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Microimm 2500 > (B) Lecture 13: Antibiotics and Antibiotic Resistance > Flashcards

(B) Lecture 13: Antibiotics and Antibiotic Resistance Flashcards

1
Q

Antimicrobial agents

A
  • disinfectants
  • antiseptics
  • antibiotics
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2
Q

Disinfectants

A

antimicrobial agents that are applied to INANIMATE OBJECTS (floors, tables, walls)

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3
Q

Antiseptics

A

antimicrobial agents that are sufficiently NONTOXIC to be applied to LIVING TISSUES (ex. hand sanitizers)

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4
Q

Antibiotics

A

antimicrobial agents produced by BACTERIA + FUNGI that are exploited by humans
- delivered topically + internally

Most effective therapeutic against bacterial infections

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5
Q

Major problems with antibiotics

A
  1. Low interest from pharmaceutical companies to develop new antibiotics (hard to make money when constantly making new antibiotics due to resistance)
  2. Bacterial resistance to antibiotics always happens
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6
Q

Misuse of antibiotics

A
  • empiric use (blinded use): don’t know specific infection
  • increased use of broad-spectrum agents: kills things you don’t want
  • pediatric use for viral infections
  • patients who don’t complete course (ex. TB)
  • antibiotics in animal feeds
  • global travel = resisted organisms/bacteria spread quickly
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7
Q

Measuring Antibiotic Activity

A

Minimum inhibitory concentration (MIC)
- MIC = point where bacteria can’t grow/ lowest conc of agent that inhibits growth
- series of culture tubes w/ diff conc. of agent + check for growth

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8
Q

How do antibiotics work?

A

Antibiotics target essential bacterial components:
- cell wall synthesis
- protein synthesis (ex. ribosomes)
- DNA/RNA synthesis
- folate synthesis
- cell membrane alteration

Targets are not present in eukaryotic cells

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9
Q

Beta Lactam Antibiotics

A

Ex. Penicillin, Methicillin

  • contains a beta lactam ring
  • INHIBITS CELL WALL SYNTHESIS in bacteria
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10
Q

Penicillin

A

a beta lactam antibiotic

Beta lactams bind bacterial “penicillin-binding proteins (PBPs)
- PBPs are transpeptidases and make peptide cross-links
- no peptide cross-links = weak cell wall = cell death

BUT some bacteria produce a beta lactamase (enzyme that destroyed ring and antibiotic)

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11
Q

Methicillin

A

a beta lactam antibiotic

  • contains a beta lactam ring
  • chemically modified penicillin
  • CAN’T be cleaved by beta lactamases

BUT some bacteria can produce a different ‘penicillin-binding protein’ (PBP2a) encoded by ‘mec’
- PBP2a doesn’t bind methicillin (or other beta lactams)

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12
Q

Vancomycin

A
  • not a great antibiotic
  • a glycopeptide antibiotic
  • inhibits cell wall synthesis in gram POSITIVES
  • often a “last resort” (ex. MRSA)

Binds peptide linkage at terminal D-Ala-D-Ala residues and inhibits transpeptidation
- resistance genes change those to D-Ala-D-Lac and vancomycin can no longer bind

Resistance is encoded by van genes

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13
Q

Bacterial strategies for antibiotic resistance

A
  • prevention of antibiotic entry (gram NEGATIVE outer membrane + mycobacteria cell envelope)
  • antibiotic modification (beta lactamase)
  • efflux of antibiotic (actively pump out the antibiotic)
  • alteration of antibiotic target (PBPs, ribosome modifications)
  • bypassing antibiotic action (use environmental folic acid)
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14
Q

Antibiotic resistance genes

A
  • many mechanisms of antibiotic resistance are GENETICALLY ENCODED (ex. mec, beta lactamase, efflux pumps)
  • can produce HIGH levels of antibiotic resistance
  • often encoded on MOBILE genetic elements (ex. plasmids, transposons) that allow for horizontal gene transfer = SUPERBUGS
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15
Q

Superbugs

A

bacteria that are resistant to MULTIPLE antibiotics

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16
Q

Horizontal gene transfer

A

new genes are acquired from another source

  1. bacterial transformation: donor cell releases DNA and recipient picks it up
  2. bacterial transduction: phage infects bacteria and phage-infected donor cell releases phage to infect a recipient cell
    - can pass on resistance genes
  3. bacterial conjugation: donor cell and recipient cell combine and plasmid moves from donor to recipient
17
Q

Klebsiella pneumoniae

A

Gram NEGATIVE

  • important cause of nosocomial pneumonia
  • produces a capsule
  • commonly resistant to multiple antibiotics
  • first documented source of NDM-1 (a carbapenemase)
  • carbapenem antibiotics are beta-lactamase resistant beta-lactams w/ broad spectrum activity
18
Q

Nosocomial

A

a disease acquired in a HEALTHCARE setting

19
Q

NDM-1

A

a carbapenemase

  • carbapenem antibiotics are beta-lactamase resistant beta-lactams w/ broad spectrum activity

Now widespread in other Gram NEGs = CRE (carbapenem-resistant Enterobacteriaceae)

20
Q

Clostridia

A
  • gram-POSITIVE, rod shaped
  • endospore-formers
  • strict ANAEROBES, vegetative cells killed by O2
  • generally found in SOIL + INTESTINAL TRACTS of animals
  • can cause life-threatening diseases mediated by EXOTOXINS

Examples
- C. difficile: pseudomembranous colitis
- C. tetani: tetanus
- C. botulinum: botulism
- C. perfringens: food-borne illness

21
Q

C. diff

A

Clostridoides difficile

Can exist as
- asymptomatic carrier in large intestine
- cause of mild to moderate diarrhea
- cause of life-threatening pseudomembranous colitis (antibiotic-associated diarrhea)

NOSOCOMIAL environments (in nursing homes + hospital environments)

ENDOSPORES can be hard to get rid of

Mode of transmission: FECAL-ORAL ROUTE

22
Q

Pseudomembranous colitis

A
  • inflammatory condition of LARGE intestine
  • most important risk factor: having recently received an antimicrobial agent
  • antibiotics suppress normal microbiota = persistence of C. diff endospores
  • when antibiotic is stopped, spores germinate; overgrowth of C. diff = toxins
  • C. diff is not invasive but EXOTOXINS cause damage + inflammation to intestinal lining of large intestine
  • diarrhea, ab pain, fever, nausea
23
Q

How does C. diff work?

A

C. diff produces A-B toxins called the LARGE CLOSTRIDIAL CYTOTOXINS

“A-B” designates two domains
- A-domain: the ACTIVE portion of the toxin that carries the enzymatic activity
- B-domain: the portion of toxin responsible for BINDING + uptake by host cell

24
Q

A-domain

A

the ACTIVE portion of the toxin that carries enzymatic activity

inactivates key regulatory proteins of host cells = dysregulation of cell processes like inflammation, cytoskeletal rearrnagements and cell death

25
Q

Diagnosis and Treatment of C. diff

A

Diagnosis
- take history (antibiotic use)
- lab tests to confirm C. diff
- endoscopy and toxin detection

Treatment
- discontinue inciting antibiotic
- fluids
- antibiotics more specific for C. diff - oral vancomycin or I.V. metronidazole
- AVOID ANTIDIARRHEAL AGENTS - would cause decreased toxin clearance

26
Q

Fecal microbiota transplantation

A

Take feces from a healthy person and transplants that into large intestine of infected person

Fixes microbiota

27
Q

Study: Duodenal Infusion of Donor feces for Recurrent C. diff

Fecal microbiota transplantation

A

Methods
- 3 therapies randomly assigned: vancomycin + bowel lavage + donor feces infusion; standard vancomycin; vancomycin + bowel lavage
- goal: resolution of diarrhea w/ C. diff w/o relapse after 10 weeks

Results
- study stopped after interim analysis
- patients who got donor-feces infusion, showed increased fecal bacteria diversity, similar to healthy ppl

Microimm 2500 (29 decks)

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