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BIOL 275 Study Questions > BIOL 275 Exam 3 Prep > Flashcards

BIOL 275 Exam 3 Prep Flashcards

1
Q

What are classification systems used for?

A
  • Order and organization
  • Predictions about structure and function
  • Understanding evolutionary connections
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2
Q

What does a bacterial strain arise from?

A

A single cell (90% similarity compared to genus or species, 70%)

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3
Q

What is the importance of rRNA and why was it used when revising the 3-domain system?

A

rRNA is found in all organisms and is required for protein synthesis so you can use rRNA for comparison

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4
Q

What are the three categories of microbial identification?

A

1.) Phenotypic
2.) Immunologic/serological tests
3.) Genotype/analysis of nucleic acids

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5
Q

Describe phenotypic methods

A

Observation of traits that are expressed:
- appearance and behavior
- type of enzymatic activities
- physical conditions it lives in
- antibiotic susceptibility
- chemical composition of its walls/structures

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6
Q

Describe immunological methods

A

Antibody response exploited - samples tested for presence of specific antibodies to pathogen
- often easier for testing for microbe itself

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7
Q

Describe genotypic methods

A

Most specific method, the more sequence provides better clarity of species/strain:
- don’t always need to culture
- can be used for microbes not easily grown in lab

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8
Q

What are some things to ensure when collecting a specimin?

A

Proper:
- collection (aseptic technique)
- transport
- storage
- labeling

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9
Q

Name some phenotypic methods?

A
  • Direct examination (microscopy, stains, etc.)
  • Selective/differential growth
  • Biochemical testing (test for enzymes)
  • Susceptibility testing (helps treatment)
  • Phage-typing
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10
Q

What are phenotypic biochemical tests used for?

A

To test for certain enzymes:
- fermentation of carbs
- utilization of substrates
- production of wastes
- fatty acid composition

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11
Q

What is a dichotomous key?

A

When using physical characteristics to identify, you use this branching decision tree that helps recognize microbe against list of known organisms.

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12
Q

In addition to helping identify microbes, what is antimicrobial susceptibility testing used for?

A

Determining which drugs to use in treatment

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13
Q

What is phage-typing?

A

Phenotypic method using bacteriophages that can infect only certain types of bacterial strains, if “plaques” appear this can help you identify bacteria

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14
Q

What are some disadvantages of phenotypic methods?

A
  • Takes 18-24 hours or longer
  • Many organisms are not culturable in a lab
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15
Q

Direct vs. indirect fluorescent antibody testing?

A

Direct - identifies presence of antigen

Indirect - identifies presence of specific antibodies

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16
Q

Name some immunologic methods

A
  • Agglutination/precipitation (clumping due to two Ab arms/smaller complexes of Ab/Ag)
  • Immunochromatography (lateral flow test like pregnancy test with colored line)
  • Florescent antibodies (direct-unknown Ag exposed to florescent Ab, or indirect-patient Ab marked with florescent Ab)
  • ELISA (Ab-Ag reaction produces color change with enzyme, indirect-Ag in well, direct-Ab in well)
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17
Q

Sensitivity vs. specificity

A

Sensitivity: small quantity of microbe required for positive result

Specificity: tests against certain Ab or Ag to return positive result

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18
Q

Some basic principles of immunological testing (AKA serological)

A

Patient antibodies unknown:
- Mix with known antigens to identify

Microbe unknown:
- Mix with known antibodies to identify

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19
Q

Name some genotypic methods

A
  • PCR (multiply DNA fragments)
  • Whole genome sequencing
  • Pulse-field gel electrophoresis (separate DNA fragments by size)
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20
Q

How many lines of defense are there and how are they categorized?

A

Nonspecific:
1st line of defense: innate immunity
2nd line of defense: innate immunity

Specific:
3rd line of defense: adaptive/acquired immunity

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21
Q

Describe the purpose of the 1st line of defense

A

Surface protection to stop microbes from entering the body. Includes:
- physical barriers (skin, mucous membranes, etc.)
- chemical barriers (stomach acid, mouth enzymes, etc.)
- microbiota barrier (antagonism)

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22
Q

Describe the purpose of the 2nd line of defense

A

Non-specifically reacts to infectious agents/pathogens that enter the body. Includes:
- phagocytosis
- inflammation/fever
- complement proteins
- antimicrobial products
- NK cells

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23
Q

Describe the purpose of the 3rd line of defense

A

Specifically recognizes and reacts to infectious agents/pathogens that enter the body. Unique reaction through specialized white blood cells:
- B lymphocytes (antibodies and humoral response)
- T lymphocytes (cell mediated response)

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24
Q

What are the functions of the immune system?

A
  • Provide surveillance
  • Recognize foreign material
  • Destroy foreign entities
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25
Q

Briefly describe the lymphatic system

A

Made of lymphatic vessels, lymph fluid carries infectious agents/pathogens to lymph nodes where lymphocytes and macrophages destroy them.

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26
Q

What are some of the contents of blood?

A

Plasma: water containing electrolytes, dissolved gasses, nutrients, and proteins

Red blood cells: carry oxygen and carbon dioxide

White blood cells: part of the immune response (2nd and 3rd line)

Platelets: stop bleeding at wounds

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27
Q

What are two main stem cells involved in hematopoiesis (production of blood cells)?

A

Myeloid stem cells

Lymphoid stem cells

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28
Q

What blood cells are derived from myeloid stem cells?

A
  • Erythrocytes (RBCs)
  • Platelets
  • Mast cells
  • Eosinophils
  • Basophils
  • Neutrophils
  • Monocytes (matures into macrophages and dendritic cells)
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29
Q

What blood cells are derived from lymphoid stem cells?

A
  • T lymphocytes
  • B lymphocytes (plasma cell when active and secreting antibodies)
  • NK cells (2nd line of defense)
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30
Q

Where do all blood cells originate?

A

They originate from hematopoietic/pluripotent stem cells located within the bone marrow.

These cells then differentiate into myeloid or lymphoid stem cells.

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31
Q

What is the function of erythrocytes? (AKA RBCs)

A

Gas transport (oxygen/carbon dioxide)

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32
Q

What is the function of platelets?

A

Blood clotting and inflammation

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33
Q

What is the function of mast cells?

A

They are involved in recruitment of other cells as well as inflammatory response

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34
Q

What are the functions of eosinophils?

A

Can leave blood via diapedesis for:
- Toxins against parasites
- Bind mitochondrial DNA to kill
- Phagocytosis
- Inflammatory response

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35
Q

What is the function of basophils?

A

Exit blood (via diapedesis) and release inflammatory chemicals (histamine)

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36
Q

What is the function of neutrophils?

A

Can leave the blood via diapedesis for:
- neutrophil extracellular traps (NET, fibers that trap pathogens)
- makes hypochlorite (bleach) to kill pathogens
- phagocytosis
- component of pus

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37
Q

What is the function of monocytes?

A

They mature into macrophages that conduct phagocytosis

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38
Q

What is the function of dendritic cells?

A

These antigen presenting cells process and carry antigens to lymph nodes and present to T-lymphocytes of adaptive immunity

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39
Q

What are the types of lymphocytes?

A
  • T cells
  • B cells
  • NK cells
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40
Q

What is the function of T-cells?

A
  • Cell-mediated response: act directly against pathogens
  • Billions of T-cell receptor (TCR) to recognize various epitopes
  • Majority of lymphocytes in blood

3 types:
- cytotoxic
- helper
- regulatory

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41
Q

What are the two pathways that cytotoxic cells (Tc) kill pathogens?

A

When activated (cell mediated response), one of two pathways are taken:

1.) perforin-granzyme pathway causes apoptosis
or
2.) CD95 pathway causes apoptosis

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42
Q

What is the difference between where adaptive and innate immunity initiates?

A

Adaptive immunity usually initiates at the lymph nodes when presented by antigen-presenting cells (APCs).

Innate immunity tends to initiate at the site of infection.

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43
Q

What are some various ways leukocytes (WBCs) can indicate different infections?

A

Eosinophils - parasitic infection or allergies

Lymphocytes - presence of viruses

Neutrophils/leukocytes - presence of bacteria

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44
Q

Why are humans naturally resistant to some species of pathogens?

A
  • Chemical receptor incompatibility
  • Environment doesn’t allow survival (pH, temp, etc.)
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45
Q

Resistance vs. susceptibility

A

Resistance - ability to ward off disease through body’s defenses
Susceptibility - lack of resistance to a disease

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46
Q

Describe the skin’s role in innate immunity

A

Two physical barriers/layers:
1.) Epidermis: outer layer of tightly packed cells
- Shedding dry, dead cells removes microbes
- Dendritic cells for phagocytosis

2.) Dermis: collagen fibers help skin resist abrasions

Chemicals:
- antimicrobial peptides by dermal cells
- sweat (salt, dermicidins, lysozyme)
- sebum/oils ( lowers pH and keeps skin pliable)

47
Q

Describe the mucous membranes’ role in innate immunity

A

Lines all body cavities open to environment. Two layers:

1.) Epithelium: thin outer layer, tightly packed
- Shedding carries away microbes
- Dendritic cells for phagocytosis
- Goblet (secrete mucous) and ciliated columnar (beating upward) cells carry trapped pathogens away

2.) Deeper connective layer: supports epithelium

48
Q

What are other physical barriers for 1st line of defense?

A

Lacrimal apparatus: tears wash away and contain lysozyme
Saliva: washes microbes off teeth
Urine: cleans urethra and flows out

49
Q

What role does normal microbiota play in innate immunity?

A

Microbial antagonism makes it hard to pathogens to compete:
- consumes nutrients
- creates unfavorable environment (pH, waste)
- stimulate 2nd line of defense
- provides vitamins and promotes health

50
Q

Name 1st line of defense chemical barriers/antimicrobial secretions?

A
  • Stomach acid
  • Gastroferritin (stomach) and transferrin (blood) sequester iron (growth factor)
  • Bile
51
Q

What are the first leukocytes that usually respond in innate immunity?

A

Neutrophils

52
Q

What structure allows macrophages to phagocytize pathogens?

A

Pseudopods

53
Q

What is the process of phagocytosis?

A

1.) Chemotaxis: pseudopods movement

2.) Adherence: bind complementary surface chemicals

3.) Ingestion: pseudopods fuse and form a food vesicle, “phagosome”

4.) Maturation: lysosome fuses with phagosome, “phagolysosome” to digest

5.) Killing: acidic pH, enzymes, and highly reactive oxygen kill pathogen

6.) Elimination: exocytosis to remove residual body

54
Q

What are some ways pathogens evade phagocytosis?

A

Virulence factors!

  • capsules
  • preventing phagosome-lysosome fusion (leukocidins)
  • lyse phagocytes
  • escape phagosome
  • surviving in phagolysosome
55
Q

Inflammation signs?

A

Redness
Heat
Swelling
Pain

56
Q

What causes redness/heat during inflammation?

A

Vasodilation
- histamine and kinin

57
Q

What causes swelling and pain during inflammation?

A

Increased permeability
- prostaglandin
- leukotriene

58
Q

What is the function of inflammation in the immune response?

A
  • Destroy agents or limit their effectiveness (fluid w/antimicrobial chemicals and neutrophils/monocytes via diapedesis)
  • Repair and/or replace damaged tissues (extra nutrients and oxygen delivered to site)
59
Q

How does a fever contribute to innate immunity?

A

Pyrogens/cytokines trigger hypothalamus to increase temp. by releasing prostaglandins.

  • enhances effect of interferons
  • inhibits growth of some pathogens
  • enhances innate/adaptive immune processes
60
Q

Describe interferons (IFN)

A

Non-specific proteins released by lymphocytes and macrophages to inhibit viral replication (I) and bacterial pathogens (II)

  • Type I (alpha/beta)
  • Type II (gamma)
61
Q

Describe type I interferons

A

Produced by virally infected cells and released. When IFN binds to uninfected cell receptors, it causes them to produce antiviral proteins (AVP) which bind to viral mRNA (to prevent replication) if/when infected.

IFN-alpha: made by epithelium and leukocytes
IFN-beta: made by fibroblasts

62
Q

Describe type II interferons

A

Cause neutrophils and macrophages to phagocytize bacteria. Can also direct cells to produce AVPs.

IFN-gamma: made by lymphocytes

63
Q

What are antiviral proteins (AVP)?

A

AVP are produced by uninfected cells when IFN type I binds to their receptors. These AVP are inactive until the cell is infected by a virus. The AVP become active and bind to viral mRNA to prevent replication.

64
Q

Describe complement (2nd line of defense)

A

Set of serum proteins that act as opsonins, chemotactic factors, trigger inflammation/fever, and destruction of pathogens via membrane attack complex.

65
Q

What are the 3 outcomes of complement activation?

A

1.) Opsonization

2.) Inflammation (via mast cell binding/histamine release)

3.) Cytolysis (via membrane attack complex)

66
Q

What are the 3 ways to activate complement?

A

1.) Classical pathway - antibodies binding to antigen activates complement cascade
(Adaptive immunity)

2.) Alternative pathway - complement proteins bind directly to antigen/pathogen to activate complement
(Innate immunity)

3.) Lectin pathway - lectins from liver bind to mannose on pathogen to activate complement
(Innate immunity)

67
Q

How is complement inactivated?

A

Proteins bind and break down activated complement proteins

68
Q

Describe complement cascade

A

Process where one complement protein reacts with another, which causes a series of exponential reactions involving different complement proteins. This may result in a membrane attack complex against the pathogen.

69
Q

What cells can kill pathogens other than phagocytosis?

A

Eosinophils - toxins kill parasites and mitochondrial DNA is used against LPS/(G-) bacteria to kill

NK lymphocytes - secrete toxins onto surface of cells with tumors/viruses. (normal body cell membranes are similar to NK and MHC-I acts as inhibitor to NK cells)

Neutrophils - makes hypochlorite (bleach) to kill pathogens and produces extracellular fibers/traps (NETs) to bind/kill

70
Q

What are Toll-Like Receptors (TLRs)? Where are they?

A

Integral proteins (in the membranes) of phagocytic cells that recognize “pathogen-associated molecular patterns” (PAMPs)
- Some are located in the cytoplasmic membrane and others are in phagosome membrane

71
Q

What are some PAMPs (pathogen-associated molecular patterns)?

A
  • Peptidoglycan
  • Lipoteichoic acid
  • Lipid A in LPS
  • Bacterial flagellin
  • dsRNA (viruses)
  • ssRNA (viral)
72
Q

What happens when TLRs are bound with PAMPs?

A
  • apoptosis
  • secretion of inflammatory chemicals (kinin, prostaglandin)
  • stimulate adaptive immune response
  • secretion of interferons
73
Q

Describe NOD proteins. Where are they? What do they trigger?

A
  • Proteins in the cytosol that bind PAMPs.
  • Trigger inflammation and apoptosis

(Mutations are associated with IBS/Crohn’s disease)

74
Q

What are the characteristics of adaptive immunity?

A

Specific - acts only against one molecular shape (think antigen / epitope)

Inducible - activated only when pathogen is present

Clonal - forms many generations of cells (copies) when induced

Unresponsive to self (AKA tolerant) - doesn’t attack itself

Memory - works quicker against pathogens previously encountered

75
Q

What are antigens? Epitopes?

A

Antigens are portions of cells or viruses that illicit immune system response.

Epitopes are what the antibodies and lymphocytes bind to on the antigen.

76
Q

What are the 3 types of antigens?

A

1.) Exogenous antigens (outside host cells) - toxins, secretions, cell walls, etc.

2.) Endogenous antigens (inside cell) - microbes that replicate inside cell or their components within a cell

3.) Autoantigens - self-antigens produced by host cells (normally removed during clonal deletion, because body shouldn’t respond to self)

77
Q

Describe adaptive immunological development process

A
  1. Lymphocyte development and clonal deletion
  2. Presentation of antigens and clonal selection
  3. Challenge B and T lymphocytes

4a. T-cell response: cell mediated
4b. B-cell response: production/activation of antibodies

78
Q

Describe antigen-independent development (before pathogen is present)

A
  1. Stem cells in bone marrow differentiate into lymphocytes

2a. Lymphocytes move to thymus and mature into T-cells. Matured T-cells move to lymph node or spleen.
2b. Lymphocytes mature in bone barrow into B-cells and move to lymph node or spleen.

  1. Antigen presence triggers response and antigen is processed by antigen-presenting cell (APC) such as dendritic or macrophage.
  2. Antigen is displayed to trigger T-cell response.

5a. Cytotoxic T-cells move to kill pathogen. Memory T-cells created.
5b. Helper T-cells activate B-cells

6a. T-cells differentiate into helper, regulatory, or cytotoxic cells.
6b. B-cells reproduce and plasma cells create antibodies to respond. Memory B-cells created.

79
Q

What are some differences between B-cells and T-cells?

A

B-cells:
- mature in bone marrow
- release antibodies (plasma cells)
- humoral response (extracellular/exogenous antigens)

T-cells:
- mature in thymus
- cell-mediated response (intracellular/endogenous antigens)
- produce cytokines (proteins that signal immune activities…ex. cytokines needed to activate Tc cells)

80
Q

What are the most common lymphocytes in blood?

A

T-cells (70-85%)

81
Q

What allows lymphocytes to bind to the epitopes of antigens?

A
  • T-cell receptors (TCR) within cytoplasmic membrane
  • B-cell receptors (BCR) within cytoplasmic membrane
82
Q

What is the role of antigen-presenting cells (APC) in adaptive immunity?

A

Dendritic cells or macrophages capture, ingest, degrade pathogens and display their antigens to T-cells to activate within the lymph nodes.

APC MHC I - presents to inactive Tc cell
APC MHC II - presents to Th cell

83
Q

What are the types of T-cells?

A

Helper T-cells (Th): help recruit adaptive response
- type 1 (Th1): assist Tc cells
- type 2 (Th2): secretion (IL-4) differentiates B-cells into plasma cells

Cytotoxic T-cells (Tc): kill targets via perforin-granzyme pathway or CD95 pathway

Regulatory T-cell (Tr): regulates response to not attack self and suppresses T-cells after infection

84
Q

Surface glycoproteins and cytokines associated with T-cells?

A

Helper T-cells: CD4, IL-2 (Th1), IL-4 (Th2), and IFN-gamma

Cytotoxic T-cells: CD8, CD95L, perforin/granzyme

Regulatory T-cells: CD25, CD4, and IL-10

85
Q

What are some examples of cytokines?

A
  • Interferons (type I or II)
  • Interleukin (IL-4 differentiates B-cells into plasma cells)
86
Q

Describe the cell-mediated immune response

A

1a. Antigen presentation by APCs in lymph nodes to Th and Tc cells.
1b. Tc cells recognize epitope

2a. Th cells differentiate into Th1 cells (using IL-12 cytokines)
2b. Th1-cells activate Tc cells (using IL-2 cytokines)

  1. Clonal expansion creates more Tc and memory T-cells
  2. Self-stimulation (active Tc cells secrete IL-2 cytokines to activate other Tc cells)

5a. Tc cell killing via CD95 or perforin-granzyme pathway

87
Q

What are the two cytotoxic T-cell pathways?

A
  1. Perforin-granzyme:
    - Vesicles containing perforin and granzyme leave via exocytosis
    - Perforin creates a pore/channel in infected cell and allows granzyme to enter
    - Granzyme activates apoptosis
  2. CD95:
    - Host cell (animal only) membranes contain CD95.
    - Tc cells bind infected cells’ CD95 with receptor proteins (CD95L) which induces apoptosis
88
Q

Describe memory T-cells

A

Memory T-cells are similar to Tc cells but to not kill.

Instead, if their T-cell receptor (TCR) contacts a complementary, previously seen antigen epitope, it will respond immediately without needing APC presentation.

Will produce active Tc cells with matching TCRs to kill pathogen.

These cells stays for months to years and result in a more effective immune response.

89
Q

What do T-cells usually require to active?

A

Signals (such as presentation of epitopes or secretion of cytokines) from APCs. If there is no signal, an immune response will not occur.

90
Q

What is the function of B-cells?

A

Activated B-cells (called plasma cells) secrete antibodies in response to a pathogen.

B-cell receptors (BCR) on a single B-cell will recognize/bind to only 1 antigen (a B-cell has many BCR that are all the same)

91
Q

Describe antibodies

A

Type of immunoglobulin made of 2 light, and 2 heavy polypeptide chains (linked by covalent bonds);
- Contains 2 antigen binding sites
- Binding sites will bind to same antigen as BCR of B-cell that produced them

92
Q

What do antibodies specifically bind to?

A

The epitopes of antigens

93
Q

What are the functions of antibodies?

A
  • Complement activation leading to inflammation: Ab bind to complement causing inflammation
  • Neutralization: Ab bind to Ag to render it neutral
  • Opsonization: Ab bind Ag to help enable phagocytosis
  • Agglutination: clumping due to multiple binding sites; makes them larger
  • Antibody dependent cell-mediated cytotoxicity (ADCC): Ab bind to Ag which are then bound by NK cells which results in apoptosis via perforin-granzyme pathway
  • Oxidation: Ab binds to Ag to produce hydrogen peroxide which can damage bacteria
94
Q

What are the 5 types of antibodies?

A

(MGAED)

IgM: first antibody produced, pentamer helps with agglutination

IgG: most common, longest-lasting, can cross placenta

IgA: associated with body secretions

IgE: involved with allergies/parasitic infections

(IgD: function unknown)

95
Q

Two types of antibodies production

A

T-dependent response: require (are dependent on) Th cells to activate B-cell

T-independent response: can respond to pathogens without Th cells (independently)

96
Q

What do most antibody immune responses depend on?

A

Helper T-cells (Th). This reliance on Th cells is called “T-dependent antibody immunity”

97
Q

Describe T-independent activation/response

A
  • BCR binds to antigen and activates B-cell
  • Activated B-cell (called plasma cell) secretes antibodies
98
Q

Describe T-dependent activation/response

A
  • APC presents antigen/epitope to Th cell
  • Th cell differentiates into Th2 cell
  • Th2 cell binds to B-cell and also releases IL-4 cytokines to activate B-cell
  • B-cell differentiates to plasma cells (which secrete antibodies) and memory cells
99
Q

When are memory B-cells made?

A

During B-cell activation

100
Q

Describe memory B-cells

A
  • Do not secrete antibodies
  • Can persist for 20 years
  • BCR is complementary to epitope that triggered their production
101
Q

Why is a secondary response faster and more effective than a primary response?

A

Memory cells are activated by contact with complementary epitope/antigen and do not need to wait for APC or Th-cells for activation

102
Q

What is the difference between passive and active vaccination?

A

Active - uses antigens to stimulate body’s immune response which creates antibodies and memory cells

Passive - administers antibodies to immediately help patient response to infection

103
Q

Types of adaptive immunity?

A

Naturally acquired active: antibodies made as a result of infection

Naturally acquired passive: maternal antibodies acquired

Artificially acquired active: vaccine introduces antigens and causes B-cell activation

Artificially acquired passive: injecting antibodies (usually due to immediate requirement to fight pathogen)

104
Q

Describe vaccination

A

The use of antigens or antibodies to provide a level of immunity:
- Provokes primary immune response
- Leads to formation of antibodies and memory cells
- Produces a rapid, intense secondary response

105
Q

What is herd immunity and why is it important?

A

Immunity in most (75%) of the population. Because immunity prevents disease, outbreaks are less likely to happen

106
Q

What are some vaccinations that the CDC recommends for children?

A
  • Hepatitis A and B
  • DTaP
  • MMR
  • Varicella
  • Rotavirus
  • Influenza
  • HiB
  • IPV
  • PCV13
107
Q

What are some types of vaccines?

A
  • live-attenuated
  • inactivated/killed
  • subunit
  • toxoid
  • virus-like particles
  • DNA/RNA
  • viral vector
108
Q

Describe attenuated vaccines

A
  • Uses pathogen with reduced virulence (attenuated)
  • Stimulates strong response
  • May produce contact immunity (beyond patient)
109
Q

Describe inactivated vaccines

A

Whole agent - pathogen but deactivated or killed

Subunit - antigenic fragment of pathogen

Conjugated - proteins (strong Ag) conjugated to carbohydrates (weak Ag)

Boosters may be required for full immunity

110
Q

What are adjuvants?

A

Additives that help result in an increase of the body’s immune response to a vaccine and improve effectiveness.
(Alum is common in the US)

111
Q

What are toxoids?

A

Chemically or thermally modified toxins that can stimulate immune activity.

Require multiple doses for full immunity due to containing few epitopes.

112
Q

Some technology for producing vaccines?

A

Recombinant gene technology:
- delete gene from pathogen (produces irreversibly attenuated microbe)
- produce large amounts of antigens
- genetically alternated bacteria or virus may express antigen as live vaccine

113
Q

What are some side effects of vaccines?

A
  • Local reaction or irritation
  • Fever
  • Allergies (ex. eggs in influenza due to culturing)

BIOL 275 Study Questions (4 decks)

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