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Microbiology post midterm > Lecture 29 and 30 > Flashcards

Lecture 29 and 30 Flashcards

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1
Q

What caused the two dips in the human population?

A
  • Black plague

- Spanish flue (Influenza) affected young people

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2
Q

What was the major cause of death before vaccines and antibiotics?

A
  • A simple cut
  • Tooth decay
  • Surgery was the last resort
  • Parents had to have many children
  • Childhood infections
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3
Q

Sterilization

A

-The process by which all living cells, spores and viruses are destroyed on an object

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4
Q

Disinfection

A
  • The killing or removal of disease-producing organisms from inanimate surfaces
  • Pathogens are killed-other microbes may survive
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5
Q

Antisepsis

A
  • Removing pathogens from the surface of living things-skin

- not as toxic as disinfectants

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6
Q

Sanitation

A

-Reduction of the microbial population to safe levels

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7
Q

Why don’t all members of the targe population succumb instantly?

A

-Genetics differences, mutations,
duration of exposure
-different growth phases

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8
Q

Cells that are treated with antimicrobials die at what rate?

A
  • They die at an exponential rate
  • Exposure to microbes to lethal chemicals does not cause instantaneous death
  • The efficiency of an antimicrobial is measured as a decimal reduction time (D-VALUE)
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9
Q

What is the D-value?

A
  • It is the length of time it takes an agent or condition to kills 90% of the population
  • Influenced by
    1. duration of exposure
    2. population size
    3. concentration of antimicrobial agent
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10
Q

What are the five physical agents that kill microbes?

A
  1. High temperature and pressure
  2. Pasteurization
  3. Cold temperatures
  4. Filtration
  5. Irradiation
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11
Q

High temperature and pressure

A
  • Moist heat is a more effective killing agent than dry heat

- An autoclave combines moist heat (steam) with high pressure to effectively kill even endospores

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12
Q

Pasteurization

A
  • Louis Pasteur who wanted to save french wine
  • Involves heating a food to a specific temperature for a short time to kill Coxiella burnetii the most heat resistant non-spore forming bacterium known.
  • Low t/long time-63 for 30min
  • Ultra high temperature-134 for 1-2s
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13
Q

Cold temperature

A
  • Most pathogens grow poorly at 4-8C

- refrigeration is an effective way to preserve food

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14
Q

Filtration

A
  • What do you do if your solution is sensitive to heat?
  • Filtration

Filtration through 0.2micron pore size filters is effective at removing most cellular microbes
-Doesn’t remove viruses

-Biological safety cabinets use air filtration to protect the worker from bacterial contamination

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15
Q

Irradiation

A
  • Bombardment of food with high energy eletromagnetic radiation
  • UV, GAMMA, X-RAY, ELECTRON BEAMS
  • It needs to expose microbes to radiation at a dose of that is millions of times higher than typical exposure for a chest x ray
  • because the target cell is so smaller
  • we need high conc. of irradiation
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16
Q

What about chemical agents?

A
  • Lister introduced the use of phenol as a disinfectant
  • phenol can be pretty toxic so it is no longer used
  • used as a great benchmark for an effective disinfectant
  • Phenol coefficient test
  • Higher the number the more effective the disinfectant
  • Formalin even though it got a low score it needs a longer exposure time to work
17
Q

Commercial disinfectants

A
  • Cause damage to proteins, lipids and DNA
  • include ethanol, chlorine, iodine and surfactants
  • Aldehydes such as formaldehyde are effective.
  • Items that cannot be sterilized using liquids or heat may be sterilized using a gas such as ETHYLENE OXIDE or betaproteolactone
  • good penetrance and very effective.
18
Q

Copper

A
  • An antimicrobial metal
  • Copper ions are toxic to bacteria
  • Incorporating copper into easily contaminated surfaces (doorknobs, beds, handrails) is an effective measure against microbial contamination.
  • Fresher water
19
Q

Biofilms

A
  • Provide resistance against chemical disinfectants
  • Extracellular matrix proteins and polysaccharides bind disinfectant, slowing penetration into the biofilm
  • This allows time for viable cells inside the biofilm to activate stress response systems
  • Mixed species biofilms containing resistant microbes may act as shields for less resistant biofilm members.
20
Q

What is an antibiotic, who discovered it?

A
  • A compound that kills or inhibits the growth of microorganisms
  • produced by a microbial species
  • Synthetic agents
  • Duchesne, Fleming, Florey, Chain.
21
Q

How are antibiotic made?

A
  • They are natural products
  • Produced by other microbes (bacteria or fungi)
  • Particularly in soil
  • Probably used to establish territory
  • Present in much lower concentrations than are used in medicine.
22
Q

Main properties of antibiotics

A
  1. Selective toxicity
    - Must not affect humans or animals
    - Should target microbial physiology
    - Specific bacterial property which humans don’t have
  2. Broad vs Narrow Spectrum
    - The range of species of bacteria affected
    - Broad-spectrum is effective against many species
    - Narrow spectrum is effective against a few/single species

The problem with A is that they have a lot of off-targets.

23
Q

What is the difference between bactericidal and bacteriostatic?

A
  1. Bactericidal
    - Kills the target bacteria
  2. Bacteriostatic
    - Inhibits growth, immune system clears the infection
    - slows their growth so the immune system can attack them.
24
Q

What is Minimum Inhibitory Concentration?

A
  • MIC
  • the lowest concentration of the antibiotic that will prevent the growth of the organism
  • The measure of the relative effectiveness of different antibiotics
  • What does will be effective
  • Consider achievable concentration in tissues
  • Must reach a bright point in a lawn and then it is effective.
25
Q

What are the mechanisms of action?

A

-Classic Targets
1. Cell wall synthesis
2. Peptidoglycan
-Nucleic acid synthesis
-DNA AND RNA SYNTHESIS
-Protein synthesis
Metabolism
-Cell membrane

26
Q

Target: Cell wall synthesis

A
  • Example (Penicillin B-lactam)
  • Chemical structure of penicillin resembles the D-ALA-D-Ala component of peptidoglycan (the part that interacts with the penicillin-binding proteins)
  • Penicillin-binding proteins bind to penicillin instead of peptidoglycan
  • Stops peptidoglycan synthesis
  • Penicillin also activates autolysin
27
Q

Gram negative vs gram positive

A
  • Gram negative thin peptidoglycan wall and an outer membrane
  • insensitive to b-lactam

-Gram positive-most effective

28
Q

Target: Cell Wall synthesis (Vancomycin)

A
  • Glycopeptidde antibiotic that binds to D-Ala-D-Ala
  • Prevents the action of the transglycosylases and transpeptidases
  • Stops peptidoglycan synthesis
29
Q

TARGET: DNA Synthesis

A

-Quinolones

  • They bind and inhibit gyrase
  • Gyrase functions to relieve the strain on the DNA as it is being unwound by helicase during replication
  • Quinolones bind to gyrase and stabilize the complex
30
Q

Target: RNA Synthesis

A
  • Rifampin
  • Binds RNA polymerase to prevent transcription
  • Obstructs the exit opening of the RNA polymerase
31
Q

Target: Protein synthesis

A

-Streptomycin

  • Binds 30S ribosomal subunit
  • Interferes with translation by causing misreading of the mRNA resulting in misfolded proteins
  • Changes the shape of the ribosomal subunit

Tetracycline

  • Also binds the 30S ribosomal subunit
  • Prevents attachment of the trna molecules to the mRNA complex stopping translation
32
Q

What is resistance?

A

-The ability of microorganisms to resist the effects of antimicrobial agents (one or more) that they were originally sensitive to

33
Q

Why does resistance happen?

A

-Antibiotics have been overused and misused
-selective pressure for resistance
-Resistance can occur by:
DNA mutations
Acquiring new genes through horizontal gene transfer
-Conjugation, transformation and transduction

34
Q

Mechanism 1: Alter the Target

A

-This strategy involves modifying the target so it no longer binds to or is recognized by the antibiotic

  • Vancomycin Resistance in Enterococcus faecium (VRE)
  • VRE has genes that produced D-ALA-D-LAC instead of D-ALA-D-ALA
35
Q

Mechanism 2: Destroy the Antibiotic

A
  • Before it gets into the cell or it causes damage to the cell
  • Resistance to B-Lactam antibiotics
  • B0lactamase producing E.coli
  • The B-lactamase enzyme cleaves the B-lactam ring
36
Q

Mechanism 3: Modify the Antibiotic

A
  • Modify the antibiotic so it is no longer functional
  • Example:
  • Streptomycin resistance in Pseudomonas aeuruginosa
  • Aminoglycoside phosphotransferase modifies streptomycin so that it cannot bind to the target (30S ribosomal subunit)
  • Translation proceeds as usual
  • Acetyltransferases and adenyltransferases
37
Q

Mechanism 4: Pump Antibiotics out of the cell

A
  • Efflux pumps/multidrug exporter
  • Functions in the extrusion of substances toxic to the cell
  • Multidrug resistance conferred by a proteinaceous pump that spans the cell wall

3 components:

  • Inner membrane pump protein
  • Accessory protein
  • Outer membrane channel

Example: MexXY OprM efflux pump conferring aminoglycoside resistance in Pseudomonas aeruginosa

Microbiology post midterm (5 decks)

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