoniazid will inhibit Cyp450 so you need to check for drug interactions and potential (blank) as a side effect
hepatitis
254
What are the five general mechanisms of abx resistance?
1. enzymatic inactivation of abx
2. decreased permeability
3. efflux of abx
4. mod of molecular target
5. failure to convert prodrug to active form
255
What are the two ways that an abx is enzymatically modified so it doesn't work?
it is either destroyed or modded so it fails to reach/bind its target
256
What are the two locations for decreased permeability?
outer membrane permeability (gram neg) or inner (cytoplasmic) membrane permeability (gram neg or pos)
257
What are some of the modifications to the molecular target of an abx to create resistance?
1. altered binding site for abx
2. protection of binding site
3. overproduction of target (think vancomycin)
4. binding up of abx
258
Resistance to what types of abx is controlled by enzymatic alteration of the abx?
B-lactams and aminoglycosides
259
Resistance to what types of abx is controlled by efflux of abx?
tetracylcine
260
Resistance to what types of abx is controlled by altered abx binding site?
B-lactams, glycopeptides, quinolones, rifampin, macrolides, lincosamides, and sulfa/trimeth
261
T/F: it is always best to choose the shortest effective abx regimen
true
262
What factor should you consider when prescribing empirically?
local susceptibility trends
263
What is an abx diffusion test?
Spread isolate on plate, drop on the abx discs, and measure the diameter of inhibition
264
What does a diffusion test tell you?
estimates the minimum inhibitory concentration of an abx
265
WHat are the disadvantages to a diffusion test?
non-quantitative interpretation
does not measure bacteriCIDAL activity
inappropriate for slow growers and slow diffusers
266
In a dilution test, are you diluting solutions of bacteria or abx?
abx
267
What are you able to calculate using a dilution test?
minimum bactericidal concentratoin--the least amount of abx needed to kill the bacteria
268
Does a dilution or diffusion test determine bactericidal activity?
dilution test
269
The (blank) test is influenced by growth rate while the (blank) is not
diffusion is, dilution is not
270
Which bacterial assay provides quantitative results?
dilution testing
271
Automated tests are mechanized (blank) tests
dilution
272
in automated tests, bacterial growth is determined by (blank)
reduction in light transmittance or increase in scattering
273
What is the advantage of automated tests?
better standardization, produces more info, and rapid results
