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My Packs: (UWO) (MICROIMM 2500) > (Section C: Bacteriology) Lecture 20 > Flashcards

(Section C: Bacteriology) Lecture 20 Flashcards

1
Q

What are the 3 classifications of antimicrobial agents?

A
  1. Disinfectants
  2. Antiseptics
  3. Antibiotics
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2
Q

Disinfectants

A

Antimicrobial agents that are applied to inanimate objects
* Floors, tables, walls etc.

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3
Q

Antiseptics

A

Antimicrobial agents that are sufficiently nontoxic to be applied to living tissues
* E.g. Hand sanitizers

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4
Q

Antibiotics

A

Antimicrobial agents produced by bacteria and fungi that are exploited by humans

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5
Q

How are antibiotics delivered/administered?

A
  • Topically
  • Internally
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6
Q

What are 2 major problems with antibiotics?

A
  1. Diminished interest from pharmaceutical companies to develop new antibiotics
  2. Bacterial resistance to antibiotics always happens
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7
Q

What are 5 examples of misuse of antibiotics?

A
  1. Empiric/blinded use
  2. Increased use of broad-spectrum agents
  3. Pediatric use for viral infections
  4. Patients who do not complete course of treatment
  5. Antibiotics in animal feeds
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8
Q

Blinded use

A

Using random antibiotics for diseases

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9
Q

Increased use of broad-spectrum agents

A

Antibiotic that is effective against wide variety of bacteria
* Causes large-scale development of resistance

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10
Q

Pediatric use for viral infections

A

Misuse, not useful for viral infections and may cause resistance to develop by bacteria

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11
Q

Patients who do not complete course of treatment

A

E.g. Tuberculosis
* Treatment usually lasts 6 months or more
* Bacteria may develop resistance if the treatment is not carried through all the way

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12
Q

Antibiotics in animal feeds

A

Spreads to environment through defecation
* Causes bacteria in the environment to gain resistance

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13
Q

How is antibiotic activity measured?

A

Minimum inhibitory concentration (MIC)

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14
Q

What is the MIC defined as?

A

The lowest concentration of agent that inhibits growth completely

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15
Q

How is MIC conducted (traditionally)?

A

Series of culture tubes with varying concentration of antibiotic
* MIC is the lowest concentration where there is no growth of bacteria

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16
Q

How is MIC conducted (modern)?

A

Antibiotic strips
* Faster to do
* Can test multiple antibiotics at the same time

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17
Q

How do antibiotics work?

A

Target essential bacterial components

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18
Q

What components do antibiotics target?

A
  1. Cell wall synthesis
  2. Protein synthesis
  3. DNA/RNA synthesis
  4. Folate Synthesis
  5. Cell membrane alteration
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19
Q

How do antibiotics ensure they target bacterial cells?

A

Targets are either
* Not present in eukaryotic cells
* Different in eukaryotic cells

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20
Q

β Lactam Antibodies
* Example
* Structure
* Function

A

* Penicillin, Methicillin
* Contain a "β Lactam ring"
* Function to inhibit cell wall synthesis in bacteria

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21
Q

How do β Lactam antibiotics work to inhibit cell wall synthesis?

A
  • Bind to bacterial “penicillin-binding proteins” (PBPs)
  • PBPs are transpeptidases
  • No peptide cross links = Weak cell wall = Cell death
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22
Q

How do bacteria counter β Lactam Antibiotics?

(Unmodified, use penicillin as example)

A

Produce β Lactamase
* Enzyme that destroys the β Lactam ring

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23
Q

How is methicillin different from penicillin?

A
  • Chemically modified penicillin
  • Cannot be cleaved by β lactamases
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24
Q

How do bacteria counter β Lactam Antibiotics?

(Modified, use methicillin as example)

A

Produce a different “penicillin-binding protein” (PBP)
* Called PBP2a or ‘mec’
* Doesn’t bind to methicillin or other β lactams

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25
Q

Vancomycin
* Type of antibiotic
* Function

A
  • Glycopeptide antibiotic
  • Inhibits cell wall synthesis in Gram positives
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26
Q

True or False:

Vancomycin is used last in a treatment

A

True, it is a drug of “last resort”

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27
Q

How does Vancomycin work?

A

Binds the peptide linkage at terminal D-Ala-D-Ala residues
* Inhibits transpeptidation, weakens cell walls

28
Q

How do bacteria counter Vancomycin?

A

Changes terminal to D-Ala-D-Lac
* Vancomycin can no longer bind
* Encoded by ‘van’ genes

29
Q

What are methods that bacteria use for antibiotic resistance?

A
  1. Prevention of antibiotic entry
  2. Antibiotic modification
  3. Efflux of antibiotic
  4. Alteration of antibiotic target
  5. Bypassing the antibiotic action
30
Q

Examples:

Prevention of antibiotic entry

A
  • Gram negative outer membrane
  • Mycobacteria cell envelope
31
Q

Examples:

Antibiotic modification

A

β lactamase

32
Q

Definition:

Efflux of antibiotic

A

Actively pumping out the antibiotic

33
Q

Examples:

Alteration of antibiotic targett

A
  • PBPs
  • Ribosome modifications
34
Q

Examples:

Bypassing the antibiotic action

A

Using environmental folic acid

35
Q

True or False:

Many mechanisms of antibiotic resistance are genetically encoded

A

True

36
Q

Where are antibiotic resistance mechanisms encoded on?

A

Mobile genetic elements (plasmids)
* Allows for horizontal gene transfer

37
Q

What can horizontal gene transfer create?

A

Superbugs

38
Q

What is horizontal gene transfer?

A

New genes are acquired from another source
* Not acquired through gene mutations

39
Q

What are forms of horizontal gene transfer? Explain each

A
  1. Bacterial transformation: Cell lysis releases genes to other cells
  2. Bacterial transduction: Virus picks up gene and implants in another cell
  3. Bacterial conjugation: Gene directly transferred to another cell when they join
40
Q

Klebsiella pneumoniae
* Type
* Disease it causes
* Antibiotic

A
  • Gram negative
  • Causes nosocomial pneumonia
  • Carbapenem antibiotics
41
Q

What are carbapenem antibiotics?

A

β lactamse resistant β-lactams with broad spectrum activity

42
Q

What does Klebsiella pneumoniae do in its life cycle?

A

Produces a capsule

43
Q

How is Klebsiella penumoniae resistant to carbapenem?

A

“NDM-1” enzyme
* Known as carbapenemase

44
Q

True or False:

NDM-1 is only present in Klebsiella pneumoniae

A

False, it is now widespread in other Gram negatives too (e.x. CRE - carbapenem resistant Entrobacteriaceae)

45
Q

Clostridia
* Type
* Shape
* Characteristics

A
  • Gram positive
  • Rod shaped
  • Endospore formers, strict anaerobes
46
Q

Where is Clostridia generally found?

A
  • Soil
  • Intestinal tracts of animals
47
Q

List:

Important human pathogens in Clostridia

A
  • Clostridiodes difficile (pseudomembraneous colitis)
  • Clostridium tetani (tetanus)
  • Clostridium botulinum (botulism)
  • Clostridium perfringens (food-borne illness, gas gangrene)
48
Q

How do Clostridia cause life threatening disease?

A

Exotoxins

49
Q

How can Clostridioides difficile exist as?

A
  • Asymptomatic carrier state in the large intestine
  • Cause of mild/moderate diarrhea
  • Cause of life-threatening pseudomembranous colitis
50
Q

What type of pathogen is C. difficile? Where is it often found?

A

A nosocomial pathogen
* Nursing homes, hospital environments

51
Q

Why is C. difficile so difficult to eradicate?

A

Endospores are difficult to eradicate
* Cultured from floor, bed pans, toilets, hands, and clothing of medical personnel

52
Q

Mode of transmission of C. difficile

A

Fecal-oral route

53
Q

What condition can C. difficile cause?

A

Pseudomembraneous colitis (aka Antibiotic-associated diarrhea)

54
Q

What is pseudomembraneous colitis?

A

Inflammatory condition of the large intestine
* Risks: Recently received an antimicrobial agent

55
Q

Signs/symptoms of pseudomembranous colitis

A
  • Diarrhea
  • Abdominal pain
  • Fever
  • Nausea
  • Dehydration
56
Q

How long does it take for signs/symptoms of pseudomembranous colitis to show?

A

May occur
* 1-2 days after antibiotics
* Several weeks after the antibiotic is discontinued

57
Q

What do endoscopy in pseudomembranous colitis patients show?

A

Characteristic lesions
* Enlarge to cover substantial portions of inflamed mucosa
* Can be stripped off

58
Q

What is the etiology behind pseudomembranous colitis?

A

Antibiotics cure infections, but also kill normal microbiota
* Suppression of normal microbiota + Persistence of C. difficile endospores = Pseudomembraneous colitis

59
Q

Is C. difficile considered an invasive bacterium?

A

No
* Exotoxins cause damage and inflammation to the intestinal lining of the large intestine

60
Q

What toxins do C. difficile produce?

A

A-B toxins known as “Large clostidial cytotoxins”

61
Q

What does the “A-B” stand for in A-B toxins?

A
  • A domain: Active portion of the toxin that carries the enzymatic activity
  • B domain: Binding portion, responsible for binding and uptake by the host cells
62
Q

How does the A domain work in large clostridial cytotoxins?

A

Inactivates key regulatory proteins of host cells
* Causes dysregulation of multiple cell processes including cytoskeletal rearrangements, cell death and inflammation

63
Q

How is pseudomembraneous colitis diagnosed?

A
  • History: Antibiotic use
  • Symptoms
  • Laboratory tests: C. difficile
  • Endoscopy
  • Toxin detection assays
64
Q

What is the treatment for pseudomembranous colitis?

A
  • Discontinue antibiotic
  • Fluids
  • Use antibiotics specific for C. difficile (oral vancomycin or I.V. metronidazole)
65
Q

Why should antidiarrheal agents be avoided in pseudomembranous colitis?

A

Would cause decreased toxin clearance

66
Q

What is a new treatment method for pseudomembranous colitis?

A

Fecal microbiota transplantation

67
Q

What is fecal microbiota transplantation? Why is it used?

A

Literally taking fecal matter from healthy patient and implanting into patients with pseudomembranous colitis
* Builds the microbiota lost to antibiotic use

My Packs: (UWO) (MICROIMM 2500) (30 decks)

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