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microbio km > microbio lecture 18 chapter 20 > Flashcards

microbio lecture 18 chapter 20 Flashcards

1
Q

Who was Paul Ehrlich (165-1915)?

A

German physician and bacteriologist

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2
Q

What did Ehrlich do?

A

Observed some dyes stain bacterial but not animal cells

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3
Q

Ehrlich found fundamental difference between

A

cell types

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4
Q

Ehrlich searched for ______ _______ that would kill microbial pathogens without harming human host

A

“magic bullet”

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5
Q

Ehrlich tested _______ _____________ to treat syphilis, caused by spirochete Treponema pallidum

A

arsenic compounds

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6
Q

The ______ _______ compound proved effective in laboratory animals

A

606th tested: it was Arsphenamine, named Salvarsan

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7
Q

Arsphenamine, Salvarsan is potentially ________ for patients but did cure infections previously considered hopeless

A

lethal,

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8
Q

Arsphenamine proved….

A

some chemicals could selectively kill microbes

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9
Q

first documented case of antimicrobial medications

A

Salvarsan (Paul Ehrlich 1910)

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10
Q

Red dye Prontosil

A

Gerhard Domagk, 1932; used to treat streptococcal infections in animals

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11
Q

red dye prontosil has no effect in

A

test tubes: enzymes in blood split to produce sulfanilamide, the first sulfa drug

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12
Q

red dye prontosil and salvarsan are

A

chemotherapeutic agents: chemicals used to treat disesase

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13
Q

synonyms of chemotherapeutic agents

A

antimicrobial medications, antimicrobial drugs, antimicrobials

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14
Q

Discovery of antibiotics

A

In 1928, Fleming identified mold Penicillium secreting compound toxic to Staphylococcus (penicillin) - he couldn’t purify it

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15
Q

penicillin showed effective in

A

killing many bacterial species

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16
Q

Chain and Florey purified penicillin and tested compounds in 1941 on police officer with
Staphylococcus aureus infection. It led to

A

Patient improvement but supply of purified penicillin ran out and he later died

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17
Q

WWII spurred research and
development of penicillin G, the

A

first antibiotic

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18
Q

antibiotic

A

naturally-produced antimicrobial

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19
Q

Selman Waksman purified ________ from soil bacterium Streptomyces griseus

A

streptomycin

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20
Q

researchers began screening

A

hundreds of thousands of
microbes for antibiotics

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21
Q

pharmaceutical companies today examine

A

soil samples from around world

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22
Q

Selective toxicity

A

causes greater harm to microbes than to
human host

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23
Q

toxicity interferes with essential structures or properties common in

A

microbes
but not human cells

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24
Q

toxicity is relative and expressed as

A

therapeutic index

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25
Q

therapeutic index calculated as the

A

lowest dost toxic to patient divided by dose used for therapy

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26
Q

penicillin g useful to humans and has high therapeutic index because it

A

interferes with cell wall synthesis, a process not present in humans

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27
Q

penicillin g also has a high therapeutic window, which is

A

the range between the therapeutic dose and the toxic dose

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28
Q

medications too toxic for systemic use may be used

A

topically (body surface application)

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29
Q

TI is the ratio of

A

the doses of toxic and the desired responses

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30
Q

TI is used as an

A

index of comparative toxicity of two different materials for relative safety of drug

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31
Q

larger the TI ratio, the _____ the relative safety

A

greater

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32
Q

bacteriostatic antimicrobial agents

A

chemicals inhibit bacterial growth
* Patient’s defenses must eliminate pathogen (sulfa drugs)

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33
Q

bactericidal agents

A

chemicals kill bacteria
* Sometimes only inhibitory depending upon drug
concentration and stage of microbial growth

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34
Q

Broad-spectrum antimicrobials

A

affect a wide range and are important for treating acute life-threatening diseases (especially when no time to culture for identification/susceptibility)

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35
Q

negative side effect of broad-spectrum antimicrobials

A

Can disrupt microbiome that helps keep out other
pathogens (dysbiosis)

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36
Q

narrow spectrum antimicrobials

A

affect limited range, requires identification and susceptibility of pathogen, less disruptive to microbiome

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37
Q

Patients may be started on broad-spectrum antimicrobial and later
switched to

A

narrow-spectrum once more is known about the pathogen

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38
Q

Antimicrobial behaviors differ in body

A

Only some can access the brain; only some can withstand stomach acid

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39
Q

Half-life of medication is

A

time it takes for serum concentration to
decrease by 50%

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40
Q

half-life dictates

A

frequency of doses required to maintain effective level in body

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41
Q

penicillin V is taken ___ times a day

A

4

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42
Q

azithromycin is taken no more than____ a day

A

once

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43
Q

Patients with kidney or liver dysfunction excrete or metabolize

A

medications more slowly; must adjust dosage to avoid toxic levels

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44
Q

Antimicrobials have saved countless lives when properly prescribed and used, however,

A

toxicity and intolerance can be significant issues

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45
Q

allergic reactions

A

May be life-threatening; may wear bracelet alert

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46
Q

Toxic effects

A
  • Monitor those taking low therapeutic index drugs
  • Some side effects are life-threatening (chloramphenicol may cause
    aplastic anemia)
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47
Q

Dysbiosis

A

imbalance in the microbiome

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48
Q

dysbiosis example

A

broad-spectrum antimicrobials may allow growth of
Clostridium difficile without competition, resulting in diarrhea or colitis

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49
Q

Certain bacteria have

A

intrinsic (innate) resistance

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50
Q

example of innate resistance

A

Mycoplasma lack cell wall, resistant to penicillin that
interferes with peptidoglycan synthesis

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51
Q

Outer membrane of Gram-negatives

A

blocks many medications

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52
Q

Pseudomonas species have very narrow

A

porin diameter (channel through outer membrane)

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53
Q

Bacteria may develop acquired resistance through

A
  • Spontaneous mutations
  • Horizontal gene transfer (drug resistance plasmids, transposons, etc.)
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54
Q

Antibacterial medications target specific bacterial processes and structures* (Selective toxicity)

A
  • Cell wall synthesis
  • Protein synthesis
  • Nucleic acid synthesis
  • Metabolic pathways
  • Cell membranes
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55
Q

antibacterial medications inhibiting cell wall synthesis due to unique bac cell walls w peptidoglycan

A

Include Beta-lactam
antibiotics, glycopeptide
antibiotics, and bacitracin

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56
Q

beta-lactam antibiotics all have

A

b lactam ring and high therapeutic index

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57
Q

beta lactam antibiotic examples

A

Penicillin, cephalosporins, carbapenems, monobactams

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58
Q

the beta-lactam antibiotics competitively inhibit with

A

penicillin-binding
proteins (PBPs) that
catalyze formation of
peptide bridges between
adjacent glycan strands;
disrupt cell wall synthesis

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59
Q

beta-lactam antibiotics are only effective against

A

actively growing cells

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60
Q

beta-lactam antibiotics also vary in

A

activity

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61
Q

when peptidoglycan of gram pos exposed, susceptible to

A

beta-lactam antibiotics, whereas outer membrane of gram-negatives block

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62
Q

PBPs different in Gram-positives versus

A

Gram-negatives; also aerobes
versus anaerobes, and in different species

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63
Q

some bacteria synthesize a b-lactamase which breaks

A

b-lactam ring destroying activity of antibiotic

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64
Q

penicillinase

A

inactivates members of penicillin family

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65
Q

extended spectrum b lactamases (ESBLS) inactivate

A

a wide variety of B lactam medications

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66
Q

gram negatives produce a more extensive array of __________ than gram positives

A

b lactamase

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67
Q

penicillinase is a

A

beta-lactamase

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68
Q

Broad-spectrum penicillins act against

A

Gram-positives and many Gram-
negatives (ampicillin, amoxicillin)

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69
Q

these penicillins inactivated by many

A

b lactamases

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70
Q

Extended-spectrum penicillins have
greater activity against

A

Enterobacteriaceae, Pseudomonas species

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71
Q

extended spec penicillins have reduced activity against

A

gram-positives

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72
Q

Augmentin: Penicillin + Beta-
lactamase inhibitor (clavulanic
acid) added to protect

A

penicillin from being degraded
by bacterial beta-lactamase

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73
Q

Cephalosporins

A

Structure makes resistant to some B lactamases

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74
Q

some cephalosporins have low affinity for

A

PBPs of gram-positives

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75
Q

chemical modifications have led to

A

five generations, where later generates more effect against gram-negs and resist b-lactamases

76
Q

fifth generation is effective against

A

MRSA

77
Q

other cephalosporins available with

A

B- lactamase inhibitor

78
Q

zerbaxa was first medication approved under

A

GAIN act

79
Q

Gain Act

A

Generating Antibiotic Incentives Now (GAIN) Act was passed by U.S. Congress in 2012
as part of the Food and Drug Administration Safety and Innovation Act (FDASIA). It
addresses the public health threat of antibacterial drug resistance by stimulating the
development and approval of new antibacterial and antifungal drugs.

80
Q

Glycopeptide antibiotics

A

Bind to amino acid side chain of NAM molecules; block peptidoglycan synthesis

81
Q

Glycopeptide antibiotics effective only against

A

Gram-positives; does not cross outer
membrane of Gram-negatives

82
Q

side effects of glycopeptide antibiotics

A

give low therapeutic index

83
Q

vancomycin is most widely

A

used glycopeptide

84
Q

vancomycin poorly absorbed from

A

intestinal tract, usually administered via IV except
for intestinal infections

85
Q

vancomycin often antibiotic of last resort to

A

treat Gram-positives resistant to beta-
lactam antibiotics

86
Q

vancomycin can be VERY

A

toxic; requires close monitoring of dose and blood levels to
guard against acute renal failure and cardiac toxicity.

87
Q

Bacitracin

A

toxicity limits to topical applications

88
Q

bacitracin interferes with

A

transport of peptidoglycan precursors across
membrane
* Common in first-aid skin ointments

89
Q

Inhibit protein synthesis

A
  • Generally bacteriostatic
  • aminoglycosides bactericidal
90
Q

aminoglycosides bactericidal

A

Can exploit differences
between prokaryotic and
eukaryotic ribosomes

91
Q

Prokaryotes have

A

70S ribosomes

92
Q

eukaryotes have

A

80S ribosomes

93
Q

mitochondria also have

A

70S ribosomes

94
Q

differences in ribosomes may account for

A

toxicity of some of these
antibiotics

95
Q

Aminoglycosides

A

gentamicin, amikacin, tobramycin, neomycin, and
streptomycin

96
Q

Aminoglycosides inhibit

A

Protein Synthesis

97
Q

Aminoglycosides Irreversibly bind to 30S ribosomal subunit, causing it to

A

malfunction; bacteriocidal

98
Q

malfunctional binding blocks

A

initiation of translation; causes misreading of mRNA by ribosomes past initiation

99
Q

aminoglycosides are often

A

toxic and generally used when alternatives unavailable

100
Q

Aminoglycosides are generally ineffective against

A

anaerobes, enterococci, and streptococci because they do not enter these cells efficientyl

101
Q

Sometimes aminoglycosides used synergistically with a penicillin that allows

A

the aminoglycoside to enter cells

102
Q

Inhaled form of tobramycin treats

A

Pseudomonas lung infections
in cystic fibrosis patients

103
Q

Neomycin too toxic for systemic use but common

A

in first-aid skin
ointments

104
Q

Tetracyclines reversibly bind to

A

30S ribosomal subunit
(thus bacteriostatic

105
Q

tetracyclines block

A

tRNA attachment; prevent translation

106
Q

tetracyclines are effective against

A

certain Gram-positives and Gram-negatives

107
Q

some tetracyclines have longer half-life meaning less

A

frequent doses

108
Q

resistances comes from either

A

decreased uptake or increased excretion

109
Q

the glycylcyclines are related to

A

the tetracyclines

110
Q

relation of glycylcyclines and tetracyclines

A

Wider activity
* Effective against bacteria resistant to the tetracyclines
* Relatively new, so acquired resistance is rare

111
Q

__________ is the only one currently approved

A

tigecycline

112
Q

Macrolides: Erythromycin and Azithromycin

A

Reversibly bind to 50S subunit; prevent continuation of translation

113
Q

Macrolides: Erythromycin and Azithromycin often antibiotic of choice for

A

patients allergic to penicillin

114
Q

macrolides are bacteriostatic against

A

many Gram-positives and most common causes
of atypical pneumonia
* Outer membrane of Enterobacteriaceae blocks

115
Q

resistance to macrolides occurs from

A

modification of ribosomal RNA target, enzyme
that modifies chemical, and decreased uptake

116
Q

Chloramphenicol

A

Binds to 50S ribosomal subunit; blocks translation
* Active against wide range of bacteria

117
Q

chloramphenicol used as last resort due to

A

rare but lethal side effect: may cause aplastic anemia, inability to form white, red blood cells

118
Q

Fluoroquinolones and rifamycins

A

inhibit nucleic acid synthesis

119
Q

fluoroquinolones

A

Inhibit topoisomerases, enzymes that maintain supercoiling of DNA; bactericidal against wide variety of bacteria
* DNA gyrase breaks, rejoins strands to relieve strain from localized unwinding of DNA; function is essential

120
Q

resistant to Fluoroquinolones

A

due to alteration in DNA gyrase target

121
Q

Rifamycin’s

A

Block prokaryotic RNA polymerase; prevents initiation of transcription

122
Q

Rifamycin is bactericidal against

A

Gram-positives, some Gram-negatives,
Mycobacterium

123
Q

resistance to rifamycin develops quickly due to

A

mutation in RNA polymerase gene

124
Q

folate inhibitors are most useful to

A

interfere with metabolic pathways

125
Q

folate inhibitors inhibit steps in

A

synthesis
of folate and ultimately
synthesis of coenzyme
required for nucleotide
biosynthesis

126
Q

animals lack enzymes to

A

synthesize folate; required in diet

127
Q

sulfonamides, trimetoprim inhibit

A

different steps in synthesis

128
Q

Sulfonamides and related are called

A

sulfa drugs

129
Q

sulfonamides inhibit many

A

Gram-positives and Gram-negatives

130
Q

sulfonamides structurally similar to

A

PABA, so enzyme binds chemical
* Example of competitive inhibition
* Human cells lack enzyme

131
Q

trimethoprim inhibits

A

enzyme in later step and has little effect on enzyme’s counterpart in human cells

132
Q

Combination of trimethoprim and sulfonamide has

A

synergistic effect; co-trimoxazole

133
Q

A few antimicrobials damage bacterial membranes causing cells to

A

leak, leading to cell death

134
Q

Daptomycin

A

inserts into cytoplasmic membrane and is Used against Gram-positives resistant to other antibiotics

135
Q

daptomycine ineffective against

A

Gram-negatives; cannot penetrate outer membrane

136
Q

Polymyxins bind to membranes of

A

Gram-negatives, limits usefulness to topical applications

137
Q

polymyxins also bind to

A

eukaryotic cells, though to a lesser extent

138
Q

Newest glycopeptide antibiotics disrupt

A

cell membranes (albavancin, oritavancin)

139
Q

Few antimicrobials effective against

A

Mycobacterium

140
Q

waxy cells of mycobacterium

A

prevents entry of many chemicals; slow growth

141
Q

First-line drugs are

A

most effective, least toxic
* Combination therapy decreases chance of development of resistant
mutants

142
Q

Second-line drugs given for strains resistant

A

to first-line drugs
* Less effective or have greater toxicity risk1

143
Q

some drugs target

A

unique cell wall of mycobacteria

144
Q

examples of drugs targeting unique processes of mycobacteria

A

Isoniazid inhibits mycolic acid synthesis; ethambutol inhibits enzymes required for synthesis of other cell wall components; pyrazinamide
interferes with protein synthesis

145
Q

Kirby-Bauer disc diffusion test

A

Conventional disc diffusion method routinely used to determine susceptibility of bacterial strain to antibiotics

146
Q

Standard sample of strain uniformly spread on agar plate in Kirby-Bauer, discs
containing ________ __________- placed on surface

A

different antibiotics

147
Q

in Kirby-Bauer test, drugs

A

diffuse outward, establish concentration gradients

148
Q

diffusion of drugs results in

A

zone of inhibition
compared with specially
prepared charts to determine
whether strain is susceptible,
intermediate, or resistant

149
Q

drug characteristics must be taken into acct, for example

A

molecular weight,
stability, amount

150
Q

minimum inhibitory concentration (MIC) is

A

lowest concentration that prevents growth in vitro

151
Q

Serial dilutions of chemical in suitable growth medium used;

A

cultures added, incubated, examined for turbidity

152
Q

inhibition does not necessarily mean

A

successful treatment; level
may not be achieved in person’s blood

153
Q

Microbes with MIC between susceptible (treatable) and resistant (untreatable) are

A

intermediate

154
Q

Minimum bacterial concentration (MBC) is

A

lowest concentration that kills 99.9% of cells in vitro

155
Q

MBC determined from plate count prepared from

A

tubes with no
growth in MIC test

156
Q

MIC techniques precise but

A

labor-intense, expensive

157
Q

Commercial modifications of susceptibility testing are

A

Less labor-intensive, often faster results

158
Q

One automated system determines growth rate via

A

turbidity in cards,
interprets results to determine MICs in 6 to 15 hours

159
Q

E test is modification of disc diffusion test, uses

A

strip with gradient of antibiotic; intersection of zone of inhibition indicates MIC

160
Q

New systems detect

A

genes encoding antibiotic resistance

161
Q

increasing use of antimicrobials, misuse selects for

A

resistant microorganisms

162
Q

only 3% of S. aureus originally resistant to penicllin G; now,

A

more than 90% are resistant

163
Q

Antimicrobial resistance alarming and has impact on

A

cost, complications, and
outcomes of treatment

164
Q

dealing with problem requires

A

understanding of mechanisms and spread
of resistance

165
Q

Mechanisms of acquired resistance

A

Antibiotic-inactivating enzymes & Antibiotic-inactivating enzymes & Decreased uptake of the
medication & Increased elimination of
medication

166
Q

Antibiotic-inactivating enzymes

A

Bacteria produce enzymes
that interfere with drug

167
Q

Antibiotic-inactivating enzymes examples

A

Penicillinase, extended
spectrum B lactamase,
chloramphenicol
acetyltransferase

168
Q

Alteration in target molecule

A

Minor structural changes can
prevent binding

169
Q

things that can cause alterations

A

PBPs (B lacatam antibiotics)
ribosomal RNA (macrolides,
lincosamides, streptogramins)

170
Q

Decreased uptake of the
medication

A

Changes in porin
proteins of outer
membrane of Gram-
negatives

171
Q

Increased elimination of
medication

A
  • Efflux pumps remove
    compounds from cell
  • Increased production or
    structural changes of pumps
    allows faster removal
  • Resistance to range of
    antimicrobials
172
Q

Acquisition of resistance

A

Spontaneous mutations that happen at low rate during replication that can still have significant effect

173
Q

just a single base-pair change in gene encoding a ribosomal proteins yields

A

resistance to streptomycin

174
Q

in a population of 10^9 cells, at least one likely has

A

that resistance mutation; if
streptomycin is added, only that cell and progeny will replicate,
yielding resistant population

175
Q

Spontaneous resistance to antibiotics with several different targets
or multiple binding sites is

A

less likely

176
Q

Combination therapy of multiple antibiotics is

A

often used; unlikely cells will simultaneously develop resistance

177
Q

Gene transfer: Genes encoding resistance can spread to

A

different strains, species, even genera

178
Q

most common spread through

A

conjugative transfer of R plasmids, which often carry several different resistance genes

179
Q

Resistance genes on R plasmids originate from

A
  • Spontaneous mutations
  • Microbes that naturally produce the antibiotic
180
Q

Gene coding for enzyme that modifies aminoglycoside likely originated from

A

the Streptomyces species that produces the antibiotic

181
Q

Responsibilities of patients to prevent resistance

A

Carefully follow instructions even if inconvenient
* Essential to maintain adequate blood levels of antibiotic; skipping a dose may reduce levels, allowing less-sensitive microbes a chance to grow and
spread
* Failure to complete treatment may not kill least-sensitive organisms, allowing subsequent spread

182
Q

The importance of an educated public

A

Antibiotics ineffective against viruses; cannot cure common cold!
* Misuse selects for antibiotic-resistant bacteria in normal microbiota; they
can eventually transfer R plasmids to pathogens

183
Q

Global impacts of the use of antimicrobial medications

A

Overuse is a worldwide concern; resistant microbes recognize no political boundaries
* Antimicrobial antibiotics available without prescription in many parts of the world, may allow improper use

184
Q

Antimicrobial antibiotics used in animal feeds at low levels to enhance growth;

A

selects for antibiotic-resistant microbes (ex. Resistant Salmonella strains linked to animals)

185
Q

phage therapeutics

A

new dawn in combatting multi-drug resistant bacteria by killing them

microbio km (6 decks)

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