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BIO 230 DCCC Suran > Exam IV > Flashcards

Exam IV Flashcards

1
Q

What is MHC?

A

Major Histocompatibility Complex protein

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2
Q

Where is MHC located?

A

On the surface of plasma membrane of cells

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3
Q

Which type of T cells do MHC class I and MHC class II interacts with?

A 
MHC Class I = Tc and CTL cells
MHC class II = Th cells.
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4
Q

What happens when an MHC class I protein is bound to an antigen?

A

It interacts with a Tc or CTL cell

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5
Q

What happens when an MHC class I protein is not bound to an antigen?

A

It keeps NK cells from killing the cell.

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6
Q

What type of cells are MHC class II proteins found on?

A

APC cells including dendritic, macrophages and B cells.

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7
Q

On what type of cells are MHC class I proteins found on?

A

On all cells.

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8
Q

When an MHC class II protein is bound to an antigen, what does it do?

A

Interacts with Th cells.

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9
Q

What is TCR?

A

T cell receptor.

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10
Q

What does a TCR do?

A

A TCR (T cell receptor) is used by T cells to interact with antigens displayed by MHC.

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11
Q

What is used by T cells to interact with antigens displayed by MHC?

A

TCR (T cell receptor)

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12
Q

What are CDs?

A

Clusters of differentiation

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13
Q

What are clusters of differentiation (CDs) used for and what are the types?

A

CDs are co-receptors that help T cells distinguish between MHC I and II proteins.
CD4 and CD8

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14
Q

What is CD4 used for?

A

CD4 is a cluster of differentiation that is found on Th cells to distinguish MHC class II cells.

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15
Q

What cluster of differentiation is found on Th cells to distinguish MHC class II cells?

A

CD4

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16
Q

What is CD8 used for?

A

CD8 is a cluster of differentiation that is found on Tc cells and recognizes MHC class I proteins.

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17
Q

What type of cluster of differentiation is found on Tc cells and recognizes MHC class I proteins?

A

CD8

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18
Q

Th are what?

A

T helper cells

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19
Q

What do T helpers do?

A

Th cells recognize an antigen presented by an APC on an MHC class II protein.

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20
Q

What type of cell recognizes an antigen presented by an APC on an MHC class II protein?

A

T helper

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21
Q

What do cytotoxic T cells do?

A

Tc cells recognize an antigen presented by an APC on an MHC class I protein (all cells).

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22
Q

What cells recognize an antigen presented by an APC on an MHC class I protein (all cells)?

A

Cytotoxic T cells (Tc)

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23
Q

What do activated T helper cells do?

A

Divide and differentiate into several cell types, including memory cells.

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24
Q

What type of T cell when activated divides and differentiate into several cell types, including memory cells?

A

T helper cells

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25
Q

What do activated cytotoxic T cells do?

A

Differentiate into CTLs (Cytotoxic T lymphocytes).

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26
Q

What type of cells differentiate into CTLs (Cytotoxic T lymphocytes) when activated?

A

Cytotoxic T cells (Tc)

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27
Q

What class of MHC protein are CTLs associated with?

A

MHC class I

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28
Q

What do CTLs do?

A

CTLs recognize antigens displayed by MHC class I proteins on the surface of a cell.

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29
Q

What happens when a CTL attaches to cell?

A

Releases:
Perforin (pore-forming protein)
granzymes and proteases that cause apoptosis (programmed cell death)

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30
Q 
What cells release:
Perforin (pore-forming protein)
Granzymes
Proteases
That cause apoptosis (programmed cell death)
A

CTLs

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31
Q

When does a cytotoxic T cell become a CTL?

A

When the Tc recognizes the antigen displayed by an MHC class I cell, it differentiates into a cytotoxic T lymphocytes (CTL).

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32
Q

What are B cells covered with?

A

One type of antibody: IgD

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33
Q

What do B cells do?

A

IgD antibody binds to antigen.
B cell presents to T helper cells
B cell becomes activated by Th cells
B cell divides and differentiates into memory and plasma cells.

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34
Q

What do B memory cells do?

A

Remain dormant until exposed to antigen in the future. Then divide and differentiate into plasma cells when exposed to the antigen in the future.

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35
Q

What do plasma cells do?

A

Produce lots of antibodies and secrete them into the blood.

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36
Q

Where do plasma cells secrete antibodies?

A

Into the blood

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37
Q

What do memory B cells do when exposed to the antigen for which they were first made?

A

They divide and differentiate into plasma cells.

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38
Q

Memory B cells are long lived? T/F

A

True

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39
Q

What cells are long lived and can divide and differentiate into plasma cells at a later date when exposed to the same antigen?

A

Memory B cells

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40
Q

What is an epitope?

A

The part of an antigen that binds to a specific antigen receptor on a B cell.

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41
Q

What is a part of an antigen that binds to a specific antigen receptor on a B cell?

A

An epitope.

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42
Q

What are immunoglobulins?

A

Antibodies.

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43
Q

What initiates B cell activation?

A

The antibody (immunoglobulin) on the B cell surface binds to the epitope (specific receptor on the antigen) and both antigen and antibody are taken into the B cell.

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44
Q

What happens to the antigen/antibody complex once it’s taken into a B cell?

A

It is processed into smaller pieces and then a fragment of the antigen is presented on the B cell surface on an MHC class II protein to attract a T helper cell. Then the Th cell produces cytokines that activate the B cell.

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45
Q

What type of antibody do plasma cells secrete large amounts of?

A

IgG specific to the activated B cell

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46
Q

What type of cell produces large amounts of IgG antibodies?

A

Plasma cells

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47
Q

What do antigens need to have to stimulate B cells without Th cells?

A

Repeating subunits that can bind to multiple B cell receptors

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48
Q

What can antigens that have repeating subunits do when binding to multiple B cell receptors?

A

Eliminate the need for T helper cell activation of the B cell.

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49
Q

What do all of the activation methods of the complement system lead to activation of?

A

C3

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50
Q

What are opsonins?

A

Antibodies or other substances that bind to antigens making them more susceptible to phagocytosis (IgG antibodies and the C3b molecules of the complement system).

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51
Q

What is opsonization?

A

A process where antigens are marked for phagocytosis.

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52
Q

What happens to C3 to activate it?

A

C3 is cleaved into C3a and C3b.

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53
Q

What does C3b do?

A

As the activated part of C3:
C3b binds to an antigen surface to aid in attachment of phagocytes (opsonization)
C3b cleaves C5 into C5a and C5b

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54
Q

What do C3a and C5a do?

A

Bind to mast cells and stimulate the release of histamine and other chemicals to increase vessel permeability during inflammation.

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55
Q

In the complement system, what happens to C5b, C6, C7 and C8?

A

C5b, C6, C7 and C8 bind together (form a complex) and insert into the membrane of bacterial cells.

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56
Q

What does the C5b, C6, C7 and C8 complex act as?

A

Acts as a receptor that attracts C9.

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57
Q

How does C9 behave in the complement system?

A

Multiple C9 fragments form a transmembrane channel. C9 fragments, together with the C5b, C6, C7 and C8 complex, form the MAC (membrane attack complex).

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58
Q

What is the MAC and what does it do?

A

The MAC (membrane attack complex) is an end product of the complement system whereby the C5b, C6, C7 and C8 complex and the C9 fragments join forces. This acts as a channel which leads to cytolysis of the bacterial cell.

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59
Q

What are the protective outcomes of each part of the complement system?

A

Opsonization: C3 cleaves into C3a and C3b, where C3b binds to membrane of microbe (opsonin) to facilitate attachment of phagocytes.

Inflammation: C3a and C5a bind to mast cells and stimulate histamine release to increase vessel permeability during inflammation.

Cytolysis: C5b, C6, C7 and C8 combine with C9 fragments to create the MAC (membrane attack complex) that acts as a channel into the bacteria cell which leads to cell lysis.

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60
Q

Define each protective outcomes of the complement system.

A

Opsonization: C3 cleaves into C3a and C3b, where C3b binds to membrane of microbe (opsonin) to facilitate attachment of phagocytes.

Inflammation: C3a and C5a bind to mast cells and stimulate histamine release to increase vessel permeability during inflammation.

Cytolysis: C5b, C6, C7 and C8 combine with C9 fragments to create the MAC (membrane attack complex) that acts as a channel into the bacteria cell which leads to cell lysis.

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61
Q

What system do opsonization, inflammation and cytolysis signify?

A

The complement system

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62
Q

What are three ways the complement system can be activated?

A

Classical, alternative and lectin pathways

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63
Q

What controls the classical activation pathway of the complement system?

A

Antibodies

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64
Q

What happens in the classical activation pathway of the complement system?

A

Antibodies attach to antigens on the surface of the microbe.

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65
Q

When antibodies attach to antigens on the surface of microbes, what is recruited in the classical pathway of the complement system?

A

C1
C1 cleaves C2 to C2a and C2b and C4 to C4a and C4b
C2a and C4b combine and activate C3 by cleaving it into C3a and C3b

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66
Q

What has to happen at the end of each pathway–classical, alternative and lectin–of the complement system to achieve activation?

A

C3 must be cleaved into C3a and C3b

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67
Q

What substances are employed in the alternative pathway of the complement system?

A

Protein factors, specifically Factor B, factor D and factor P

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68
Q

To what system are Factor B, factor D and factor P important?

A

The alternative pathway of the complement system

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69
Q

What are lectins?

A

Proteins that bind to carbohydrates found on the surface of microbes.

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70
Q

What are lectins produced by and when are they produced?

A

Lectins are produced by the liver in response to cytokine release by macrophages after they ingest bacteria, viruses or foreign matter.

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71
Q

When do macrophages release cytokines?

A

After they ingest microorganisms or foreign matter.

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72
Q

Are lectins specific to certain carbohydrates?

A

Yes, specific lectins bind to specific carbohydrates.

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73
Q

What is an example of lectins that bind to a specific carbohydrate?

A

Mannose-binding lectin binds to the carb mannose found in cell walls and viral particles. It cleaves C2 and C4, C2a and C4b combine to split C3 into C3a and C3b (as in the classical pathway).

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74
Q

In the complement system alternative pathway, how do the protein factors activate C3?

A

Protein factors B, D and P recruit C3 and cleave it into C3a and C3b.

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75
Q

What do the classical and lectin pathways of the complement system have in common when activating C3?

A

The classical starts with C1 and the lectin starts with C2, but they both cleave C2 and C4 and end with C2a and C4b combining to cleave C3 into C3a and C3b.

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76
Q

In the complement system, how does the alternative pathway differ in the activation of C3 from the classical and lectin pathways?

A

The alternative pathway protein factors directly recruit C3 and cleave it into C3a and C3b.

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77
Q

Name three ways that microbes evolved to avoid the complement system.

A

Capsules that can prevent complement activation.

Sialic acid in capsules discourages opsonization and MAC formation.

Some gram + cocci release an enzyme that breaks down C5a (w/ C3a binds with mast cells) which stops the activation cascade.

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78
Q

Capsules, sialic acid, and gram + cocci enzymes are examples of what?

A

Ways in which microbes have evolved to avoid the complement system.

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79
Q

What is the innate immune system?

A

That part of the immune system that people are born with that does not depend on B or T cells. It includes the 1st and 2nd lines of defense.

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80
Q

Granulocytes and agranulocytes are involved in what segment of immunity?

A

Innate - 2nd line of defense

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81
Q

Name 3 types of granulocytes

A

Neutrophils, eosinophils, basophils

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82
Q

What is a neutrophil?

A

A type of granulocyte that is highly phagocytic and motile, can leave the blood and travel into the tissues to destroy microbes and foreign particles.

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83
Q

What is a basophil?

A

A type of granulocyte that releases histamine for the inflammation and allergic response.

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84
Q

What is an eosinophil?

A

A type of granulocyte that has phagocytic properties and can leave the blood (like neutrophils). Major function is to produce toxic proteins to defend against parasites (like helminths).

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85
Q

How do eosinophils attack parasites?

A

Attach to the surface of the parasite and discharge peroxide ions and digestive enzymes.

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86
Q

Name three types of agranulocytes.

A

Monocytes, dendritic cells and lymphocytes.

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87
Q

What types of blood cells are highly phagocytic?

A

Neutrophils and macrophages

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88
Q

Is a monocyte phagocytic?

A

Not actively phagocytic until it matures into a macrophage.

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89
Q

What is a monocyte?

A

A slightly phagocytic agranulocyte that matures into a macrophage when leaving the blood and entering the tissues.

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90
Q

What are macrophages?

A

Highly phagocytic antigen presenting cells that matured from monocytes in the blood when they entered the tissues. Have MHC class II proteins on membrane that interact with T helper cells.

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91
Q

What is a dendritic cell?

A

An agranulocyte with long extension like a nerve cell that destroy microbes by phagocytosis and initiate adaptive immunity responses. Have MHC class II proteins on plasma membrane that interact with T helper cells.

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92
Q

What are lymphocytes?

A

Agranular blood cells that include NK cells that check for non-self cells (MHC class I - Tc cells), T cells that regulate adaptive immune response and are responsible for cellular immunity, and B cells that produce antibodies in humoral or antibody-mediated immunity in adaptive immunity.

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93
Q

NK, B and T cells are what type of blood cells?

A

Lymphocytes

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94
Q

List 5 classes of antibodies

A

IgG, IgD, IgE, IgA, IgM

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95
Q

What are IgG antibodies?

A

IgG are monomers produced by plasma cells (most common - 80%)

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96
Q

What are IgD antibodies?

A

IgD are monomers similar to IgG found on B cell surface in blood and lymph. Involved in immune response initiation in B cells.

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97
Q

Which antibody is responsible for immune response initiation in B cells?

A

IgD, because they cover B cell surface membrane.

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98
Q

What are IgE antibodies?

A

Monomers slightly larger than IgG, very rare in serum. Fc (stem) of IgE bound to receptors on mast cell and basophils (allergic rxs). Binding of IgE to attached cell releases histamine and mediators to provoke an allergic response.

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99
Q

What are IgM antibodies?

A

Pentameter - Five monomers joined by polypeptide J chain. Causes clumping of bound antigens (agglutination).

Many antigen-binding sites.

Appear first in immune response and are short lived.

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100
Q

What antibody appears first in an immune response and is short lived?

A

IgM

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101
Q

What antibody is a pentameter?

A

IgM

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102
Q

What antibody that binds to a cell releases histamine?

A

IgE (mast cells and basophils)

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103
Q

What antibody causes agglutination?

A

IgM - the pentameter

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104
Q

Which antibody has many antigen-binding sites?

A

IgM

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105
Q

Which antibodies are most common?

A

IgG

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106
Q

What antibodies are produced by plasma cells?

A

IgG

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107
Q

What is an IgA antibody?

A

Two monomers joined by J chain a polypeptide called secretory component that protects IgA from enzymatic degradation. Most common in secretions (mucus, saliva, tears and breast milk). Protects newborns from gastrointestinal infection.

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108
Q

What antibody is made of two monomers?

A

IgA

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109
Q

What antibody has a polypeptide called secretory component and what does it do?

A

IgA, protects IgA from enzymatic degradation.

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110
Q

What type of macromolecule is secretory component of IgA antibodies?

A

Polypeptide

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111
Q

What is the most common antibody in bodily secretions including breast milk?

A

IgA

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112
Q

Which antibodies are monomers?

A

IgG, IgE, IgD

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113
Q

Which antibodies are not monomers?

A

IgM - pentameter

IgA - two monomers

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114
Q

What antibody is found on the surface of B cells?

A

IgD

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115
Q

What is an antigen?

A

Anything that causes antibody formation.

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116
Q

What is anything that causes antibody formation?

A

An antigen

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117
Q

What macromolecules are most antigens made of?

A

Polypeptides (large proteins) or polysaccharides.

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118
Q

What region of an antigen do antibodies interact with?

A

The epitope or antigenic determinant.

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119
Q

What is the antigenic determinant?

A

The epitope or the region of an antigen that antibodies interact with

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120
Q

What is the relationship between antibodies and antigens?

A

Antigens have an epitope or antigenic determinant that is recognized by and interacts with the antibody.

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121
Q

Essay:

What are five protective outcomes of antigen-antibody binding?

A

Agglutination (IgM)

Opsonization (IgD)

Neutralization

Antibody-dependent cell-mediated cytotoxicity (eosinophils)

Activation of complement system (MAC, opsonization, inflammatory response (basophils))

122
Q

How does antibody-antigen agglutination offer protective outcome?

A

Antibodies cause antigens to clump together to make easier to ingest by phagocytes (IgM ).

123
Q

How does antibody-antigen opsonization offer protective outcomes?

A

Antigen is coated with antibodies (opsonins) that bind to phagocytes and aid in ingestion and lysis by phagocytic cells.

124
Q

How does antibody-antigen neutralization offer protective outcomes?

A

Antibodies inactivate microbes by disrupting their shape, make external antigen structures nonfunctional, prevent virions from binding to host, neutralize exotoxins by block binding to substrate.

125
Q

How does antibody-dependent cell-mediated cytotoxicity offer protective outcomes?

A

Signal eosinophils to release enzymes that kill the parasite (microbe).

126
Q

How does activation of the complement system offer protective outcomes?

A

Activates complement system to kill invading cells by cytolysis (from MAC) opsonization and activation of the inflammatory response.

127
Q

What is humoral immunity?

A

Immunity bought about by antibodies dissolved in body fluids, mediated by B cells (also antibody-mediated immunity).

128
Q

What is cellular immunity?

A

The immune response that involves cytotoxic T cells binding to antigens presented on antigen-presenting cells. Tc causes infected cell to go through apoptosis (controlled suicide)

129
Q

What type of lymphocyte is cellular immunity based on?

A

Cytotoxic T cells

130
Q

Cytotoxic T cells are involved in what type of immunity?

A

Cellular immunity or cell-mediated immunity

131
Q

B cells are involved in what type of immunity?

A

Antibody-mediated or humoral immunity

132
Q

What is apoptosis?

A

Cellular suicide cause by cytotoxic T cells in cellular or cell-mediated immunity

133
Q

What is chemotaxis?

A

Chemical attraction of phagocytes to microorganisms.

134
Q

What chemicals can cause chemotaxis?

A

Cytokines produced by WBCs, peptides derived from complement system, components of white blood cells and damaged tissue.

135
Q

What are the four steps in phagocytosis and intracellular digestion?

A

Chemotaxis, adherence, ingestion, digestion.

136
Q

What happens during phagocytosis with adherence?

A

Attachment of the phagocyte’s plasma membrane receptors to the surface of the microorganism.
Facilitated by attachment of pathogen-associated molecular patterns (PAMS) to receptors (i.e, Toll-like receptors on surface of phagocytes). Opsonins promote attachment through opsonization.

137
Q

What happens during phagocytosis in ingestion?

A

The plasma membrane of the phagocyte extends pseudopods meet and fuse, around the microbe within a vesicle called
a phagosome.

138
Q

Where in phagocytosis and intercellular digestion does a vesicle called a phagosome house the invading microbe?

A

During ingestion.

139
Q

What is a phagosome?

A

A vesicle that is created by the meeting and fusing of the pseudopod around the invading microbe within the phagocyte.

140
Q

What happens in the digestion phase of phagocytosis or intercellular digestion?

A

The phagosome fuses with lysosomes to form phagolysosome. After digestion, remaining undigestible content (residual body) is discharged from cell.

141
Q

What are lysosomes in intercellular digestion?

A

Vesicles that contain digestive enzymes used in digestion of intercellular contents.

142
Q

What is a phagolysosome?

A

The combination of the phagosome (the cell that will phagocytize the microbe) and the enzymes (lysosomes) that will digest the microbe.

143
Q

Two ways microbes avoid phagocytosis.

A

Bacteria have structures that resist adherence. Other microbes kill the phagocyte from the inside by releasing proteins that disrupt the plasma membrane..

144
Q

Essay question: Koch’s four postulates

A
  1. Every case
  2. Pure culture
  3. Injected
  4. Isolated
  5. Same pathogen must be present in every case of the disease.
  6. Pathogen must be isolated from diseased host and grown in pure culture.
  7. Pathogen from pure culture must cause the disease when injected into new healthy, susceptible lab animal.
  8. Pathogen must be isolated from the diseased animal and shown to be the original microbe.
145
Q

Put Koch’s postulates in correct order:

  1. Pathogen must be isolated from diseased host and grown in pure culture.
  2. Pathogen from pure culture must cause the disease when injected into new healthy, susceptible lab animal.
  3. Same pathogen must be present in every case of the disease.
  4. Pathogen must be isolated from the diseased animal and shown to be the original microbe.
A

3, 1, 2, 4

146
Q

What is the procedure for Koch’s postulate?

A
  1. Microorganisms are isolated from a diseased or dead individual.
  2. The microorganisms are grown in pure culture and individually identified.
  3. The microorganisms are individually introduced into new, healthy test organisms. Test organisms are observed for development of signs that are similar to those experienced by first organism.
  4. Microorganisms are isolated from test organisms that develop similar signs to the original organism to show that the injected microorganisms multiplied inside the test organism (causing the disease signs).
147
Q

Four situations where Koch’s postulates don’t apply

A
  1. Organism cannot be cultured in the lab.
  2. Several different types of organisms cause the same signs.
  3. Several disease conditions are caused by some microorganisms.
  4. Some microorganisms have no other known host (other than humans)
148
Q

Five stages of disease

A 
Incubation
Prodromal
Illness
Decline
Convalescence
149
Q

What is the incubation period of disease?

A

Interval between initial infection and the appearance of symptoms.

150
Q

What is the prodromal period of disease?

A

Short period following incubation characterized by early, mild symptoms.

151
Q

What is the level of microbes in the prodromal period of disease?

A

Low number of microbes but increasing

152
Q

What happens in the period of illness stage of the five stages of disease?

A

Signs and symptoms most severe: fever, chills, muscle pain, sensitivity to light, sore throat, lymph node enlargement, gastrointestinal disturbances. If disease is not successfully overcome, death occurs.

153
Q

At what stage of the five stages of disease does death occur?

A

Illness stage

154
Q

In what state of the five stages of disease is the level of microbes the highest?

A

The illness stage

155
Q

What happens in the period of decline in the five stages of disease?

A

Signs and symptoms subside. Number of microbes peaks and declines. Lasts less than 24 hours to several days.

156
Q

In what stage of the five stages of disease do microbes peak and decline?

A

Period of decline

157
Q

What happens in the period of convalescence in the five stages of disease?

A

Person regains strength and body returns to pre-disease state. Number of infecting microbes decreases to zero.

158
Q

What is the level of microbes in the period of convalescence?

A

Zero

159
Q

What are the level of microbes in each of the five stages of disease?

A 
Incubation period - Very low
Prodromal period - Low but increasing
Period of illness - Highest
Period of decline - Peak and decline
Convalescence - Zero
160
Q

Put the stage of disease in the correct order:

  1. Prodromal
  2. Illness
  3. Convalescence
  4. Incubation
  5. Decline
A 
Incubation
Prodromal
Illness
Decline
Convalescence
161
Q

Two organizations that monitor disease

A

CDC - National, source of epidemiological information. Publishes MMWR (morbidity, mortality)
WHO - Global, tracks and studies emerging infectious diseases

162
Q

What is a reservoir of infection?

A

A continually source of disease-causing organisms.

163
Q

Three different types of reservoirs of infection.

A

Human, animal, nonliving.

164
Q

What is a carrier of disease?

A

People that harbor pathogens and transmit them without exhibiting any signs of illness.

165
Q

What is a nosocomial infection?

A

Infections spread via healthcare settings

166
Q

What are infections spread in healthcare settings called?

A

Nosocomial infections

167
Q

Animal reservoirs of infection include what two types of animals?

A

Wild and domestic

168
Q

What are Zoonosis diseases?

A

Diseases that occur in wild and domestic animals that can be transmitted to humans

169
Q

What are diseases that occur in animals that can be transmitted to humans?

A

Zoonosis diseases

170
Q

What represents nonliving disease reservoirs?

A

Soil and water

171
Q

Three microbe portals of entry

A

Mucous membranes
Skin
Perenteral route

172
Q

Name the mucous membranes

A

Lining of respiratory tract, GI tract, genitourinary tract, conjunctiva

173
Q

What qualities of skin provides a portal of microbe entry?

A

Skin is impenetrable but some microbes find entry through sweat gland ducts, hair follicles. Hookworm larvae bore through skin; some fungi grow on keratin.

174
Q

What portals of entry of parenteral routes do microbes use for entry?

A

When deposited directly into tissues beneath skin via punctures, injections, bites, cuts, wound, surgery and splitting of skin or mucous membranes from swelling/drying.

175
Q

Punctures, injections, bites, cuts, wound, surgery and splitting of skin are examples of what type of microbe portals of entry?

A

Parenteral

176
Q

Hookworms and fungi are examples of what type of microbe portals of entry?

A

Skin

177
Q

Microbes entering the GI tract via dirty fingers are an example of what type of portal of entry?

A

Mucous membranes

178
Q

Microbes that are killed by hydrochloric acid, bile and enzymes were located in what parts of the GI tract?

A

Hydrochloric acid - stomach

Bile, enzymes - small intestine

179
Q

How do bacteria use capsules to penetrate host defenses?

A

Capsules resists phagocytosis. Opsonins may be able to bind to capsule to allow attachment of phagocytes.

180
Q

How do bacteria use cell wall components to penetrate host defenses?

A

Cell walls contain chemical components that enhance virulence.

181
Q

What are examples of cell wall components that are used to penetrate host defenses?

A

M protein of Streptococcus pyogenes resist heat/acid that assist in attachment and resists phagocytosis.

Opa protein in Neisseria gonorrhoeae grows inside human epithelial cells and leukocytes.

Mycobacterium tuberculosis, mycolic acid in cell wall makes it resistant to phagocytosis

182
Q

Give examples of enzymes used by bacteria to penetrate host defenses.

A

Extracellular enzymes (exoenzymes) can digest materials between cells and form or digest blood clots.

183
Q

Three examples of enzymes used by bacteria to penetrate host defenses.

A

Coagulase (forms blood clots)

Fibrinolysin - digests clots

Hyaluronidase - breaks down molecules that hold CT together.

184
Q

What is antigenic variation?

A

Ability of some pathogens to alter surface antigens to avoid specific antibodies.

185
Q

How do bacteria penetrate host defenses by using penetration into host cell cytoskeleton?

A

Allows microbes to avoid immune system components (invasins, listeria)

186
Q

What are examples of bacteria that penetrate host defenses by penetrating into host cell cytoskeleton?

A

Invasins - proteins that rearrange nearby host actin filaments to cause ruffle and engulf bacteria.

Listeria - intracellular parasite that polymerizes actin for propulsion and to transfer to new cells.

187
Q

What do invasins do to allow bacteria to penetrate host defenses?

A

Cause ruffle near site of attachment of membrane and allow cell to engulf bacteria.

188
Q

Three ways bacterial pathogens damage host tissues.

A

Siderophores, direct damage, toxins (endo and exotoxins)

189
Q

What are siderophores?

A

Molecules that allow bacteria to steal iron from host.

190
Q

Pathogens that multiply inside host cells can do what to host tissues?

A

Damage them

191
Q

What are three ways bacteria damage host cells?

A

Siderophores, direct damage, toxins

192
Q

Siderophores, direct damage and toxins are three ways for bacteria to do what?

A

Damage host cells

193
Q

What is a bacterial exotoxin?

A

Destroy part of host cell or inhibit metabolic function. Because are enzymes can catabolize reactions repeatedly, can cause large effects in small amounts.

194
Q

Exotoxins are enzymes. Why are they so destructive?

A

Because they can catabolize the same reaction repeatedly.

195
Q

Exotoxins are what type of molecule?

A

Enzyme

196
Q

How is immunity to exotoxins induced?

A

Through vaccinating with heat-denatured exotoxins (toxoids)

197
Q

What type of molecule are endotoxins?

A

Lipopolysaccharides (LPS) that are part of the cell wall of gram negative bacteria.

198
Q

When are endotoxins released?

A

When the cell dies and the wall undergoes lysis.

199
Q

What cells do endotoxins stimulate?

A

Macrophages that produce cytokines at toxic levels.

200
Q

All endotoxins produce the same signs and symptoms. What are they?

A

Chills, fever, weakness generalized aches.

201
Q

Why do all endotoxins cause the same symptoms?

A

Because endotoxins stimulate macrophages to produce cytokines at toxic levels.

202
Q

What do cytocidal viruses cause?

A

Cause macromolecular synthesis to stop in host cell.

203
Q

How do cytocidal viruses cause destruction of intracellular contents?

A

Cause cell’s lysosomes to release enzymes

204
Q

Five cytopathic effects of viral infections

A

Cytocidal viruses destruction of intracellular contents:
- Inclusion bodies
- Adjacent cell agglutination (form syncytium)
- Antigenic changes on cell surface
- Oncogenic viruses (chromosome
changes)
- Contact inhibition

205
Q

What are these examples of:

  • Inclusion bodies
  • Adjacent cell agglutination (form syncytium)
  • Antigenic changes on cell surface
  • Oncogenic viruses (in chromosome
    changes)
  • Contact inhibition
A

Cytopathic effects of viruses

206
Q

What does cytopathic mean?

A

Producing damage to living cells

207
Q

Three organisms that commonly produce antibiotics

A

Streptomyces (from soil)
Endospore-forming bacillus
Molds (Penicillium and Cephalosporum)

208
Q

These organisms are examples of what?

Streptomyces (from soil)
Endospore-forming bacillus
Mols (Penicillium and Cephalosporium)

A

Three organisms that commonly produce antibiotics.

209
Q

Five actions of antibiotic drug action

A

Inhibition of:

Cell wall synthesis
Protein synthesis
Nucleic acid synthesis
Essential metabolite synthesis
Injuring plasma membrane
210
Q

Inhibition of:

Cell wall synthesis
Protein synthesis
Nucleic acid synthesis
Essential metabolite synthesis and 
Injuring plasma membrane
are examples of what?
A

Mechanisms of antibiotic drugs

211
Q

What type of drug is built around a beta-lactam ring?

A

Pencilliln

212
Q

Essay question:

Two methods to reduce antibiotic resistance.

A

Patients:

  • Finish full course to discourage survival and proliferation of resistant microbes
  • Never use leftover antibiotics to treat new illnesses
  • Never use antibiotics prescribed for someone else.

Healthcare workers:

  • Avoid unnecessary prescriptions
  • Ensure choice and dosage are appropriate to situation
  • Prescribe most specific antibiotic possible to decrease resistance in patient’s flora.
213
Q

What are three ways patients can avoid antibiotic resistant strains?

A

Patients:

  • Finish full course to discourage survival and proliferation of resistant microbes
  • Never use leftover antibiotics to treat new illnesses
  • Never use antibiotics prescribed for someone else.
214
Q

What are three things healthcare workers can do to avoid antibiotic resistant strains?

A

Healthcare workers:

  • Avoid unnecessary prescriptions
  • Ensure choice and dosage are appropriate to situation
  • Prescribe most specific antibiotic possible to decrease resistance in patient’s flora.
215
Q

2 mechanisms of antiviral drugs

A

Entry/fusion inhibitors
Assembly/exit inhibitors
Uncoating, genome integration and nuclei acid synthesis inhibitors
Interferons, activate antiviral host defenses

216
Q

E tests exhibit what concept?

A

Minimum inhibitory concentration (MIC)

217
Q

What is MIC (minimum inhibitory concentration) and what test is it associated with?

A

E tests, plastic strips that test antibiotic effectiveness.
MIC - lowest concentration that inhibits growth and is highest concentration where bacteria can grow directly next to plastic strip.

218
Q

What tests uses the zone of inhibition?

A

Kirby-Bauer assay (disk diffusion method)

219
Q

Four mechanisms used by bacteria to resist antibiotics

A 
Blocking entry (especially gram negative)
Modify pores
inactivating enzymes
Altering drug target site
Rapid efflux (ejection)
220
Q

What are the following an example of?

Blocking entry (especially gram negative)
Modify pores
inactivating enzymes
Altering drug target site
Rapid efflux (ejection)
A

Ways in which bacteria evade antibiotics

221
Q

Two means of research for new chemotherapeutic drugs

A

Antimicrobial peptides - small protein chains in bird, amphibians, plants, mammals.
Directly damage bacteria, viruses, fungi or stimulate host immune system.
(Peptide DRGN-1 from Komono dragon displayed antimicrobial activity against Pseudomonas aeroginosa and Staphylococcus aureus and aided in health of wounds.)

Phage therapy - Use phages to kill bacteria, used in 2017 successfully. Few potential disadvantages: immune system kills it in secondary response. Don’t spread as well in host.

222
Q

The peptide DRGN-1 is an example of what?

A

New chemotherapeutic drugs called antimicrobial peptides

223
Q

What is phage therapy an example of?

A

New chemotherapeutic drugs

224
Q

T/F The skin acts as a direct barrier to microbial entry.

A

True

225
Q

What are the two layers of the mucous membranes?

A

Epithelial and underlying connective tissue.

226
Q

What do mucous membranes line?

A

GI tract, genitourinary tract, respiratory tract.

227
Q

What does the epithelial lining of the mucous membranes secrete?

A

Mucous

228
Q

What is a viscous glycoprotein produced by goblet cells?

A

Mucous

229
Q

What is mucous produced by?

A

Goblet cells

230
Q

How does mucous protect against infections?

A

Keeping membranes from drying out and traps pathogens

231
Q

What keeps membranes from drying out and traps pathogens?

A

Mucous

232
Q

What does the lacrimal apparatus do?

A

Maintains and drains away tears.

233
Q

What anatomical structure does the lacrimal apparatus protect?

A

The eyes

234
Q

How does the lacrimal apparatus protect the eyes?

A

It provides continual washing action to keep microbes from settling on the surface of the eye.

235
Q

Name the chemical components of the first line of defense

A

Sebum - unsaturated fatty acids, maintains acidic pH.
Perspiration - flush microbes, lysozyme
Lysozyme - breaks down cell walls of gram+ and some gram-negative bacteria in tears, saliva, nasal secretions, tissue fluids, urine.
Gastric juices - pH 1.2 - 3
Vaginal secretions - contain glycogen, broken down by Lactobacillus acidophilus to make acidic pH.
Cervical mucus - antibacterial properties
Urine - contains lysozyme, acid pH, urea that inhibit bacteria growth

236
Q

Sebum, perspiration, lysozyme, gastric juices, vaginal secretions and cervical mucus are examples of what?

A

Chemical components of first line of defense

237
Q

Stages of the inflammatory response

A 
Vasodilation
Increased permeability
Phagocyte migration
Phagocytosis
Tissue repair
238
Q

Immediately following tissue damage, what happens to blood vessels?

A

Vessels dilate which increased blood flow to the area increases permeability.

239
Q

How does increased permeability contribute to the inflammatory response?

A

Permits substances normally retained in the blood to pass through the walls of the vessels to the injured tissue.

240
Q

Edema is the result of what inflammatory response?

A

Permeability

241
Q

Which two chemicals are responsible for vasodilation and increased permeability in injured tissue?

A

Histamine and cytokines

242
Q

What produces histamine?

A

Injured cells and the complement system

243
Q

What produces cytokines?

A

Activated fixed macrophages

244
Q

When do phagocytes generally arrive at the site of injury?

A

Within an hour

245
Q

What do phagocytes do at an injury site to initiate their response?

A

Stick to inner surface of endothelium of vessels in response to cytokines.

246
Q

How do phagocytes arrive at injured tissue?

A

Squeeze through endothelial cells of blood vessels and then begin destroying invading microorganisms.

247
Q

What does tissue repair do?

A

Replace dead or damaged cells with new ones.

248
Q

Tissue is repaired when stroma or parenchyma produce what?

A

New cells

249
Q

What is the difference between the stoma and the parenchyma cells?

A

Stroma - connective tissue

Parenchyma - functioning part of tissue

250
Q

What is a fever?

A

Systemic response of the body to injury

251
Q

What part of the brain controls the body temperature?

A

Hypothalamus

252
Q

What is one chemical that the hypothalamus responds to?

A

Cytokines

253
Q

What does the hypothalamus do in response to cytokines?

A

Increases body temperature

254
Q

How does the hypothalamus increase body temperature?

A

Sends out chemicals that constrict vessels, increase metabolism and cause shivering.

255
Q

What are the three things the hypothalamus does to increase body temperature?

A

Constricts blood vessels, increase metabolism, cause shivering.

256
Q

What is the initial phase of a fever?

A

Chill

257
Q

What happens during a chill that starts a fever?

A

Body temp is rising, skin is cold, shivering continues.

258
Q

During a chill, body temp is rising, skin is cold, shivering continues until what?

A

The temp that the hypothalamus sets is reached.

259
Q

When does the chill of a fever disappear?

A

When the temp set by the hypothalamus is reached.

260
Q

When the infecting agent is eliminated from the body, what part of the fever process stops?

A

Cytokine signaling to the hypothalamus

261
Q

When cytokines cease signaling the hypothalamus during a fever, what does the hypothalamus do?

A

Reset to 37° C

262
Q

What phase of a fever starts when the hypothalamus resets to normal body temp?

A

Crisis phase

263
Q

What is the crisis phase of a fever?

A

Skin warms, person sweats to shed heat, temp returns to normal.

264
Q

In what phase of a fever do these happen? Skin warms, person sweats to shed heat, temp returns to normal.

A

Crisis phase

265
Q

What are three benefits of a fever?

A

Lower growth of microbes
Intensifies effect of antiviral and antimicrobial agents
Speeds up body’s reactions (may help tissues heal faster)

266
Q

The following are benefits of what physiologic action?
Lower growth of microbes
Intensifies effect of antiviral and antimicrobial agents
Speeds up body’s reactions (may help tissues heal faster)

A

Fever

267
Q

Name the four parts of an antibody

A

Heavy chains
Light chains
Variable regions
Constant regions

268
Q

How are the heavy and light chains bonded in an antibody?

A

Disulfide bonds

269
Q

Two longer amino acids on the inside of an antibody monomer are?

A

Heavy chains

270
Q

Which chains of an antibody consist of the inner half of each arm and the stem region?

A

Heavy chains

271
Q

In an antibody, which chains in are connected to each other and to the light chains via disulfide bonds?

A

Heavy chains

272
Q

In an antibody, which chains make up the outer region of the arm and are connected to the heavy chain?

A

Light chains

273
Q

By what bond are light chains connected to heavy chains in an antibody?

A

Disulfide bonds

274
Q

The antigen-binding sites of an antibody are located on what chains?

A

On both the light and heavy chains

275
Q

The antigen-binding sites of an antibody are called what?

A

Variable regions

276
Q

T/F Antibodies produced by different B cells have different amino acid sequences in their variable region.

A

True

277
Q

What is a constant region on an antibody?

A

The remainder of the heavy and light chains outside of the antigen-binding sites.

278
Q

The remainder of the heavy and light chains outside of the antigen-binding sites on an antibody are called what?

A

Constant regions

279
Q

Antibodies produced by different B cells have different amino acids in their variable regions but the same what?

A

Amino acids in their constant regions.

280
Q

Which region in an amino acid carries the same amino acids when produced by different B cells?

A

Constant region

281
Q

The antibody-mediated immune response intensifies when?

A

After a second exposure to an antigen.

282
Q

Which response, the primary or secondary is slower and less intense?

A

Primary

283
Q

After initial exposure to an antigen, there are no detectable antibodies for how long?

A

4-7 days, slow rise afterwards

284
Q

Which class of antibodies are produced first in the adaptive immune response?

A

IgM

285
Q

What class of antibodies following the production of IgM in the primary response of the adaptive immune response?

A

IgG

286
Q

When does antibody production peak in the primary response?

A

10-17 days

287
Q

What’s another name for the secondary immune response?

A

The anamnestic response

288
Q

Which response, the primary or secondary is faster and more intense?

A

The secondary

289
Q

Compared to the primary response, in how many days does the secondary response begin antibody production?

A

2-7 days

Primary = 4-7 days

290
Q

Antibody production lasts many days in what part of the antibody-mediated immune response?

A

Secondary

291
Q

In which phase of antibody-mediated immune response, the primary or secondary, is the level of antibodies higher?

A

Secondary

292
Q

What cells are responsible for the difference in the immune response from the primary to secondary in the antibody-mediated immune respone?

A

B and T cells

293
Q

When stimulated by an antigen, which cells rapidly differentiate into antibody-producing cells?

A

B cells

294
Q

Which cells are also necessary for establishing memory in the antibody-mediated immune response?

A

T cells

295
Q

In what phase of the antibody-mediated immune response are memory cells present?

A

The secondary. The primary is required to generate them.

296
Q

In what part of the immune system hierarchy are vaccinations listed?

A

Adaptive-immunity: artificially acquired, active immunity

297
Q

The difference in magnitude between the primary and secondary responses in antibody-mediated immunity is why what artificially-induced process can work?

A

Vaccinations

298
Q

The objective of vaccination is to introduce an antigen to induce the primary response to create what type of cells?

A

Memory cells

299
Q

T/F The entire antigen is required to stimulate an immune response by the body.

A

False. Only antigens associated with the pathogen are required to stimulate an immune response (e.g. macromolecules proteins/carbs)

300
Q

The goal of vaccination is to introduce antigens without introducing the pathogen to stimulate which immune response?

A

Primary response

301
Q

In vaccination, an antigen is introduced without the entire pathogen to stimulate the primary response. If encountered again, it hopefully stimulates what response?

A

The secondary response

BIO 230 DCCC Suran (6 decks)

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