Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microimm 2500 > Antibiotics and Antibiotic Resistance > Flashcards

Antibiotics and Antibiotic Resistance Flashcards

1
Q

Disinfectants

A

antimicrobial agents that are applied to inanimate objects (e.g. floors, tables, walls)

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

Antiseptics

A

antimicrobial agents that are sufficiently nontoxic to be applied to living tissues (e.g hand sanitizers)

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

Antibiotics

A

antimicrobial agents produced by bacteria and fungi that are exploited by humans (delivered topically and internally)

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

Who is Alexander Fleming?

A
  • discovered penicillin in 1928
  • produced from Penicillium
  • colonies of staphylococci couldn’t grow around a contaminating mold
  • Nobel Prize in Physiology and Medicine (1945)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are two major problems related to antibiotics?

A
  1. Diminished interest from pharmaceutical companies to develop new antibiotics
  2. Bacterial resistance to antibiotics always happens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is antibiotic overused/misused?

A
  • Empiric use (blinded use)
  • Increased use of broad spectrum agents
  • Pediatric use for viral infections
  • Patients who do not complete course (chronic disease, e.g. TB)
  • Antibiotics in animal feeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Minimum Inhibitory Concentration (MIC) purpose

A
  • used to measure antibiotic activity

- lowest amount of antibiotic that will inhibit growth

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

What was the old way to test MIC

A

Have aSeries of culture tubes with varying concentration of agent and see which one is effective at the lowest concentration

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

Modern way to test MIC

A
  • Use antibiotic strips
  • Plate bacteria
  • Put antibiotic strips (multiple antibiotics)
  • Allow bacteria to grow
  • Zone of inhibition - where bacteria cannot grow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do antibiotics target?

A
  • Cell wall synthesis
  • Protein synthesis
  • DNA/RNA synthesis
  • Folate Synthesis
  • Cell membrane alteration
  • targets are not present (or are different) in eukaryotic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

B - Lactam Antibiotics

A
  • e.g. Penicillin
  • contain a “β lactam ring”
  • function to inhibit cell wall synthesis in bacteria
    β lactams bind the bacterial “penicillin-binding proteins (PBPs)”
  • PBPs are transpeptidases
  • no peptide cross-links = weak cell wall = cell death
  • but some bacteria can produce a β lactamase, an enzyme that destroys the ring and thus the antibiotic (bacteria select against this antibiotic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Modified B Lactam Antibiotics

A
  • e.g. Methicillin
  • contains a “ β lactam ring”
  • chemically modified penicillin
  • can’t be cleaved by β lactamases
  • but some bacteria can produce a different “penicillin-binding protein” (e.g. PBP2a) – encoded by ‘mec’
  • PBP2a doesn’t bind methicillin (or other β lactams), so antibiotic no longer works
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F: antibiotic resistance is always present

A

TRUE: it is always present, but the use of the antibiotic makes it favoured it in the environment and therefore selects for it

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

Vancomycin

A
  • a glycopeptide antibiotic
  • inhibits cell wall synthesis in Gram positives
  • often a drug of “last resort” (e.g. HA-MRSA)
  • Vancomycin binds the peptide linkage at terminal D-Ala-D-Ala residues and inhibits transpeptidation
  • resistance genes change these to D-Ala-D-Lac and vancomycin can no longer bind
  • resistance is encoded by the van genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Protein Synthesis Inhibitors

A
  • Bacteria contain 70S (30S+50S) ribosomes
  • Eukaryotes contain 80S (40S+60S) ribosomes

Many antibiotics target bacterial ribosomes and block translation (inhibit the synthesis of proteins)

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

Name two 50s inhibitors

A

Erythromycin, Chloramphenicol

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

Name two 30s inhibitors

A

Tetracycline, Kanamycin

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

Folic Acid Synthesis Inhibitors

A
  • e.g. Trimethoprim and Sulfonamides
  • folic acid is a vitamin (B9) for humans that we consume
  • bacteria need folic acid for thymidine synthesis
  • but bacteria cannot absorb folic acid so they must synthesize their own
  • inhibition of folic acid synthesis blocks DNA replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

DNA/RNA Synthesis Inhibitors - Fluoroquinolones

A
  • interfere with DNA gyrase needed for supercoiling of DNA
20
Q

DNA/RNA Synthesis Inhibitors - Rifampicin

A

inhibits bacterial RNA polymerase

21
Q

Cell Membrane Alteration

A
  • e.g. Polymyxin B (polysporin has this)
  • used for Gram negatives
    bind to LPS
  • hydrophobic tail inserts and disrupts outer and inner membranes
22
Q

Selection for Antibiotics

A

Paradoxically, the use of antibiotics actively selects for antibiotic resistant bacteria

  • NO antibiotic: the number of resistant bacteria remain the same (very low population)
  • WITH antibiotic: eventually the whole population is only resistant bacteria
  • Same thing can happen in an infectious environment
23
Q

Bacterial Strategies for Antibiotic resistance

A

Prevention of antibiotic entry
- Gram negative outer membrane and mycobacteria cell wall

Antibiotic modification
- β lactamase (enzyme destroys antibiotic)

Efflux of antibiotic
- actively pump out the antibiotic

Alteration of antibiotic target
- PBPs, Ribosome modifications

Bypassing the antibiotic action
- use environmental folic acid

24
Q

Which class of bacteria is more resistant to antibiotics (gram neg or pos) and why?

A

Gram negative, because it is harder to get through the membrane

25
Q

Antibiotic resistance genes

A
  • many mechanisms of antibiotic resistance are genetically encoded (e.g. mec, β lactamase, efflux pumps)
  • can produce very high levels of antibiotic resistance
  • often encoded on mobile genetic elements (e.g. plasmids) allowing for horizontal gene transfer “superbugs”
26
Q

Horizontal Gene Transfer

A

rather than alter gene function through mutations, new genes are acquired from another source

27
Q

Name the three methods of HGT

A

Transformation, transduction, conjugation

28
Q

Transformation

A

– recipient cell takes up DNA from donor cell (dead) in the the environment – not passive diffusion, there are mechanisms that do this

29
Q

Transduction

A
  • transfer of DNA via virus (bacteriophage)
  • donor cell has resistant gene
  • gets infected with virus
  • package genome into virus particle during replication
  • sometimes, they make mistakes and package pieces of chromosome in there
  • virus get out, and inject resistant gene into another cell
30
Q

Conjugation

A
  • typically on plasmid, machinery that actively moves DNA across and to a recipient cell
  • very high efficiency
31
Q

Klebsiella pneumoniae

A
  • Gram negative
  • an important cause of nosocomial pneumonia
  • produces a capsule and is commonly resistant to multiple antibiotics
  • first documented source of “NDM-1” (New Delhi Metallo-beta-lactamase-1)
  • also known as a carbapenemase (enzyme)
32
Q

What are carbapenem antibiotics

A
  • carbapenem antibiotics are β-lactamase resistant β-lactams with broad spectrum activity
  • NDM-1 is now widespread in other Gram negatives
    = CRE (carbapenem resistant Enterobacteriaceae)
33
Q

Clostridia

A
  • Gram-positive, rod shaped, endospore-formers
  • Strict anaerobes, vegetative cells killed by O2
  • Generally found in soil and intestinal tracts of animals
  • can cause life threatening diseases mediated by exotoxins
34
Q

what does clostridium difficile cause?

A

pseudomembranous colitis

35
Q

what does Clostridium tetani cause?

A

tetnus

36
Q

what does clostridium botulinum cause?

A

botulism

37
Q

what does perfringens cause?

A

food-borne illness and gas gangrene

38
Q

Clostridium difficile (“C. diff”) exists as:

A
  • asymptomatic carrier state in the large intestine (most common)
  • cause of mild to moderate diarrhea
  • cause of life-threatening pseudomembranous colitis
39
Q

Where is C. diff often found?

A
  • often found in nursing homes and hospital environments

- a nosocomial pathogen

40
Q

What is the mode of transmission of C. diff?

A

through the spore: fecal-oral route

41
Q

T/F: Endospores are very difficult to eradicate from the environment.

A

TRUE: can be cultured from floor, bed pans, toilets, hands and clothing of medical personnel

42
Q

Pseudomembranous colitis - most important risk factor

A
  • most symptomatic patients have recently received an antimicrobial agent
43
Q

What is pseudomembranous colitis?

A
  • an inflammatory condition of the large intestine
  • offensive smelling diarrhea, abdominal pain, fever, nausea, dehydration
  • symptoms may occur 1-2 days after antibiotics or several weeks after the antibiotic is discontinued
  • endoscopy can show characteristic yellow lesions
  • lesions can enlarge to cover substantial portions of inflamed mucosa and can be stripped off (the pseudomembrane)
44
Q

How does the disease, pseuduomembranous colitis manifest?

A
  • antibiotics are used to cure infections, but they also kill the normal microbiota
  • suppression of normal microbiota + persistence of C. difficile endospores
  • after the antibiotic is stopped, spores germinate, overgrowth of C. difficile occurs with production of toxins
  • C. difficile does not itself invade, but the toxins damage the intestinal lining of the large intestine
45
Q

How does C.diff cause damage?

A
  • C. difficile produces A-B toxins called the large clostridial cytotoxins
  • “A-B” serves to designate two domains
  • The A (active) domain denotes the active portion of the toxin that carries the enzymatic activity
  • The B (binding) domain denotes the portion of the toxin molecule responsible for binding and uptake by the host cell
  • “A” domain functions to inactivate key regulatory proteins of host cells which causes disregulation of multiple cell processes including cytoskeletal rearrangements, cell death and inflammation
46
Q

Diagnosis and Treatment of Pseudomembranous Colitis

A
  • history (antibiotic use), symptoms and laboratory tests to confirm C. difficile
  • endoscopy and toxin detection assays
  • discontinue inciting antibiotic if still being used
    fluids
  • antibiotics more specific for “C. diff” – oral vancomycin or I.V. metronidazole
  • avoid antidiarrheal agents (would cause decreased toxin clearance)
47
Q

Fecal Microbiota Transplantation

A
  • Treatment: transferring someone else’s fecal microbiota into your intestine
  • Get microbiota from healthy patient, and see if you can cure C diff. (it works!) –> New England Journal study

Microimm 2500 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions