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Biology 3/4 > Unit 3 AoS 2- INFECTION AND DISEASE > Flashcards

Unit 3 AoS 2- INFECTION AND DISEASE Flashcards

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1
Q

Difference between a pathogen and a pathogenic agent?

A

Pathogens are cellular agents (bacteria, fungus, protozoans, parasites) whereas pathogenic agents refers to non-cellular agents (viruses, prions, viroids).

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2
Q

What are the 3 different shapes of bacteria?

A

Coccus (round-shaped), spirochaete (spiral-shaped) and bacillus (rod-shaped).

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3
Q

What is a vector?

A

An animal (usually an insect) that carries pathogens from one host to another and is not affected by it.

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4
Q

What is a parasite?

A

An organism that lives in or on a host organism, obtaining food and/or shelter, and contributing nothing to the host’s welfare. Not necessarily pathogenic. (Parasites don’t necessarily kill their hosts, as their food source would ultimately be destroyed).

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5
Q

What is an endoparasite?

A

Parasite that lives within the host (e.g. tapeworm)

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6
Q

What is an ectoparasite?

A

Parasite that lives on the surface of the host (e.g. flea)

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7
Q

What is a disease?

A

Any body abnormality or failure to function properly in an organism (such as incorrect metabolism, injury, infection) except that resulting directly from physical injury.

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8
Q

What is an infectious disease?

A

A disease caused by the invasion and growth of a pathogen within an organism and is contagious.

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9
Q

What is a non-infectious disease?

A

A disease caused by any other source than infection/ e.g. by the environment (UV light effect on skin cancer, cyanide poisoning), poor nutrition (scurvy, obesity), genetic disorders (cystic fibrosis, Huntington’s disease) etc.

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10
Q

What is a host?

A

The organism in or upon which a parasite feeds. In some life cycles, more than one host is required by the parasite species.

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11
Q

What is a primary host?

A

Organism where pathogen lives in the adult form and reproduces (usually shows disease sympoms)

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12
Q

What is a secondary (intermediate) host?

A

Organism in which the parasite passes through its larval or asexual stages only (e.g. sheep or human in hydatid tapeworm lifecycle).

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13
Q

What is a carrier?

A

An individual that is host to a pathogen, but does not experience signs or symptoms of infection, yet can transmit the disease to others.

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14
Q

What is an infection?

A

The invasion and growth of a harmful cellular/non-cellular agent within the body of a host.

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15
Q

How do bacteria replicate?

A

Bacteria reproduce asexually by binary fission.

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16
Q

What is a leucocyte?

A

White blood cell.

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17
Q

In what ways can an infectious disease be transmitted from individual to individual?

A 
Direct contact 
Indirect contact 
Water
Air
Food
Vectors
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18
Q

Examples of direct contact?

A
  • Touching, kissing (e.g. measles, fungal infections, colds)

* Exchange of bodily fluids (e.g. AIDS, hepatitis)

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19
Q

Examples of indirect contact?

A

*Bed linen, contact with soil (e.g. diphtheria)

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20
Q

Examples of transmitted disease through consumption of contaminated water?

A
  • Typhoid

* Cholera

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21
Q

Examples of transmitted disease through air droplets (ie sneezing, inhalation)?

A
  • Influenza
  • Pneumonia
  • Chicken pox
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22
Q

Examples of transmitted disease through consumption of contaminated food?

A
  • Salmonella

* Hepatitis

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23
Q

Examples of transmitted disease through vectors?

A
  • Malaria (Mosquitoes)

* African Sleeping Sickness Trypanosome (Tsetse fly)

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24
Q

What is the difference between an infectious and a non-infectious disease?

A

An infectious disease is caused by a pathogen or pathogenic agent and can be passed on from one person to another, while a non-infectious disease cannot be passed on from one person to another and is caused by factors other than pathogens, e.g. dietary diseases, inherited diseases or exposure to mutagens.

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25
Q

Examples of pathogens?

A
  • Bacteria
  • Protozoa
  • Fungi
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26
Q

Examples of pathogenic agents?

A
  • Virus (protein coat surrounding RNA or DNA)
  • Prion (protein)
  • Viroid (small piece of RNA)
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27
Q

What is a viroid?

A
  • Smallest known infectious agent
  • Small piece of RNA (no protein)
  • Only known pathogens found in plants such as potatoes, tomatoes and grape vines.
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28
Q

What is a prion?

A

A prion is an abnormal and infectious folded piece of protein.

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29
Q

Diseases caused by prions?

A

TSE (mad cow disease)
Scrapie (sheep)
Creutzfeldt- Jakob disease and kuru (humans)

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30
Q

What is a virus?

A

A particle lacking cellular organisation and consisting of genetic material (RNA/DNA) surrounded by a protein coat and only reproduces in a host cell.

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31
Q

Role/function of the bloodstream in the immune system?

A

Carries immune cells like phagocytes and other proteins like complement proteins, blood clotting proteins such as prothrombin and fibrinogen.

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32
Q

Role/function of non-self antigen in the immune system?

A

Form of identification to inform cells in the body that a foreign body has entered.

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33
Q

Role/function of self antigen (eg MHC marker) in the immune system?

A

Form of identification for self-cells- so that immune cells do not attack them.

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34
Q

Complement proteins

A

*Group of proteins that assist phagocytes in recognising pathogens (continually circulate in blood plasma)
*Help in bacterial infection by attracting phagocytes to site of infection.
*Bind to bacteria and lyse cell membrane, make it easier for bacteria to be recognised by phagocytes and call more phagocytes to the area
*They can also directly lyse the membrane of bacterial cell (NOT cell walls) causing leakage of cell contents in order
to attract more phagocytes to area
*Promote inflammation (by increasing local permeability of capillaries and attracting phagocytes)

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35
Q

Phagocyte

A

A white blood cell that is able to engulf and ingest foreign bodies.
Examples: macrophages, monocytes, neutrophils, eosinophils
Part of the non-specific immune response

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36
Q

Macrophage

A

A type of phagocyte. In the bloodstream, this cell is the monocyte and when it leaves the bloodstream, it matures into this cell.
Part of the non-speicific immune response

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37
Q

Dendritic cell

A

A type of phagocyte.

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38
Q

Interferons

A

Proteins released by virus-infected cells and immune cells which warn surrounding uninfected cells of virus and increase the resistance of the uninfected cells so that the virus remains outside the cell where it is more susceptible to phagocytosis.

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39
Q

T cells

A

Cells which are produced in bone marrow but mature in the thymus gland. They are important immune cells in third line of defence.

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40
Q

T helper cell

A
  • Specialised lymphocyte that helps in recognising foreign antigen and stimulating the T cytotoxic cells and B cells.
  • Regulatory cells that, when stimulated by antigen, produce and release cytokine molecules that control development and function of other T and B cells, and phagocytes
  • Also release interferon.
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41
Q

Antigen presentation

A

Process where macrophage displays the foreign antigen on its cell membrane and presents it to the T helper cell to trigger 3rd line of defence.

1) Phagocyte engulfs and ingests pathogen
2) Parts of the pathogen (non-self antigen) goes to the surface of the phagocyte
3) The phagocyte presents the antigen to a T helper cell
4) T-helper cell is activated

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42
Q

T cytotoxic cells

A

Specialised lymphocyte that recognises and destroys viral infected cells, cancer cells and foreign eukaryotic cells (ie protists and fungi).
Cytotoxic T cells lyse infected cells with perforin and toxic granules to destroy the cell and its contents.
*The release of cytokines further stimulates phagocytosis by macrophages.
*Can also release interferon.

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43
Q

B cells

A

A lymphocyte that has a unique antibody that can recognise specific antigen

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44
Q

Antibody

A

An immunoglobin with two antigen-binding sites.

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45
Q

Immunoglobulin G (IgG)

A

A type of antibody

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46
Q

Clonal Selection/ Clonal Expansion/ Differentiation

A

When a B lymphocyte is triggered by the binding of the antigen (with the help of T helper cell), it is activated to form clones of cells, some of which become B plasma cells and some of which become B memory cells.

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47
Q

B memory cell

A

A lymphocyte that is produced during the first infection, to retain information about the pathogenic agent and it helps the body to ‘fight back’ even stronger and faster in subsequent infections.

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48
Q

B plasma cell

A

A type of lymphocyte that can produce massive amounts of antibodies

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49
Q

Antibody round- up/ Agglutination

A
  • Agglutination occurs when an antibody-antigen complex forms–> attracts macrophages
  • Process of gathering of antigens by the antibodies.
  • Specific Antigens bind to the specific antibodies, which block antigens from binding to its target or attracts phagocytes/ macrophage
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50
Q

Tears/ Saliva

A

Contain the enzyme lysozyme which may cause the bacteria to lyse/burst and tears wash bacteria away from the body.

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51
Q

Sneezing

A

sneeze out bacteria

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52
Q

Mucus

A

Traps bacteria and stops them from entering into the body

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53
Q

Cilia

A

Filter air passing through respiratory system.

Guides pathogens trapped in mucus towards the nose/mouth.

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54
Q

Intact Skin

A

acts as a physical barrier to stop bacteria from entering body

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55
Q

Stomach acid

A

may kill bacteria– acid denatures proteins in cell membranes of bacteria

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56
Q

Platelets

A

Platelets clot blood.

  • When they come into contact with damaged cells they release an enzyme called thromokinase (1 mark).
  • This converts prothrombin to thrombin, which catalyses the conversion of fibrinogen to fibrin.
  • Fibrin is an insoluble protein that traps blood cells (1 mark), causing a blood clot which plugs holes in tissues damaged as bacteria entered, or prevents bacteria from entering the body (1 mark)
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57
Q

What does the first line of defence include?

A

External barriers of the body, including:

  • Intact skin (relatively tough and impermeable unless broken)
  • Tears (contains lysozymes)
  • Saliva (contains amylase)
  • Mucus (traps micro- organisms)
  • Sweat (acidic, dehydrating repellent)
  • Nasal hair (filter air)
  • Ear wax (traps pathogens)
  • Cilia
  • Stomach acid kills most pathogens that enter
  • Blood clotting
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58
Q

Histamines

A

released from damaged tissues when bacteria enter the body –dilate blood vessels which brings more phagocytes/ macrophages to the area

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59
Q

Phagocyte

eg neutrophil/ monocyte

A

recognise non-self antigens on bacteria and engulf bacteria

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60
Q

Macrophage

A
  • engulf bacteria in surrounding tissues as they recognise non-self antigens on the surface of the pathogens (1 mark) * may present antigens to THelper cell (Antigen Presenting Cell) (1 mark)
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61
Q

Inflammation

A
  • Inflammation is triggered by histamines released from mast cells, platelets and cytokines from damaged cells
  • Results in:
  • increased blood flow to area (1 mark),
  • increased permeability of blood vessels so phagocytes and macrophages can enter tissues to fight the bacteria, as well as antibodies and complement proteins (1 mark).
  • Increased phagocytosis in area results in pus formation.
  • Inflammation causes heat, swelling, pain and reduced movement.
  • The stimulated macrophages release chemicals such as cytokines which affect the control of temperature by the hypothalamus, leading to fever.
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62
Q

Interferon

A
  • Warns of viral infection to neighbouring uninfected cells, when infected cell is destroyed – not released with bacteria.
  • Interferons also stimulate the production of antiviral proteins.
  • A class of cytokines
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63
Q

Cytokines

A
  • glycoproteins that act as signalling molecules (chemical messengers) in the immune system
  • only act on cells locally with specific receptors
  • released by cells after tissue injury or infection
  • trigger both specific and non-specific responses such as:
  • promote growth of lymphocytes,
  • induce fever,
  • activate macrophages,
  • initiate inflammation,
  • allow communication between cells involved with the immune system
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64
Q

Fever

A
  • Fever is triggered by bacterial toxins ie pyrogens (toxins released by bacteria that act on the brain) and cytokines (released by stimulated macrophages which travel from blood to brain)
  • released from macrophages (during inflammatory response)
  • Increase in body temperature eg above 37.8ºC, resulting from the resetting of the body temperature set-point in the hypothalamus.
  • higher temperature inhibits reproduction of most bacteria
  • Increase in temperature increases enzyme activity improving the inflammatory response.
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65
Q

Natural Killer Cells

A
  • Detect cancerous and virus-infected cells by changes in carbohydrate molecules on surface of body cells
  • Lyse cell membranes of any virus infected cells (and microbial infection)
  • Part of the non-specific immune response
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66
Q

What does the second line of defence include?

A
  • Phagocytes (engulf invaders)
  • Complement proteins (assist in identifying invading pathogens by coating bacterial cells, stimulating histamines and attract phagocytes).
  • Inflammation (increase blood supply)
  • Histamines (attract phagocytes)
  • Natural killer cells (NK) (kill virus infected cells but non-specific)
  • Interferon (makes uninfected cells more resistant to viruses)
  • Fever
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67
Q

What is an antigen?

A
  • A compound, usually a protein, that can trigger the immune system to respond in various ways, including antibody production
  • Binds to specific antibodies
  • Allows the body to distinguish from self and non-self
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68
Q

What are MHC markers?

A

MHC are the genes that code for the proteins on the cell membranes that act as “markers”. These proteins are called “MHC markers”.
It is the combination of antigens (proteins) on the outer surface of the cell membrane that are ‘self’

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69
Q

On what cells can Class 1 MHC markers be found?

A

All cells except red blood cells

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70
Q

On what cells can Class 2 MHC markers be found?

A

On immune cells such as T lymphocytes, B lymphocytes and some macrophages

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71
Q

What types of cells can be antigen presenting cells?

A

B cells, macrophages, phagocytes and dendritic cells

72
Q

Lymph System

A

 Includes all of the structures dedicated to the production and circulation of lymphocytes
 Clear fluid moves in one direction only
 Movement of fluid in the veins relies on muscular movements to squeeze the fluid along towards the heart
 Veins (like veins in the circulatory system) contain one-way valves that keep the fluid moving in one direction
 Transport of antigen presenting cells such as dendritic cells, to the lymph nodes where an immune response is stimulated

73
Q

Lymph nodes

A

*fibrous nodules
*Found along the length of lymph vessels in special regions
*They filter the lymph before it can be returned to the circulatory system.
*The nodes contain macrophages, phagocytic cells that engulf and destroy bacteria, dead tissue, and other foreign matter, removing them from the bloodstream.
*Phagocytes filter out foreign matter
*Contain T and B lymphocytes
*T and B cells respond to presence of foreign antigens in lymph fluid by multiplying rapidly in lymph nodes
*Much of the adaptive immune response is initiated in the lymph nodes
(There are between 600-700 lymph nodes present in the average human body).

74
Q

What is lymph?

A

Fluid containing plasma proteins that circulates in the lymphatic system.

75
Q

What are the two main functions of lymph vessels?

A
  • To drain the interstitial fluid

* To transport cells (especially B cells and T cells) around the body to the lymph nodes

76
Q

Function of lymph nodes?

A
  • Extracellular fluid is filtered in the lymph nodes.

* The lymph nodes contain many dendritic cells, antigen presenting cells, B cells and T cells

77
Q

Function of inflammation?

A
  • Destruction of the cause and products of an infection
  • Confining the infection to a small area
  • Increase in rate at which damaged cells are repaired or replaced
78
Q

How do cells determine which cells are theirs and which cells are foreign?

A
  • Cells in an organism have their own particular molecules (self antigens) on the surface. (ie MHC markers)
  • Cells with different molecules on their surface (non-self antigens) are recognised as foreign and are attacked by the immune system.
79
Q

Difference between antibodies and antigens and how do they relate to each other?

A

An antigen is a molecule that provokes the production of antibodies .
Antibodies are produced by B cells and are designed to damage pathogens.
A specific antigen will provoke the production of one type of antibody.

80
Q

Cell mediated immunity

A

Involves the resistance to disease resulting from the action of cells.
Involves attacks on pathogens which are inside cells.

81
Q

What is a retrovirus?

A

A virus whose genetic material is RNA; the RNA is changed into a molecule of DNA that is inserted into a host cell’s DNA when the retrovirus enters the host cell.

82
Q

How does the HIV virus reproduce?

A
  • HIV enters the host cell (viral RNA is injected into the host cell)
  • Reverse transcriptase catalyses reverse transcription, synthesising a DNA strand which is complementary to the viral RNA.
  • Integrase integrates the viral DNA into the cell genome
  • Proviral genes are transcribed into RNA molecules.
  • The viral mRNA strand leaves the nucleus and is translated into HIV proteins.
  • Protease cuts up the protein and the virus protein is reconstructed (assembled around viral genomes and reverse transcriptase molecules)
  • The new virus buds off from the host cell.
83
Q

Allergic response

A
  • Upon first exposure, antigen causes B cell to produce IgE antibodies
  • Large number of IgE antibodies bind to mast cells
  • There may be no reaction during first exposure to allergen
  • Upon subsequent exposure to antigen, the antigen binds to IgE antibodies on mast cells.
  • When there is cross linking of the IgE antibodies and the allergen molecules, mast cells secrete histamines that cause an allergic response.
  • Results in vasodilation, mucous secretion, smooth muscle contraction which can lead to runny nose, itchiness, breathlessness and anaphylaxis.
84
Q

What is an allergy?

A

An excessive immune response upon renewed exposure to usually harmless antigens (allergens)

85
Q

What are antihistamines?

A
  • drugs that block the body’s receptors for histamine

* counteract the effects of histamine –> suppress some allergic symptoms

86
Q

What is an allergen?

A
  • A substance(antigen) which stimulates a sufficient number of IgE antibodies to create an allergic response, eg penicillin, pollen, nuts, bee venom, dust mite faeces, etc
  • Creates an allergic response when it binds to IgE antibodies anchored in the cell membranes of mast cells
87
Q

What is anaphylaxis (anaphylactic shock)?

A

An extreme and generalised allergic reaction in which widespread release of histamine can be life threatening.

  • circulating histamines and other released mediators cause bronchioles to constrict, blood vessels to dilate and loss of fluid to the tissues so that blood pressure falls dramatically
  • can be controlled by immediate injection of adrenaline (epinephrine)  EpiPen
88
Q

What can anaphylactic shock result in?

A

The release of large quantities of histamines can lead to:

  • Constriction of bronchioles, leading to suffocation
  • Vasodilation, resulting in loss of fluid from capillaries into surrounding tissues, swelling, fall in blood pressure and heart failure.
89
Q

In an allergic reaction, what can increased levels of histamine result in?

A
  • Dilation of blood vessels resulting in localised swelling, inflammation and decrease in blood pressure (which can lead to less oxygen being transported via RBC to the brain–> dizziness and faintness.)
  • Swelling is a result of blood plasma leaking out of blood vessels into tissue–> phagocytes move into affected area.
  • Contraction of smooth muscle in the lungs leading to a decrease in the diameter of bronchioles and consequent breathing problems etc
90
Q

Humoral immunity

A

Humoral immunity involves the resistance to disease by the production of antibodies (immunoglobulins) that bind to specific antigens

91
Q

What are the ways in which drug design slow down reproduction of HIV virus?

A

*Blocking protein enzyme Reverse Transcriptase so it can’t convert RNA into DNA ie Sustiva
*Protease inhibitors stop protease enzymes so they can’t cut up the proteins that need to be packaged into the virus ie Kaletra
*Block virus from entering the host cell ie Fuzeon
*

92
Q

How is Influenza virus prevented?

A

Relenza (drug) works by inhibiting viral enzyme called neuraminidase (found on surface of Influenza A Virus) to prevent the release of newly synthesized viruses from leaving the infected cells.

93
Q

Why are booster shots/immunisations required?

A

Booster shots allow the body to keep a good memory (by production of B memory cells) of pathogen/pathogenic agent so immune system can quickly recognise invader and act on it.

  • Also to protect against mutated strains
  • Sometimes B memory cells can be short lived
  • Protect against mutated strains
  • Greater production of antibodies leads to immediate / faster response
94
Q

Where does humoral immunity take place?

A

In the lymph node

95
Q

Describe process of humoral immunity.

A
  • Macrophage engulfs and ingests pathogen/pathogenic agent.
  • Macrophage displays non-self antigen on MHC marker on surface of cell membrane. This is called antigen presentation.
  • This is recognised by the T-helper cell.
  • T- helper cell activates a B cell that has an antibody specific to the non-self antigen and the non-self antigen binds to the B cell’s antibody-like receptor simultaneously.
  • The activated B cell undergoes clonal selection to produce B plasma cells (which produce lots of antibodies) and B memory cells (which have antibodies on the cell surface and retain information about the encountered infection; long lived.)
96
Q

Describe the process of cell-mediated immunity

A
  • Infected cells display antigen- MHC complex.
  • T-helper cells are activated by the antigen-MHC complex
  • T-helper cells stimulate cytotoxic T cells to destroy infected cells.
97
Q

What is an auto immune response?

A

The loss of ability of the immune system to differentiate between self and non-self. Self cells are destroyed. Eg of autoimmune diseases are multiple sclerosis, Type I Diabetes and rheumatoid arthritis.

  • Could be a result of MHS marker changed in a particular tissue
  • Non-self receptors could become distorted and accept self antigens
98
Q

Rejection of organ transplants

A
  • Transplanted organ is recognised as non-self (except when received from identical twin).
  • Immune suppressant drugs can be administered e.g cyclosporin which acts against T cells.
  • The degree of match between the donor’s and recipient’s tissues will determine the success of the transplant.
99
Q

Immune deficiency diseases

A
  • A deficiency or malfunction in one or more of the components of the immune system.
  • Could be inherited or acquired ie AIDS
100
Q

What are antibodies?

A

Large globular proteins called immunoglobulins which are produced by animals in response to non-self antigens.

101
Q

What are the two types of immunity?

A

Active immunity and passive immunity

102
Q

Active immunity

A

Immunity that develops when an organism makes its own antibodies; antibodies may be produced naturally in response to chance infection (natural active immunity) or may be induced by vaccination (induced/artificial active immunity)
*B memory cells produced

103
Q

Passive immunity

A

Immunity provided when an individual receives antibodies made by another organism; antibodies may be received through injection (induced/artificial passive) or naturally, as when a baby receives them from its mother across the placenta or in breast milk (natural passive)
*B memory cells are not produced

104
Q

What is a vaccine?

A

Suspension of attenuated living, dead microorganisms, toxins produced by organisms, non-pathogenic form of bacteria, or closely related variant of bacterium that, when injected into a person, stimulates the immune system to produce specific antibodies.

105
Q

Rhesus incompatibility

A
  • In pregnancies/blood transfusions
  • Problems arise when an Rh negative person receives Rh positive blood or when an Rh negative mother carries a Rh positive fetus for a second or subsequent time.
106
Q

Blood clotting

A
  • Creates a ‘plug’ to stop blood flow, repair breaks in the bloodstream
  • Non-specific
  • Occurs when platelets come into contact with damaged blood vessels, damaged blood vessels release thromokinase which converts prothrombin (blood protein) to thrombin,
  • thrombin converts fibrinogen (blood protein) into fibrin (an insoluble protein) which forms the clot (mesh)
107
Q

What are plant physical defence mechanisms?

A
  • Dropping infected leaves
  • Galls [roots]- used to enclose and entrap parasites and prevent further infection of pathogens
  • Thick waxy cuticle of leaves, thickened bark of stems
  • Epidermal layer of cells (e.g. with sunken stomata)
  • Cuticle and epidermal cells form a protective barrier
  • Silicon in leaves make them resistant to pathogen’s enzymes
  • Thickened cell walls
  • Hairy or spiny leaves to deter vectors of disease
108
Q

What are plant chemical defence mechanisms?

A
  • Sticky resins
  • Antibiotics and toxins produced by the plant.
  • Chemicals that protect against some fungi and bacteria
  • Enzymes which digest fungus cell walls
  • High levels of toxins in leaves
  • Some trees, e.g. lemon and mint, produce oils that repel some insect pests
  • Secrete gum e.g. stone fruit trees- seal off an infected area
109
Q

What is a viroid?

A
  • Smallest known infectious agents
  • Short pieces of naked RNA
  • Depend on host cell for reproduction
  • Believed to only infect plants
110
Q

Describe series of events upon an individual’s first exposure to an allergen.

A

1) Antigen stimulates B cell to produce IgE antibodies.
2) A large number of IgE antibodies are embedded onto mast cells.
* There may not be a reaction upon first exposure to the allergen.

111
Q

Describe series of events upon subsequent exposure to an allergen.

A

1) Upon subsequent exposure to the allergen, the antigen binds to IgE antibodies on the mast cells.
2) The cross-linking of the antigens on the IgE antibodies of the mast cells, causes histamine to be released which results in an allergic response.

112
Q

What happens when we come into contact with a prion protein?

A
  • If we become infected with a defective prion it converts normal protein into abnormal prion protein (scrapie prion sPrP) –> prion ‘replicates’
  • Contact between sPrP and nPrP causes nPrP to flip into disease shape
  • Chain of amino acids that make up protein become folded in an abnormal way
  • Prions eventually cause cell to burst (‘holes’ in infected brains) and are free to infect other cells
113
Q

What causes TSE?

A
  • Too many infectious prions cause neurons to burst, making the brain appear to have holes in it.
  • Abnormal and infectious proteins called prions cause these degenerative neurological diseases, also called transmissable spongiform encephalopathies (TSE)
114
Q

How is the HIV Virus transmitted from person to person?

A

Sharing of bodily fluids, eg sexual contact, sharing needles, blood transfusions, mothers may pass the HIV virus through the placenta to their unborn children

115
Q

What is drug design?

A

A drug that has been man made to prevent the action of a particular infective agent and hence prevents the development of the particular disease.

116
Q

Why do lymph nodes swell during an infection?

A

Lymph nodes swell during an infection, as the particular type of white blood cell responsible for fighting the infection (ie B cell, T cytotoxic cell etc) multiplies rapidly in order to overcome and destroy the invader, typically a virus or bacterium.

117
Q

What is a bacteriophage?

A

Viruses that infect bacteria.

118
Q

Examples of bacterial diseases?

A
  • Typhoid
  • Pneumonia
  • Gonorrhoea
  • Syphilis
  • Tetanus
119
Q

How does Relenza (drug designed for Influenza) work?

A

Works by inhibiting a viral enzyme called neuraminidase. By inhibiting this enzyme, Relenza helps to prevent the release of the virus from infected cells. It does not directly help the cells that have already been infected; instead, it prevents other cells from being infected as well.

120
Q

Characteristics of bacteria?

A 
Shape
Organisation
Presence/absence of capsule
Requirement for oxygen
Nutritional requirements
Gram staining techniques
121
Q

What damage does bacteria cause to host cells?

A
  • secrete enzymes that digest material that holds cells together.
  • release toxins (inhibit protein synthesis, damage cell membranes or disrupt cell transport, interfere with nerve function).
122
Q

What is an antibiotic?

A

Naturally occurring compound that is effective against disease-causing agents, that have been extracted from bacteria and fungi

123
Q

Protozoan

A
  • Unicellular eukaryotic organism

* Most protozoans are carried by a vector

124
Q

What environmental conditions does a fungus require in order to grow?

A

Dark, moist environment

Ringworms are fungus

125
Q

Result of fungal infection in plants?

A

Hyphae entering through stomata

Decrease in cellular respiration, decrease in photosynthesis

126
Q

What are some of the structural adaptations for the tapeworm?

A

Hooks onto small intestines where nutrients are
Hermaphrodite–>can make own eggs and sperms–> can have own babies, can also undergo sexual reproduction
Long and thin–> increase SA area to vol ratio–>diffusion made easier

127
Q

Differences between specific and non-specific defences?

A

Non-specific responses respond in the same way to all infections, have no ‘memory’ about prior infections and the level of response same for each infection of same organism.
Specific defences react in a specific way to each infection, have a ‘memory’ about prior infections and there is a much greater response on a second infection by the same organism.

128
Q

What is the role of the lymphatic system in defence?

A

Continuous movement of fluid through tissues and back into lymphatic and circulatory systems provide means for the immune system to routinely screen body for foreign materials

129
Q

Primary lymphoid organs

A
  • Bone marrow and thymus

* Produce new lymphocytes

130
Q

Secondary lymphoid organs

A
  • lymph nodes,
  • spleen,
  • tonsils,
  • adenoids
  • appendix
  • Where immune responses occur.
131
Q

What happens when a phagocyte engulfs a pathogen?

A
  • When a phagocyte ingests an invader, it travels to nearest lymph node to present information about captured antigen (antigen presentation: when phagocyte displays an antigen fragment from an invader on its own surface)
  • when receptor of helper T cells recognises the antigen fragment, T cell is activated –> produces proteins (cytokines) that activate B, T and other immune cells
132
Q

Incubation period

A
  • Incubation period is generally between one to three days.
  • Patients usually present with fever, headache, muscle ache, blocked or runny nose, sore-throat, cough and tiredness, etc.
133
Q

What happens when a macrophage encounters a bacterium?

A
  • Macrophage recognizes bacterium as non-self
  • Macrophage envelopes bacterium with its cell membrane
  • Vacuole forms around bacterium
  • Lysosomes fuse with vacuole
  • Powerful enzymes digest bacterium
134
Q

What is an antibody?

A
  • A SPECIFIC protein produced by lymphocytes in response to a SPECIFIC antigen, with which it binds.
  • Large globular glycoproteins (immunoglobulins) produced by lymphocytes and released into bloodstream
135
Q

Structure of antibody

A

Y-shaped, with two identical antigen-binding sites

136
Q

Antivenom

A
  • Antivenoms contain antibodies that act specifically against the snake venom.
  • These are produced by rabbits or horses that have been injected with the venom.
137
Q

Why aren’t the rabbits/horses that the venom is injected into, killed?

A
  • Initial dose is so small that rabbits survive and are able to produce antivenom
  • A slightly higher dose of venom is then injected into rabbits which respond by producing higher level of antivenom
138
Q

Endemic

A

A disease that exists permanently in a particular region or population. Malaria is a constant worry in parts of Africa.

139
Q

Epidemic

A

An outbreak of disease that attacks many people at about the same time and may spread through one or several communities.

140
Q

Pandemic

A

When an epidemic spreads throughout the world.

141
Q

How is rhesus incompatibility prevented?

A

Through providing the mother with anti-Rh antibodies so that she uses passive immunity.

142
Q

Placenta

A
  • Placenta acts as a selective barrier against most antibodies, only allowing some to cross.
  • An antibody blocking factor is also present in the maternal serum
143
Q

Autoimmune disease

A

A condition whereby the immune system attacks tissues belonging to the organism it is supposed to defend i.e. attacking of tissues with self molecules or MHC markers

144
Q

Immunodeficiency disease

A

A disease resulting in the failure of one or both branches of the immune system; may be genetic or acquired.

145
Q

Hypersensitivity

A

Caused by excess immune activity

146
Q

Type II Hypersensitivity

A

*Seen in blood transfusion recipients e.g. ABO incompatibility – IgM antibodies cause lysis of red blood cells, Rhesus incompatibility, IgG antibodies cause destruction of foetal blood

147
Q

Examples of autoimmune disease?

A
  • Insulin-Dependent Diabetes (Type 1)
  • Rheumatoid arthritis
  • Multiple Sclerosis
148
Q

Primary immunodeficiency

A
  • congenital (child born with deficiency, due to genetic defect or developmental abnormality)
  • DiGeorge syndrome
  • Thymus fails to develop–> no T cells
  • ‘bubble babies’
  • no B or T cells
149
Q

Secondary immunodeficiency

A
  • as a result of severe stress or another disease

* AIDs (Acquired Immuno Deficiency Syndrome)

150
Q

AIDS

A
  • resulting from infection with HIV (human immunodeficiency virus)
  • virus is present in body fluids of infected individuals, transmission from one person to another is almost always from body fluids of one person into bloodstream of another
151
Q

Persistent inflammation

A
  • When inflammation persists, surrounding healthy tissues can also become damaged
  • Inappropriate persistence of inflammatory response contributes to a number of diverse disease conditions (heart disease, rheumatoid arthritis, severe asthma)
152
Q

Two main pathways for initiation of apoptosis?

A
  • mitochondrial pathway and death receptor pathways
  • Signals from outside cell- death receptor pathway (Extrinsic pathway)
  • Mitochondrial Pathway (Intrinsic pathway)
153
Q

General process of apoptosis?

A

Cell receives a ‘death’ signal
Cells activate caspase enzymes and send a signal to attract phagocytes to the area
Cells starts to shrink and develop small bumbs (blebs) on their surface
Caspases enter nucleus and break down the DNA and proteins inside, mitochondria also break down
Cell fragments into apoptotic bodies
Phagocyte digests cell fragments (apoptotic bodies)

154
Q

When is apoptosis initiated?

A

Cell are no longer required (eg cells between fingers and toes in developing foetus)
Cells haven’t fully developed (eg embryonic brain cells)
There are too many cells (eg overproduction of immune cells, eg Bplasma)
Damaged or old cells
To get rid of autoreactive lymphocytes- such as B cells that produce autoantibodies

155
Q

Aim of apoptosis in diseases?

A

*to remove unwanted immature B lymphocytes- those that produce autoantibodies *
*to remove unwanted T cells and B cells (such as B plasma cells) once they have fought infection, so that swollen lymph nodes return to original size
Note: These are examples of the extrinsic pathway
*Can lead to autoimmune diseases if apoptosis does not occur

156
Q

Too much apoptosis?

A

neurodegenerative diseases such as Alzheimer and Huntington’s diseases

157
Q

Too little apoptosis?

A

production of cancer and autoimmune diseases

158
Q

What is an opportunistic infection?

A

Infection occurring when normal defences are compromised in some way, such as following disruption to natural flora of body or reduced responsiveness of immune system as in AIDS.
(as AIDS patients or transplant patients receiving immunosuppressive drugs)

159
Q

Outline one way in which antivenoms are made?

A

A small ‘dose’ of the infective agent or venom is injected into an animal, such as a rabbit. Because the dose is small, it does not kill the rabbit but stimulates the production of antibodies against the infective agent. The animal is given a series of such injections, with each successive dose being higher than the previous dose. This means the animal produces higher and higher levels of antibodies able to act against the specific disease. These antibodies are extracted from the blood of the animal at regular intervals and incorporated into vaccines.

160
Q

Explain why a person suffering from an allergy may be treated with an antihistamine.

A

During an allergic response, mast cells accumulate around blood vessels and release histamine when they rupture. Histamine causes contraction of smooth muscles; for example, the muscles around tubules into lungs can contract, making breathing difficult. Antihistamines react with and reduce the effect of histamines.

161
Q

Explain why some women are given an injection of immunoglobulin shortly after the birth of a baby.

A

If a Rhesus negative woman has a Rhesus positive baby, some of the baby’s Rh positive cells may cross the placenta into the mother’s bloodstream. If this occurs, the mother produces Rh antibodies that may be fatal for a future pregnancy if the second baby is also Rhesus positive. Such a mother is given an injection of immunoglobulin, high in Rhesus antibodies after the birth of the first child. The Rh antibodies in the immunoglobulin react with any Rhesus positive cells that have entered the mother from the first baby. These cells are destroyed and so the mother’s immune system fails to be activated to produce Rhesus antibodies.

162
Q

A baby is born with a defective thymus. Comment on the baby’s ability to resist infection — immediately after birth and at six months of age.

A

During pregnancy, maternal antibodies pass across the placenta into the developing baby. Hence, at birth, a baby possesses a range of antibodies similar to those found in the mother. Also, the baby obtains more of these antibodies for as long as it is breast fed. These antibodies give the baby protection against infection by some organisms. However, when breastfeeding ceases (say, at six months), this source of protection is lost. In a baby with a defective thymus, it is likely that T cells are unable to mature. The lack of T cells makes the baby increasingly susceptible to infection as the level of maternal antibodies reduces to zero.

163
Q

Explain why it has been difficult to develop drugs against viruses.

A

Viruses cause damage inside cells. Drugs that are capable of destroying virus particles would also destroy the cells that the viruses have invaded.
(Note: Recent advances include the development of drugs that prevent entry of virus particles into cells.)

164
Q

What are the differences between the structure of a virus, a viroid and a prion?

A

Prions are abnormal protein molecules that cause degenerative neurological diseases.
Viroids are short pieces of naked RNA, thought to act as pathogens in plants.
Viruses comprise a protein coat containing a nucleic acid: DNA in some viruses but RNA in others.

165
Q

Specialised structures found in some bacteria?

A
  • flagella — thin, whip-like appendages that enable a bacterium to move
  • spore — special reproductive structure resistant to heat and drying out
  • capsule — a layer of slimy gelatinous material outside the cell wall of a bacterium.
166
Q

What is the difference between broad-spectrum and narrow-spectrum antibiotics?

A

Broad-spectrum antibiotics act against a wide range of disease-causing organisms. Narrow-spectrum antibiotics act against a limited variety.

167
Q

Why do people with HIV develop opportunistic infections?

A

HIV Virus particles target T helper cells
and
These cells are responsible for presenting antigens to immature B cells which proliferate into
many antibody producing plasma cells and a few memory cells. Killing of the T helper cells
prevents a person from producing antibodies leaving them vulnerable to infection.

168
Q

Why aren’t attenuated viruses used to innoculate people against HIV?

A

It is too dangerous to produce live vaccines for HIV as viruses frequently mutate and it is
possible that an attenuated virus would mutate into a virulent form.

169
Q

What is the link between proteomics and rational drug design?

A

Proteomics is the study of the proteins and the proteome.
Rational drug design is an outcome of proteomics. The premise behind rational drug design
is that if the shape of an antigen such as neuraminidase is known then a drug with a
complementary shape and charge can be produced which will bind to and inhibit the antigen.

170
Q

Why can a hypersensitivity reaction not occur unless an individual is sensitized to an allergen?

A

A hypersensitivity reaction cannot occur unless a B cell has previously encountered an
allergen and produced antibodies against it.

171
Q

What does type II hypersensitivity include?

A 
ABO Incompatibility (Rhesus incompatibility) 
and Autoimmune disease
172
Q

During its cycle in a cell the virus undergoes many changes in its genetic material. This has made treatment very difficult. Currently a mixture of drugs which target different stages of the viral cycle are used.
Why has this treatment been more successful than treatment with only one drug?

A

Viruses continually mutate in random ways, and increasing the number of drugs used increases the chance that one of the drugs may be able to inhibit the action caused by a random change.

173
Q

In what way is apoptosis significant in the formation of a tumour?

A

Apoptosis is programmed cell death. In the formation of a tumour, apoptosis is occurring at a slower rate than the reproduction of new cells, hence a tumour forms.

174
Q

What happens in terms of cytotoxic T cells and B cells in autoimmune diseases?

A

Cytotoxic T cells recognise self markers as foreign and attack self cells. B plasma cells produce autoantibodies that attach to self antigens. (the body usually attacks these autoantibodies through apoptosis, but if it doesn’t happen, then it results in autoimmune disease. )

175
Q

How do bacterial cells transfer plasmids with an antibiotic resistance gene to one another?

A

Through a conjugation tube (sometimes pillus is used)

176
Q

What is meant by a designed drug?

A

A drug that has been man made to prevent the action of a particular infective agent and hence prevents the development of the particular disease.

Biology 3/4 (7 decks)

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