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Biology Year 1 > 4.1.1- Communicable diseases, Prevention and Immune system > Flashcards

4.1.1- Communicable diseases, Prevention and Immune system Flashcards

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1
Q

what are the 4 different types pathogens that can cause communicable diseases?

A
  • bacteria
  • viruses
  • protoctista
  • funghi
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2
Q

what are communicable diseases?

A

a disease that is caused by a pathogen and transmitted directly between organisms.

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3
Q

what are bacteria?

A

Prokaryotic cells that have cell walls but lack organelles. Some bacteria are
pathogenic, producing toxins that damage host cells, or they can remain within body cavities/spaces

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4
Q

what is a virus?

A

Non-living infectious agents that invade host cells and take over cell metabolism, replicating within them, hijacking their machinery to replicate genetic material and proteins.
They do not have a cellular structure, so they can’t respire, produce ATP or replicate genetic material

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5
Q

what is a protoctista?

A

A group of unicelllar eukaryotic, single-celled microorganisms that may cause disease.
They digest cells and use the cell contents to reproduce

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6
Q

what is funghi?

A

Eukaryotic, often multicellular organisms that may cause disease. They digest and destroy cells, and produce spores that can spread rapidly between organisms
they have a similar structure to plants, with cell walls and large vacuoles, but their bodies are made of filaments called hyphae.

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7
Q

what does hyphae do in plants?

A

hyphae form a network and spread throughout a host/soil

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8
Q

what are the two types of transmission of communicable pathogens?

A
  • direct

- indirect

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9
Q

what is direct transmission?

A

when the communicable pathogens are transmitted from one host to another host

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10
Q

what is indirect transmission?

A

when a second organism (vector) that is unaffected by the pathogen transfers it to a new host

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11
Q

what is a vector?

A

an organism that transports pathogens from one host to another, but is not harmed by the pathogen.

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12
Q

what is disease transmission?

A

the transfer of pathogens from an infected host to an uninfected host.

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13
Q

what are spores and how are they involved in transmission?

A
  • small reproductive structures that are released into the environment, and are produced through mitosis/meisosis
  • they are dispersed via wind/water, when they have reached a food source, they begin growing
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14
Q

what are the 8 factors that affect disease transmission?

A
  • overcrowding
  • poor nutrition
  • living conditions
  • mobile vector
  • climate change
  • culture/infrastructure
  • socioeconomic
  • low genetic diversity
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15
Q

what are 4 examples of plant pathogens?

A
  • ring rot (bacteria)
  • tobacco mosaic virus (virus)
  • potato/tomato late blight (protoctista)
  • black sigatoka in bananas (funghi)
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16
Q

what are 7 examples of animal pathogens?

A
  • tuberculosis (bacteria)
  • bacterial meningitis (bacteria)
  • HIV/AIDS (virus)
  • influenza (virus)
  • malaria (protoctista)
  • ring worm (funghi)
  • athletes foot (funghi)
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17
Q

what are the two types of passive defense do plants have against pathogens?

A
  • physical barrier

- chemicals

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18
Q

what is the role of chemical defences in plants?

A
  • they prevent pathogens from growing on plant surface by creating acidic conditions, or kill them
  • repel insect vectors for diseases away from plant
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19
Q

what is the role of physical barriers in defences of plants?

A

to reduce the spread of a pathogen

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20
Q

what are some examples of chemical defences in plants?

A
  • toxic compounds
  • enzyme inhibitors
  • receptor molecules
  • sticky resin in bark
  • compounds that encourage the growth of competing microorganisms
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21
Q

what are some examples of physical barriers for defences in plants?

A
  • reinforced cell wall (funghi and bacteria)
  • narrowing of the plasmodesmata
  • ingrowths into the xylem cell, creates wall made of callose, from cytoplasm growing into xylem
  • blockage of the phloem
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22
Q

explain the callose deposition as part of a physical defence in plants?

A
  • invasion of pathogens stimulates release of callose and lignin
  • callose= a polysaccharide, forms matrix shape
  • callose and lignin is deposited between cell surface membrane and wall, both acting as barriers/lignin is a mechanically stronger barrier
  • callose also fills sieve pores of phloem, so phloem sap cannot be transported
  • callose reduces size of channels that connect neighbouring plant cells, narrowing plasmodesmata
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23
Q

how do plants recognise a pathogen attack?

A
  • receptors in cells respond to pathogen/chemicals released when cell wall is attacked
  • receptors release phytoalexin chemicals, which disrupt pathogen metabolism and bacterial cell surface membranes, delay pathogen reproduction, and stimulate the release of chitinases
  • salicylic acid and ethelyne are also released as part of signalling molecules/cell signalling
  • cellular responses are triggered, producing defences and strengthening the cell wall.
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24
Q

what are the four methods of defence in animals?

A
  • physical, body tissue act as barriers, preventing the entry of pathogens
  • cellular, cells detect/signal presence of pathogens, secreting protective substances
  • chemical, secreted substances generate an inhospitable environment for the growth of pathogens, by trapping and bursting them, preventing entry
  • commensal organisms, harmless bacteria and funghi compete with pathogens for nutrients
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25
Q

what is the non specific immune system in animals?

A

the system doesn’t distinguish between different pathogens, so the same response is given each time to the same attacking pathogen.

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26
Q

what does the first/primary line of defence in animals do?

A

-prevents the entry of pathogens

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27
Q

what are the 4 defences in the primary line of defence?

A
  • skin, acts as a physical barrier to pathogens
  • mucous membranes, move bacteria/viruses out of body
  • expulsive reflexes, coughing and sneezing
  • chemical secretions
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28
Q

how does the skin act as a physical barrier?

A
  • outer layer= hard, dry, dead cells filled with keratin
  • there are secretions of sebum that contain fatty acids which have antimicrobial properties
  • evaporation of sweat from the skin leaves behind a salt residue
  • the lack of moisture, low pH and high salinity creates an inhospitable environment for the growth of microorganisms
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29
Q

how does a mucous membrane protect animals against pathogens?

A
  • line the gut, airways and reproductive system
  • membrane consists of epithelial cells, and mucus-secreting cells, mucus is sticky due to glycoproteins/carbohydrate chain
  • muscus can trap bacteria/viruses, thenmoved up and out of tubes by cilia
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30
Q

how do expulsive reflexes protect animals against pathogens?

A
  • when a pathogen irritates the lining of an airway it can trigger an expulsive reflex; a cough or sneeze, resulting in a sudden expulsion of air.
  • -his expelled air contains secretions from the respiratory tract along with the foreign particles that have entered
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31
Q

what are the two main chemical secretions that occur within animals to protect against pathogens?

A
  • lysozymes= antimicrobial enzymes that breakdown the cell wall of bacteria, found in body fluids such as blood, tears, sweat, and breast milk
  • hydrochloric acid= produced by the cells that line the stomach, creating a low pH inside the stomach, helping kill any bacteria that has been ingested alongside food, the cells of the gut secrete mucus to prevent being damaged by hydrochloric acid
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32
Q

what does the 2nd/secondary line of defence in non-specific immunity involve?

A

phagocytic cells and antimicrobial proteins responding to the invading pathogens

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33
Q

what are the 4 examples involved in the secondary line of defence in non-specific immunity?

A
  • blood clotting
  • inflammation
  • wound repair
  • phagocytosis
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34
Q

what does blood clotting involve?

A

-a break in mucous membrane/skin, causes release of molecules that trigger a chemical cascade, resulting in blood clotting

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35
Q

what does blood clotting do?

A
  • prevents excess blood loss
  • prevents the entry of pathogens
  • provides a barrier/scab for wound healing to occur
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36
Q

what does inflammation involve?

A
  • localised response to damage/irritation from pathogen
  • pain, warmness, redness and swelling of tissue
  • chemical signalling molecules/mast cells, resulting in migration of phagocytes into tissue and increased blood flow
  • histamines and cytokines
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37
Q

what does histamines do in terms of inflammation?

A
  • cause vasodilation, increasing blood flow
  • ‘leaky’ capillaries allow fluid to enter the tissues and creating swelling, with some plasma leaving the blood
  • phagocytes leave the blood and enter the tissue to engulf foreign particles
  • cells release cytokines
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38
Q

what does cytokines do in terms of inflammation?

A

-stimulate inflammation and immune response

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39
Q

what does wound repair involve?

A
  • occurs below the scab formed by blood clotting

- stem cells divide by mitosis to heal wound

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40
Q

what are the 6 steps to wound repair?

A
  • new blood vessels form
  • collagen is produced
  • granulation tissue forms to fill the wound, made from fibrin fibres
  • stem cells move over the new tissue and divide to produce epithelial cells
  • contractile cells cause wound contraction
  • unwanted cells die
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41
Q

what are phagocytes?

A

=white blood cells that are involved in the secondary, non-specific response to infection, and are responsible for removing dead cells and invasive microorganisms

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42
Q

what are the two types of phagocytes?

A
  • neutrophils

- macrophages/antigen-presenting cells.

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43
Q

what occurs during phagocytosis?

A
  • pathogen enters, it is recognised as foreign due to it’s antigens
  • neutrophils attach to foreign antigens
  • receptors on phagocytes bind to antibodies already attached to pathogen, helping attract the phagocyte to site of infection
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44
Q

what is phagocytosis?

A

the process of recognising and engulfing a pathogen?

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45
Q

what is the mode of action of neutrophils?

A
  • chemicals released by pathogens attract neutrophils to located site, neutrophils move towards pathogens
  • receptor proteins on neutrophils recognise antibodies and attach to them
  • neutrophil’s cell surface membrane extends around pathogen, engulfing and trapping it
  • digestive enzymes destroy pathogen, then neutrophil dies
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46
Q

what is the role of macrophages?

A

-stimulate immune system

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47
Q

how do macrophages stimulate an immune response?

A
  • break up invading pathogen
  • display it’s antigens on it’s surface, recognised as lymphocytes. (known as antigen-presenting cell)
  • this initiates an immune response
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48
Q

what does the specific immunity system involve?

A
  • the recognition of antigens, which have previously entered the body
  • this gives life long immunity
49
Q

what are the two types of lymphocytes involved in the specific response?

A

T and B, both with a large round nucleus

50
Q

where do B lymphocytes mature?

A

in the bone marrow, then released into the body

51
Q

what are the three types of B lymphocytes?

A
  • plasma cells
  • B-effector cells
  • B-memory cells
52
Q

what is the role of plasma cells?

A

produce antibodies for a specific antigen,, releasing it into blood

53
Q

how many antibodies do plasma cells produce per second?

A

2000/sec

54
Q

what is the role of B-effector cells?

A
  • binds to complementary antigen, engulfing and processing it, to become ATP.
  • then divides into plasma or B-memory cells through clonal expansion
55
Q

when are B-effector cells activated?

A

when in contact with with antigen from pathogen

56
Q

what do B-effector cells divide into?

A
  • plasma cells

- B-memory cells

57
Q

what is the role of B-memory cells?

A

programmed to remember specific antigen, so will move around body to identify it
once identified, they make rapid response by dividing into plasma cells and antibodies.

58
Q

what is the memory of B-memory cells called?

A

IMMUNOLOGICAL MEMORY

59
Q

what are the 4 types of T lymphocytes?

A
  • T-helper
  • T-killer
  • T-memory
  • T-regulator
60
Q

what is the role of T-helper cells?

A
  • bind to APC

- produce interleukins, which help B lymphocytes to activate and produce antibodies.

61
Q

what is the role of T-killer cells

A
  • destroy pathogens by producing perforin

- perforin creates holes in the cell membrane

62
Q

what is the role of T-memory cells?

A
  • patrol body for complimentary antigen

- rapidly divide to loads of killer cells, to kill the pathogen

63
Q

what is the role of T-regulator cells?

A
  • supress and control the immune system
  • stop immune response once pathogen is destroyed
  • makes sure that the body recognises all self-antigen, so autoimmune response does not happen
64
Q

what is clonal selection?

A

the identification of an antibody-producing cell with complementary receptors to the shape of a specific antigen

65
Q

what is clonal expansion?

A

the mass proliferation of specific antibody-producing cells

66
Q

what is an antigen?

A

any molecule that the body recognises as foreign/non-self

usually a protein/glycoprotein in or on the surface of a pathogen

67
Q

what is an antibody?

A

a Y-shaped glycoprotein/immunoglobulins, that bind to a specific antigen that has triggered an immune response.

68
Q

what does the structure of an antibody include (4 things)?

A
  • four polypeptide chains (2 heavy, 2 light), held together by disulfide bridges
  • a variable region, shape is complimentary to shape of antigen
  • a constant region, same in all antibodies
  • a hinge region
69
Q

what does the variable region allow the antibody to do?

A

gives them specificity, so antibody only attaches to correct antigen, so an antigen-antibody complex can be formed

70
Q

what does the constant region of an antibody allow?

A

enables antibodies to bind to phagocytes and helps in the process of phagocytosis

71
Q

what does the hinge region of an antibody allow?

A

-a certain degree of flexibility to allow branches of Y-shaped molecule to move further apart to allow attachment to more than one antigen.

72
Q

what are the 4 parts of the mode of action of antibodies?

A
  • constant region binds to receptor on surface, making it easier to ingest pathogen, acting as a link.
  • agglutination= sticking together of bacteria to prevent spread
  • neutralisation= attach to antigen, preventing pathogen from binding to host cell
  • antibodies also bind to toxins released by pathogens, prevent entry to cell, also neutralised to become harmless
73
Q

what is natural active immunity?

A

immune response due to infection by a pathogen

74
Q

what is immunity?

A

to be resistant to a particular infection/toxin, owing to the presence of specific antibodies.

75
Q

what is natural passive immunity?

A

involves antibodies being passed naturally to an individual for temporary protection

76
Q

what is artificial active immunity?

A

immune response, antibodies are made due to receiving antigens in vaccination, artificial primary response

77
Q

what is artificial passive immunity?

A

involves injection of antibodies into individual for temporary protection

78
Q

what are examples of natural immunity?

A
  • active=becoming immune to an illness after contracting it a first time
  • passive=from mother to foetus across placenta, or to baby through breast milk
79
Q

what are examples of artificial immunity?

A
  • active= vaccine

- passive= tetanus injection

80
Q

what are vaccinations?

A

an artificial active immunity/deliberate exposure to antigenic material that stimulates the body to make it’s own antibodies to the antigen for a specific pathogen.

81
Q

what is an autoimmune disease?

A

a condition in which the immune system attacks and destroys healthy body tissue, because it stops recognising ‘self’ cells

82
Q

what can autoimmune diseases cause?

A

results in chronic inflammation or the breakdown/destruction of healthy tissue

83
Q

what are two examples of an autoimmune disease?

A
  • arthritis

- lupus

84
Q

what does normal treatment of autoimmune diseases include?

A

immunosuppressant drugs that prevent the immune system from working.

85
Q

what are vaccinations?

A

an artificial active immunity, that is a deliberate exposure to antigenic material, which stimulates the body to make it’s own antibodies, helping to provide immunity, without becoming infected and ill.

86
Q

what are the 5 ways that vaccines are made safe for them to be given to patients, without the risk of infection?

A
  • killed/inactive bacteria/virus
  • attenuated strains/weakened of live bacteria/virus
  • toxin molecules that have been altered/detoxified
  • antigens isolated from pathogen
  • genetically engineered antigens
87
Q

who underpinned the principles of vaccinations, and when?

A

Edward Jenner, 1700s, when he developed the first small pox vaccine

88
Q

what are vaccination programmes?

A
  • vaccines are offered to a population, as a component of health protection.
  • the young are given vaccines for diseases that were once common and harmful
  • vaccines are taken before going to certain countries, lowers risk of harm from deadly diseases
89
Q

what are routine vaccinations?

A

vaccines that are taken so often, as a booster, to ensure ongoing immunity and protection, they keep up the level of memory cells in your blood.
-eg-flu vaccine every winter in UK

90
Q

why are vaccines effective?

A
  • gives lifetime protection

- generally harmless, primary immune response

91
Q

why are some vaccines uneffective? 5?

A
  • poor response, some people’s immune system does not work properly, and cannot produce enough antibodies
  • antigenic variation, vaccines may not create immune response or vaccines may be difficult to create
  • antigenic shift, changes of disease, vaccine no longer works
  • antigenic concealment, hides from immune system
  • cross-breeding, creates new viruses
92
Q

what is herd immunity?

A

when a large proportion of a population is vaccinated and are therefore immune to a disease
-those who are unvaccinated are still protected due to the large amount of those who are

93
Q

when can herd immunity break down?

A

when vaccination rate falls below the required level

94
Q

what is ring immunity?

A

people living/working near a vulnerable (or infected) person are vaccinated in order to prevent them from catching and transmitting the disease, they do not spread the pathogen onto others, so people within the ‘ring’ are protected

95
Q

what are two reasons why eradicating disease is difficult?

A
  • unstable political situations

- lack of public health facilities, such as poor infrastructure, little trained people, and lack of financial funding.

96
Q

what are the two main sources of medicine?

A

plants and microorganisms (bacteria and funghi)

97
Q

give an example a medicine who’s source is a plant? explain the action of the drug?

A

drug=aspirin
source= compounds from sallow/willow bark
action= painkiller, anti-coagulant, anti-pyretic (reduces fever), anti-inflammatory

98
Q

give an example of a medicine who’s source is a microorganism, explain it’s action?

A 
drug= vancomycin
source= soil fungus
action= powerful antibiotic
99
Q

who discovered the first medicine and what was it?

A
  • Florey and Chain

- penicillin, extracted and processed from mould.

100
Q

what is the need to maintain biodiversity with the use of medicine?

A

allows for new plants and microorganisms to be discovered for new and improved medicine

101
Q

what is personalised medicine?

A

form of medical care that enables doctors to provide healthcare that is customised to an individual’s genotype.

102
Q

what is synthetic biology?

A

the design and construction of new biological entities, as well as the reconstruction of pre-existing natural biological systems.

103
Q

explain personalised medicine?

A
  • developed of tageted and personalised drugs to treat human diseases and development of sythetic tissue
  • information gathered from genome projects to develop genomic medicine
104
Q

what kind of information is found from genetic testing in terms of personalised medicine?

A

information used to divide the population into subgroups according to how they are likely to respond to specific drugs.
-this would ensure that individuals receive the most effective drugs that cause the least side effects

105
Q

why are individuals given medicine based on their genome?

A

between individuals, there are differences in DNA base sequences.
these differences can affect the tertiary structure of the proteins which are targeted by drugs

106
Q

explain synthetic biology?

A
  • involves assembling an entire genome, which causes a cell to operate in a novel way
  • assembly can be done using existing DNA sequences or new.
  • new sequences are written so that they produce specific proteins/transcription factors
107
Q

what is an example for the use of synthetic biology?

A

-commercial production of artemisinin, which is an antimalarial drug, that is genetically reprogrammed from E.coli and yeast, so that they produce the precursor of the drug on a large scale.

108
Q

what are antibiotics?

A

a chemical or compound produced by a living organism that kills or prevents the
growth of bacteria, but do not effect human tissue/own cells

109
Q

who discovered antibiotics/penicillin

A

Alexander Fleming

110
Q

what are the two ways that you can describe antibiotics, and what do they mean?

A
  • bactericidal (they kill)

- bacteriostatic (they inhibit growth processes)

111
Q

what is selective toxicity?

A

the idea that antibiotics affect bacterial cells but do not interfere with human cells.

112
Q

what are 3 examples of antibiotics and their mechanism of action?

A
  • penicillin= inhibits synthesis of bacterial cell wall
  • quinolones= inhibits synthesis of bacterial DNA
  • polymixin= affects cell surface membrane function
113
Q

what is the problem with antibiotics?

A

-becoming less effective due to bacteria developing resistance to them

114
Q

what are the 3 main ways in which resistance against antibiotics has come about?

A
  • overuse of antibiotics
  • random mutation during reproduction, mutations during binary fission results in some bacteria becoming immune to effects of antibiotics, natural selection then takes over, allowing for reproduction
  • public using antibiotics incorrectly, not taking the full course of treatment allows any bacteria left in the body to gain resistance
115
Q

what are two examples of antibiotic resistant bacteria?

A
  • MRSA

- C.difficile

116
Q

what is MRSA and how has it become resistant?

A

what= problem for hospitals, bacteria that is carried on the skin/nose of individuals, can cause boils, abscesses and fatal septicsaemia
-mutation produced methicillin-resistant strains, so hospitals must now swab patients before surgery to check if they’re positive

117
Q

what is C.difficile and how has it become resistant?

A 
what= common in care homes/hospitals, bacterium found in intestine/guts, toxins damage the lining of intestines, leading to diarrhoea, bleeding and death
-resistance= when commonly-used antibiotics kill off many of the 'helpful' gut bacteria, bad bacteria survives, reproduces and takes hold rapidly.
118
Q

what is antibiotic resistance?

A

when bacteria is no longer effected by the antibiotic used against it.
-not caused by B-cell, but instead by the enzymes that are made by some bacteria

Biology Year 1 (12 decks)

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