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Bio 251 > Chapters 20 & 14, Diseases > Flashcards

Chapters 20 & 14, Diseases Flashcards

1
Q

What are the four types of antimicrobials?

A
  • Antibacterial Drugs
  • Antiviral Drugs
  • Antifungal Drugs
  • Antiprotozoan Drugs/Antihelminthic Drugs
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2
Q

What are the three categories (for microbiologists) of antibacterial drugs?

A
  • Antibiotics
  • Semi-synthetics
  • Synthetics
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3
Q

What was discovered in 1670?

A

Existence of Microbes

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4
Q

What happened around 1840-1850?

A

Pasteur & his Germ Theory

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5
Q

What happened in 1880?

A

Germ Theory was proven

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6
Q

What happened in 1935?

A

First antibacterial- sulfa drugs

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7
Q

What did Paul Ehrlich and his Magic Bullet do?

A
  • development of “selective toxicity” idea

- found dyes which treated african sleeping sickness

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8
Q

What did Sahachiro Hato do?

A

Sahachiro Hato identified arsenic compounds that treated syphilis

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9
Q

What are sulfa drugs?

A

Drugs which attack the enzymes that make folic acid.

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10
Q

Why are sulfa drugs significant?

A

They only attack enzymes that make folic acid, and since humans don’t make folic acid, they have selective toxicity and don’t harm us.

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11
Q

What was the first true antibiotic?

A

Penicillin.

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12
Q

What was the first synthetic antibiotic?

A

Sulfa drug.

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13
Q

How was penicillin discovered?

A

Alexander Fleming, in 1928, observed a contaminated plate. Didn’t think it could develop more.

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14
Q

What did Selman Waksman do?

A

Discovered every major class of antibiotics. Grew bacteria and fungi from all over the world to see which produced antibiotics. Coined the term antibiotics.

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15
Q

Why would microbes be secreting toxic compounds?

A

To protect them. They want to kill off their neighbors, since it’s a big war for nutrients and space.

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16
Q

What is the drug pipeline?

A

Bringing a drug to the market.

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17
Q

What do you need in the drug pipeline?

A
  • 1 billion dollars
  • Prove it’s safe and effective
  • Clinical trials (1. Safety in humans, 2. effectiveness, 3. Relative effectiveness)
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18
Q

How long does the drug pipeline take?

A

Ten years.

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19
Q

What are the cell wall inhibitors?

A
  • Penicillins
  • Polypeptides
  • Cephalosporins
  • Antimycobacterials
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20
Q

What does natural penicillin work against?

A

Gram +

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21
Q

Is natural penicillin narrow or broad spectrum?

A

Narrow

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22
Q

Is semi-synthetic penicillin narrow or broad spectrum?

A

Broad

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23
Q

What does clavulanic Acid (Augmentin) do?

A

Will stop penicillinase, which is found in some microbes.

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24
Q

What is clavulanic acid (augmentin) composed of?

A

Amoxicillin and clavulanic acid.

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25
Q

What are the protein synthesis inhibitors?

A
  • Aminoglycosides
  • Pleuromutilins
  • Tetracyclines
  • Macrolides
  • Streptogimes
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26
Q

What are the nucleic acid inhibitors?

A

Sulfa drugs

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27
Q

What are probiotics?

A

Bacteria taken to replenish normal flora lost during antibiotic treatment.

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28
Q

What are prebiotics?

A

Nutrients taken to feed normal flora. Generally fibers that humans can’t digest.

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29
Q

What are antifungals?

A

Antimicrobials for fungus.

  • Fewer in number
  • Natural and synthetics
  • Broad spectrum
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30
Q

What are antivirals, and what types are there?

A

Antimicrobials for viruses.

  • Fusion Inhibitors
  • Nucleic acid inhibitors
  • assembly inhibitors
  • exit inhibitors
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31
Q

What is the problem with antivirals?

A

They’re extremely narrow spectrum, and only synthetic

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32
Q

What are some types of antibiotic resistance?

A

Decreased permeability
Activation of drug pumps
Change in drug binding site
Use of alternate metabolic pathway

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33
Q

What happens with decreased permeability resistance?

A

The receptor that transports the drug is altered, so the drug can’t get into the cell.

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34
Q

What happens in activation of drug pumps resistance?

A

Specialized membrane proteins are activated and continually pump the drug out of the cell. Call drug eflex pump.

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35
Q

What happens in alternate metabolic pathway resistance?

A

The drug has blocked the usual metabolic pathway, so the microbe circumvents it by using an alternate, unblocked pathway that achieves the required outcome.

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36
Q

What happens in change in drug binding site resistance?

A

The binding site on target (ribosome) is altered so the drug has no effect.

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37
Q

How are mutations spread? (There are four ways)

A
  1. Conjugation
  2. Transduction
  3. Transformation
  4. Binary Fission
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38
Q

What happens in transduction?

A

The virus take the genetic info from bacteria

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39
Q

What happens in transformation?

A

Microbe takes genetic info from dead organisms that are around

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40
Q

What happens in binary fission?

A

Sexual reproduction

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41
Q

What happens in conjugation?

A

Genetic information sharing through sex pili.

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42
Q

How can we stop resistance?

A
  • Limit use
  • Rotate Drugs
  • Appropriate dosing
  • Drug combinations
  • New variations
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43
Q

Where did our normal flora come from?

A 
Birth
Breathing
Touch
Liquids
Solid Food
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44
Q

Where are our normal flora?

A

Skin, Upper Respiratory Tract, GI Tract, urethral opening, external genitals, vagina, external ear, eye canal.

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45
Q

What are the three types of bacteria in humans?

A

Normal Flora
Pathogen
Opportunistic Pathogen

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46
Q

What is an infection, by definition?

A

Microbes reproducing in the body tissues.

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47
Q

What is a disease, by definition?

A

Disruption of normal body processes.

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48
Q

What is an infectious disease?

A

Disruption of normal body processes caused by a microbe.

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49
Q

What is a primary infection?

A

The infection caused by the original pathogen.

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50
Q

What is the secondary infection?

A

The infection caused by the second pathogen, which gained entry because of the first pathogen.

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51
Q

What are the three portals of entry?

A

Skin
Mucous Membranes
Placenta (for a fetus)

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52
Q

What is the infectious dose?

A

The number (or range) of cells needed to get a disease.

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53
Q

What are symptoms?

A

Subjective. What the patient says.

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54
Q

What are the signs?

A

Objective. What we can see.

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55
Q

What are the three types of reservoirs?

A

Human
Animal
Nonliving reservoirs

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56
Q

What are zoonoses?

A

Diseases that are transmitted from animals to humans.

57
Q

What is a communicable disease? Example?

A

Transmissible to others, but not super easily. Ex. HIV.

58
Q

What is a contagious disease? Example?

A

Easily transmissible to others. Ex. A cold.

59
Q

What is a non-communicable disease? Example?

A

Not transmissible from one person to another. Ex. Food poisoning.

60
Q

What are the three types of contact transmission?

A

Direct
Indirect
Droplet

61
Q

What’s the difference between droplet and airborne transmission?

A

Droplet is within less than three feet, airborne is more than three feet away.

62
Q

What is vehicle transmission?

A

Transmission by an inanimate reservoir.

63
Q

What are three examples of vehicle transmission?

A

Waterborne
Foodborne
Airborne

64
Q

What is vector transmission?

A

Animals/arthropods that transmit organisms

65
Q

What is the morbidity rate?

A

An incidence rate. The number of new cases in a specific time period per unit of population

66
Q

What is a mortality rate?

A

The number of deaths from a disease.

67
Q

What is a sporadic?

A

Never expected. Random case.

68
Q

What is an endemic?

A

Standard rate, which you can guess and predict. Random cases all over.

69
Q

What is an epidemic?

A

Any time there’s more than the predicted rate. Bunch of cases in one place.

70
Q

What is a pandemic?

A

An epidemic on several continents. Bunch of cases all over.

71
Q

What makes a pathogen dangerous?

A

Its virulence factors.

72
Q

What are some biological characteristics of S. aureus?

A
  • Gram +
  • Facultative Anaerobe
  • Grape-like clusters
  • Halotolerant (10% NaCl)
  • Transformation
  • Approx. 80,000 deaths/year
73
Q

What are some virulence factors of S. aureus?

A
  • It may have a capsule
  • It may have a slime layer
  • It has protein A
  • Enzymes
  • Toxins
74
Q

What is Protein A?

A

Found on the surface of the cell wall. Binds to antibodies, facing the wrong direction. FC portion of the antibody is bound to protein A.

75
Q

What enzymes does S. aureus have?

A
  • Coagulase
  • Staphylokinase
  • Hyaluronidase
  • Lipase
  • Nucleases
76
Q

What does coagulase do?

A

Has the ability to clot blood, can block himself in so WBCs can’t get in.

77
Q

What does staphylokinase do?

A

Dissolves the blood clots he made when he’s ready to leave his wall.

78
Q

What does lipase do?

A

Break down fats. Can get in all of our cells.

79
Q

What does nuclease do?

A

Chop up our DNA.

80
Q

What are cytolytic Enzymes?

A

Specifically disable red blood cells.

81
Q

What does Panton-Valene Leukocidin do?

A

Kills leukocytes

82
Q

What is exfoliative toxin?

A

Makes layers shed, like an exfoliator.

83
Q

What does hyaluronidase do?

A

Breaks down hyaluronic acid, which is cell cement, in order for S. aureus to be able to get in.

84
Q

What are enterotoxins?

A

Target our enteric system, causing severe diarrhea and vomiting.

85
Q

How much of the population are S. aureus carriers?

A

33%

86
Q

How is S. aureus transmitted?

A

Contact transmission-both direct and indirect

  • touching and droplets
  • fomites
87
Q

What is the treatment of S. aureus?

A
  • Penicillins, although 90% of S. aureus strands produce penicllinase
  • Methicillin/oxacillin
  • vancomycin
88
Q

How much of the community has MRSA in the community vs. in a hospital setting?

A
  • 2% in the community

- 50% in the hospital

89
Q

What secondary diseases can S. aureus cause?

A
  • Food poisoning
  • Skin infections/diseases
  • Pneumonia, etc.
90
Q

How does S. aureus food poisoning work?

A
  • You eat food with S. aureus in it.
  • It was improperly cooked or stored
  • You ingest their TOXINS, not it itself after you eat it
91
Q

What are the symptoms of S. aureus food poisoning?

A
  • Happens within 4 hours of ingestion
  • Projectile vomiting
  • Diarrhea
  • Headache
  • Sweating
  • Stomach pain
  • Last approx. 24 hours
92
Q

What’s the treatment for S. aurerus food poisoning?

A

There is none.

93
Q

What are some S. aureus skin diseases?

A
  • Scalded skin syndrome
  • Impetigo
  • Folliculitis
  • Boils
  • Carbuncles
94
Q

What happens with Scalded Skin Syndrome?

A
  • Exfoliative toxins, and hyyaluronidase are made
  • Blisters, skin peeling, fever
  • Dehydration
  • Secondary bacterial infections
95
Q

Who does scalded skin syndrome effect?

A

Children younger than five.

96
Q

What is the treatment for scalded skin syndrome?

A

Antibiotics and liquids/electrolytes

97
Q

What happens with Impetigo?

A
  • 80% of the time, it’s caused by S. aureus
  • Blisters on patches on skin
  • Puss and scabs with white BCs and bacteria
  • Common in children
  • Cured with antibiotics
98
Q

What happens with folliculitis?

A

The hair follicle’s entrance is blocked, so bacteria is trapped inside the hair follicle.

99
Q

What is a boil?

A

Folliculitis, but gone far. Very common and painful. Treat with antibiotics.

100
Q

What are carbuncles?

A

Coalescing of several boils. Way too many cytokines are being released.

101
Q

What is special about S. aureus skin diseases?

A

They’re pyogenic, meaning that they cause puss.

102
Q

What is sepsis?

A

Systemic response to a microbial infection.

103
Q

What happens during sepsis?

A

Fever, increased pulse rate, increased respiratory rate, alkalination, increase in WBC count, low BP,

104
Q

Why is sepsis so serious?

A

Organs start shutting down.

105
Q

What is septic shock?

A

Sepsis associated with severe refractory hypotension, multiple organ failure.

106
Q

How does influenza get in?

A

Receptors found only in the upper respiratory tract. Endocytosis, replicates in our nucleus, released from cell by budding.

107
Q

What makes you ache everywhere when you have influenza?

A

Tons of cytokines released all over your body.

108
Q

What are your symptoms caused by when you have influenza?

A

Our immune system from t-cytotoxic cell destruction.

109
Q

What is the morbidity rate of influenza?

A

5-20%

110
Q

What is the mortality rate of influenza?

A

3000-48000 cases

111
Q

What actually causes death with influenza?

A

A secondary infection like pneumonia.

112
Q

What treatment is there for influenza?

A

Antivirals. NO ASPIRIN

113
Q

What type of antivirals are there?

A
  • Neuraminidase inhibitors

- M2 Blockers

114
Q

What do neuraminidase inhibitors do?

A

Block a virus’s spikes.

115
Q

What is antigenic drift?

A

Influenza’s accumulation of mutations. This is normal evolution that’s bound to happen.

116
Q

What is antigenic shift?

A

Genetic recombination involving reassortment of genomes. Ex. Mixing human and bird virus through conjugation in a pig to make a new virus.

117
Q

What is significant about the 1918 Influenza?

A

40 million people died. It occured in people ages 20-40, when usually it’s the very old and the very young. Effected healthy people because the particular influenza strain caused the body to produce too many cytokines, called a cytokine storm.

118
Q

What kind of vaccines for influenza are there?

A

Inactivated
Recombinant
Attenuated

119
Q

What kinds of inactivated vaccines are there?

A
  • Tri-valent=3 strains

- Quadri-valent=4 strains

120
Q

What is an inactivated vaccine?

A

Dead pieces of the virus.

121
Q

What is a recombinant virus?

A

Genes of the virus put into another organism

122
Q

What is an attenuated virus?

A

Live virus-found in mists and sprays

123
Q

What is the biggest way to prevent yourself from getting influenza?

A

Get an annual vaccination

124
Q

How long does influenza last on hard surfaces (hard fomites)?

A

Two days

125
Q

How long does influenza last on soft surfaces (soft fomites)?

A

12 hours

126
Q

How long does influenza last on hands?

A

5 minutes

127
Q

What are some biological characteristics of C. diff?

A
  • Gram +
  • Endospore former
  • Anaerobic
  • Opportunistic pathogen
128
Q

What are your risk factors for getting C. diff?

A

Antibiotic treatment
Immunocompromised
Extended hospital stay
Nursing Home stay

129
Q

What do Toxins TcdA and TcdB do?

A

They target tight junctions and chemotaxis neutrophils, respectively.

130
Q

What is pseudomembranous colitis?

A

Inside of colon has been being eaten away.

131
Q

What are the symptoms of pseudosmembranous colitis?

A

Diarrhea
Cramping
Bloody/Pussy stool
Perforated bowel

132
Q

What are the treatments of C. diff?

A 
Discontinue previous antibiotics
Vancomycin/Metronidazole
Probiotics
Surgery
Fecal transplant
Bleach-based cleaner
133
Q

What was the former name of HIV?

A

Slim’s Disease

134
Q

What are some of the biological characteristics of the HIV virus?

A
  • +RNA virus
  • Retrovirus
  • Enveloped
  • Infects macrophages and T helper cells
135
Q

How does HIV enter human cells?

A

Membrane fusion

136
Q

What viral enzymes needed for replication?

A

Reverse transcriptase
Integrase
Protease

137
Q

When does HIV turn into AIDS?

A

When he’s killed enough of your T helper cells.

138
Q

What is the requirement of T helper cell count to have AIDS?

A

Less than 200 T helper cells per microliter of blood

139
Q

How do T helper cells die?

A

They get sticky and membranes fuse together. Called syncytia. Immune system them attacks syncytia.

Bio 251 (2 decks)

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