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Unit 3 Flashcards

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1
Q

What are the 4 broad kinds of defenses that God has given us against infection?

A
  1. Knowledge
  2. “innate” immunity
  3. “adaptive” immunity
  4. antimicrobial drugs
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2
Q

What is “Innate” Immunity?

A

It is a non-specific, fast acting, small-scale form of defense against microorganisms. Can result in collateral damage, it limits the spread of damage.

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3
Q

What is “adaptive” immunity?

A

It is an extremely specific, slow to develop, energy expensive defense against microorganisms. It is only acquired after being exposed to a microorganism, therefore it is useful for preventing reinfection.

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4
Q

What are the 3 places where microorganisms and body defenses can meet? (list them in the order in which they usually occur)

A
  1. body suface
  2. interstitial space
  3. bloodstream
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5
Q

What are the two types of body surfaces where body defenses and microorganisms can meet?

A
  1. External (skin)

2. Internal (linings)

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6
Q

How does the skin (external body surface) provide protection physically? 2 ways

A
  1. Its cells are multilayered, tightly attached, and closely packed - hard to get through
  2. tight, mesh-like basement membrane
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7
Q

How does the skin (external body surface) provide protection chemically? 2 ways

A
  1. it is low in nutrients and high in salts (not habitable by most microorganisms)
  2. has germicidal chemicals like oils and acids
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8
Q

How do linings (internal body surfaces) provide protection physically? 4 ways

A
  1. packed layer of cells
  2. basement membrane
  3. viscous mucous traps microorganisms
  4. mucous is constantly flowing
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9
Q

How do linings (internal body surfaces) provide a chemical protection?

A

Enzymes in the mucous called lysozymes act on microorganisms with cell walls made of peptidoglycan, by cutting up the peptidoglycan

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10
Q

How do linings (internal body surfaces) provide a biological protection?

A

The natural flora in the bodies linings compete against pathogens. This is called microbial antagonism.

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11
Q

What are the 3 types of non-specific defense that the body provides beneath either body surfaces?

A
  1. Phagocytic cells
  2. NK cells/lymphocytes
  3. inflammation
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12
Q

How do Phagocytic cells provide non-specific defense beneath body surfaces?

A

Macrophages and dendritic cells reside beneath body surfaces. They work by expressing TLR’s which they use to recognize pathogenic invaders, they respond by phagocytosing them. (small line of defense, may be overwhelmed by microorganisms)

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13
Q

How do NK cells/lymphocytes provide non-specific defense beneath body surfaces?

A

When host cells undergo ‘stress’ they secrete a ligand, called MIC/A. NK cells/lymphocytes have a receptor called NKG2D which binds to MIC/A and responds in one of two ways. 1. induce apoptosis of infected host cell OR 2. secrete proteins called perforins that punch holes in the infected host cells plasma membrane

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14
Q

What four things occur as a result of inflammation in terms of non-specific defense?

A
  1. blood vessels dilate (vasodilation)
  2. blood vessels become more permeable
  3. reconstruction is initiated
  4. non-specific systemic responses to microbial invasion occur
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15
Q

What benefits does the dilation of blood vessels during inflammation provide?

A

It allows for blood cells (specifically neutrophils) to be brought in. Neutrophils provide defense in three ways: 1. they phagocytose microorganisms

  1. they release oxidizing agents
  2. they lyse themselves, creating a DNA net that traps microorganisms (the negative charge from DNA absorbs important charged ions essential to microorganisms survival
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16
Q

How can microorganisms protect themselves from the effects of neutrophils lysing themselves?

A

If they have DNase (like staph does) than they can simply break down the DNA net formed

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17
Q

What does diapedesis mean?

A

It means movement across, specifically across a membrane

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18
Q

How can the releasing of oxidizing agents by neutrophils be bad?

A

Because it can lead to a significant amount of collateral damage.

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19
Q

Why is it important that blood vessels become more permeable during inflammation? (what important things cross out of the vessels)

A

It allows for blood proteins to escape from the capillaries and into the damaged/infected area

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20
Q

What types of blood proteins leave the capillaries during inflammation? What other substance leaves the capillaries and why?

A
  1. complement proteins
  2. clotting proteins
  3. antibodies
    fluid also escapes from the vessels due to osmosis
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21
Q

What are complement proteins /where do they come from? What do they do?

A

Complement proteins are made by the liver, it is always available and therefore provides immediate defense. It acts in two ways: 1. it attaches to microorganisms, marking them for neutrophils to phagocytose 2. bore holes in the PM which leads to lysis (could be bad bc collateral damage)

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22
Q

What type of clotting protein leaves the capillaries during vasodilation of inflammation? What does it do?

A

Fibrin, It produces a clot around the bacteria, this limits their spread. (unless the bacteria secrete fibrinolysin)

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23
Q

What do antibodies do?

A

If you have been exposed to a microorganism before, antibodies act by marking them so that they can be phagocytosed

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24
Q

Why is fluid exiting the bloodstream along with blood proteins during inflammation both good and bad?

A

It is good because along with water come nutrients. It is bad because it accumulates and causes swelling which causes pain.

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25
Q

How does inflammation initiate reconstruction of the damaged area?

A

It brings in more macrophages which remove the debris. It also brings in more platelets which produce blood clots, attracting neutrophils which stimulate stem cells to regenerate (replacing damaged cells)

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26
Q

How could chronic inflammation lead to cancer? (2 ways)

A
  1. neutrophils brought in by inflammation secrete oxidizing agents could lead to cancerous mutations
  2. replication of stem cell DNA could lead to cancerous mutations
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27
Q

What are the non-specific systemic responses to a microbial invasion?

A

cytokines production by mac/dc which leads to these 4 responses:

  1. fever: shivering + vasoconstriction leading to an increase in temp
  2. haptoglobin which absorbs Fe
  3. Energy diverted to body defenses
  4. alerts adaptive immunity that there is an infection
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28
Q

What are the 3 non-specific defenses in the blood?

A
  1. lots of neutrophils which reproduce rapidly in response to an infection
  2. macrophages, which are found in every organ that filters blood and lymph
  3. the blood has the highest conc. of antibacterial proteins (antibodies, complement, clotting factors)
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29
Q

What is leukocytosis?

A

It is a high WBC count, which indicates infection

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30
Q

What is leukopenia? How is it caused? (2 ways)

A

It is a low WBC count, it is cause by 1. an infection by bacteria secreting leukocides (virulence factor) or 2. blood cancers

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31
Q

What is septicemia?

A

Also known as sepsis, septicemia is a fatal systemic inflammation = septic shock

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32
Q

What is shock?

A

Any sudden drop in blood pressure

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33
Q

What are the 6 types of shock a person can experience?

A
  1. septic shock - widespread vasodilation
  2. hypovolemic shock - blood loss
  3. anaphylactic shock - IgE + allergen
  4. cardiogenic shock - drop in cardiac output and heart rate
  5. neurogenic shock - systemic vasodilation due to problem in CNS
  6. Insulin shock (not really shock because blood pressure stays normal) - glucose drop
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34
Q

What types of weakened defenses can lead to infections? (5)

A
  1. broken barriers (cuts, burns, punctures)
  2. impaired washing of mucous membrane (smoking, influenza leading to pneumonia)
  3. reduced number of phagocytic cells (malnutrition, cancer, chemotherapy)
  4. low energy level (fatigue, stress, lack of sleep)
  5. inflammation reduced by aspirin or ibuprofen
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35
Q

Which type of WBC secretes anitbodies?

A

B lymphocytes

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36
Q

What is the primary way that antibodies attack microorganisms?

A

By tagging them for phagocytosis

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37
Q

What are the 4 primary groups of cells in adaptive (specific) immunity?

A
  1. B lymphocytes
  2. Cytotoxic T lymphocytes
  3. Helper and Regulatory (administrative) lymphocytes
  4. phagocytic cells
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38
Q

Characteristics of B lymphocytes include (structure)?

A

They are small cells with a large nucleus, and they have hundreds of BCR receptors

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39
Q

What are B lymphocytes primarily useful in attacking? What specific type of immunity do they provide?

A

microorganisms outside of host cells are most commonly targeted by B lymphocytes. They provide humoral immunity

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40
Q

What are the BCR receptors on B lymphocytes for?

A

They are for matching with the pieces of the microorganism selected. Stimulating secretion of antibodies by B lymphocytes into the bloodstream.

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41
Q

Another name for Cytotoxic T Lymphocytes (CTL’s) is…

A

killer cells

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42
Q

What is the difference between CTL’s and NK cells?

A

CTL’s are very specific have a higher affinity and work on a larger scale.

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43
Q

What types of microorganisms do CTL’s primarily defend against? How do they provide this attack? What type of immunity is this?

A

They attack intracellular microorganisms, they do this by inducing apoptosis. This is called cell-mediated immunity

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44
Q

How do CTL’s induce apoptosis of infected host cells?

A

Via a protein called CD178

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45
Q

What are tCR receptors for? What types of cells can they be found on?

A

They are used to match with pieces of of a selected microorganism so that the T cell can respond. They are found on CTL’s, T helper and T regulatory cells.

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46
Q

What do T helper cells do?

A

They secrete an interleukin which stimulates both B lymphocytes and CTL’s to proliferate.

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47
Q

What do T regulatory cells do?

A

They suppress or inhibit immune responses against normal, uninfected host cells. They do this by secreting an interleukin that inhibits the T helper cells secretion of their interleukin

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48
Q

How long after infection does it take the adaptive immunity to respond?

A

It takes 7-10 days.

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49
Q

What role do macrophages and dendritic cells play in adaptive immunity?

A

They begin the immune response by phagocytosing, processing, and presenting the microorganism

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50
Q

How do macrophages and dendritic cells process microorganisms?

A

Through lysosomes

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51
Q

How do neutrophils and macrophages respond to humoral immunity?

A

By phagocytosing microorganisms tagged with antibodies

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52
Q

How do macrophages and dendritic cells know what to phagocytose in the first place?

A

Because they have TLR receptors which are pattern recognition receptors.

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53
Q

How many cells are saved as memory cells? Why are they kept?

A

10 % of all of the proliferated cells, they are saved in order to prevent reinfected.

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54
Q

What are antigens? What types of cells respond to antigens?

A

Antigens are foreign surface proteins ( or polysaccharides) TLR’s on macrophages and dendritic cells recognize antigens as do BCR’s on B cells and TCR’s on T cells.

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55
Q

How do neutrophils recognize foreign microorganisms?

A

Because of complement or because of antibodies.

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56
Q

Which part of the antibody is known as the constant region and which is the variable region?https://www.brainscape.com/profiles/2558605

A

The constant region is the two heavy amino acid chains, it is the Fc region. The variable region is the one made up of the to light chains.

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57
Q

What is opsinization?

A

It is the “gluing” of an antigen to an antibody

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58
Q

What type of cell has Fc receptors?

A

neutrophils

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59
Q

Each variable region on an antibody matches a specific…

A

antigen

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60
Q

How are antibody classes categorized?

A

each antibody class has a different constant region and therefore some unique function.

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61
Q

All antibodies are made by?

A

B lymphocytes

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62
Q

What is another synonym for the word antibody?

A

Immunoglobin

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63
Q

How many types of immunoglobin (antibody) classes are their in humans?

A

5

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64
Q

What is the largest antibody (immunoglobin) class?

A

IgG

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65
Q

What are IgG molecules like structurally?

A

They are single, Y-shaped molecules that are relatively small, they are monomers.

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66
Q

Where do IgG antibodies come from? Where do they go?

A

They are secreted by B cells from the spleen and lymph nodes into the blood stream. They are small enough however to cross capillaries and end up interstitial spaces.

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67
Q

How do IgG antibodies work? (3 mechanisms of attack)

A
  1. They enhance phagocytosis by opsonizing (neutrophils will then attach to Fc region)
  2. They prevent uOs from attaching to host cells by attaching to their pili and spike proteins (neutralization)
  3. Paired with complement they are able to puncture and therefore lyse uOs directly
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68
Q

What is the structure of IgM antibodies?

A

5 Y-shaped molecules bonded together by their Fc regions (pentamer)

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69
Q

What is agglutination?

A

It is the clumping of antigen-bearing microorganisms

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70
Q

Where can IgM antibodies be found?

A

Because of their large size they cannot escape the bloodstream, so they would be located in the bloodstream.

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71
Q

How do IgM antibodies work? ( 4 mechanisms of attack)

A
  1. They bind up to 10-antigen containing uOs making phagocytosis way more efficient
  2. opsonization
  3. neutralization
  4. activates complement
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72
Q

What is the structure of IgA antibodies?

A

It is a dimer, two Y-shaped molecules bonded together

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73
Q

Where can IgA be found?

A

They are transported by epithelial cells into mucous secretions

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74
Q

How do IgA antibodies work?

A

They provide mucosal immunity by neutralizing uOs before they are able to attach to mucous membrane cells, causing them to simply be washed away.

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75
Q

What is the structure of IgD antibodies?

A

They are single Y-shaped monomers

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76
Q

Where can IgD be found?

A

Imbedded in the membranes of B cells by transmembrane domains on its H chains (not secreted)

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77
Q

How do IgD antibodies work?

A

They serve as B cell receptors for antigens (IgD = BCR)

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78
Q

Why do not all people have IgE antibodies?

A

Because they are the source of allergen responses, and not all people have allergies

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79
Q

What type of cell bind IgE antibodies? Why only this cell type?

A

Mast cells, because the Fc region of IgE is unique from the Fc region of antibodies

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80
Q

How does IgE work?

A

When it attaches to mast cells it causes them to exocytose massive amounts of histamine which causes inflammation

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81
Q

What makes up immunity?

A

Antiobodies (IgA, IgG, and IgM) and or memory cells

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82
Q

What are the 4 basic ways to acquire immunity?

A
  1. natural active immunity
  2. artificial active immunity
  3. natural passive immunity
  4. artificial passive immunity
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83
Q

What is natural active immunity?

A

Immunity acquired by being exposed to a reservoir, getting sick, and then recovering (takes a week before you have any significant amount of immunity)

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84
Q

What is artificial active immunity?

A

Immunity acquired by vaccination. Exposure to an unharmful amount of uO, threat is perceived and immune system is activated, producing memory cells, however host does not get sick in this process.

85
Q

What were the 5 vaccine types given in class?

A
  1. dead uOs
  2. Live but weakened (attenuated) uOs
  3. parts of uOs
  4. recombinant vaccines
  5. DNA - with only the antigen genes
86
Q

What is natural passive immunity?

A

Immunity acquired by the transfer of antibodies from a mother to her child. This is effective immediately, but also temporary (about 2 weeks) because no memory cells are being passed to the baby.

87
Q

What types of antibodies are passed from mother to baby in natural passive immunity? How are these transferred to the baby?

A
  1. IgG is passed across the placenta during pregnancy

2. IgA is passed from the mother to the baby through breast milk

88
Q

What is artificial passive immunity?

A

Immunity acquired by the transfer of antibodies by injection from immunized donor. Immunity is immediate, but temporary because these antibodies would eventually wear out.

89
Q

How would antibodies from artificial passive immunity protect you?

A

Even though they are temporary, they can help to neutralize the uO (examples, rabies and hepatitis patients receiving antibodies)

90
Q

What types of cells produce immune system cells (as well as all other blood cells)?

A

Hemocytoblasts - pluripotent stem cells

91
Q

Where are hemocytoblasts located?

A

Bone marrow

92
Q

Where do hemocytoblast daughters that eventually become T lymphocytes mature?

A

In the thymus

93
Q

Where do the hemocytoblast daughters that eventually become B lymphocytes mature?

A

In the bone marrow

94
Q

Where are mature T and B cells stored?

A

In lymphoid organs, where they wait for their antigen to appear, they occasionally circulate the bloodstream

95
Q

What are the lymphoid organs?

A

Spleen, tonsils, lymph nodes, (some examples)

96
Q

When an antigen appears which are the first IS to detect is?

A

Macrophages/dendritic cells, they will then carry it to the nearest lymphoid organ

97
Q

What types of IS become memory cells?

A

CTL’s and B lymphocytes

98
Q

Why is it that memory cells are able to prevent reinfection?

A

Because if the antigen-carrying uO were to ever reappear they would be able to mount a quick, large-scale attack.

99
Q

What is pathogenesis?

A

It means “suffering generation” and it is the process by which symptoms are produced

100
Q

What are the 4 steps that make uOs able to eventually cause symptoms?

A
  1. Entry into host
  2. Adhere to host cells
  3. Resist host defenses
  4. Damage host cells
101
Q

How does a uO gain access into a host?

A

Their are two primary portals of entry: 1. skin “front door” and 2. mucous membranes “back door”

102
Q

What is a parenteral route of entry?

A

It is a direct deposit of uOs beneath the skin

103
Q

What is the prevalence of different mucous membrane portal entries?

A

respiratory > genitourinary > digestive

104
Q

What are opportunisitc microorganisms?

A

They are uOs that wait for a break of some kind in order to cross a front line

105
Q

What is the difference between a portal of entry and a route of transmission?

A

A route of transmission is how a uO get ONTO you, whereas a portal of entry is how a uO gets INTO you.

106
Q

Why do microorganisms have preferred portals of entry?

A

Because uOs tend to be found in places that meet their specific growth requirements

107
Q

What are examples of uO preferred portals of entry?

A

Clostridium tetani requires anaerobic environments and a parenteral route of entry.
URT infections require lower temperatures

108
Q

What do microorganisms use to adhere to host cells?

A

virulence factors

109
Q

What are the 5 ways that microorganisms resist host defenses?

A
  1. producing a capsule
  2. secreting certain enzymes
  3. growing inside of host cells
  4. changing its surface proteins/antigens
  5. coating itself with its host’s proteins
110
Q

How does producing a capsule aid uOs in resisting host defenses?

A
  1. it retards phagocytic cells from adhering to it, allowing it to slip away
  2. it covers its surface proteins, therefore it will not be detected (by TLR’s) and attacked
111
Q

What are the 6 different enzymes that a uO can secrete in order to resist host cell defenses?

A
  1. leukocides 2. coagulase 3. fibrinolysin 4. protease 5. collagenase 6. DNase
112
Q

What type of host cell defense resistance does leukocide secretion produce?

A

leukocides are injected into neutrophils via a hollow pillus (type III secretion system), this will kill the neutrophils by blocking their ribosomes

113
Q

What type of host cell defense resistance does coagulase secretion produce?

A

coagulase promotes blood clot formation, this blood clot can surround the uOs and protect them from phagocytosis and immune system attacks

114
Q

What type of host cell defense resistance does finbrinolysin secretion produce?

A

It breaks down blood clots formed by the body, allowing the uO to spread

115
Q

What type of host cell defense resistance does protease secretion produce?

A
  1. if extracellular - it destroys antibodies and complement thereby reducing phagocytosis
  2. if intracellular - it destroys internal signalling proteins, like the used to stimulate interleukin synthesis
116
Q

What type of host cell defense resistance does collagenase secretion produce?

A

It breaks down collagen fibers in the host’s basement membranes beneath body linings as well as around capillaries, allowing for great uO spread

117
Q

What type of host cell defense resistance does DNase secretion produce?

A

It breaks down the DNA net that neutrophils create to entangle the uOs

118
Q

What types of uOs grow inside of host cells in order to evade host cell defenses?

A

viruses, Plasmodium (which is a protozoan), and some bacteria

119
Q

What type of host cell defense resistance does growing inside of host cells provide?

A

It causes a shield from humoral defenses (because of host cell PM), leaving defense up to cell-mediated immunity only

120
Q

What are the two ways in which uOs change their surface proteins/antigens in order to evade host cell defenses?

A
  1. antigenic shift = radically changing form and surface proteins (like Plasmodium does in Malaria)
  2. antigenic drift = smaller changes caused by mutating the genes for those antigens
121
Q

What benefit does coating itself with its host’s proteins provide a microorganism?

A

It causes it to appear the same as the host cells, therefore it will not be attacked by the immune system

122
Q

What are the 4 ways in which microorganisms cause damage to host cells?

A
  1. Lysing them
  2. Secreting exotoxins
  3. Secreting endotoxins
  4. Stimulating inflammation or an immune response
123
Q

What types of uOs damage host cells by lysing them?

A

Most viruses as well as Plasmodium

124
Q

What are exotoxins (“ouside toxins”)?

A

They are proteins produced by certain gram+ bacteria which are often coded for by genes on plasmids (easily transferred) and are soluble in both water and the bloodstream (can spread rapidly + widely)

125
Q

What are the effects of exotoxins?

A

They cause severe and sometimes lethal effects to specific host cells

126
Q

What are two examples of the effects of exotoxins?

A
  1. tetanus toxin - blocks the NT release of neurons which inhibit muscle contraction resulting in rigid paralysis
  2. botulinum toxin - blocks release of ACh at neuro-muscular junction causing flaccid paralysis
127
Q

What is the effect of cooking food containing exotoxins?

A

The exotoxins will be denatured by the heating

128
Q

What are endotoxins (“inside toxins”)?

A

They are lipopolysaccharides released from gram- bacteria when they die and break apart

129
Q

What are the effects of endotoxins?

A

They all produce the same general symptoms (e.g. fever, nausea, fatigue)

130
Q

Why are anti-inflammatory drugs given along with antibiotics for G- bacterial infections?

A

Because endotoxins have been suggested to provoke inflammation

131
Q

What is the effect of cooking food containing endotoxins?

A

The endotoxins will not be destroyed

132
Q

Which is more toxic, exotoxins or endotoxins?

A

exotoxins

133
Q

Why does stimulating inflammation or immune response lead to damage of host cells?

A

Because infected host cells must be killed, and there is collateral damage in immune defense (e.g. neutrophils releasing oxidizing agents/lysosomal enzymes

134
Q

What are the 10 requirements for an ideal antimicrobial drug?

A
  1. toxic to uOs
  2. although foreign, should not stimulate allergic response from host’s IS
  3. soluble in body fluids (polar)
  4. soluble in lipids (nonpolar)
  5. stable = not broken down rapidly
  6. unaffected by microbial resistance mechanisms
  7. minimal side effects
  8. affordable
  9. narrow spectrum of activity - specific
  10. doesn’t interact with other drugs
135
Q

How do you make an antimicrobial drug toxic to a microorganism?

A

By finding a unique property of that microorganism to exploit

136
Q

Why do antimicrobial drugs have to be small?

A

So that they can get through basement membranes and so that they don’t stimulate the IS

137
Q

Can a host become allergic to an drug? Can a host become resistant to a drug?

A

A host may become allergic to a drug but only microorganisms become resistant to drugs

138
Q

Why is it important for drugs to be soluble in body fluids (water)?

A

So that they can diffuse to wherever they need to go (plasma, interstitial fluid, cytoplasm, etc.)

139
Q

Why is it important for drugs to be soluble in lipids?

A

So that they can cross the host cell’s PM but also the PM/OM of uOs as well

140
Q

What does it mean to say that a drug is in vivo?

A

that it has already been administered

141
Q

What are the two main reasons why drugs need to be stable?

A
  1. In order to have some sort of storage life

2. So that it lasts long enough after administered to actually have an effect

142
Q

What all does a drug have to go through before it actually even gets to the bloodstream?

A

mouth - stomach (acid) - intestines (absorption) - liver (enzymes) - kidneys (which filter)

143
Q

When drugs interact with other drugs what two negative things could occur?

A
  1. synergism leading to an overdose

2. antagonism leading to no effect

144
Q

Why could a broad spectrum drug be bad?

A

It could kill your normal flora

145
Q

What causes an IS response towards antibiotics?

A

When your body encounters foreign molecules it will either attack them or ignore them, if they attack them and you are repeatedly exposed it generally leads to IgE production resulting in inflammation

146
Q

What are the 3 sources of antibiotic production?

A
  1. discovered by accident
  2. made by modifying “natural” antibiotics (improving their characteristics)
  3. rational drug design
147
Q

How could an antibiotic be discovered by accident?

A
  1. screening of plant and exotic animal extracts that they use to defend against uOs
  2. by making chemicals by combinatorial (random combinations) chemistry
  3. test chemicals by trial and error
148
Q

How does rational drug design occur?

A

By making/designing a drug to match the exact shape of the active site of a uO enzyme

149
Q

What are the 5 current modes of action in antimicrobial drugs?

A
  1. inhibit synthesis of peptidoglycan cell wall
  2. inhibit protein synthesis
  3. injury to the plasma membrane
  4. inhibit synthesis of RNA or DNA
  5. inhibit synthesis of other essential molecules
150
Q

How do drugs inhibit the synthesis of peptidoglycan cell wall?

A

They inhibit the enzyme transpeptidase or glycosyltransferase, this would only effect multiplying bacteria

151
Q

What are some examples of drugs that inhibit synthesis of peptidoglycan cell wall?

A

“cillins”, cephalosporins, vancomycin

152
Q

How do drugs inhibit protein synthesis?

A

They inhibit protease, making synthesized polyproteins useless, they also inhibit peptide deformylase

153
Q

What are some examples of drugs that inhibit protein synthesis?

A

streptomycin and tetracycline

154
Q

Why would protein inhibition drugs not effect host cells?

A

Because host cells have larger ribosomes made of different proteins and rRNA’s

155
Q

How do drugs injure the plasma membrane of uOs?

A
  1. inhibit ergosterol synthesis

2. disrupt cell’s selectively permeable barrier

156
Q

What are some examples of drugs that inhibit protein synthesis?

A

antibacterial - polymyxin B
antifungal - amphotericin B
antimalarial - chloroquinine, artemesinin

157
Q

How do drugs inhibit the synthesis of RNA or DNA?

A
  1. inhibit DNA gyrase

2. by using base analogs to introduce a dead end

158
Q

What are some examples of drugs that inhibit RNA/DNA protein synthesis?

A

rifampin, ciprofloxacin, acylovir and AZT

159
Q

Why would drugs that inhibit RNA/DNA synthesis not effect host cells?

A

Because host cells use different enzymes in RNA/DNA synthesis

160
Q

What type of drugs inhibit synthesis of essential molecules (like folic acid)?

A

sulfa drugs

161
Q

What are the 7 mechanisms by which uOs display drug resistance?

A
  1. secrete enzymes that destroy or inhibit drug
  2. change the lipid composition of OM/PM so drug cannot enter into uO
  3. Mutate channels - too narrow for drug to enter
  4. synthesize more natural substrate to out-compete competitive inhibitor
  5. synthesize more enzyme than the inhibitor can block
  6. Synthesize a mutant enzyme that drug can no longer attach to but natural substrate can
  7. drug-efflux pumps
162
Q

How does a uO use enzymes to resist drugs?

A
  1. It can use enzymes to cut bonds in the drug - altering its shape - drug can no longer bind
  2. It can attach a glucose to the drug (glycosylation) - drug can no longer bind
163
Q

Mutations for drug resistance occur by accident ( and are sometimes bad ) however the uO do respond to changes in their environment in 2 ways:

A
  1. They increase their mutation rate

2. sense damage and stop cell division to repair damage

164
Q

Why are combinations of drugs often more effective than single drugs?

A
  1. synergism - greater attack on uO
  2. lower doses = less side effects
  3. less chance of resistance
165
Q

What are the odds of mutation against one drug?

A

10^-6

166
Q

What 7 factors determine what the dose of the drug should be?

A
  1. expected % to be destroyed by stomach
  2. expected % that won’t be absorbed by intestine
  3. expected % to survive passage through liver
  4. expected % not bound to plasma proteins
  5. the size of the patient
  6. min conc. required to be effective
  7. max conc. which can be tolerated
167
Q

Usually, how much of the drug is actually free (and therefore available) by the time it gets to the bloodstream?

A

10%

168
Q

The averaged sized patient has how many liters of plasma + ISF in which the drug will be diluted?

A

14 liters

169
Q

What are the 5 principles of antimicrobial drug use?

A
  1. combinations of drugs are often more effective
  2. dose of drug must be estimated based on 7 factors
  3. conc. of drug must be maintained long enough to act on most or all uOs
  4. route of administration is important
  5. drugs can be used at 2 different times
170
Q

What impacts the concentration of an administered drug?

A

rate of excretion by kidneys and rate of neutralization by liver

171
Q

What is done in order to ensure that the conc. of the drug is maintained enough to be effective?

A

The frequency of the dosage is kept constant

172
Q

What are the two routes of antimicrobial drug administration?

A
  1. injection

2. oral drugs

173
Q

Why are injections of drugs good/bad?

A

They are the most rapid route but they are inconvinient

174
Q

Why are oral drugs good/bad?

A

They are convenient but they have to be ale to withstand stomach acid and be absorbed by intestines. It is also hard to ensure compliance with oral drugs

175
Q

What are the 2 different times at which drugs can be taken?

A
  1. therapeutically - after infection has begun

2. prophylactically - prevention from infection occurring in the first place

176
Q

What are the 2 possible relationships between HIV and AIDS?

A
  1. HIV infection alone causes AIDS

2. HIV requires a cofactor to cause AIDS

177
Q

Who was the codiscoverer of the view that HIV alone causes AIDS?

A

Robert Gallo

178
Q

What is AIDS made up of?

A

opportunistic infections

179
Q

How does HIV infection alone cause AIDS?

A

HIV virus attacks T helper cells, therefore opportunistic infections are not able to be stopped because B cells and CTL’s are not being stimulated to proliferate

180
Q

How does HIV with a cofactor cause AIDS?

A

The cofactor which is already suppressing the adaptive immune system provides an opportunity for opportunistic HIV which will then cause AIDS (also opportunistic)

181
Q

What type of cofactors would suppress the IS and allow for HIV to occur?

A

another infection, malaria, TB, STD’s, poor nutrition, drug abuse

182
Q

Why is the view of HIV along with a cofactor causes AIDS important?

A

Because if you prevent the cofactors, you can prevent AIDS

183
Q

Where is the HIV thought to have come from (reservoir) as of the the 1940-1950’s?

A

Chimpanzees infected with SIV, mutations in spike proteins allowing it to attache to receptors on human cells. Exposure to chimp blood during hunting, butchering, or eating.

184
Q

What are the 6 reasons for the HIV epidemic (because of accelerated transmission?

A
  1. increased international travel
  2. increased promiscuity
  3. increased anal sex
  4. increased drug abuse
  5. increased STD’s
  6. increased in a worldview which worships freedom
185
Q

What is the Ro for HIV?

A

4

186
Q

How many times greater is HIV transmission risk in anal sex than vaginal?

A

18X

187
Q

What are the three phases of AIDS pathogenesis (after HIV)? How long is each phase?

A
  1. acute - 12 weeks
  2. chronic - 10 years
  3. terminal
188
Q

What occurs during the acuter (phase I) phase of HIV?

A
  1. HIV infects T helper cells, it replicates rapidly and immediately, if it is not eliminated by innate immunity, prodromal symptoms (mono - like) will begin to develop after the incubation period. The person may also experience lymphadenopathy = swollen lymph nodes due to lymphocyte proliferation/inflammation due to damaged lymphocytes. There will also be a CTL response
189
Q

What is the incubation period for AIDS.

A

2-6 weeks

190
Q

At what point can HIV be detected in an infected person?

A

within 3-8 weeks, (7-10 days after incubation period) antibodies are produced and the person can be deemed HIV+

191
Q

What part of innate immunity is able to eliminate HIV?

A

An aggressive NK cell response

192
Q

What occurs during the chronic (phase II) phase of HIV?

A
  1. There is a low HIV load because their is still rapid HIV replication, but there is also rapid HIV virus removal.
  2. gradual depletion of T helper cells
  3. few or minor symptoms
193
Q

What is the cause of T helper cell death?

A

Only 10% is actually dying because of infection, the other 90% is dying for unknown reasons

194
Q

What occurs during the terminal (phase III) phase of HIV?

A

At this point there are too few T helper cells and the opportunistic infections take over = AIDS

195
Q

What types of cells does HIV infect?

A

primarily T helper cells, but also infects macrophages, endothelial cells and neurons. (this leads to other symptoms being caused)

196
Q

When does HIV become impossible to remove?

A

When it splices into the chromosome of the host’s neurons, this creates an internal reservoir by which the person can infect themselves

197
Q

What are the 3 immune responses against HIV?

A
  1. antibodies should neutralize HIV
  2. antibodies and phagocytic cells may destroy free virus, but not infected cells, or “virus factories”
  3. CTLs destroy virus factories
198
Q

What are the 4 routes of transmission for AIDS?

Blood - to - blood contact

A
  1. IV drug abuse
  2. promiscuity
  3. neonatal AIDS
  4. transfusions
199
Q

If you can get exposed to HIV from other bodily fluids, why don’t you get aids from these?

A

Probably because the viral load is low, and there are no cofactors.

200
Q

What does PrEP stand for?

A

pre-exposure prophylaxis

201
Q

What are AZT drugs used for regarding AIDS?

A

They are a prophylatic drug that acts as a base analog, it blocks HIV’s reverse transcriptast preventing it from transcribing is vRNA to ssDNA (e.g. given to HIV+ mom’s in labor in order to protect baby)

202
Q

What do integrase inhibitors do to prevent HIV?

A

They prevent dsDNA from HIV to splice into the host cell chromosomes

203
Q

What do protease inhibitors do in HIV therapy?

A

They keep polyproteins from being broken down into proteins (this will prevent more cells from becoming infected)

204
Q

What are antiretroviral drugs for?

A

They are used in HIV prevention

205
Q

What are the 4 problems presented when dealing with HIV/AIDS drugs?

A
  1. resistance
  2. Once virus splices into neuron, irreversible
  3. expensive
  4. compliance = getting people to take their drugs (side-effects reduce compliance)
206
Q

Why is resistance to the drugs especially a problem regarding HIV?

A

Because mutations occur especially rapidly in HIV 10/9200 bp (1,000 times that of bacterial infections)

207
Q

What are the vaccine problems presented when dealing with HIV/AIDS?

A
  1. most vaccines stimulate the production of antibodies
  2. mutations may render vaccines useless (harder than developing a flu shot)
  3. who would you test the vaccine on?
  4. who would develop such a high-risk vaccine (not really a problem anymore)
208
Q

What are some ways to prevent AIDS?

A
  1. avoid reservoir
  2. avoid route of transmission
  3. avoid co-factors
    AIDS is mostly a behavioral disease…

Microbiology (13 decks)

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