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Microbiology > Chapter 20 Micro > Flashcards

Chapter 20 Micro Flashcards

1
Q

What is selective toxicity?

A

the idea of a drug killing pathogens without damaging the host (concept popularized by Paul Ehrlich)

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2
Q

What is chemotherapy?

A

the use of drugs/chemicals to treat any disease (broad historical term coined by Paul

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3
Q

What are antimicrobial drugs?

A

compounds that interfere with the growth of microbes within a host

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4
Q

What are some disadvantages of natural penicillin?

A

narrow spectrum of activity (only gram-positive bacteria)
(not always a disadvantage)
• susceptibility to penicillinases (b-lactamases)
- most common form of resistance to penicillins

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5
Q

What is an antibiotic?

A

substance produced by a microbe that, in small amounts, inhibits another microbe (a strict definition from the text of chapter 20)

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6
Q

When was first antibiotic discovered?

A 
1928: Fleming 
discovered penicillin, 
produced by a mold 
from the genus 
Penicillium
§1940: Scientists led 
by Ernst Chain and  
Howard Florey began 
first clinical trials of 
penicillin
The first antibiotic discovered
S. aureus colonies
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7
Q

Why have pharmaceutical companies put very little investment in the development of new antibiotics?

A
  1. generate small revenue

2. difficult to identify new mechanisms to kill pathogens

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8
Q

What is antibiosis?

A

an association of two organisms in

which one is harmed or killed by the other

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9
Q

Which genus produces more than half of our antibiotics?

A

Streptomyces

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10
Q

What two characteristics do almost all antibiotic producing microbes have in common?

A
  1. commonly found in soil

2. All have spores

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11
Q

What are broad spectrum antimicrobials?

A

act against a wide range of microbes

gram positive and negative

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12
Q

What are narrow spectrum antimicrobials?

A

effective against specific groups of

microbes

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13
Q

Why is the LPS outer layer a primary factor in antibiotic selective toxicity?

A

Additional barrier that the pathogen has to get through

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14
Q

What is the advantage/disadvantage of treating a bacterial infection with broad spectrum antibiotic?

A

Advantage: effective treatment more likely when the identify of the pathogen is not yet known
Disadvantage:
destroys normal microbiota that ordinarily compete with and check the growth of pathogens and other microbes

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15
Q

What is a super infection?

A

a second infection occurring during the course of an
existing infection, usually caused by the antibiotic
destruction of the normal microbiota and overgrowth of
opportunistic pathogens unaffected by the antibiotic (i.e.
gut overgrowth of Clostridium difficile and/or Candida
albicans)

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16
Q

Why are these organisms generally not affected by initial antimicrobial treatment?

A

One is naturally resistant and the other is a yeast so antimicrobial drugs would not be of assistance

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17
Q

What does bactericidal mean?

A

Kill microbes directly

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18
Q

What does bacteriostatic mean?

A

Prevent microbes from growing
–Host’s defenses (antibody production and
phagocytosis) usually destroy organisms

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19
Q

What are the five ways antimicrobial drugs act?

A
  1. inhibition of cell wall synthesis: penicillins
  2. Inhibition of protein synthesis: chloramphenicol
  3. Inhibition of nucleic acids replication and transcription: rifampin
  4. Injury to plasma membrane: polymyxin B
  5. Inhibition of essential metabolite synthesis: sulfonamide
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20
Q

Why is is more difficult to find or develop antimicrobials effective against fungi?

A

More targets for selective toxicity in bacteria

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21
Q

There is concern that antibiotics that target bacterial ribosomes could adversely affect cells of the host. Why?

A

Mitochondria of eukaryotic cells contain 70 s ribosomes

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22
Q

What is a common antimicrobial target in fungal plasma

membranes?

A

Sterols

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23
Q

Why does penicillin only affect actively growing cells?

A

Only target peptidoglycan synthesis

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24
Q

Antimicrobials that target replication and transcription

generally have limited medical usefulness. Why?

A

Interferes with mammalian DNA

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25
Q

What are some inhibitors of cell wall synthesis?

A 
-Penicillin (over 50 chemically related antibiotics 
with a common core structure)
§Natural penicillins
§Semisynthetic penicillins
-Extended-spectrum
-Penicillinase resistant
§Carbapenems
§Monobactams
§Cephalosporins
§Polypeptide Antibiotics
§Vancomycin
§Bacitracin
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26
Q

What are tetracyclines?

A

• Broad spectrum (gram + and -)
• Bind to 30S ribosomal subunit and interfere with tRNA-codon
attachment
• Natural tetracylines are produced by Streptomyces and include
tetracycline, chlorotetracycline, and oxytetracycline
• Semisynthetic tetracyclines (i.e. doxycycline) have longer
retention times in the body
• Selective toxicity due to both greater bacterial ribosome sensitivity and poor penetration into mammalian cells
• Treatment disadvantages:
suppress normal intestinal
microbiota, may brown children’s
(< 8 yrs) teeth, or cause liver
damage in pregnant women

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27
Q

What are macrolides?

A

• Named for the presence of a macrocyclic lactone ring
• Binds 50S subunit; prevents translocation (blocks exit
tunnel)
• Natural and first member of this class is erythromycin.
- similar spectrum to Penicillin G (can’t penetrate gram-
negative LPS) but can be taken orally
• Newer members are
derived from erythromycin
and have a broader
spectrum

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28
Q

What are streptogramins?

A

Cyclic peptides
• Gram positive spectrum
• The only approved streptogramin, is a mixture of two
streptogramins (quinupristin and dalfopristin)

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29
Q

How do streptogramins work?

A

• These streptogramins act synergistically at two uniquely
different points on the 50S ribosomal subunit, which together
causes premature protein termination.
- dalfopristin blocks an early translational step
- quinopristin blocks a later translational step
• Major clinical use is treatment of gram
positive infections, particularily Vancomycin-
resistant Staphylococcus aureus (VRSA) and
Vancomycin-resistant enterococcus (VRE)

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30
Q

What are oxazolidinones?

A

-it is a totally synthetic antimicrobial, which may lessen
resistance rate
• unique target and mechanism – prevents formation
of a functional 70S-initiation complex by binding the
50S subunit near 30S interface
• linezolid is a member of this group

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31
Q

How does linezolid work?

A

interacts with the peptidyl-tRNA binding P site at the
50S subunit and prevents binding of fMet-tRNA to this site
during the formation of the initiation complex

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32
Q

Some antibiotics target what?

A

fatty acid

biosynthesis

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33
Q

What is the function of polymyxin B?

A

-binds LPS of gram negative bacteria then alters both inner and outer membranes, making them more permeable
-little to no effect on gram-positives, since thicker cell wall
prevents access to membrane
*Neosporin!

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34
Q

What is rifamycin?

A

– Members are produced naturally by the bacterium
Amycolatopsis (am′ē-kō-la-top′sis) mediterranei, or
artificially.
– inhibits transcription by binding prokaryotic RNA
polymerase
– Semisynthetic Rifampin/Rifampicin is the best known family
member
–Key use is as part of the
antibiotic cocktail for treating
Mycobacterium infections,
including tuberculosis and
leprosy

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35
Q

What are quinolones?

A

-family of synthetic broad-spectrum antibiotics
– inhibits DNA gyrase
– first member was Nalidixic acid (early 1960’s)
– historically used to treat urinary infections but members are
rarely used today, naladixic acid listed as a carcinogen in
1998.

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36
Q

What are fluroquinolones?

A

– fluorinated quinolones
– divided into generations based on progressively
broader spectrum of activities
– group is relatively non-toxic but resistance can develop
rapidly, even during treatment
- Treatment of choice for urinary tract infections

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37
Q

what are sulfonamides?

A 
Among the first synthetic anti-
microbial drugs
-Structurally similar to para-
aminobenzoic acid
-Interfere with conversion of 
PABA to folate
-Bacteriostatic
-Broad spectrum
-Most widely used sulfa drug 
is used as a combination of 
the sulfonamide 
sulfamethoxazole with 
trimethoprim (TMP-SMZ)
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38
Q

Why are only bacteria affected by sulfa drugs?

A

Bacteria synthesize folic acid starting with
PABA (folic acid can’t cross bacterial cell
walls). Humans ingest folic acid already
formed (lack the enzymes to convert PABA to
folic acid)

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39
Q

What are anti fungal drug targets?

A
  • Fungal Sterols
  • Fungal Cell Walls
  • Nucleic Acids
  • Other fungal targets
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40
Q

What are fungal sterols?

A
  • The principal sterol in fungal plasma membranes isergosterol (cholesterol in humans)
  • Several antifungal drug groups target ergosterol
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41
Q

What are polyenes?

A

polyenes (polyunsaturated organic acids)
- Amphotericin B, produced by Streptomyces, is the
most commonly used member
- Binds to ergosterol and forms a transmembrane
channel that leads to leakage

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42
Q

What are azoles?

A

• inhibit ergosterol synthesis
• contains some of the most widely used antifungal drugs
- imidazoles: (miconazole, clotrimazole, ketoconazole etc.)
are commonly used topically without prescription for
localized surface infections (i.e. athlete’s foot and vaginal
yeast infections
- triazoles: (fluconazole, voriconazole etc.) are used for
invasive life-threatening fungal infections.

43
Q

What are allylamines?

A
  • inhibit a different enzyme (than the azoles) in the
    ergosterol biosynthetic pathway
  • Terbinafine is a representative member
44
Q

What are thiocarbamates?

A

inhibits same enzyme as allyamines
- Tolnaftate is a representative member
- common alternative to miconazole as a topical
treatment for athlete’s foot.

45
Q

What are fungal cell walls composed of?

A

tight, semipermeable
fibrous network of polymers such as chitin, b-glucan, other
polysaccharides and mannoproteins.

46
Q

What are fungal nucleic acids?

A

Flucytosine is a synthetic analog of the pyrimidine
cytosine (prodrug)
• In fungi, flucytosine is converted to 5-fluorouracil è
5-FUMP èè5-FUTP
- 5-FUTP can be incorporated into RNA and inhibit
translation or further metabolized to 5-FdUMP, a potent
inhibitor of thymidylate synthase and thus DNA
synthesis.
• mammalian cells lack the flucytosine converting
enzyme

47
Q

What is Griseofulvin?

A

binds to fungal tubulin interfering with
microtubule assembly and subsequently mitosis.
Produced by a species of Penicillium

48
Q

What is undecylenic?

A

is an organic unsaturated fatty acid.
Active against athletes foot but not as effective as
tolnafate or miconazole. Mechanism of action
unknown.

49
Q

What is pentamidine?

A

is used to treat Pneumocystis
pneumonia, a complication of AIDS. (caused by a
fungi called Pneumocytosis jirovecci) Mechanism of
action unknown

50
Q

Why is Gentamicin spelled with an “i”?

A

Aminoglycosides from bacterias of the Streptomyces genus are names with suffix mycin whereas those from Micromonospora species are given the suffix micin

51
Q

What are HIV targeted antivirals?

A
  • reverse transcription
  • protease inhibitors
  • cell entry inhibitors
  • integrase inhibitors
52
Q

What is acyclovir?

A

structurally resembles the nucleoside
deoxyguanosine.
- generally useful for treating herpesvirus infections
• Several other nucleoside and nucleotide analogs
are commercially available

53
Q

What is zanamivir and oseltamivir?

A

inhibit the

enzyme neuramindase of Influenza virus

54
Q

Cells produce ____ to prevent the spread of viruses to new cells.

A

interferons

55
Q

What is the mechanism of blocking cell entry?

A

Drug targeting the host cell CCR5 receptor used for viral entry
- Synthetic peptide that inhibits fusion by mimicking a region of
the gp41 HIV-1 envelope protein.

56
Q

What are reverse transcription inhibitors?

A
  • nucleoside (azidothymidine/AZT) and nucleotide (tenofovir)
    analogs. Thymidine and Adenosine chain terminators,
    respectively
  • non-nucleotide agents (inhibits reverse transcriptase)
57
Q

What are integrase inhibitors?

A
  • inhibit enzyme that integrates viral DNA into the

genome of the infected cell

58
Q

What is the weakness of targeting the fatty acid biosynthetic pathway to kill pathogens?

A

targeting pathogens and pathogens can use fatty acids from the host. Dependent upon pathogen

59
Q

What is quinine?

A

– Isolated from the cinchona tree
- Used to treat malaria
– Mechanism of action not fully resolved
– Now largely replaced by synthetic derivatives used to
treat a variety of protozoan and amoebic diseases.

60
Q

What is metronidazole?

A

selective for anaerobic bacteria and protozoa due to
their ability to intracellularly reduce metronidazole to its
active form. Reduced metronidazole covalently binds to
DNA and disrupts synthesis

61
Q

What is the E test?

A

a gradient diffusion method that determines the antibiotic
sensitivity and estimates minimal inhibitory concentration (MIC).
• plastic strips placed on a lawn of cells contain an increasing
gradient of the antibiotic

62
Q

What are mechanisms of antibiotic resistance?

A
  1. Prevention of drug penetration
  2. Enzymatic destruction or inactivation of drug
  3. Alteration of drug’s target site
  4. Rapid efflux of the drug
  5. Other mechanisms
63
Q

What is the prevention of drug penetration?

A
  • Gram-negative cells are inherently more resistant to antibiotics. The outer
    membrane provides a barrier which restricts access to porins
  • Porin mutations can further restrict antibiotic entry to periplasmic space
64
Q

what is enzymatic destruction or inactivation of drug?

A
  • Nearly 200 b-lactamases known

- Other types of inactivation

65
Q

What is alteration of the drugs target site?

A
  • rpsL
  • another Penicillin binding protein (PBP)
    • MRSA (express a foreign PBP that is unaffected by methicillin)
66
Q

What is rapid efflux of the drug?

A
  • pumps present in the plasma membranes of gram-negative bacteria
  • confers resistance to practically all major classes of antibiotics
67
Q

What are the functions of other mechanisms for antibiotic resistance?

A
  • Produce large amounts of target enzyme/molecule
  • Produce less of the target enzyme/molecule (i.e. polyene antibiotics and
    sterols)
68
Q

Antibiotic misuse selects for resistance mutants include:

A

– Using outdated, impure or counterfeit antibiotics
– Using antibiotics for the common cold and other
inappropriate conditions
-Using antibiotics in animal feed (see book)
– Failing to complete the prescribed regimen
– Using someone else’s leftover prescription

69
Q

What is synergism?

A

occurs when the effect of two
drugs together is greater than the effect of
either alone

70
Q

What is antagonism?

A

occurs when the effect of two
drugs together is less than the effect of either
alone

71
Q

What is the Therapeutic index?

A

A comparison of the amount of a therapeutic agent that
produces the therapeutic effect to the amount that causes death.
The Therapeutic Index is often defined in terms of a comparison
of the average toxic dose vs. average effective dose, i.e. TI =
TD50/ED50. A higher index is preferable to a lower one.

72
Q

What is the research on new chemotherapeutic agents?

A

1) Antimicrobial peptides
– part of innate immune systems of higher organisms
– generally 100 a.a. or less and carry a positive charge
(cationic peptides)
– mechanisms of action
• most disrupt microbial and viral enveloped membranes
rich in anionic phospholipids (Primary target)
• a variety other targets
-2) Phage therapy
– use of bacteriophages to treat pathogenic bacterial
infections. Although used and developed mainly in former Soviet
Union countries for more than 50 years, still being tested
elsewhere. Theoretically, could specifically target bacterial cells.
Generally used in the US as a last-ditch effort after antibiotics fail.

73
Q

What is the Kirby bauer test?

A 
-The diameter of the zone 
of inhibition is measured. 
-In general, the larger the 
zone, the more sensitive 
the microbe
-zones can be compared to chart of other bacteria to be judged as sensitive, intermediate or resistant
74
Q

What is not always true about the Kirby Bauer test?

A

The size of the zone does not always relative to sensitivity of the microbe

75
Q

How can the minimal bacteriocidal concentration

(MBC) be determined from the previous test?

A

Wells lacking growth are cultured in broth/agar plates lacking the drug
-Growth occurs if the drug is not bacteriocidal

76
Q

Why is it important to know the MIC/MBC?

A

To avoid antibiotic over usage; expensive and potential for toxic side effects

77
Q

What is an antibiogram?

A

-Sum report of antimicrobial susceptibility testing data from patients

78
Q

Tetracycline sometimes interferes with the

activity of penicillin. How?

A

Bacteriostatic. Action of penicillin requires bacterial growth

79
Q

What is the Therapeutic index?

A

A comparison of the amount of a therapeutic agent that
produces the therapeutic effect to the amount that causes death.
The Therapeutic Index is often defined in terms of a comparison
of the average toxic dose vs. average effective dose, i.e. TI =
TD50/ED50. A higher index is preferable to a lower one.

80
Q

What do antimicrobial peptides do?

A

– part of innate immune systems of higher organisms
– generally 100 a.a. or less and carry a positive charge
(cationic peptides)
– mechanisms of action
• most disrupt microbial and viral enveloped membranes
rich in anionic phospholipids (Primary target)
• a variety other targets

81
Q

What is phage therapy?

A

Phage therapy
– use of bacteriophages to treat pathogenic bacterial
infections. Although used and developed mainly in former Soviet
Union countries for more than 50 years, still being tested
elsewhere. Theoretically, could specifically target bacterial cells.
Generally used in the US as a last-ditch effort after antibiotics fail.

82
Q

What are the two natural penicillins?

A 
Penicillin G(injection)
Penicillin V(oral)
83
Q

What are the most often used pencillins?

A

G and V
G: gold standard
V: to feed or eat

84
Q

Why is natural penicillin effective against gram positive but not gram negative bacteria?

A

Natural penicillin can’t penetrate the membrane

85
Q

What are semisynthetic penicillins?

A

Natural penicillins that have been chemically modified.
• Alternative side chains are chemically added to a common penicillin
nucleus to
- extend antibiotic spectrum
- increase resistance to penicillinase.
• A common penicillin nucleus is obtained by either
1) Interrupting the organisms synthesis of penicillin or
2) removing the side chains from the completed natural molecule

86
Q

How are penicillins generally modified to

increase their resistance to β-lactamases?

A

Bulky side chain hinder beta lactamase access to the B ring

87
Q

What modification increases outer membrane permeability?

A

Less bulky side group, additional hydrophilic/polar groups to allow passage through pore

88
Q

What are extended spectrum penicillins?

A

Semi-synthetic penicillins effective against many gram-negative
bacteria as well as gram-positive bacteria
• Not resistant to penicillinases
• Different classes produced over the years. A broader spectrum
of activity achieved with each group (listed in order)
- aminopenicillins (ampicillin and amoxicillin)
- carboxypenicillins (carbenicillin)
- ureidopenicillins (mezlocillin and azlocillin)

89
Q

What are beta lactamase inhibitors?

A

• A strategy to overcome penicillinases is to combine penicillins
with potassium clavulanate.
- produced by a Streptomycete
- irreversible inhibitor of b-lactamase (suicide inhibitor)
- despite having a β-lactam ring it has negligible intrinsic
antimicrobial activity

90
Q

What is MRSA?

A

I. Staphylcoccal infections rapidly became resistant to
Penicillin due to a plasmid borne ß-lactamase gene
II. Semisynthetic Penicillin antibiotics relatively resistant
to ß-lactamase (i.e. methicillin) were introduced
III.S. aureus strains resistant to methicillin appeared, and
were termed MRSA
- resistance is so common that methicillin use has been
discontinued in the US
• MRSA is now applied to describe S. aureus strains that
have developed resistance to 1) other penicillin resistant
penicillins, 2) penicillins combined with ß-lactamase
inhibitors and 3) cephalosporins.

91
Q

What are carbapenems?

A

Class of b-lactam antibiotics that swap a C and S in the
common penicillin nucleus and add a double bond
• Broadest spectrum of activity of b-lactam antibiotics
(active against 98% of hospital patient isolated organisms)
• resistant to penicillinases but carbapenamases have arisen
• Imipenem is representative of the group. Is effective alone or
can be given with cilastatin
(Imipenem is degraded in the kidneys by dehydropeptidase and
its activity can be prolonged by combining with cilastatin)

92
Q

What are monobactams?

A

Class of monocyclic b-lactam antibiotics
• Produced by several bacterial species but synthetic
Aztreonam is the only monobactam used clinically

93
Q

Why is activity of monobactams limited to certain gram neg bacteria?

A

Poorly binds penicillin binding proteins of gram pos and anaerobic bacteria

94
Q

What are cephalosporins?

A 
Activity and b-
lactam ring
structure matches
penicillin
• Although portions
of the common
nucleus differ
from penicillin, b-
lactamases have
arisen that 
inactivate them
95
Q

What are the generations of cephalosporins?

A

A very extensive class grouped by generations, which reflect
increased spectrums as development continued
– First-generation: Narrow spectrum, gram-positive
– Second-generation: Extended spectrum includes some
gram-negative
– Third-generation: increased gram-negative spectrum.
Includes some Pseudomonads
– Fourth-generation: most extended spectrum of activity
– Fifth-generation: also active against Methicillin-resistant
S. aureus (MRSA) and E. faecalis

96
Q

What is bacitracin?

A 
Mixture of related cyclic 
polypeptides from Bacillus 
subtilus isolated from the 
infected compound fracture 
from a girl named Tracy
§interferes with the transport 
of peptidoglycan precursors 
(NAG and NAM monomers) 
across the cytoplasmic 
membrane 
§use restricted to topical 
application (toxic orally)
§narrow spectrum (gram 
positives)
97
Q

What is vancomycin?

A

named for the word “vanquish”(vanquished MRSA)
§Traditionally used as a drug of last resort against
antibiotic-resistant S. aureus (MRSA)
§Binds NAG and NAM subunits to prevent their
incorporation into the peptidoglycan matrix (same
target as Teixobactin but different mode of action)
§Glycopeptide derived from Streptomyces
§Widespread use has led to the appearance of
vancomycin-resistant Staphylococcus aureus (VRSA)
and vancomycin-resistant enterococci (VRE)
§Both Vancomycin and Teixobactin are Narrow
spectrum (gram positives)

98
Q

What is isoniazid?

A 
Inhibits mycolic acid synthesis
• never used on its own to treat 
active tuberculosis because 
resistance quickly develops
• Used with rifampin (rifampicin) 
and/or ethambutol etc. (different 
regimens employed to treat TB)
99
Q

What is ethambutol?

A 
Inhibits incorporation of mycolic 
acid into the cell wall
• Comparatively weak 
antitubercular drug that is used as 
a secondary drug to reduce 
resistance problems
100
Q

Why is resistance a concern

when using a weak antibiotic?

A

unable to kill every pathogen, grows slowly and leads to resistance

101
Q 
Does 
oxygen 
influence 
antibiotic 
activity?
A

Oxygen is required for uptake of aminoglycosides

102
Q

What are aminoglycosides?

A

Streptomycin, Neomycin, Gentamicin, Tobramycin
• Gram-negative spectrum but not anaerobes
• Changes shape of 30S subunit causing translation errors
• Rapid development of resistance and side-effects led to
reduced use in 1970s and 1980s. Nevertheless, today they are
still the most used antibiotics worldwide due to their high
efficacy and low cost.

103
Q

What is chloramphenicol?

A

Low cost: simple structure can be chemically synthesized
rather than isolated from Streptomyces
- Broad spectrum (gram + and -)
- Binds 50S subunit; inhibits peptide bond formation
- Chloramphenicol and metronidazole have potent anaerobic
activity

104
Q

What are some inhibitors of protein synthesis?

A 
Chloramphenicol
• Aminoglycosides
• Tetracyclines
• Macrolides
• Streptogramins
• Oxazolidinones

Microbiology (7 decks)

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