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Microbiology LECTURE > Chapter 20 > Flashcards

Chapter 20 Flashcards

Antimicrobial drugs

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1
Q

Antibiosis

A

A mechanism of inhibition that inhibits reaction between colonies on solid media

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2
Q

Antibiotic

A

A substance produced by microorganisms that in small amounts inhibits another microorganism

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3
Q

Sulfa drug

A

A synthetic drug. Active compound sulfanilamide.

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4
Q

What are most of our antibiotics produced by

A

More than half–> Streptomyces: filamentous bacteria that commonly inhabit soil
Bacillus–> endospore forming bacteria
Molds–> penicillin, cephalosporium

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5
Q

How do prokaryotic and eukaryotic cells of humans differ

A

In the presence or absence of cell walls, the fine structure of their ribosomes, the details of their metabolism

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6
Q

Which organisms pose a problem when attempting to treat humans against an infection Why

A

When the pathogen is a eukaryotic cell such as a fungus, protozoan, or helminth. Because at the cellular level these organisms resemble a human cell much more closely.

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7
Q

Why are viral infections particularly difficult to treat in humans

A

Because the pathogen is within the humans host’s cells and because the genetic information of the virus is directing the human cell to make viruses rather than to synthesize normal cellular materials.

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8
Q

Narrow spectrum of microbial activity, example

A

Drugs that have a limited range of microbes they effect. Such as PCN G, affects gram positive bacteria and very few gram negative bacteria

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9
Q

Broad spectrum antibiotics

A

Antibiotics that affect a broad range of gram positive or gram negative bacteria

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10
Q

What is a primary factor involved in the selective toxicity of antibacterial action

A

This lies in the lipopolysaccharide outer layer of gram negative bacteria and the porins that form water filled channels across this layer. Drugs that pass through these channels must be relatively small and preferably hydrophilic.

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11
Q

What happens if drugs are lipophilic

A

They have an affinity for lipids or especially large, do not enter gram negative bacteria readily

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12
Q

Why are broad spectrum drug used more frequently in treating a disease

A

Because they save valuable time and because the identity of the pathogen is not always immediately known.

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13
Q

What are the disadvantages of a broad spectrum drug

A

This drug destroys many normal microbiota of the host, the normal microbiota ordinarily compete with and check the growth of pathogens or other microbes

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14
Q

How do opportunistic pathogens develop as a result of antibiotic use

A

If the antibiotic does not just kill certain organisms, but also destroys the normal microbiota and does not destroy their competitors, the survivors may flourish and become opportunistic pathogens

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15
Q

An example of an opportunistic pathogen

A

Overgrowth by the yeast like fungus, Candida albicans, which is not sensitive to bacterial antibiotics

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16
Q

Superinfection, example

A

A term applied to growth of a target pathogen that has developed resistance to the antibiotic. Candida albicans

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17
Q

Major action modes of antimicrobial drugs

A
  1. Inhibition of cell wall synthesis
  2. Inhibition of protein synthesis
  3. Inhibition of nucleic acid replication and transcription
  4. Injury to plasma membrane
  5. Inhibition of essential metabolite synthesis
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18
Q

Antibacterial drugs are either ___________ or ___________

A

Bactercidal

Bacteriostatic

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19
Q

How do antimicrobials that are bacteriostatic help prevent microbes from growing

A

It allows the host’s own defenses such as phagocytosis and antibody production to destroy the microorganisms

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20
Q

Which antibiotics inhibit cell wall synthesis

A

Penicillins, cephalosporins, bacitracin, vancomycin

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21
Q

Which antimicrobial drugs inhibit protein synthesis

A

Chloramphenicol, erythromycin, tetracyclines, streptomycin

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22
Q

Which anti microbial drugs inhibit metabolite synthesis

A

Sulfanilamide, trimethoprim

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23
Q

Which antimicrobial drugs inhibit nucleic acid replication and transcription

A

Quinolones, rifampin

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24
Q

What antimicrobial drug causes injury to plasma membrane

A

Polymycin B

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25
Q

Antimicrobial drugs target certain __________ ___________ of the microbe

A

Essential functions

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26
Q

The key to antimicrobial treatment is

A

To not interfere with essential functions of the microbe’s host

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27
Q

How do antimicrobial drugs inhibit cell wall synthesis

A

These antibiotics prevent the synthesis of intact peptidoglycan found only in bacterial cell walls. They weaken the cell walls and the cell undergoes lysis. It it only targets the synthesis process. Only actively growing cells are affected by this.

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28
Q

Why are drugs that inhibit cell wall synthesis not toxic to humans

A

Because humans do not have peptidoglycan cell walls

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29
Q

In regards to protein synthesis, what is the difference between prokaryotes and eukaryotes

A

The structure of ribosomes. Eukaryotic cells have 80S ribosomes, prokaryotic cells have 70S (50s and 30s subunits) ribosomes

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30
Q

Are antibiotics that inhibit protein synthesis selectively toxic

A

Antibiotics targeting the 70S ribosomes are selectively toxic in that they are preventing protein synthesis of bacterial cells, but can have adverse effects on the cells of the host due to eukaryotic mitochondria also possessing 70s ribosomes.

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31
Q

Which type of antibiotics cause the most damage to the plasma membrane

A

Polypeptide antibiotics, they result in the loss of important metabolites from the microbial cell due to increasing plasma membrane permeability

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32
Q

How do antifungals affect fungal plasma membrane

A

These drugs combine with sterols in the fungal plasma membrane to disrupt the membrane

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33
Q

What flaw do antimicrobials that inhibit nucleic acid synthesis have

A

Some drugs have an extremely limited usefulness because they interfere with mammalian DNA and RNA as well

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34
Q

How does a competitive inhibitors work

A

Enzymatic activity of a microorganism can be competitively inhibited by a substance that closely resembles the normal substrate for the enzyme.

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35
Q

What do you call a substance that closely resembles the normal substrate for an enzyme that competitively inhibits the activity of a particular enzyme

A

Antimetabolite

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36
Q

What is an example of competitive inhibition of an antimetabolite

A

The relationship between the antimetabolite sulfanilamide and para-aminobenzoic acid (PABA)

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37
Q

What is PABA’s function in a bacterial cell

A

It is the substrate for an enzymematic reaction leading to the synthesis of folic acid

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38
Q

What role does folic acid have in bacterial cells

A

It is a vitamin that functions as a coenzyme for the synthesis of purine and pyrimidine bases of nucleic acids and many amino acids

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39
Q

What is needed for antibiotics to function as a magic bullet

A

They must target microbial structures whose functions are not shared with mammalian structures or functions

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40
Q

Why is the microbial cell wall an attractive target for the action of antibiotics

A

Eukaryotic mammalian cell usually does not have a cell wall, only a plasma membrane.

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41
Q

What is the common core structure of all penicillins? How are they differentiated?

A

B-lactam ring called the nucleus. They are differentiated by the chemical side chain attached to their nuclei

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42
Q

What do penicillins prevent and how does that affect a bacterial cell

A

They prevent the cross linking of the peptidoglycans which interferes with the final stages of the construction of the cell walls, primarily of gram positive bacteria

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43
Q

What are the different categories of penicillin

A
  1. Natural
  2. Semisynthetic
  3. Extended spectrum
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44
Q

Natural penicillins

A

Penicillin G–> sensitive to stomach acid

Penicillin V–> resistant to stomach acid

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45
Q

What is a disadvantage of natural penicillin

A

They have a narrow spectrum of activity and are susceptible to penicillinases, enzymes produced by many bacteria, such as Staphylococcus species

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46
Q

What do penicillinases do to penicillin

A

They cleave the B-lactam ring

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47
Q

How are semisynthetic penicillins developed to overcome the disadvantages of natural penicillins

A
  1. They can interrupt synthesis of the molecule by penicillium and obtain only the common penicillin nucleus for use
  2. They can remove the side chains from the complete to natural molecules and then chemically at other chains that make them more resistant to penicillinase
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48
Q

What are semi synthetic penicillins made of

A

Part mold and part is added synthetically

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49
Q

Name semisynthetic penicillins

A
  1. Oxacillin–>narrow spectrum–>g+–>resistant PCNase

2. Ampicillin–> Extended spectrum, many gram negatives

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50
Q

Extended spectrum penicillins

A

Broader spectrum semi synthetic penicillin, effective against many gram negative bacteria as well as gram positive ones, not resistant to penicillinases

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51
Q

What is the most common form of resistance to penicillins

A

Penicillinase

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52
Q

Penicillins plus B-Lactamase inhibitors

A

Penicillin with potassium clavulanate, a noncompetitive inhibitor of penicillinase with no antimicrobial activity

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53
Q

B-Lactam antibiotics

A
  1. Penicillin: PNCase resistant, + B-lactamase inhibitors
  2. Carbapenems
  3. Monobactam
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54
Q

Carbapenems

A

Class B-lactam antibiotic that substitute a carbon atom for a sulfur atom and add a double bond to penicillin nucleus

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55
Q

Monobactam

A

B-lactam antibiotic, synthetic drug with a single ring rather than conventional B-lactam double ring

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56
Q

Cephalosporins

A

The nuclei structure resemble those of penicillin. They inhibit cell wall synthesis the same way penicillins do. They’re more widely used. B-lactam ring differs from PCN.

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57
Q

How are the Cephalosporins grouped

A

According to their generations

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58
Q

First generation

A

Narrow spectrum, gram positive

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59
Q

2nd generation

A

Extended spectrum includes gram negative

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60
Q

3rd generation

A

Includes pseudomonads, injected

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61
Q

Pseudomonads

A

Hospital acquired infections, difficult to treat, attacks immunocompromised, not a true pathogen

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62
Q

4th generation

A

Can be taken orally

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63
Q

Polypeptide antibiotics

A

Bacitracin and Vancomycin

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64
Q

Bacitracin

A

Topical application, works against gram positives. Inhibit cell wall synthesis at an early stage.

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65
Q

Vancomycin

A

Glycopeptide (Polypeptide) antibiotics, Narrow spectrum of activity inhibits cell wall synthesis, Last line of antibiotic defense for treating Staphylococcus aureus infections that are resistant to other antibiotics.

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66
Q

Vancomycin resistant entercocci (VRE)

A

The widespread use of Vancomycin to treat MRSA has led to the appearance of this. It is an opportunistic gram positive pathogen that is particularly troublesome in hospital settings so

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67
Q

Antimycobacterial antibiotics

A

Isoniazid (INH)

Etambutol

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68
Q

INH

A

Effective synthetic antimicrobial drug against mycobacterium tuberculosis. Inhibits the synthesis of mycolic acids.

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69
Q

Why do INH drugs need to be taken with other drugs? What are they?

A

This minimizes development of drug resistance. The tubercle bacilli is usually found only within macrophages or walled off in tissue, any antitubercular drug must be able to penetrate into such sites.
Rifampin or ethambutol

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70
Q

Ethambutol

A

Affective only against mycobacteria. Inhibits incorporation of mycolic acid into the cell wall. It is a weak antitubercular drug. It is used as a secondary drug to avoid resistance problems.

71
Q

Chloramphenicol

A

Inhibits the formation of peptide bonds in the growing polypeptide chain by reacting with the 50S portion of the 70S prokaryotic ribosome. Broad spectrum.

72
Q

How do Aminoglycosides work

A

They interfere with the initial steps of protein synthesis by changing the shape of the 30S portion of the 70S prokaryotic ribosome. This causes the genetic code of the mRNA to be read incorrectly. Significant activity against gram negative bacteria. Broad spectrum.

73
Q

Aminoglycosides

A

Streptomycin, neomycin, gentamicin

74
Q

Tetracyclines

A

Broad spectrum. Interferes with the attachment of the tRNA carrying the amino acids to the ribosome at the 30S portion of the 70S ribosome, preventing the addition of amino acids to the growing polypeptide chain.

75
Q

Why is it that tetracyclines do not interfere with mammalian ribosomes

A

Because they do not penetrate very well into intact mammalian cells, small amounts are able to enter the host cell. They are selectively toxic because of the greater sensitivity of the bacteria at the ribosomal level.

76
Q

Tetracyclines are effective against

A

Gram positive and gram negative bacteria, Intracellular rikketsias and chlamydias. They are broad spectrum.

77
Q

Macrolides, example

A

Named for the presence of a macrocyclic lactone ring. It inhibits protein synthesis. It is not able to penetrate the cell walls of most gram negative bacilli. Use for treatment against gram positives

78
Q

Example if Macrolides

A

Erythromycin

79
Q

How does Streptogramins work

A

A unique group of antibiotics. They block protein synthesis by attaching to the 50S portion of the ribosome One cyclic peptide blocks the early step of protein synthesis and that other blocks a later step, inhibiting translation

80
Q

What do Streptogramins work against

A

A broad range of gram positive bacteria that are usually resistant to other antibiotics

81
Q

The synthesis of bacterial plasma membranes requires the synthesis of

A

Fatty acids as building blocks

82
Q

What are successful antimicrobial that target fatty acid synthesis

A

Isoniazid and antibacterial triclosan

83
Q

Polymyxin B

A

A bactercidal antibiotic effective against gram negative bacteria such as pseudomonas, now seldomly used for this and more as a topical treatment. It targets the synthesis of the plasma membrane.

84
Q

What is Polymyxin B combined with

A

Bacitracin and neomycin

85
Q

Rifamycins

A

Inhibit the synthesis of mRNA. Used in the treatment of tuberculosis and leprosy. Has ability to penetrate tissues and reach therapeutic levels in CSF and abcesses.

86
Q

Antituberculosis drug that is derived from Rifamycin

A

Rifampin

87
Q

Quinolones and Fluoroquinolones

A

It has a unique bactericidal effect by selectively inhibiting an enzyme (DNA gyrase), needed for the replication of DNA.

88
Q

Nalidixic acid

A

The 1st of the group of quinolone anti microbials. Limited to use for treatment of urinary tract infections.

89
Q

Fluoroquinolones

A

A synthetic quinolone. It’s divided into groups each of which has a progressively broader spectrum of activity.

90
Q

What are most Fluoroquinolones used to treat

A

Urinary tract infections and certain types of pneumonia

91
Q

What is the most commonly publicized Fluoroquinolone and what does it treat that makes it most publicized

A

Cipro

Anthrax

92
Q

Sulfonamides

A

Sulfa drug. One of the 1st synthetic anti microbial drugs. Usually bacteriostatic. Has a structural similarity to PABA. Used against bacteria that must synthesize their own PABA. Broad spectrum, inhibit folic acid synthesis.

93
Q

Why are fungal infections becoming more frequent

A

Because of their role as opportunistic infections in immunosuppressed individuals

94
Q

Why is it more difficult to find a point of selective toxicity in fungal infections vs bacterial infections

A

Because they are eukaryotes and they use the same mechanisms to synthesize proteins and nucleic acids as higher animals

95
Q

What do antifungal agents that affect the plasma membrane target

A

The biosynthesis of the sterol, ergosterol, in plasma membrane of fungi, is interrupted. This causes a membrane to become excessively permeable, killing the cell.

96
Q

What is the most commonly used member of the antifungal polyenes and what is its mode of action

A

Amphotericin B

Inhibition if ergosterol synthesis: plasma membrane

97
Q

Azoles , Examples

A

Affects synthesis of fungal sterols. Most widely used.

Miconazole and Triazoles

98
Q

Allylamines

A

Class of antifungals that inhibit the biosynthesis of ergosterols in a manner that is functionally distinct. Frequently used when resistance to azole type antifungals arise.

99
Q

What antifungal agent affects cell walls

A

Echinocandins

100
Q

How does Echinocandins work

A

It targets the B-glucan by inhibiting their biosynthesis, resulting in an incomplete cell wall synthesis and cell lysis.

101
Q

What is a member of Echinocandin group and what is it used against

A

Candida

Candida and Pneumocystis

102
Q

Why is it difficult to target a virus without damaging the host’s cellular machinery

A

Because viruses replicate within the host’s cells, very often using the genetic and metabolic mechanisms of the host’s own cells

103
Q

What are many of today’s antivirals

A

Analogs of components of viral DNA or RNA.

104
Q

What was an early and obvious target for antiviral drugs

A

The reverse transcriptase step found in RNA viruses and not used in human DNA

105
Q

Anitiviral drugs have consisted mostly of

A

Nucleoside and nucleotide analogs

106
Q

Which nucleoside analog is commonly used and how does it work

A

Acyclovir. It’s structurally resembles the nucleoside deoxyguanosine. The thymidine kinase is altered and converts the acyclovir to a false nucleotide, which blocks DNA synthesis by DNA polymerase.

107
Q

Zanamivir

A

Antiviral drug used in the treatment of influenza. It
works by binding to the active site of the neuraminidase protein, rendering the influenza virus unable to escape its host cell. It inhibits attachment and enzymes.

108
Q

What are interferons

A

There are classified as cytokines. They are produced when cells are infected by a virus. They inhibit further spread of the infection

109
Q

Alpha interferon

A

A drug of choice for viral hepatitis infections. It works by preventing the spread of viruses to new cells

110
Q

What kind of virus is HIV

A

It is an RNA virus and its reproduction depends on the enzyme reverse transcriptase which controls the synthesis of RNA from dna.

111
Q

Antiretroviral

A

Implies that a drug is used to treat HIV infections

112
Q

When the host cell of an HIV infected person makes a new virus it must begin by

A

Cutting up large proteins with protease enzymes. The resulting fragments are then used to assemble new viruses.

113
Q

What do analogs of amino acid sequences in the large proteins serve as

A

Inhibitors of proteases, made at the direction of the infecting HIV, by competitively interfering with their activity

114
Q

Protease inhibitor

A

Indinavir (for HIV)

115
Q

Integrate inhibitors function

A

Inhibits an enzyme that integrates viral DNA into the DNA of the infected cell

116
Q

Entry Inhibitors

A

Antivirals that target the receptors that HIV uses to bind to the cell before entry

117
Q

What is an example of an Entry inhibitor

A

CCR5

118
Q

Fusion inhibitors

A

Entry of HIV into the cell is blocked by a synthetic peptide that blocks cell fusion and entry by mimicking a region of the viral envelope

119
Q

Example of fusion inhibitor

A

Enfuvirtide

120
Q

Amantadine

A

Inhibits the replication of influenza A by interfering with the uncoating of the virus inside the cell

121
Q

Chloroquine

A

A synthetic derivative of quinine used to control the protozoan disease malaria by inhibiting DNA synthesis

122
Q

Metronidazole

A

Aka Flagyl. Widely used antiprotozoan drugs Acts not only against parasitic protozoa but also against obligately anaerobic bacteria. Interferes with anaerobic metabolism and damages DNA.

123
Q

What is Metronidazole used for

A

Entamoeba and Trichomonas

124
Q

Nitazoxanide

A

An antiprotozoan agent. Also it interferes with metabolism of anaerobes and effective against helminthic diseases.

125
Q

Mebendazole

A

A broad spectrum antihelminthic used to treat intestinal roundworm infections. It works by inhibiting the formation of microtubules in the cytoplasm, which interferes with the absorption of nutrients by the parasite.

126
Q

Invermectin

A

It has a wide range of applications. It is effective against round worms and several mites. It results and paralysis of intestinal worms.

127
Q

Chemotherapy

A

The use of drugs to treat a disease caused by genetics, infection, or non infectious disease.

128
Q

Antimicrobial drugs

A

Interfere with the growth of microbes within the host. The treatment of a disease caused by microbes.

129
Q

Selective toxicity

A

A drug that kills harmful microbes without damaging the host. It inhibits or kills pathogens.

130
Q

What things must be taken into consideration in regards to the selective toxicity of a drug

A
  1. The anti microbial agent must harm the microbes without causing significant damage to the host.
  2. Toxic dosage level.
  3. Therapeutic dosage level must be maintained at a constant level for the entire time of treatment.
131
Q

What did Fleming discover in 1928

A

Penicillin produced by penicillum

132
Q

What did Howard Florey and Ernst Chain perform in 1940

A

First clinical trials rials of penicillin

133
Q

A physician must know the _____________ of the pathogen before ____________ can be started

A

Sensitivities

Treatment

134
Q

If a physician cannot wait for sensitivity tests and must begin treatment based on their _____________ estimation of the most likely pathogen causing the illness

A

Best guess

135
Q

When are tests necessary

A

When susceptibility is not predictable or when antibiotic resistance problems develop

136
Q

Disk diffusion method

A

Kirby Bauer test. Most widely used.
It is a petri plate containing an agar medium and it is inoculated uniformly over the entire surface with a standard amount of a test organism. Filter paper disks are impregnated with known concentrations of chemotherapeutic agent on the solidified agar surface. The farther the agent diffuses from the disk, the lower its concentration.

137
Q

Zone of inhibition

A

A clear zone that forms around the disk containing a chemical agent, after a standardized incubation. The larger this zone the more sensitive the microbe is to that agent. The organism is reported as sensitive, intermediate, or resistant.

138
Q

E test

A

A more advanced diffusion method enables the lab technician to estimate the minimal inhibitory concentration that prevents visible bacterial growth.

139
Q

MIC

A

Minimal inhibitory concentration. The lowest antibiotic concentration that prevents visible bacterial growth.

140
Q

Broth dilution test

A

Useful in determining that MIC and the MBC of antimicrobial drugs. A suspension of the test organism is prepared and inoculated into wells that contain drug agent. After incubation the turbidity may be read visually. The wells that do not show growth can be cultured in broth or on agar plates free of the drug. If growth occurs, drug is not bactercidal and MBC can be determined.

141
Q

MBC

A

Minimal bactercidal concentration needed to kill bacteria.

142
Q

Why is determining the MIC and MBC important

A

Because it avoids the excessive or erroneous use of expensive antibiotics and minimizes the chance of toxic reactions that larger than necessary doses might cause

143
Q

Do we want to use am MIC or MBC for treatment and why

A

MIC. Because we want to use inhibitory instead of killing and that way we can allow the immune system to produce antibodies to prevent future infections and it is also safer.

144
Q

Antibiogram

A

Infection control reports that record the susceptibility of organisms encountered clinically. Written by hospital personnel responsible for infection control periodically. These reports are especially useful for detecting the emergence of strains of pathogens resistant to the antibiotics used in these institution.

145
Q

Where do the genetic characteristics that account for the survival of microbes and their progeny come from

A

These arise from random mutations that are spread horizontally among bacteria by processes such as conjugation and transduction. The resistance can be carried by plasmids or transposons. The mutation can also be transmitted vertically; through reproduction.

146
Q

Superbugs, Example

A

Bacteria that are resistant to large numbers of antibiotics.

MRSA

147
Q

What are the 5 mechanisms of resistance to antibiotics

A
  1. Inactivating enzymes
  2. Blocking entry
  3. Alteration of target molecule
  4. Efflux of antibiotic
  5. Abandoning metabolic pathway
148
Q

Enzymatic destruction or inactivation of the drug

A

It affects natural products; antibiotics. There are various variations of the enzyme, B-Lactamase, that selectively hydrolyze the B-Lactam ring structure of antibiotics such as PCN, cephalosporins, carbapenems

149
Q

Prevention of drug penetration to the target site within the microbe

A

Gram negative bacteria cell walls restrict absorption of many molecules to movement through porins. Some bacterial mutants modify the porin openings preventing entry to periplasmic space. When B-Lactamase is present in periplasmic space, the antibiotic remains outside and it the reaches it and inactivates it.

150
Q

Alteration of the drugs target site

A

Minor modifications of the target site neutralize the effects of antibiotics without significantly affecting cellular function. The target site can be eliminated or changed. Change affinity to substrate molecule.

151
Q

Rapid efflux or ejection of the antibiotic

A

Certain proteins in the plasma membranes of gram negative bacteria act as pumps that expel antibiotics preventing them from reaching an effective concentration.

152
Q

What type of bacteria are relatively more resistant to antibiotics and why

A

Gram negative bacteria because of their cell wall

153
Q

Alteration of the metabolic pathways of the host

A

Changes in regulatory networks of the cell

154
Q

How are antibiotics misused and how does this contribute to antibiotic resistance

A

In less developed countries prescriptions are not required and are used for inappropriate uses. The dose regimens are usually shorter and thereby encourages survival of resistant strains of bacteria. Outdated antibiotics are common. Prescriptions are given for common colds, sore throats, or ear infections. There used in animal feeds to promote growth.

155
Q

How does cost affect resistance of antibiotics

A

The drugs are expensive and difficult to afford. This causes people to discontinue medications as soon as symptoms improve, leftover medications are used to treat other illnesses

156
Q

What can help minimize the resistance of drugs

A

Avoiding broad spectrum drugs and prescribing the most specific antibiotic possible. Healthcare workers can prevent inhalation of aerosolized antibiotics.

157
Q

Therapeutic index

A

This involves assessing risks against benefits. This compares the toxic dosage level and the therapeutic dosage level. (Toxic level ÷ therapeutic level).

158
Q

Synergism

A

The chemotherapeutic effect of two drugs given simultaneously is sometimes greater than the effect of either given alone.

159
Q

Antagonism

A

The simultaneous use of two drugs is often less effective than when either drug is used alone

160
Q

How do you know the therapeutic index is safe

A

The larger the therapeutic index (TI), the safer the drug is. If the TI is small (the difference between the two concentrations is very small), the drug must be dosed carefully and the person receiving the drug should be monitored closely for any signs of drug toxicity.

161
Q

What are the effects of premature termination of antibiotic treatment

A

A super infection can develop, Endospores can survive and can cause an infection later, The normal flora is killed and creates no competition for the more resistant organisms

162
Q

What can happen the next time antibiotics are taken when one previously terminated antibiotic treatment prematurely

A

Bacteria might have higher threshold, requiring a different concentration of an antibiotic. This could require a different antibiotic, different dose, a longer regimen. This can increase that toxicity. Recombination could also occur producing resistant flora.

163
Q

Antibiotics serum levels must be…

A

Consistently at a therapeutic level for the specified duration to get rid of pathogen.

164
Q

What is the order that the different types of organisms are eradicated during an antibiotic treatment

A

1st are highly sensitive organisms

Then intermediate organisms

Finally highly resistant organisms

165
Q

How can a synergistic antibiotic be beneficial

A
  1. It can stop the emergence of resistant varieties
  2. You can give low dose of both medications which would increase the therapeutic index
  3. You can increase the effectiveness of the medication and kill both regular and resistant strains if microorganisms
  4. Signs and symptoms of illness can decrease sooner
166
Q

Selective pressure

A

is any phenomena which alters the behavior and fitness of living organisms within a given environment. It is the driving force of evolution and naturalselection, and it can be divided into two types ofpressure: biotic or abiotic

167
Q

What is selective pressure in bacteria

A

In the case of antibiotic resistance, antibiotics cause aselective pressureby killing susceptiblebacteria, allowing antibiotic-resistantbacteriato survive and multiply.Selection pressurecan be regarded as a force that causes a particular organism to evolve in a certain direction.

168
Q

Antibiotics that inhibits cell wall synthesis

A
  • Penicillins
  • Carbapenems
  • Monobactam
  • Cephalosporins
  • Polypeptide antibiotics: bacitracin, Vancomycin
  • Antimycobacterials: INH, ethambutol
169
Q

Antibiotics that inhibit protein synthesis

A
  • Chloramphenical
  • Aminoglycosides
  • Tetracyclines
  • Streptogramins
  • Macrolides
170
Q

Antibiotics that cause injury to plasma membrane

A

Polymyxin

171
Q

Inhibitors of nucleic acid synthesis

A
  • Rifampin

* Quinolones an Fluoroquinolones

172
Q

Competitive inhibitors

A

Sulfanilamides

173
Q

How does an antibiotic inhibit the synthesis of essential protein

A
  • chloramphenical–> Binds to 50S portion and inhibits formation of peptide bond
  • Aminoglycosides (streptomycin)–> Changes shape of 30S portion, causing code on mRNA to be read incorrectly
  • tetracycline–> Interferes with attachment of tRNA to mRNA ribosome complex
  • Streptogramins–> binds 50S subunit, inhibits translation
  • Macrolides (erythromycin)–> binds 50S subunit, prevents translocation

Microbiology LECTURE (13 decks)

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