Mod 4: Communicable diseases Flashcards

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1
Q

Vectors

A

Vectors carry pathogens from one organism to another, eg water and insects

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2
Q

Two ways that bacteria can be classified

A

Two ways that bacteria can be classified:
-By their basic shapes - rod shaped (bacilli), spherical (cocci), comma shaped (vibrios), spiralled (spirilla) and corkscrew (spirochaetes)
-By their cell walls - two main types that react differently with Gram staining

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3
Q

Gram staining cell walls of bacteria

A

Gram staining cell walls of bacteria:
-Gram positive bacteria look purple-blue under the light microscope eg MRSA
-Gram negative bacteria appear red - eg E.coli

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4
Q

Why is identifiying cell walls of bacteria with gram staining useful?

A

Gram staining is useful because the type of cell wall affects how bacteria react to different antibiotics

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5
Q

What are antibiotics?

A

Antiobiotics = a compound that kills or inhibits the growth of bacteria

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6
Q

Features of viruses

A

Viruses:
-About 0.02-0.3 micrometers in diameter (50 times smaller than average bacterium)
-Invade living cells where genetic material of virus takes over the biochemistry of the host to cell to make more viruses
-Reproduce rapidly
-Evolve by developing adaptations to the host
-Considered by scientists to be the ultimate parasites

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7
Q

Viruses that attack bacteria

A

Viruses that attack bacteria are called bacteriophages :
-They take over the bacterial cells and use them to replicate, destroying the bacteria at the same time
-Now used to identify and treat some disease, and are important in scientific research

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8
Q

Protoctist/Protista features

A

Protoctist/Protista features:
-Small percentage act as pathogens
-Protists which cause disease are parasitic (they use people or animals as their host organism)
-Pathogenic protists may need a vector to transfer them to their hosts eg malaria or may enter body directly through polluted water eg giardia

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9
Q

Fungi features

A

Fungi:
-Eukaryotic organisms often multicellular (Excluding yeast)
-Cannot photosynthesis
-Digest their food extracellularly before absorbing nutrients
-Many are saprophytes (feed on decaying matter) but some are parasitic (feed on living plants and animals) -> these are the pathogenic fungi that cause communicable diseases
-When fungi reproduce they produce millions of tiny spores that spread huge distances meaning they spread fast

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10
Q

Ways that viruses damage the host tissue directly

A

Ways that viruses damage the host tissue directly:
-Viruses - take over the cell metabolism - viral genetic material gets into the host cell and is inserted into the host DNA - virus then uses host cell to make new viruses which then burst out the cell, destroying it and then spread to infect other cells

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11
Q

Ways that protoctista damage the host tissue directly

A

Ways that protoctista damage the host tissue directly:
-Take over cells and break them open as the new generation emerge, but htey do not take over the genetic material of the cell - they simply digest and use the cell contents as they reproduce - malaria is an example of this

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12
Q

How fungi damages host tissue directly

A

How fungi damages host tissue directly:
-Fungi digest living cells and destroy them -> this combined with the response of the body to the damage caused by the fungus gives the symptoms of disease

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13
Q

Producing toxins which damage host tissues

A

-Most bacteria produce toxins that poison or damage the host cells in some way, causing disease -> some bacterial toxins damage the host cells by breaking down the cell membranes, some damage or inactivate enzymes and some interfere with the host cell genetic material so that the cells cannot divide
-Some fungi produce toxins which affect host cells and cause disease

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14
Q

Process of a virus destroying a bacterial cell (bacteriophage)

A

Process of a virus destroying a bacterial cell (bacteriophage) :
1). Attachment of virus to host cell
2). Insertion of viral nucleic acid
3). Replication of viral nucleic acid
4). Synthesis of viral protein
5). Assembly of virus particles
6). Lysis of host cells

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15
Q

Bacterial shapes

A

Bacterial shapes (which they can be classified by):
Their basic shapes - rod shaped (bacilli), spherical (cocci), comma shaped (vibrios), spiralled (spirilla) and corkscrew (spirochaetes)

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16
Q

Ring rot in plants cause

A

Ring rot in plants:
-Bacterial disease of potatoes, tomatoes and aubergines caused by the Gram positive bacterium (clavibacter michiganensis)

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17
Q

Effect of ring rot in plants

A

Effect of ring rot in plants:
-Damages leaves, tubers and fruit - can destroy up to 80% of the crop and there is no cure
-Once bacterial ring rot infects a field it cannot be used to grow potatoes again for at least two years

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18
Q

Cause of tobacco mosaic virus (TMV) in plants

A

Cause of tobacco mosaic virus in plants (TMV):
-Virus that infects tobacco plants and 150 other plant species

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19
Q

Effect of TMV on plants

A

Effect of TMV on plants:
-Damages leaves, flowers and fruit, stunting growth and reducing yields, and can lead to an almost total crop loss
-Resistant crop strains available but there is no cure

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20
Q

What causes potato blight ?

A

Cause of potato blight in plants:
-Caused by fungus-like protoctist oomycete (phytopathora infestans)

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21
Q

Effect of potato blight on plants

A

Effect of potato blight on plants:
-The hyphae penetrates host cells, destroying leaves, tubers and fruit causing lots of crop damage
-No cure, but resistant strains, careful management and chemical treatments can reduce infection risk

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22
Q

What is black sigatoka caused by?

A

Black sigatoka is caused by the fungus mycospharella fijiensis, which attacks and destroys the leaves
-Disease that affects bananas

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23
Q

Black sigatoka effect on banana plants

A

Effect of black sigatoka on banana plants:
-Hyphae penetrates and digests cells, turning the leaves lack
-If plants are infected, it can cause a 50% reduction in yield
-Resistant strains are being developed - good husbandry and fingicise treatment can control spread of disease but there is no cure

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24
Q

What is husbandry in agriculture?

A

Husbandry = the cultivation and production of edible crops or of animals for food

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25
Q

What is tubercolosis (TB) caused by?

A

TB is a bacterial disease of humans, cows, pigs, badgers and deers commonly caused by mycobacterium tuberculosis and M.bovis

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26
Q

Effect of tubercolosis (TB)

A

TB effect:
-Damages and destroys lung tissue and suppresses the immune system, so the body is less able to fight off other diseases
-People with HIV/AIDS are much more likely to develop TB
-TB is curable by antibiotics and preventable by improving living standards and vaccination

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27
Q

What is bacterial meningitis caused by?

A

Bacterial meningitis - a bacterial infection (commonly streptococcus pneumoniae or neisseria menigitidis) on the meninges of the brain, which can spread into the rest of the body causing septicaemia (blood poisioning) + rapid death

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28
Q

What are the meninges of the brain?

A

The meninges of the brain are protective membranes on the surface of the brain

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29
Q

Effect of bacterial meningitis

A

Bacterial meningitis effect:
-Mainly effects young children and teens
-Blotchy red/purple rash that does not dissapear when a glass is pressed against it
-Up to 25% of people who recover have some permanent damage
-Antibiotics cure the disease if early, and vaccines can protec against some forms of bacterial meningitis

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30
Q

What is HIV/AIDS caused by? (acquired immunodeficiency syndrome)

A

-Caused by HIV (human immunodeficiency virus) - targets T cells in immune system - gradually destroys immune system to people are more prone to secondary infections
-Virus is passed on in bodily fluids, most commonly through unprotected sex, shared needs, contaminated blood products and from mothers to babies during pregnancy, birth or breast feeding

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31
Q

Process of HIV infection

A

HIV:
-Retrovirus with RNA as its genetic material
-Contains enzyme reverse transcriptase, which transcribes the RNA to a single strand of DNA to produce a single strand of DNA in the host cell
-This DNA interacts with the genetic material of the hose cell

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32
Q

Effect of HIV/AIDS

A

HIV/AIDS effect:
-Weakens the immune system
-No vaccine or cure, but treated with anti-retrovrial drugs

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33
Q

Cause of influenza/flu

A

Cause of influenza:
-Viral infection (orthomyxoviridae spp.) of the ciliated epithelial cells in the gas exchange system - kills them and leaves the airways open to secondary infection
-Three main strains (A, B and C)
-Flu viruses mutate regularly
-Major changes in surface antigens heralds a flu epidemic/pandemic as no antibodies available

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34
Q

Effect of influenza/flu

A

Influenza effect:
-Can be fatal, young children, old people and people with chronic illness are most vulnerable -> mostly from the secondary infections

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35
Q

Strain A of influenza

A

Strain A viruses - most virulent - classified further by proteins on their surfaces eg A (H1N1) and A (H3N3)

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36
Q

Cause of malaria

A

Cause of malaria:
-Caused by the protoctista plasmodium and spread by bites of infected anopheles mosquitoes
-Plasmodium parasites has complex life cycle - two hosts - mosquito and people
-Female mosquito takes two blood meals to provide her with proteins before laying her eggs - which is when plasmodium is passed onto people, which invades rbc, livers and brain

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37
Q

Effect of malaria

A

Effect of malaria:
-Diseases recurs, making people weak and vulnerable to other infections
-No vaccine against malaria and limited cures, but can be prevented by controlling the vectors
-> eg insectidies to destroy the mosquitos, mosquito nets, window and door screens, long sleeved clothing, etc

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38
Q

What is ring worm caused by in mammals?

A

Ring worm is a fungal disease affecting mammals inclugin cattle,d ogs, cats and humans
-Different fungi infect different species
-In cattle -> trichophyton verrucosum

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39
Q

Effect of ring worm in mammals?

A

Ring worm effect:
-Causes grey-white, crusty, infectiours, circular areas of skin
-Itchy but not damaging
-Treated with antifungal creams

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40
Q

What is athlete’s foot caused by?

A

Athlete’s foot is caused by a human fungal disease caused by tinia pedia

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41
Q

Effect of athlete’s foot

A

Athlete’s foot effect;
-Form of human ring worm that grows on and digests the warm, moist skin between the twos
-Causes cracking and scaling, which is itchy and may become sore
-Treated with antifungal creams

42
Q

Direct methods of disease transmission between animals

A

Direct methods of disease transmission between animals:
-Direct contact
-Inoculation
-Ingestion

43
Q

Examples of direct contact of disease transmission between animals

A

Examples of direct contact of disease transmission between animals:
-Kissing/exchange of bodily fluids (eg bacterial meningitis, STI’s
-Direct skin to skin contact (eg ring worm and athlete’s foot)
-Microorganisms from faeces transmitted on the hands (eg diarrhoeal diseases

44
Q

Examples of inoculation as a way to transmit disease between animals

A

Examples of inoculation as a way to transmit disease between animals:
-Through a break in the skin (eg during sex, HIV/AIDS)
-From an animal bite (eg rabies)
-Through a puncture wound or through sharing needs (eg septicaemia)

45
Q

Examples of ingestion as a way to transmit disease between animals

A

Examples of ingestion as a way to transmit disease between animals:
-Taking in contaminated food or drink
-Transferring pathogens to the mouth from the hands (amoebic dysentry, diarrhoeal diseases)

46
Q

Indirect methods of disease transmission between animals

A

Indirect methods of disease transmission between animals:
-Fomites
-Droplet infection/inhalation
-Vectors

47
Q

Fomites as an indirect method of disease transmission between animals

A

Fomites as an indirect method of disease transmission between animals:
-Inanimate objects such as bedding, socks or cosmetics can transfer pathogens (eg athletes foot, gas gangrene and staphylococcus infections)

48
Q

Droplet infection/inhalation as an indirect method of disease transmission between animals

A

Droplet infection/inhalation as an indirect method of disease transmission between animals:
-Minute droplets of saliva and mucus are expelled from your mouth as you talk, cough or sneeze (eg influenza and tuberculosis)

49
Q

Vectors an indirect method of disease transmission between animals

A

Vectors an indirect method of disease transmission between animals:
-Transmits communicable pathogens from one host to another
-Often, but not always animals - eg malaria
-Water can act as a vector - eg diarrhoeal diseases

50
Q

Factors affecting transmission of disease

A

Factors affecting transmission of disease:
-Overcrowded living and working conditions
-Poor nutrition
-Compromised immune system
-Poor disposal of waste
-Climate change (introduces new vectors and diseases)
-Culture and infrastructure
-Socioeconomic factors

51
Q

Direct transmission of disease between plants

A

Direct transmission between plants:
-Involves the direct contact of a healthy plant with any part of a disease plant
-Eg: ring rot, TMV, tomato and potato blight and black sigatoka

52
Q

Indirect transmission of disease between plants

A

Indirect transmission of disease between plants:
-Soil contamination
-Vectors (eg wind, water, animals and humans)

53
Q

Soil contamination as an indirect method of disease transmission between plants

A

Soil contamination as an indirect method of disease transmission between plants:
-Infected plants leaving pathogens (bacteria or viruses) or reproductive spores (protoctista or fungi) in the soil -> infects the next crop -> eg black sigatoka spores, ring rot bacteria, spores of P.infestans and TMV

54
Q

Wind as a vector for plant transmission between plants

A

Wind as a vector for plant transmission between plants:
-Bacteria, virus and fungal or oomycete spores may be carried in the wind
-Eg black sigatoka blown between carribean islands

55
Q

Water as a vector that carries diseases between plants

A

Water as a vector that carries diseases between plants:
-Spores swim in the surface film of water on leaves
-Raindrop splashes carry pathogens and spores etc

56
Q

Animals as a vector that transmits disease between plants

A

Animals as a vector that transmits disease between plants:
-Insects and bires carry pathogens and spores from one plant to another as they feed
-Insects such as aphids inoculate pathogens directly into plant tissues

57
Q

Humans as a vector that transmits diseases between plants

A

Humans as a vector that transmits diseases between plants:
-Pathogens and spores are transmitted by hands, clothing, fomites, farming practices and by transporting plants and crops around the world eg TMV survives for years in tobacco products

58
Q

Factors affecting the transmission of communicable diseases in plants

A

Factors affecting the transmission of communicable diseases in plants:
-Planting varieties of crops that are susceptible to disease
-Overcrowding increases the likelihood of contact
-Poor mineral nutrition reduces resistance of plants
-Damp, warm conditions increase the survival and spread of pathogens and spores
-Climate change - increased rainfall and wind promote the spread of diseases; changing conditions allow animal vectors to spread to new areas; drier conditions may reduce the spread of disease

59
Q

How do plants recognise an attack from pathogens?

A

Plants recognising an attack from pathogens:
-Receptors in cells respond to molecules from pathogens
-This stimulates the release of signalling molecules that appear to switch on genes in the nucleus
-This triggers cellular responses

60
Q

Cellular responses from plants when being attacked by pathogens

A

Cellular responses from plants when being attacked by pathogens:
-Producing defensive chemicals
-Sending alarm signals to unaffected cells to trigger their defences
-Physically strengthening the cell walls

61
Q

Callose

A

Callose:
-Polysaccharide which contains beta 1,3 linkages and beta 1,6 linkages between the glucose monomers

62
Q

How does callose act as a physical defence for plants against invading pathogens?

A

How does callose act as a physical defence for plants against invading pathogens:
-Callose synthesised and deposited between cell walls and cell membranes in cells next to infected cells -> acts as barriers to prevent pathogens entering plant cells
-Continuosly depostited in cell walls -> lignin added to make mechanical barrier thicker and stronger
-Callose blocks sieve plants in phloem, sealing off the infected part and preventing the spread of pathogens
-Callose is deposited in the plasmodesmata between infected cells and their neighbours, sealing them off from the healthy cells and helping to prevent the pathogen spreading

63
Q

Examples of plant defensive chemicals

A

Examples of plant defensive chemicals:
-Insect repellants eg pine resin
-Insecticides eg caffeine which is toxic to insects and funi
-Antibacterial compounds including antibiotics eg lysosomes which release enzymes that break down bacterial cell walls
-Antifungal compounds eg chitinases which break down chitin in fungal cell walls
-Anti-oomycetes - eg glucanases that break down glucans
-General toxins - can be broken down into cyanide which is toxic to most living things

64
Q

Barriers found within the body which blocks pathogens from entering

A

Barriers found within the body which blocks pathogens from entering:
-Skin covers the body and prevents entry of pathogens - it has a skin flora of healthy microorganisms that out compete pathogens for space on the body surface - skin also produces sebum, an oily substance that inhibits the growth of pathogens
-Many of body tracts including airways are lined with mucous membranes that secret mucus - traps micoorganisms and contains lysozymes which destroy bacterial and fungal cell walls, mucus also contains phagocytes
-Lysozymes in tears and urine, and the acid in stomach prevents pathogen entry also

65
Q

Expulsive reflexes of the body to remove pathogens

A

Expulsive reflexes of the body to remove pathogens:
-Coughs and sneezes eject pathogen-laden mucus from the gas exchange system, while vomiting and diarrhoea expel the contents of the gut along with any infective pathogens

66
Q

Blood clotting and wound repair

A

Blood clotting and wound repair:
-Platelets come into contact with collage in skin or wall of damaged vessel, adhere and secrete substances, most importantly:
~Thrombloplastin
~Serotonin

67
Q

Thromboplastin

A

Thromboplastin: an enzyme that triggers a cascade of reactions resulting in the formation of a blood clot

68
Q

Serotonin role on wound repair

A

Serotonin:
Makes the smooth muscle in the walls of the blood vessels contract, so they narrow and reduce the supply of blood to the area

69
Q

Stages of wound repair

A

Stages of wound repair:
-Blood clot dries out, forming hard tough scab that keeps pathogens out
-Epidermal cells below the stab start to grow, sealing the wound permanetly while damaged blood vessels regrow
-Collagen fibres are deposited to give the new tissue strength
-One the new epidermis reaches normal thickness, the scab sloughs off and the wound is healed

70
Q

Inflammatory response

A

Inflammatory response is a localised response to pathogens (or damage or irritants) resulting in inflammation at the sit of the found
-Characterised by pain, heat, redness and swelling of tissue
-Most cells are activated in damaged tissue and release chemicals called histamines and cytokines

71
Q

Histamines (involved in the inflammatory response)

A

Histamines:
-Histamines make the blood vessels dilate, causing localised heat and redness. The raised temperature helps prevent pathogens reproducing
-Histamines make blood vessel walls more leaky so blood plasma is forced out, once forced out of the blood it is known as tissue fluid. Tissue fluid causes swelling (oedema) and pain

72
Q

Cytokines involvement in the inflammatory response

A

Cytokines:
-Cytokines attract white blood cells (phagocytes) to the site. They dispose of pathogens by phagocytosis

73
Q

Why is fevers/increasing body temperature from 37 degree celcius a useful adaptation?

A

Fevers:
-Most pathogens reproduce best at or below 37 degree celcius - higher temps inhibit pathogen reproduction
-The specific immune system works faster at higher temperature

74
Q

Phagocytes

A

Phagocytes are specialised white cells that engulf and destroy pathogens. There are two main types of phagocytes - neutrophils and macrophages

75
Q

Two main types of phagocytes

A

There are two main types of phagocytes - neutrophils and macrophages

76
Q

Stages of phagocytosis

A

Stages of phagocytosis:
1). Pathogens produce chemicals that attract phagocytes
2).Phagocytes recognise non-human proteins on the pathogen. This is a response not to a specific type of pathogen, but simply a cell or organism that is non-self
3). The phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome
4). The phagosome combines with a lysosome to form a phagolysosome
5). Enzymes from the lysosome digest and destroy the pathogen

77
Q

Macrophages

A

-Type of phagocyte
-Complex long process
-When a macrophage has digested a pathogen, it combines with antigens from the pathogen surface membrane with special glycoproteins in the cytoplasm called the major histompatibility complex (MHC) - the MHC complex moves these pathogen antigens to the macrophage’s own surface membrane, becoming an antigen-presenting cell (APC). These antigens now stimulate other cells involved in the specific immune system response

78
Q

Major histocompatibility complex (MHC)

A

Major histocompatibility complex (MHC): glycoproteins found in the cytoplasm of macrophages, which moves pathogen antigens to the macrophage’s own surface membrane

79
Q

What does a macrophages become when the MHC has moved the pathogen antigens onto its own surface membrane?

A

Macrophages become an antigen-presenting cell (APC) once the pathogen antigen has been moved by the MHC onto it’s own surface membrane

80
Q

Why are blood smears stained when observed under the microscope to count blood cells?

A

Blood smears are stained to show up the nuclei of the lymphocytes, making them easier to identify
-Identifying the numbers of different types of lymphocytes in a blood smear indicates if a non-specific or specific immune response is taking place

81
Q

Function of cytokines

A

Cytokines act as cell-signalling molecules, informing other phagocytes that the body is under attack and stimulating them to move to the site of infection or inflammation
-Cytokines can also increase body temperature and stimulate the specific immune system

82
Q

Function of opsonins

A

Opsonins are chemicals that bind to pathogens and tag them so they can be more easily recognised by phagocytes - phagocytes have receptors on the cell membranes that bind to common opsonins, and the phagocytes then engulfs the pathogen
-There are a number of different opsonins, but antibodies such as immunoglobulin G (IgG) and immunoglobulin M (IgM) have the strongest effect

83
Q

What are antibodies?

A

Antibodies are Y-shaped glycoproteins called immunoglobulins - binds to a specific antigen on the pathogen or toxin that has triggered the immune response

84
Q

What are antibodies made up from?

A

Antibodies are made up of two identical long polypeptide chains called the heavy chains, and two much shorter identical chains called the light chains
-Chains are held together by disulfide bridges and there are also disulfide bridges within the polypeptide chains holding them in shape

85
Q

Antibody function

A

Antibodies bind to antigens with a protein-based ‘locka nd key’ mechanism -> binding site is an area of 110 amino acids on both the heacy and the light chains, known as the variable region -> it is a different shape on each antibody and gives the antibody its specificity -> rest of the antibody molecule is always the same, so it is called the constant region

86
Q

Antigen-antibody complex

A

Antigen-antibody complex:
-When an antibody binds to an antigen it forms an antigen-antibody complex
-The hinge region of the antibody proved the molecule with flexibility, allowing it to bind two separate antigens, one at each of its antigen-binding sites

87
Q

Hinge region of an antibody

A

-The hinge region of the antibody proved the molecule with flexibility, allowing it to bind two separate antigens, one at each of its antigen-binding sites

88
Q

How do antibodies defend the body?

A

Antibodies defending the body:
1). The antibody of the antigen-antibody complex acts as an opsonin so the complex is easily engulfed and digested phagocytes
2). Most pathogens can no longer effectively invade the host cells once they are part of an antigen-antibody complex
3). Antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together. This prevents them spreading through the body and makes it easier for phagocytes to engulf a number of pathogens at the same time

89
Q

Where do B lymphocytes mature?

A

B lymphocytes mature in the bone marrow

90
Q

Where do T lymphocytes mature

A

T lymphocytes mature in the thymus gland

91
Q

Main types of T lymphocytes

A

Main types of T lymphocytes:
-T helper cells
-T killer cells
-T memory cells
-T regulator cells

92
Q

T helper cells

A

T helper cells:
-Has CD4 receptors on their cell surface membranes, which bind to the surface antigens on APCs
-They produce interleukins -> Stimulates the activity of B cells -> increases antibody production -> stimulates production of other types of T cells and attracts and stimulates macrophages to ingest pathogens with antigen-anitbody complexes

93
Q

Interleukins

A

Interleukins:
-Type of cytokine (cell-signalling molecule)
-Made by the T helper cells
-Stimulates the activity of B cells -> increases antibody production -> stimulates production of other types of T cells and attracts and stimulates macrophages to ingest pathogens with antigen-anitbody complexes

94
Q

T killer cells

A

T killer cells:
-Destroyes the pathogen carrying the antigen
-Produces a chemical called perforin which kills the pathogen by making holes in the cell membrane so it is freely permeable

95
Q

Perforin

A

Perforin:
-Chemical produced by T killer cells
-Kills pathogens by making holes in the cell membrane so it is freely permeable

96
Q

T memory cells

A

T memory cells:
-Live for a long time
-Part of the immunological memory
-If they meet an antigen the second time, they divide rapidly to form a huge number of clones of T killer cells that destroy the pathogen

97
Q

T regulator cells

A

T regulator cells:
-Suppress the immune system, acting to control and regulate it
-Stops the immune response once a pathogen has been eliminated
-Makes sure the body recognizes self antigens and does not set up an autoimmune response
-Interleukins are important in this control

98
Q

Main types of B lymphocytes

A

Main types of B lymphocytes:
-Plasma cells
-B effector cells
-B memory cells

99
Q

Plasma cells

A

Plasma cells - these produce antibodies to a particular antigen and release them into the circulation
-An active plasma cell only lives for a few days but produces around 2000 antibodies per second while it is alive and active

100
Q

B effector cells

A

B effector cells - these divide to form the plasma cell clones

101
Q

B memory cells

A

B memory cells - these live for a very long time and provide the immunological memory
-They are programmed to remember a specific antigen and enable the body to make a very rapid response when a pathogen carrying that antigen is encountered again