Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Microbiology > Chapter 27 > Flashcards

Chapter 27 Flashcards

(95 cards)

Start Studying
1
Q

Who purified penicillin in the 1940s

A

Florey and Chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why do fungi and bacteria produce antibiotics?

A

To compete for limited nutrients by inhibiting or killing rival microbes in their environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What evolutionary pressure drives the production of antibiotics by microbes?

A

Competition—because there is a finite amount of nutrients available in their environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

If microbes produce antibiotics, what must they also do to survive?

A

They must protect themselves from the antibiotics they produce.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What group of organisms produces over 50% of clinically available antibiotics?

A

Actinomycetes, a group of soil-dwelling bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What key concept does the statement “We didn’t invent antibiotics… we discovered them” emphasize?

A

That antibiotics are natural products evolved by microbes, and humans simply found and harnessed them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is selective toxicity in the context of antibiotics?

A

The ability of an antibiotic to inhibit or kill microbes without harming the host.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What makes a good antibiotic besides effectiveness?

A

It must be safe, with low toxicity and minimal patient sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What major bacterial structure do penicillins and cephalosporins target?

A

Peptidoglycan synthesis (cell wall synthesis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which antibiotic class targets the cell membrane?

A

Polymyxins, daptomycin, and gramicidin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name two protein synthesis inhibitors and their ribosomal subunit targets.

A

Aminoglycosides → 30S

Macrolides (e.g., erythromycin) → 50S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the target of quinolones?

A

DNA replication, specifically DNA gyrase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do rifampin and pyronins inhibit?

A

RNA polymerase (transcription).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What metabolic pathway do sulfonamides inhibit?

A

Folate synthesis (a metabolic process essential for DNA and RNA production).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What structure do cell wall synthesis inhibitors target?

A

They target the peptidoglycan layer of bacterial cell walls, disrupting its synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do β-lactam antibiotics (like penicillin) work?

A

They block transpeptidase enzymes that cross-link peptidoglycan chains, weakening the cell wall and causing cell lysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What specific peptide bond does penicillin block?

A

The bond between the D-alanine residues during cross-bridge formation in peptidoglycan.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What enzyme catalyzes the cross-bridge formation that is blocked by β-lactams?

A

Penicillin-binding proteins (PBPs), also known as transpeptidases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens to a bacterial cell if peptidoglycan cross-linking is inhibited?

A

The cell becomes osmotically unstable and may lyse, especially in hypotonic environments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which two amino acids are involved at the terminal end of the peptide chain in peptidoglycan?

A

D-alanine - D-alanine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which step in peptidoglycan synthesis does penicillin block?

A

Penicillin blocks the action of the transpeptidase enzyme, preventing the formation of peptide cross-bridges between D-alanine residues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What specific amino acids are involved in the cross-linking step targeted by penicillin?

A

Penicillin inhibits the connection between the terminal D-alanine and D-alanine of neighboring peptidoglycan strands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens to the bacterial cell wall when penicillin inhibits transpeptidase?

A

The cell wall becomes weakened due to lack of cross-linking, leading to osmotic lysis of the bacterium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why is penicillin selectively toxic to bacteria but not humans?

A

Humans do not have peptidoglycan cell walls, so penicillin does not affect human cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What structural feature is essential for beta-lactam antibiotics to function?
The beta-lactam ring, which mimics the two terminal D-alanines in the peptidoglycan chain.
26
How do beta-lactam antibiotics disrupt bacterial cell wall synthesis?
They bind to transpeptidase enzymes, preventing them from linking the peptide side chains in peptidoglycan.
27
What is the result of beta-lactam antibiotics binding to transpeptidases?
Peptidoglycan cross-links fail to form, weakening the cell wall and leading to bacterial lysis.
28
Name the four major groups of beta-lactam antibiotics.
Penicillins Cephalosporins Monobactams Carbapenems
29
What structural similarity allows beta-lactams to block transpeptidases?
Beta-lactams structurally mimic D-alanine–D-alanine, tricking the enzyme into binding the antibiotic instead of its true substrate.
30
Why are there so many different kinds of beta-lactam antibiotics?
Because natural antibiotics can be chemically modified to create new, improved variants that retain their essential function but gain enhanced properties.
31
What organism produces natural penicillin?
The mold Penicillium.
32
What are semisynthetic beta-lactam antibiotics?
They are modified natural antibiotics where the beta-lactam ring is preserved, but chemical groups are altered to improve activity, spectrum, or stability.
33
What is retained in semisynthetic beta-lactams to ensure function?
The beta-lactam ring, which is crucial for binding to transpeptidase.
34
Give examples of semisynthetic beta-lactam antibiotics
Ampicillin, Methicillin, and Carbenicillin.
35
What makes Ampicillin and Methicillin semi-synthetic antibiotics?
They have a natural beta-lactam ring structure, but their R groups are chemically modified to enhance function, stability, or resistance to degradation.
36
What structural feature is retained in Ampicillin and Methicillin from natural penicillin?
The beta-lactam ring, which is essential for antibacterial activity.
37
What is the purpose of modifying the R group in beta-lactam antibiotics?
To improve drug properties such as spectrum of activity, resistance to beta-lactamases, or oral bioavailability.
38
Which parts of Methicillin and Ampicillin are chemically altered compared to Penicillin G?
Their R groups are different—Methicillin has methoxy groups, while Ampicillin has an amino group.
39
Why does natural penicillin have a limited spectrum of activity?
It cannot penetrate the outer membrane of Gram-negative bacteria, limiting its effectiveness to mostly Gram-positive organisms.
40
How does ampicillin overcome the limitation of natural penicillin?
Ampicillin has chemical modifications that allow it to pass through porins in the outer membrane of Gram-negative bacteria.
41
What kind of antibiotic is ampicillin, and what structural feature enables its broader activity?
Ampicillin is a semi-synthetic beta-lactam antibiotic; its modified R group helps it access Gram-negative cells by fitting through general porins.
42
Why was methicillin developed?
Methicillin was created to resist degradation by penicillinase (beta-lactamases), which are enzymes produced by bacteria to destroy penicillin.
43
What do beta-lactamases do?
Beta-lactamases cleave the beta-lactam ring of antibiotics, making drugs like penicillin ineffective.
44
During which bacterial growth phase are antibiotics that target cell wall synthesis most effective?
Antibiotics are most effective during the exponential (log) phase, when bacteria are actively dividing and synthesizing new cell walls.
45
Why are cell wall-targeting antibiotics like penicillin less effective in the stationary phase?
In the stationary phase, bacterial growth slows, and cell wall synthesis decreases, making antibiotics that target peptidoglycan formation less effective.
46
Which two antibiotics target bacterial cell membranes and are typically used only topically?
Gramicidin and Polymyxin target bacterial cell membranes and are used only for topical application.
47
Why are Gramicidin and Polymyxin only used topically and not internally?
They can disrupt human cell membranes as well, making them toxic when used systemically. Therefore, they are limited to external use like in ointments (e.g., Neosporin).
48
What is the mechanism of action of sulfonamides (sulfa drugs)?
Sulfonamides (like sulfanilamide) mimic para-aminobenzoic acid (PABA) and block folic acid synthesis by competitively inhibiting the enzyme that uses PABA.
49
Why is blocking folic acid synthesis effective against bacteria but not harmful to humans?
Humans do not synthesize folic acid—they obtain it from their diet. Bacteria, however, must synthesize it, so sulfa drugs specifically target bacterial metabolism without harming human cells.
50
What is the combination of drugs in Bactrim and how do they work together?
Bactrim combines sulfamethoxazole (a sulfonamide) and trimethoprim. They act synergistically to block two different steps in folic acid synthesis, making the treatment more effective.
51
What class of antibiotics inhibits DNA synthesis by targeting DNA gyrase?
Quinolones and Fluoroquinolones, such as ciprofloxacin, inhibit DNA synthesis by blocking DNA gyrase and topoisomerase IV, enzymes essential for bacterial DNA replication.
52
How do quinolones work at the molecular level?
They bind to DNA gyrase or topoisomerase, causing breaks in the bacterial DNA and preventing it from being properly replicated or repaired.
53
Why are fluoroquinolones effective antibiotics?
They are broad-spectrum, highly potent, and bactericidal, making them effective against a wide range of Gram-positive and Gram-negative bacteria.
54
What is the target of antibiotics that inhibit protein synthesis?
They target the bacterial ribosome, specifically the 30S or 50S subunits, interfering with translation without affecting eukaryotic ribosomes.
55
How does chloramphenicol inhibit protein synthesis?
Chloramphenicol binds to the 50S ribosomal subunit and inhibits peptide bond formation, blocking elongation of the protein chain.
56
What do tetracyclines (like doxycycline) do?
Tetracyclines bind to the 30S ribosomal subunit and prevent the attachment of tRNA to the mRNA-ribosome complex, halting translation.
57
How does streptomycin inhibit translation?
Streptomycin binds to the 30S subunit and changes its shape, causing mRNA to be read incorrectly (misreading of the genetic code).
58
What part of the ribosome do tetracyclines like doxycycline target?
They target the small subunit (SSU) of the ribosome.
59
What is the specific mechanism of action for doxycycline?
Doxycycline binds to the A-site of the ribosome and prevents amino-acylated tRNA from binding, halting protein elongation.
60
What types of antimicrobial agents are included in protein synthesis inhibitors?
They include natural, semi-synthetic, and fully synthetic agents.
61
Can protein synthesis inhibitors act on both ribosomal subunits?
Yes, they may affect either the small (30S) or large (50S) subunit.
62
What historical impact did the discovery of antibiotics have on human health?
It coincided with a significant increase in life expectancy.
63
What major problem is caused by the overuse of antibiotics?
Antibiotic resistance—indiscriminate use promotes the spread of resistant microbes.
64
What does the rise of resistant organisms like MRSA indicate about antibiotic use?
That we may be approaching the end of the "glory days" of antibiotics, and new strategies are needed.
65
What is a key example of a clinically significant resistant organism?
Methicillin-resistant Staphylococcus aureus (MRSA).
66
What warning did the WHO issue regarding antibiotic use?
The WHO warned of a "post-antibiotic era", where common infections could become deadly due to widespread antibiotic resistance.
67
What is intrinsic antibiotic resistance?
Intrinsic resistance means the resistance is built into the organism's structure and is not acquired from another source.
68
Give examples of intrinsic resistance features in bacteria.
Outer membrane of Gram-negative bacteria Capsules Mycomembranes (e.g., in mycobacteria)
69
What is acquired antibiotic resistance?
Acquired resistance means a bacterium gained resistance genes it did not originally have, often through horizontal gene transfer.
70
How do bacteria typically acquire resistance genes?
Through horizontal gene transfer—e.g., transformation, transduction, or conjugation.
71
What do beta-lactamase enzymes do?
They cleave the beta-lactam ring, making beta-lactam antibiotics non-functional.
72
H
A
73
What does ESBL stand for and why is it important?
ESBL = Extended Spectrum Beta-Lactamase. These enzymes can inactivate a wide range of beta-lactam antibiotics, making infections harder to treat.
74
Why are ESBL-producing bacteria a clinical concern?
They are resistant to most beta-lactams, often found in healthcare settings, and may require complex or last-resort treatments.
75
How can bacteria become resistant to beta-lactams without using beta-lactamase?
Through mutations in the transpeptidase (PBP) enzyme, which prevent the antibiotic from binding.
76
p
77
How do these mutations confer resistance without losing enzyme function?
The enzyme still works in cell wall synthesis, but the beta-lactam can no longer bind to block it.
78
What is the function of a multidrug efflux pump in bacteria?
It actively exports antibiotics and other toxic compounds out of the bacterial cell, reducing intracellular drug concentration.
79
In what types of bacteria are multidrug efflux pumps commonly found?
They are commonly found in Gram-negative bacteria.
80
What are the three major components of a multidrug efflux system?
Transporter protein (in cytoplasmic membrane) Accessory protein (in periplasm) Outer membrane channel
81
Why are efflux pumps problematic for antibiotic treatment?
Because they can pump out multiple classes of antibiotics, leading to multidrug resistance (MDR).
82
T
83
What happens when antibiotics are taken?
Antibiotics kill both pathogenic and helpful bacteria, but drug-resistant bacteria survive.
84
What occurs after drug-resistant bacteria survive treatment?
They are allowed to grow and take over because the competition has been removed.
85
o
86
What is combination therapy in the context of antibiotic resistance?
It involves using multiple antibiotics at once to reduce the chances of bacteria developing resistance to all agents.
87
How does phage therapy work?
Bacteriophages, which are viruses that infect bacteria, are used to target and destroy specific bacterial pathogens, including drug-resistant strains.
88
Why might scientists modify current antibiotics?
To overcome resistance mechanisms and make the antibiotic effective again against resistant bacteria.
89
What is the goal of identifying new targets in fighting drug resistance?
To find previously unexploited bacterial functions or structures that antibiotics can act upon.
90
What does it mean to “link antibiotics”?
It refers to chemically combining two different antibiotics into a single molecule to enhance effectiveness and reduce resistance.
91
What are the four major mechanisms by which bacteria become resistant to antibiotics?
Modify the target Destroy the antibiotic Modify the antibiotic Remove the antibiotic
92
What does "modify the target" mean in antibiotic resistance?
The bacterial cell changes the structure of the antibiotic’s target (e.g., ribosome or enzyme) so the drug can no longer bind effectively.
93
What is meant by "destroy the antibiotic"?
Bacteria produce enzymes (like beta-lactamases) that chemically break down or inactivate the antibiotic before it can act.
94
How does a bacterium "modify the antibiotic"?
It chemically alters the antibiotic molecule, making it ineffective without destroying it (e.g., by adding a functional group).
95
Ef

Microbiology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions