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BIO111: Microbiology > Chapter 20 & 19 > Flashcards

Chapter 20 & 19 Flashcards

1
Q

Father of Chemotherapy

A

Paul Ehrlich
German, 1910
-drug treatment for syphillis
-Selective toxicity

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2
Q

Chemotherapy

A

Use of chemicals to treat a disease

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3
Q

selective toxicity

A

toxic to microbe, but not host cells

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4
Q

Domagk

A 
1935 - Sulfa drugs 
-first major class of drugs with widespread clinical use
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5
Q

Antibiotics

A

antibacterial compounds produced naturally by a microorganism

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6
Q

father of penicillin

A

Flemming 1928

in Penicillium mold

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7
Q

father of streptomycin

A

Waksman - 1943

from soil bacteria Streptomyces griseus

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8
Q

Antimicrobial chemotherapy

A

use of drugs to destroy or inhibit the growth of microbes that are causing disease

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9
Q

Antimicrobic

A

a word that incorporates all types of antimicrobial drugs, regardless of origin

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10
Q

Synthetic

A

antimicrobial chemical produced in the lab (sulfa drug)

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11
Q

Semisynthetic

A

antibiotic that has been chemically altered

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12
Q

Types of antimicrobial drugs (4)

A

Antimicrobic
Antibiotic
Synthetic
Semisynthetic

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13
Q

Therapeutic Index (TI)

A

lowest dose toxic to patient divided by normal dose used for therapy
-OR toxic dose divided by therapeutic dose

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14
Q

Minimum Inhibitory Concentration (MIC)

A

lowest dose that prevents growth of the microbe (=normal dose used for therapy)
- TI= lowest dose toxic to patient divided by MIC

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15
Q

High TI

A

antimicrobics are usually less toxic to host.

  • good ratio is 10:1
  • usually because they are specific to non-host processes
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16
Q

Low TI

A

antimicrobics are potentially toxic to heat

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17
Q

Spectrum of Activity

A

Broad spectrum

Narrow spectrum

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18
Q

broad spectrum

A

affects a wide range of bacteria

  • use if microbe is unknown and infection is serious
  • usually have a low TI
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19
Q

Narrow spectrum

A

affects a limited range of bacteria

  • used if bacteria pathogen has been identified
  • Usually have a high TI
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20
Q

Half-life

A

time it takes for a drug to decrease in body by 50% = describes the rate of elimination.
- Determines the amount of drug given and how often

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21
Q

Tissue distribution

A
  • Antibiotic characteristics determine which tissue can be entered and how drug id given
  • Ex. to cross blood/brain barrier antibiotics are lipid soluble and smaller molecules
    ex. Penicillin G given IV - not stable in low pH of stomach
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22
Q

Resistance to antimicrobials

A

Intrinsic (innate) resistance

acquired resistance

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23
Q

intrinsic (innate) resistance

A

natural resistance based on bacteria’s characteristics

ex. mycoplasma (no cell wall) is not affected by antibiotics specific to peptidoglycan

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24
Q

acquired resistance

A

resistance gained through mutation or genetic exchange

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25
Q

allergies

A

some antibiotics cause hypersensitivity in patient, resulting in immune responses or allergies
- most common - penicillin, cephalosporins, sulfas

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26
Q

Toxic effects

A

some antibiotics can cause damage to host often when used at high concentrations
-ex. streptomycin at high levels can damage kidneys

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27
Q

Antagonistic

A

two drugs make each other less effective.

- Ex. bacteriostatic drugs (prevent binary fission) interfere with Penicillin

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28
Q

Synergistic

A

drugs are more effective when taken together

ex. action of penicillin allows streptomycin to enter cell more easily

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29
Q

Additive

A

no drug interaction, drug combinations are neither antagonistic nor synergistic

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30
Q

Which microbes are easiest to treat using antimicrobial medication?

A

Prokaryote cells

because of selective toxicity, unique cellular targets different from host must be found

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31
Q

Targets of antimicrobial drugs

A

synthesis, structure, function of:

  • cell wall
  • cell membrane
  • proteins
  • nucleic acids
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32
Q

Cell Wall Synthesis

Target

A
  • formation of cell wall is inhibited
  • if cell wall is not intact, osmotic pressure will cause bacteria to lyse
  • high TI b/c we do not have cell walls
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33
Q

Cell Membrane: function

target

A
  • drugs bind to cell membrane and produce large holes
  • causes “leaky” cells and cell death
  • very low TI b/c we also have cell membranes
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34
Q

proteins: metabolic pathways

target

A
  • some drugs target unique metabolic pathways

- high TI

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35
Q

proteins: synthesis/transcription

target

A

Transcription (DNA to mRNA) is prevented by inhibition of RNA polymerase
- low TI b/c our RNA polymerase is similar to microbes so it could affect us as well

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36
Q

Proteins: synthesis/translation

target

A
  • protein synthesis is stopped by disrupting the ribosome
  • drugs attach to bacteria 70S ribosomes
  • Medium/high TI b/c ribosomes found in mitochondria are also 70S so they may be affected
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37
Q

Nucleic acids: DNA synthesis

target

A
  • inhibition of bacterial enzymes needed for DNA synthesis (DNA polymerase, gyrase)
  • low TI b/c our cells also have those cells to go through DNA synthesis
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38
Q

Antibacterial drug families

A
  • Sulfonamides
  • B-lactams
  • Glycopeptides
  • Aminoglycosides
  • Tetracyclines
  • Macrolides
  • Rifamycins
  • Quinolones
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39
Q

Sulfonamides

A

-Synthetic

Broad spectrum - both Gram - and +

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40
Q

Mode of Action for SULFONAMIDES

A
  • competitive inhibitor in METABOLIC PATHWAY that synthesized folic acid
  • human cells do not make folic acid
  • Same pathway makes precursors to proteins and nucleic acids for bacteria
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41
Q

Toxicity of SULFONAMIDES

A

nearly harmless to humans
High TI
- Some allergic reactions

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42
Q

B- Lactams

A
  • contain B-lactam ring
  • antibiotics produced by fungi/molds
  • many semi-synthetic versions (methicillin)
  • used for first time in 1941, very important in WWII
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43
Q

Mode of action of B-LACTAMS

A

interferes with CELL WALL SYNTHESIS, causes bacteria cell to lyse

  • inhibits enzymes that form peptide bridges between glycan chains
  • only work on actively growing cells
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44
Q

Toxicity of B- LACTAMS

A

very little - high TI

  • animal cells do not have cell walls or peptidoglycan
  • sever allergies to penicillin possible
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45
Q

Current effectiveness of B-LACTAMS

A
  • usually more effective against Gram+ bacteria
  • difficult for B-lactams to penetrate Gram - outer membrane, but some can.
  • Broad and narrow spectrum
  • older and newer penicillins
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46
Q

Glycopeptides

A
  • usually injected - is not absorbed well through intestines

- can be taken orally for intestinal pathogens

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47
Q

Mode of Action of GLYCOPEPTIDES

A
  • inhibits CELL WALL SYNTHESIS by binging to peptidoglycan
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48
Q

Toxicity of GLYCOPEPTIDES

A

low toxicity, high TI

- serious side-effects can include nausea and hearing loss

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49
Q

Current effectiveness of GLYCOPEPTIDES

A 
Narrow spectrum (Gram + only)
- usually little resistance, although some seen with S.A and intestinal pahtogens
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50
Q

Aminoglycosides

A
  • from filamentous soil bacteria Streptomyces griseus
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51
Q

mode of action of AMINOGLYCOSIDES

A
  • inhibit TRANSLATION by attaching to 30S subunit of bacterial ribosomes, mRNA is misread and proteins are synthesized incorrectly
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52
Q

Toxicity of AMINOGLYCOSIDES

A
  • severe = low TI
  • used in low doses
  • severs side-effects include kidney and inner ear damage
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53
Q

Current effectiveness of AMINOGLYCOSIDES

A
  • broad spectrum
  • many bacteria are resistant, so not used much
  • often used with other antibiotics (PENICILLIN)
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54
Q

Tetracyclines

A

from streptomyces species and semi-synthetic

-drug of choice for un-diagnosed diseases

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55
Q

Mode of action of TETRACYCLINES

A
  • inhibit TRANSLATION by attaching to 30S subunit of bacterial ribosomes, precents attachment of tRNA, protein synthesis completely blocked
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56
Q

Toxicity of TETRACYCLINES

A
  • low = high TI, but not given to patients with liver and kidney damage or are pregnant
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57
Q

Current effectiveness of TETRACYCLINES

A

Very broad spectrum, resistance is common

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58
Q

Macrolides

A

-often used when patient is allergic to penicillin

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59
Q

mode of action of MACROLIDES

A
  • prevents TRANSLATION by binding to 50S subunit of ribosome
60
Q

Toxicity of MACROLIDES

A

little = high TI

- gastric distress, reversible liver damage

61
Q

current effectiveness of MACROLIDES

A 
narrow spectrum (gram + and mycoplasma)
- gram - are resistant b/c macrolides can't pass their cell wall (intrinsic resistance)
62
Q

Rifamycins

A

-from streptomyces bacteria

63
Q

mode of action of RIFAMYCINS

A

prevents RNA polymerase from starting transcription

64
Q

toxicity of RIFAMYCINS

A

low = high TI

- specific to bacteria RNA polymerase

65
Q

Current effectiveness of RIFAMYCINS

A

broad spectrum, Gram +, some Gram - , used for mycobacterium tuberculosis, resistance develops easily

66
Q

Quinolones

67
Q

Mode of action of QUINOLONES

A
  • inhibits gyrase (DNA SYNTHESIS)
68
Q

Toxicity of QUINOLONES

A

little = high TI

eukaryotes have different enzyme

69
Q

Current effectiveness of QUINOLONES

A

Broad spectrum
Gram + more resistant, overuse causing some resistance.
-Used for UTI and anthrax

70
Q

Triple Antibiotic Lotions

A

Neomycin - aminoglycoside - affects translation
Polymyxin - affects cell membrane
Bacitracin - affects cell wall
Topical because of low TI

71
Q

Antifungal drugs

A
  • most are very toxic and have low TI
  • Usually given topically
  • ex. Polyenes, Flucytosine
72
Q

Polyenes

A

made by streptomyces species, disrupt fungal CELL MEMBRANE and cause leakage, amphoterican B used systemically (IV drop) only for life-threatening infections, nystatin used topically

73
Q

Flucytosine

A

inhibits NUCLEIC ACID SYNTHESIS, synthetic version of cytosine, effective against yeast cells only and used for severs/systemic yeast infections, taken orally.

74
Q

Drugs that treat Anthrax

A

tetracyclines

quinolones

75
Q

Drugs that treat E.coli

A

no antibiotics used unless very severe b/c of resistance

76
Q

Drugs for HIV/AIDS

A

antiviral cocktail

77
Q

Drugs for Staph

A

vancomycin, resistant to penicillin & B-lactams

78
Q

Example of B-Lactams

A

Penicillin, Cephalosporin

79
Q

Example of Glycopeptides

A

Vancomycin

80
Q

Example of Aminoglycosides

A

Streptomycin, Gentamicin

81
Q

Example of tetracyclines

A

tetracycline, doxycycline, oxytetracycline

82
Q

Example of macrolides

A

erythromycin, azithromycin

83
Q

example of rifamycins

84
Q

example of quinolones

A

ciprofloxacin

85
Q

Types of Antiviral Drugs

A

Nucleotide analogs
Amantadine and Rimantadine
Reverse transcriptase inhibitors
others

86
Q

Nucleotide analogs

A

AZT, ddl, acyclovir

  • Have similar structure to nucleotides
  • halts DNA SYNTHESIS
  • low TI
  • exception acyclovir: few side effects bc only activated by viral coded enzymes
87
Q

Amantadine and Rimantadine

A
  • prevent uncoating of influenza virus
  • helps alleviate symptoms
  • must be given in early stages of infection
88
Q

Revers transcriptase inhibitors

A
  • prevents DNA synthesis in HIV virus
89
Q

Others (antiviral)

A

-prevent transcription and translation or prevent maturation of viruses

90
Q

Properties of Antiviral Drugs

A
  • Do not give a cure - only slow progression of disease
  • “Drug cocktails” use 3-4 different antiviral compounds for AIDS patients, lowers the number of replicating viruses, can greatly improve life for patient, but if treatment is stopped viruses return
91
Q

Bacterial resistance types

A

Intrinsic (innate) resistance

Acquired resistance

92
Q

Acquired resistance

A

resistance from mutation or genetic exchange (conjugation/ R plasmid)

93
Q

Mechanisms of Acquired resistance

A
  • Alteration of target molecule
  • alteration of drug
  • decreased uptake of drug
  • prevention of competitive inhibitors
94
Q

Alteration of target molecule

A

can prevent drug from binding to target
ex. tetracycline binds to 30S subunit of ribosome, a change in the ribosome molecular structure could prevent tetracycline from binding

95
Q

Alteration of drug

A

bacteria produces enzymes that alter, destroy or attach to drug
Ex. penicillinase produced by bacteria can destroy penicllin

96
Q

Decreased uptake of drug

A

alteration of permeability of bacteria membrane
-especially true of Gram - bacteria
Ex. these changes can prevent streptomycin from entering bacteria cells

97
Q

Prevention of Competitive inhibitors

A

if bacteria produces a large amount of affected enzyme the metabolic pathways is not inhibited
-ex Sulfa drugs need to be in a very high concentration to inhibit large amounts of PABA enzyme

98
Q

Consequences of overuse of antibiotics

A

Hypersensitivites (allergies)

  • toxicity
  • Secondary infections
  • production of resistant strains
99
Q

Immunity

A

stimulating the body’s natural ability to combat infection (infection can provide immunity)

100
Q

Immunization

A

producing immunity by providing exposure to altered organisms that do not cause disease

101
Q

Vaccine

A

preparation of a pathogen or its products to provide immunity

102
Q

Cowpox and Smallpox in milkmaids

A

Edward Jenner 1796

103
Q

Anthrax and rabies vaccination

A

Pasteur 1881,1184

104
Q

Attenuated vaccine

A

weakened form of pathogen that is unable to cause the disease

105
Q

Inactivated vaccine

A

unable to replicate but can still trigger immunity response - killed bacteria, inactive toxins, pieces of pathogen

106
Q

Which drugs affect Protein metabolic pathways

A

Sulfa drugs

107
Q

Which drugs affect Cell wall synthesis

A

B-Lactams

Glycopeptides

108
Q

Which drugs affect Translation

A

Aminoglycosides
Macrolides
Tetracyclines

109
Q

Which drugs affect Transcription

110
Q

Which drugs affect DNA synthesis

A

Quinolones

111
Q

Epidemiology

A

The study of the cause, frequency and distribution of disease in a population

112
Q

What does an epidemiologist do?

A

Collect and interpret data to control, prevent or predict diseases

113
Q

Hantavirus

A

1993 southwestern US

  • Acute respiratory failure caused by unknown type of hantavirus- severe pneumonia
  • virus carried by mice
  • increased food sources led to increased population of mice
  • transmitted through air in dust of urine and feces
  • search led to similar cases as far back as 1959
114
Q

Communicable disease

A

an infectious disease caused by a pathogen that can be transmitted from one host to another = contagious

115
Q

Non-communicable diseases

A

does not spread from one host to another

116
Q

Example of Non-communicable microbes

A

botulism, tetanus, Toxic Shock Syndrome

117
Q

Rate of Disease

A

the proportion (percentage) of a population who have the disease.

118
Q

Attack rate of disease

A

percentage of population that develop the disease after they have been directly exposed to the pathogen

119
Q

Morbitity

A

rate of new cases of a disease in a specific time period in a certain population

120
Q

which diseases have high morbitity rate?

A

contagious diseases

121
Q

Mortality

A

overall death rate in a population

122
Q

Endemic

A

diseases that are constantly present in a population

ex. cold and flu

123
Q

Epidemic

A

disease in unusually high frequencies in a population

ex. ebola in certain African countries

124
Q

Pandemic

A

epidemic that has spread world-wide (AIDS)

125
Q

Transmission of Disease (chain of infection)

A
  • Reservoir
  • Portal of exit
  • Mode of transmission
  • portal of entry
126
Q

Reservoir

A
  • environment where pathogen can live, grow and spread to other hosts
127
Q

Types of Reservoir

A
  1. Human reservoir - most common
  2. Other animal (zoonotic diseases)
  3. Environmental - microbes in soil, water, etc
128
Q

Anthrax is what kind of reservoir

A

environment and zoonotic

129
Q

Portal of Exit

A

Ex. Digestive system - anus or mouth
Urinary system - urethra
Respiratory system - mouth, nose
etc

130
Q

Mode of Transmission

A

feces, vomit
urine
mucous, droplets

131
Q

Portal of entry

A

similar routes of exit, not necessarily same route in as out.

132
Q

Mode of Transmission

A
  • Direct contact
  • Indirect contact
  • Non-contact sources
133
Q

Direct contact

A

any physical contact

-ex. Fecal-oral transmission

134
Q

Indirect contact

A

-From a non-human source

Vector, Fomite, or Droplet transmission

135
Q

Vector

A

living organism that carries disease-causing microbes

136
Q

Fomite

A

inanimate object that could carry the microbe

137
Q

Non-contact sources

A

air transmission, food and water contamination

138
Q

Incubation period

A

length of time between exposure to the pathogen and onset of disease symptoms

139
Q

Symptomatic

A

host shows symptoms

140
Q

Asymptomatic

A

host does not show symptoms, but can possibly transmit the disease

141
Q

Dosage

A

the number of pathogens the host is originally exposed to

142
Q

Large dosage

A

more likely to cause disease, will shorten incubation time

143
Q

Small dosage

A

less likely to cause disease or will lengthen incubation time

144
Q

Immunity to Pathogen

A

immunity through previous exposure or immunization decreases the possible reservoirs

145
Q

Herd immunity

A

susceptible (non-immune) hosts are protected because disease cannot spread in a population where the majority of individuals are immune

146
Q

What certain characteristics of the population can increase susceptibility to a disease?

A
  • malnutrition
  • crowding
  • fatigue
  • stress
  • age
  • gender
  • genetics

BIO111: Microbiology (12 decks)

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