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Microbiology > Chapter 10 Videos > Flashcards

Chapter 10 Videos Flashcards

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Biology 101 flashcards
1
Q

Define Chemotherapeutic agents.

A

Drugs that act against diseases

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2
Q

Define Antimicrobial agents.

A

Drugs that treat infections

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3
Q

Define Antibiotics

A

Antimicrobial agents produced naturally by organisms.

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4
Q

Define Semisynthetics.

A

Chemically altered antibiotics that are more effective, longer lasting, or easier to administer than naturally occurring ones

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5
Q

Define Synthetics.

A

Antimicrobials that are completely synthesized in a lab

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6
Q

What makes a successful chemotherapy?

A

Successful chemotherapy requires selective toxicity
* must be more toxic to a pathogen than to the pathogen’s host

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7
Q

Define selective toxicity.

A

must be more toxic to a pathogen than to the pathogen’s host

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8
Q

How can selective toxicity be achieved during the design of an antimicrobial drug?

A

Differences in structure or metabolism between the pathogen and its host

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9
Q

Antibacterial drugs constitute the largest number and diversity of antimicrobial agents. Why?

A

The differences between the host and the pathogen allow for more chances for selective toxicity.

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10
Q

Fewer drugs to treat eukaryotic infections. Why?

A

There are few differences between eukaryotic cells, making it more difficult for selective toxicity.

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11
Q

Antiviral drugs are limited. Why?

A

Viruses take everything from the host to replicate.

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12
Q

Define Spectrum of Action.

A

Number of different pathogens a drug acts against

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13
Q

Define Narrow-spectrum and Broad-spectrum

A
  • Narrow-spectrum: effective against few organisms
  • Broad-spectrum: effective against many organisms
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14
Q

Disadvantages of Broad- spectrum drugs.

A
  • May allow for secondary or superinfections to develop
  • Killing of normal flora reduces microbial antagonism
    (Causes competition between normal microbes and pathogens for nutrients and space.)
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15
Q

What microbial antagonism?

A

Competition between normal microbes and pathogens for nutrients and space.

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16
Q

How is antimicrobial effectiveness measured?

A
  • Efficacy of antimicrobials assessed by a variety of tests

A) Diffusion susceptibility test
Example: Kirby-Bauer test

B.) Minimum inhibitory concentration test (MIC)
* Attempt to quantify the smallest amount of a drug that will inhibit the growth and reproduction of the pathogen

Can be determined by:
* Broth dilution test
* Etest

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17
Q

What are three pathogen classifications?

A

Susceptible, intermediate, resistant.

18
Q

What are the routes of administration?

A

Topical application of drug for external infections
* Ex. Athlete’s foot

The oral route requires no needles and is self-administered

intramuscular administration delivers the drug via a needle into the muscle

Intravenous administration delivers the drug directly to the bloodstream

19
Q

Describe toxicity in drugs.

A

Toxicity
* Drugs may be toxic (to cause harmful effects) to kidneys, liver, or nerves

  • Example: Polymyxin- permanent damage to kidneys
  • Example: Flagyl- temporary damage
    “black hairy tongue”
20
Q

Describe allergy considerations when taking drugs.

A
  • Hypersensitivity of your immune response
  • Allergic reactions are rare but may be life-threatening
  • Anaphylactic shock-
  • swelling of the tongue and breathing tubes, low blood pressure, heart failure, and death
21
Q

What can happen when there is a Disruption of normal microbiota?

A
  • May result in secondary infections
  • Overgrowth of normal flora, causing superinfection
22
Q

What are the six mechanisms of antimicrobial action?

A
  • Inhibition of Cell Wall Synthesis
  • Inhibition of Protein Synthesis
  • Inhibition of Cytoplasmic Membrane
  • Inhibition of Metabolic Pathways
  • Inhibition of DNA or RNA Synthesis
  • Inhibition of Pathogen’s Attachment or Entry into Cell Host
23
Q

Inhibition of cell wall synthesis methods.

A
  1. Inhibition of synthesis of bacterial walls
    * Most common agents prevent cross-linkage of NAM
    subunits
    * Beta-lactams are most prominent in this group
    * Functional groups are beta-lactam rings
    * Cause: They act by preventing the cross-linkage of NAM subunits
    * Effect: Bacteria have weakened cell walls and eventually lyse

Lipoglycopeptides: Vancomycin and cycloserine
* Interfere with particular alanine-alanine bridges that link NAM subunits in many Gram-positive bacteria

Bacitracin
* Blocks transport of NAG and NAM from cytoplasm

Isoniazid and ethambutol
* Disrupt mycolic acid formation in mycobacterial species

24
Q

Inhibition of Protein Synthesis Methods.

A
  • Prokaryotic ribosomes are 70S (30S and 50S)
  • Eukaryotic ribosomes are 80S (40S and 60S)
  • Mitochondria of animals and humans contain 70S
    ribosomes
  • Can be harmful to animals and humans, specially very active cells in the liver and bone marrow.
25
Q

Disruption of Cytoplasmic Membranes methods

A
  • Some drugs form channel through cytoplasmic membrane and damage its integrity
  • Polyenes (Amphotericin B)
  • attaches to ergosterol in fungal membranes
  • Disrupting the membrane and causing lysis
26
Q

Inhibition of Metabolic Pathways Methods

A
  • Antimetabolic agents can be effective when pathogen and host metabolic processes differ
  • Metabolic antagonists
  • Antimetabolic agents
  • Example: Sulfonomides (sulfa drugs)
  • They are structurally analog
  • As analog they compete for the active site of the enzyme for a specific pathway
  • Effect: termination of metabolism - cell death
27
Q

Inhibition of Nucleic Acid Synthesis

A
  • Several drugs block DNA replication or RNA
    transcription
  • Drugs often affect both eukaryotic and prokaryotic cells
  • Not normally used to treat infections
  • Used primarily in research and perhaps to slow cancer cell replication
  • Quinolones and fluoroquinolones
  • Act against prokaryotic DNA gyrase
  • Inhibitors of RNA polymerase
  • Reverse transcriptase inhibitors
  • Act against an enzyme HIV uses in its replication cycle
  • Do not harm people because humans lack reverse transcriptase
  • Examples: Nucleotide or nucleoside analogs
  • Interfere with function of nucleic acids
  • Distort shapes of nucleic acid molecules and prevent further replication, transcription, or translation
  • Most often used against viruses
  • Effective against rapidly dividing cancer cells
28
Q

Prevention of Virus Attachment and Entry Methods

A
  • Attachment is an essential step during the virus replication
  • Attachment of viruses can be blocked ther by interrupting the viral replication
  • Example: Attachment antagonists
  • Pleconaril (to treat some cold viruses)
29
Q

What is drug resistance?

A
  • Some pathogens are naturally resistant
  • In nature, microbes are constantly evolving in order to overcome the antimicrobial compounds produced by other microorganisms.
  • Human development of antimicrobial drugs and their widespread clinical use has simply provided another selective pressure that promotes further evolution.
30
Q

What Drug Resistance Means?

A
  • Antibiotic resistance does not mean that your body is becoming resistant to antibiotics;
  • it is that bacteria (microbes) have become resistant to the antibiotics designed to kill them.
  • Antibiotic resistant infection are:
  • Difficult, and sometimes impossible, to treat
  • Can require extended hospital stays
  • additional follow-up doctor visits
  • costly and toxic alternatives.
31
Q

Bacteria acquire resistance in two ways

A
  1. New chromosomal mutations
    * Can be transferred vertically to subsequent microbial generations
  2. Acquisition of R
    plasmids
    * via horizontal gene transfer
32
Q

How does antibiotic resistance happen?

A
  1. Lots of germs. A few are drug-resistant.
  2. Antibiotics kill bacteria that cause illness, and good bacteria protect the body from infection.
  3. The drug-resistant bacteria are now allowed to grow and take over.
  4. Some bacteria give their drug-resistance to other bacteria, causing more problems.
33
Q

Drug modification or inactivation
(resistance mechanism)

A
  • Microbes change or destroy the antibiotics with enzymes, proteins that break down the drug.
  • Example: beta-lactamase or penicillinase

Once the B-lactam bond is broken, the drug loses its antibacterial activity.

34
Q

Block Penetration
(resistance mechanism)

A

Slow or prevent entry of drug into the cell
* Microbes restrict access by changing the entryways or limiting the number of entryways.
* Microbes change the structure or electrical charge of cytoplasmic membrane proteins
* Example: Porins

35
Q

Target Modification
(resistance mechanism)

A

Drug Binding Site Alter
* Microbes change the antibiotic’s target so the drug can no longer fit and do its job.
* Preventing drug binding
* Example: Genetic changes impacting the active site of penicillin-binding proteins (PBPs) can inhibit the binding of B-lactam drugs and provide resistance to multiple drugs within this class.

36
Q

Alternate metabolic pathway
(resistance mechanism)

A
  • By increasing the concentration of targeted enzymes
  • overproduce the target enzyme such that there is a sufficient amount of antimicrobial-free enzyme to carry out the proper enzymatic reaction.
  • By developing new cell processes that avoid using the antibiotic’s target.
  • By absorbing its product from the environment.
37
Q

Drug Pumps
(resistance mechanism)

A

Prevention of Cellular Uptake or Efflux
* Microbes get rid of antibiotics using pumps in their cell walls to remove antibiotic drugs that enter the cell.

  • One single efflux pump can have the ability to translocate multiple types of antimicrobials.
  • Example: Efflux Pumps
  • actively transport an antimicrobial drug out of the cell and prevent the accumulation of drug to a level that would be antibacterial.
38
Q

Biofilms
(resistance mechanism)

A
  • bacteria in biofilms can resist antimicrobials
  • Retard diffusion of the drugs
  • Slow metabolic rate reduces drug effectiveness
39
Q

Target Mimicry
(resistance mechanism)

A
  • Microbes produces a protein (mimics the target) that binds to the target of an antimicrobial drug
  • Preventing the drugs from binding to their target.
  • Example: Mycobacterium tuberculosis produces MfpA protein, that binds DNA gyrase, preventing the binding of fluoroquinolone drugs
40
Q

Describe Multiple Resistance and Cross Resistance.

A

Multiple resistance:
* Pathogen can acquire resistance to more than one drug
* Resistant to three or more different drugs
Cross-resistance:
* Pathogen can acquire resistance to similar drugs
* This occurs when drugs are similar in structure.

41
Q

Retarding Resistance:
Solutions

A
  • Synergism:
  • One drug enhance the effect of a second drug
  • Use antimicrobials only when necessary
  • limiting usage of antibiotics in health care, agriculture industry, animal husbandry
  • Develop new variations of existing drugs
  • Search for new antibiotics, semisynthetics, and synthetics

Microbiology (23 decks)

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