Chapter 20 & 19 Flashcards Preview

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Flashcards in Chapter 20 & 19 Deck (146):
1

Father of Chemotherapy

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

2

Chemotherapy

Use of chemicals to treat a disease

3

selective toxicity

toxic to microbe, but not host cells

4

Domagk

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

5

Antibiotics

antibacterial compounds produced naturally by a microorganism

6

father of penicillin

Flemming 1928
in Penicillium mold

7

father of streptomycin

Waksman - 1943
from soil bacteria Streptomyces griseus

8

Antimicrobial chemotherapy

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

9

Antimicrobic

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

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Synthetic

antimicrobial chemical produced in the lab (sulfa drug)

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Semisynthetic

antibiotic that has been chemically altered

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Types of antimicrobial drugs (4)

Antimicrobic
Antibiotic
Synthetic
Semisynthetic

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Therapeutic Index (TI)

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

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Minimum Inhibitory Concentration (MIC)

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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High TI

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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Low TI

antimicrobics are potentially toxic to heat

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Spectrum of Activity

Broad spectrum
Narrow spectrum

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broad spectrum

affects a wide range of bacteria
- use if microbe is unknown and infection is serious
- usually have a low TI

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Narrow spectrum

affects a limited range of bacteria
- used if bacteria pathogen has been identified
- Usually have a high TI

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Half-life

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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Tissue distribution

-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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Resistance to antimicrobials

Intrinsic (innate) resistance
acquired resistance

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intrinsic (innate) resistance

natural resistance based on bacteria's characteristics
ex. mycoplasma (no cell wall) is not affected by antibiotics specific to peptidoglycan

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acquired resistance

resistance gained through mutation or genetic exchange

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allergies

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

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Toxic effects

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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Antagonistic

two drugs make each other less effective.
- Ex. bacteriostatic drugs (prevent binary fission) interfere with Penicillin

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Synergistic

drugs are more effective when taken together
ex. action of penicillin allows streptomycin to enter cell more easily

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Additive

no drug interaction, drug combinations are neither antagonistic nor synergistic

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Which microbes are easiest to treat using antimicrobial medication?

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

31

Targets of antimicrobial drugs

synthesis, structure, function of:
- cell wall
- cell membrane
- proteins
- nucleic acids

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Cell Wall Synthesis
(Target)

-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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Cell Membrane: function
(target)

-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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proteins: metabolic pathways
(target)

-some drugs target unique metabolic pathways
- high TI

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proteins: synthesis/transcription
(target)

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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Proteins: synthesis/translation
(target)

- 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

37

Nucleic acids: DNA synthesis
(target)

- 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

38

Antibacterial drug families

-Sulfonamides
-B-lactams
-Glycopeptides
-Aminoglycosides
-Tetracyclines
-Macrolides
-Rifamycins
-Quinolones

39

Sulfonamides

-Synthetic
Broad spectrum - both Gram - and +

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Mode of Action for SULFONAMIDES

- 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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Toxicity of SULFONAMIDES

nearly harmless to humans
High TI
- Some allergic reactions

42

B- Lactams

- 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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Mode of action of B-LACTAMS

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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Toxicity of B- LACTAMS

very little - high TI
- animal cells do not have cell walls or peptidoglycan
-sever allergies to penicillin possible

45

Current effectiveness of B-LACTAMS

- 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

46

Glycopeptides

-usually injected - is not absorbed well through intestines
- can be taken orally for intestinal pathogens

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Mode of Action of GLYCOPEPTIDES

- inhibits CELL WALL SYNTHESIS by binging to peptidoglycan

48

Toxicity of GLYCOPEPTIDES

low toxicity, high TI
- serious side-effects can include nausea and hearing loss

49

Current effectiveness of GLYCOPEPTIDES

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

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Aminoglycosides

- from filamentous soil bacteria Streptomyces griseus

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mode of action of AMINOGLYCOSIDES

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

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Toxicity of AMINOGLYCOSIDES

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

53

Current effectiveness of AMINOGLYCOSIDES

- broad spectrum
- many bacteria are resistant, so not used much
- often used with other antibiotics (PENICILLIN)

54

Tetracyclines

from streptomyces species and semi-synthetic
-drug of choice for un-diagnosed diseases

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Mode of action of TETRACYCLINES

- inhibit TRANSLATION by attaching to 30S subunit of bacterial ribosomes, precents attachment of tRNA, protein synthesis completely blocked

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Toxicity of TETRACYCLINES

- low = high TI, but not given to patients with liver and kidney damage or are pregnant

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Current effectiveness of TETRACYCLINES

Very broad spectrum, resistance is common

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Macrolides

-often used when patient is allergic to penicillin

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mode of action of MACROLIDES

- prevents TRANSLATION by binding to 50S subunit of ribosome

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Toxicity of MACROLIDES

little = high TI
- gastric distress, reversible liver damage

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current effectiveness of MACROLIDES

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

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Rifamycins

-from streptomyces bacteria

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mode of action of RIFAMYCINS

prevents RNA polymerase from starting transcription

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toxicity of RIFAMYCINS

low = high TI
- specific to bacteria RNA polymerase

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Current effectiveness of RIFAMYCINS

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

66

Quinolones

Sythetic

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Mode of action of QUINOLONES

- inhibits gyrase (DNA SYNTHESIS)

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Toxicity of QUINOLONES

little = high TI
eukaryotes have different enzyme

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Current effectiveness of QUINOLONES

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

70

Triple Antibiotic Lotions

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

71

Antifungal drugs

-most are very toxic and have low TI
- Usually given topically
- ex. Polyenes, Flucytosine

72

Polyenes

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

Flucytosine

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

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Drugs that treat Anthrax

tetracyclines
quinolones

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Drugs that treat E.coli

no antibiotics used unless very severe b/c of resistance

76

Drugs for HIV/AIDS

antiviral cocktail

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Drugs for Staph

vancomycin, resistant to penicillin & B-lactams

78

Example of B-Lactams

Penicillin, Cephalosporin

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Example of Glycopeptides

Vancomycin

80

Example of Aminoglycosides

Streptomycin, Gentamicin

81

Example of tetracyclines

tetracycline, doxycycline, oxytetracycline

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Example of macrolides

erythromycin, azithromycin

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example of rifamycins

rifampin

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example of quinolones

ciprofloxacin

85

Types of Antiviral Drugs

Nucleotide analogs
Amantadine and Rimantadine
Reverse transcriptase inhibitors
others

86

Nucleotide analogs

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

Amantadine and Rimantadine

- prevent uncoating of influenza virus
-helps alleviate symptoms
- must be given in early stages of infection

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Revers transcriptase inhibitors

- prevents DNA synthesis in HIV virus

89

Others (antiviral)

-prevent transcription and translation or prevent maturation of viruses

90

Properties of Antiviral Drugs

- 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

Bacterial resistance types

Intrinsic (innate) resistance
Acquired resistance

92

Acquired resistance

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

93

Mechanisms of Acquired resistance

-Alteration of target molecule
- alteration of drug
- decreased uptake of drug
- prevention of competitive inhibitors

94

Alteration of target molecule

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

Alteration of drug

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

96

Decreased uptake of drug

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

97

Prevention of Competitive inhibitors

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

Consequences of overuse of antibiotics

Hypersensitivites (allergies)
- toxicity
-Secondary infections
- production of resistant strains

99

Immunity

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

100

Immunization

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

101

Vaccine

preparation of a pathogen or its products to provide immunity

102

Cowpox and Smallpox in milkmaids

Edward Jenner 1796

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Anthrax and rabies vaccination

Pasteur 1881,1184

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Attenuated vaccine

weakened form of pathogen that is unable to cause the disease

105

Inactivated vaccine

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

106

Which drugs affect Protein metabolic pathways

Sulfa drugs

107

Which drugs affect Cell wall synthesis

B-Lactams
Glycopeptides

108

Which drugs affect Translation

Aminoglycosides
Macrolides
Tetracyclines

109

Which drugs affect Transcription

Rifamycin

110

Which drugs affect DNA synthesis

Quinolones

111

Epidemiology

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

112

What does an epidemiologist do?

Collect and interpret data to control, prevent or predict diseases

113

Hantavirus

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

Communicable disease

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

115

Non-communicable diseases

does not spread from one host to another

116

Example of Non-communicable microbes

botulism, tetanus, Toxic Shock Syndrome

117

Rate of Disease

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

118

Attack rate of disease

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

119

Morbitity

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

120

which diseases have high morbitity rate?

contagious diseases

121

Mortality

overall death rate in a population

122

Endemic

diseases that are constantly present in a population
ex. cold and flu

123

Epidemic

disease in unusually high frequencies in a population
ex. ebola in certain African countries

124

Pandemic

epidemic that has spread world-wide (AIDS)

125

Transmission of Disease (chain of infection)

- Reservoir
- Portal of exit
- Mode of transmission
- portal of entry

126

Reservoir

- environment where pathogen can live, grow and spread to other hosts

127

Types of Reservoir

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

128

Anthrax is what kind of reservoir

environment and zoonotic

129

Portal of Exit

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

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Mode of Transmission

feces, vomit
urine
mucous, droplets

131

Portal of entry

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

132

Mode of Transmission

-Direct contact
- Indirect contact
- Non-contact sources

133

Direct contact

any physical contact
-ex. Fecal-oral transmission

134

Indirect contact

-From a non-human source
Vector, Fomite, or Droplet transmission

135

Vector

living organism that carries disease-causing microbes

136

Fomite

inanimate object that could carry the microbe

137

Non-contact sources

air transmission, food and water contamination

138

Incubation period

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

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Symptomatic

host shows symptoms

140

Asymptomatic

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

141

Dosage

the number of pathogens the host is originally exposed to

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Large dosage

more likely to cause disease, will shorten incubation time

143

Small dosage

less likely to cause disease or will lengthen incubation time

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Immunity to Pathogen

immunity through previous exposure or immunization decreases the possible reservoirs

145

Herd immunity

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

146

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

- malnutrition
-crowding
-fatigue
- stress
-age
- gender
-genetics