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ABHAYS A-LEVEL BIO FLASHCARDS > M4, C12 Communicable Diseases > Flashcards

M4, C12 Communicable Diseases Flashcards

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1
Q

what are the main pathogens and give examples of diseases they cause

A

bacteria – tuberculosis (TB), bacterial meningitis, ring rot (potatoes, tomatoes)

virus – HIV/AIDS (human), influenza (animals), Tobacco Mosaic Virus (plants)

protoctista – malaria, potato/tomato late blight,

fungi – black sigatoka (bananas), ring worm (cattle), athlete’s foot (humans).

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2
Q

Define

a) communicable disease
b) pathogen
c) vectors

A

Communicable disease – can be passed from one organism to another

Pathogen – disease causing micro-organism

Vectors – carry pathogens from one organism to another (water/insects)

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3
Q

How do viruses cause disease?

A

Viruses insert their genetic material into the hosts cells DNA. They then use the host cell to replicate.

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4
Q

How do protoctista work?

A

Take over cells
Break them open as a new generation emerge
They DO NOT take over the genetic material
They just digest and use the cell contents to reproduce

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5
Q

how do fungi work

A

digest living cells and destroy them

some produce toxins which break down the cell membrane of cells and inactivate enzymes

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6
Q

how does bacteria work?

A

Produce toxins that break down cell membranes and Inactivate enzymes
The toxins can also interfere with the host cell’s genetic material so they cannot divide

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7
Q

how are bacteria classified?

A

Shape – rod, spherical, comma, spiralled, corkscrew
Cell walls – have different structures and react with gram staining differently, which affects how they react to antibiotics
Gram positive bacteria – purple under light microscope (MRSA)
Gram negative bacteria – red under light microscope (E.coli)

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8
Q

what is the smallest pathogen

A

virus

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9
Q

what pathogen is a Saprophytic eukaryote

A

fungi

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10
Q

why are plant diseases such a concern for humans

A

Plants provide food-people may starve
Plants provide building materials
Plants provide medicines
Plants are the start of all food chains-without them, the food chain is disrupted and the whole ecosystem suffers

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11
Q

what is ringrot?

A

bacteria
damages leaves, tubers and fruits
Can remain in soil for 2 years so plants cannot be grown in the same soil for the next two years
no cure

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12
Q

what is tabacco mosaic virus

A

virus
damages leaves, roots and stems stunting the growth of the plant
resistant crop chains are available but no cure

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13
Q

what is potato blight

A

protoctist
destroy leaves, tubers causing vast crop loss
no cure but resistant strains, careful management and chemical treatments can reduce infection risk

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14
Q

what is black sigatoka

A

a banana disease caused by fungi
attacks and destroys leaves and turns them black
resistant strains are being developed - good husbandry and fungicide treatment can control the spread of disease but there is no cure

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15
Q 
what is TB?
who gets it?
what does it damage
is there a cure?
caused by?
stats?
A

Bacterial disease
Humans, cows, pigs, badgers and deer get it
Caused by mycobacterium TB and M.Bovis
Damages and destroys lung tissue and slows the immune system
Cured by antibiotics which are taken for 6 months
Prevented by vaccination

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16
Q 
what is bacterial meningitis?
who gets it?
what does it damage
is there a cure?
caused by?
stats?
A

Bacterial infection fo the meninges of the brain (membranes on the surface)
Can spread to rest of body causing blood poisoning and rapid death
Affects young children and teens 15-19
Causes a blotchy red/purple rash
Symptoms include fever, drowsiness, rapid breathing and stiff neck

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17
Q 
what is HIV/AIDS?
who gets it?
what does it damage
is there a cure?
caused by?
stats?
A

Human immunodeficiency virus
Targets T helper cells in the immune system
Gradually destroys immune system so you are open to other infection
Affects humans and primates
Passed on through bodily fluids - sex, needles, blood or breast milk
2012 - 35 million people had HIV, 1.6 million died
No vaccine or no cure
Anti-retroviral drugs slow the progress of the disease
Females in Africa are at a high risk because of female genital mutilation
Contains the enzyme transcriptase which transcribes RNA to DNA in the host cell

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18
Q 
Malaria:
what causes it?
how does a mosquito become infected?
how does a human become infected?
what does it do inside humans?
cure?
A

Caused by protoctista called Plasmodium
Enters a mosquito when it eats on something that is already infected. The plasmodium reproduces in the mosquito and goes to the salivary glands.
When a mosquito bites a human the plasmodium enters the bloodstream.
It invades the red blood cells, liver and brain.
No cure or vaccine so you have to control the vector by mosquito nets

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19
Q 
Influenza:
who gets it?
what does it damage
is there a cure?
caused by?
A

Viral infection of the ciliated epithelial cells
Affects mammals
Leaves airways open to infection
Fatal for young children, elderly or people with chronic illnesses
3 strains
They mutate regularly so no cure but there is a vaccine

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20
Q

Give details about ring worm

A

Fungal disease affecting mammals
Different fungi for different species
Causes grey-white, crusty, infectious, circular areas of skin
Anti fungal creams are a cure

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21
Q

Give details about athlete’s foot

A

Fungal disease caused by Tinia pedia
Form of ringworm that grows on and digests warm, moist skin between toes
Causes cracking and scaling which is itchy and sore
Anti fungal creams - cure

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22
Q

what are examples of direct transmission between animals

A
  • Kissing/contact with body fluids (bacterial meningitis/STDs)
  • Animal bite (rabies)

Puncture wound/sharing needles (septicaemia)

Ingestion of contaminated food/drink or transferring pathogens from hands to mouth

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23
Q

what are examples of indirect transmission between animals

A

Fomites
-Inanimate objects e.g. bedding, socks, cosmetics (athletes foot, gangrene, staphylococcus infections)
Droplet infection (inhalation)
-Droplets of saliva and mucus – talking, coughing, sneezing (Flu, TB)
Vectors
-Transmit pathogens from one host to another, normally animals (mosquitoes – malaria, rat fleas = bubonic plague)
-Water (diarrhoeal disease)

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24
Q

what increases the risk of catching a disease in animals

A
  • Overcrowded working and living conditions
  • Poor nutrition
  • Compromised immune system (HIV)
  • Poor sanitation
  • Breeding sites for vectors
  • Climate change – introduce new vectors/disease
  • Cultural beliefs – traditional medicine
  • Socioeconomic factors – lack of doctors/nurses/public warnings
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25
Q

How does disease directly transmit in plants

A

Direct contact of the healthy plant against any part of the diseased plant = ring rot, TMV, black sigatoka

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26
Q

How does disease indirectly transmit in plants

A 
Soil contamination
-Infected plants leave pathogens or reproductive spores in soil
Vectors
-Wind
-Water
-Animals
-Humans
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27
Q

what increases the risk of catching a disease in plants

A
  • Planting varieties of crops susceptible to disease
  • Overcrowding
  • Damp, warm conditions increase survival of pathogens
  • Climate change – increased rainfall + wind, promote the spread
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28
Q

how does a plant know its infected

A

The pathogen may release molecules which are recognised by receptors on the plant cell surface membrane

The pathogen may damage the cellulose cell wall. The products of this breakdown may be recognised by receptors on the cell surface membrane

Detection of either of these things will trigger either physical or chemical defences.

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29
Q

what is callose

A

a polysaccharide
made of beta glucose with 1-3 and 1-6 glycosidic bonds

a physical defence a plant uses

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30
Q

what does callose do and how does this help a plant defend itself

A

Callose deposited between the cell walls and cell membrane in cells beside infected ones
-Acts as a barrier preventing pathogens entering cells around infection site

Callose builds up and blocks sieve plates in the phloem
-Seals off infected part of plant and prevents spread of pathogens in the phloem

Callose deposited in plasmodesmata between infected cells and healthy neighbouring cells
-Seals off infected cells to prevent spread of pathogen

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31
Q

give examples of chemicals these plants produce

a) lemongrass
b) cocoa beans
c) almonds
d) cotton

A

a) citronella
b) caffeine
c) cyanide
d) gossypol

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32
Q

what are examples of chemical defences in plants

A

insect repellents

insecticides - act as insect neurotoxins

antibacterial compounds - break down bacterial cell walls

antifungal compounds - interfere with fungal cell membranes

anti-oomycetes - break down glucans

general toxins - cyanide which is toxic for pathogens

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33
Q

what are the two lines of defence in mammals

A

The primary non-specific defence (always present/activated rapidly)
The specific immune response (specific to each pathogen)

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34
Q

how does skin keep pathogens out

A

prevents entry, has skin flora (healthy microorganisms that outcompete pathogens, produces sebum (inhibits growth)

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35
Q

how does mucus membrane keep pathogens out

A

secrete sticky mucus, traps pathogens (contains phagocytes), contains lysozyme (destroys cell walls)

36
Q

how does tears and urine keep pathogens out

A

contains lysosomes

37
Q

how does stomach acid keep pathogens out

A

kills pathogens

38
Q

what expulsive reflexes does our body do

A

Coughs and sneezes from gas exchange system

Diarrhoea and vomiting expel contents of gut

39
Q

what is the process of blood clotting

A

When you cut yourself:
-Platelets come in contact with collagen in the skin
-Platelets stick to each other
-Secrete several substance
Thromboplastin – enzyme that leads to the formation of a blood clot
Serotonin – causes smooth muscle in walls to contract (narrowing reduces blood supply to area
-Clot dries out, forming a hard, tough scab
-Epidermal cells below start to grow, sealing wound permanently
-Damages blood vessels regrow
-Collagen fibres deposited to give new tissue strength

40
Q

what is

  • thromboplastin
  • prothrombin
  • thrombin
  • fibrinogen
  • fibrin
A

Thromboplastin - enzyme
Prothrombin - clotting factors made by the liver
Thrombin - enzyme that converts fibrinogen to fibrin
Fibrinogen - is a glycoprotein
Fibrin - is a fibrous, non-globular protein

41
Q

what is the body’s inflammatory response

A

= Pain, heat, redness and swelling of tissue

Mast cells (type of WBC) in damaged tissue release

–Histamine
Causes blood vessels to dilate and walls to become leaky

–Cytokines
Attract phagocytes

42
Q

How does histamine cause the symptoms of inflammation?

A

Blood vessels dilating, causes localised redness and heat, so raises temperature to prevent pathogen reproducing

Blood vessels leaky to force blood plasma out, tissue fluid causes swelling and pain

43
Q

what is the process of phagocytosis

A

1) phagocyte is attracted by chemicals produced by the pathogen
2) phagocyte recognises pathogen as non-self and binds to it
3) phagocyte engulfs the pathogen to form phagosome - lysosome moves towards phagosome and combines with it forming a phagolysosome
4) In phagolysosome, enzymes break down the pathogen
5) Digested pathogen absorbed by phagocyte - antigens combine with MHC in the cytoplasm
6) MHC is displayed on phagocyte membrane, making an antigen presenting cell (APC)

44
Q

what is cytokines

A

A chemical produced by phagocytes that have engulfed a pathogen
They act as cell-signalling molecules, informing other phagocytes that the body is under attack and it stimulates them to move to the site of infection/inflammation
They can also increase body temp

45
Q

what is opsonins

A

chemicals that bind to pathogens and ‘tag’ them so they can be more easily recognised by phagocytes.

phagocytes have receptors on their cell membranes that bind to common opsonins and the phagocyte then engulfs the pathogen.

46
Q

what are antibodies made up of

A

two identical long polypeptide chains called the heavy chains and to much shorter identical chains called light chains.
they are held together by disulphide bridges and there are also disulphide bridges between the polypeptide chains to hold them in shape

47
Q

how do antibodies bind to antigens

A

lock and key mechanism
the variable region of the antibody is the binding site and this gives the antibody a different shape to other antibodies because each antibody is specific to an antigen
the rest of the antibody is called the constant region as its always the same

when an antibody binds to an antigen it forms an antigen-antibody complex

48
Q

what are the 4 ways in which antibodies defend the body

A

1) the antibody acts as an opsonin so the pathogen is easily engulfed and digested by phagocytes
2) stop them entering host cells
3) antibodies act as agglutinins which cause pathogens to clump together which stops them spreading and so phagocytes can engulf them at the same time
4) they act as antitoxins which bind to toxins produced by the pathogens and make them harmless

49
Q

what are the two types of lymphocytes and where are they made

A

B lymphocytes - mature in the bone marrow

T lymphocytes - mature in the thymus gland

50
Q

what are the main types of T lymphocytes

A

T helper cells
T killer cells
T memory cells
T regulator cells

51
Q

what are the main types of B lymphocytes

A

plasma cells
B effector cells
B memory cells

52
Q

what are T helper cells

A

they have receptors on their cell-surface membrane which bind the surface antigens on APCs
they produce interleukins which are a type of cytokine - they stimulate activity of B cells which increases antibody production ad stmulates other types of T cells
attracts and stimulates macrophages to ingest pathogens

53
Q

what are T killer cells

A

destroy the pathogen carrying the antigen

produce a chemical called perforin which makes holes the cell surface membrane of the pathogen so it is freely permeable

54
Q

what are T memory cells

A

part of the immunological memory

if they meet a pathogen for a second time they divide rapidly to form a huge number of clones to kill the pathogen

55
Q

what are T regulator cells

A

they suppress the immune system - control and regulate it
stop the immune response once a pathogen has been eliminated
makes sure the body recognises self antigens and doesn’t set up an autoimmune response

56
Q

what are plasma cells

A

produce antibodies to a particular antigen and release them into circulation
produces 2000 antibodies per second

57
Q

what are B effector cells

A

divide to from plasma cell clones

58
Q

what are B memory cells

A

provide immunological memory
programmed to remember a specific antigen and enable the body to make a rapid response when that antigen on a pathogen is encountered again

59
Q

in cell-mediated immunity how could cells have been changed

A

viral infection
mutation
antigen processing

60
Q

what happens in the response to cell-mediated immunity

A

1) APC presents the antigen on the surface of the cell
2) T helper cells have receptors which complement the antigen
3) when the t helper cell binds to the antigen, the t helper cell becomes activated (clonal selection)
4) They produce interleukins
5) this stimulates more T cells that are specific to the antigen to divide and form clones (clonal expansion)
6) the clones then do one of four things:
- produce interleukins to stimulate phagocytosis
- produce interleukins to stimulate B cells to divide
- differentiate into T killer cells
- differentiate into T memory cells

61
Q

whats the difference between cell mediated immunity and humoral immunity

A

cell-mediated immunity - responses to cells that have been changed in some way

humoral immunity - response to antigens found outside of cells in body fluids (bacteria and fungi)

62
Q

how does the body respond to humoral immunity?

A

1) B lymphocytes covered in antibodies bind to specific antigens (clonal selection) OR B lymphocytes engulfs the pathogen and present the antigen on the surface
2) With the help from the T helper cell interleukins, the B cells are activated and divide by clonal expansion
3) the clones develop into either plasma cells producing antibodies or into memory cells

63
Q

what is the difference between the primary and secondary immune response

A

primary response - when the pathogen enters for the first time, you have a slow recovery, B and T lymphocytes are activated and you get symptoms

secondary response - when the pathogen enters for the 2nd time, fast recovery, memory cells are activated and you have no symptoms

64
Q

What is active immunity

A

Memory cells are produced
Long term protection
Protection has to develop
Requires exposure to antigens

65
Q

What is passive immunity

A

No memory cells produced
Short term protection
Immediate protection
No exposure to antigen

66
Q

Give an example of:

  • natural active immunity
  • natural passive
  • artificial active
  • artificial passive
A

Natural active - secondary response to antigen entering the body for second time

Natural passive - antibodies from mother passing into baby in breast milk

Artificial active - vaccine with dead pathogens injected into person

Artificial passive - vaccine containing antibodies injected into person

67
Q

What is in vaccines

A

Dead pathogens
Attenuated (reduced) pathogens
Detoxified toxins
Isolated antigens

68
Q

How do vaccines work

A

A dead or inactive pathogen enters the body. It contains the antigens from the pathogen. Antibodies are produced by the white blood cells. These bind to the antigens of the vaccine. Memory cells now know the antigen so if the pathogen returns the body can produce the right white blood cells quickly to destroy the pathogen.

69
Q

Define epidemic

Define pandemic

A

Epidemic - when a communicable disease spreads rapidly to a lot of people locally or nationally

Pandemic - when the same disease spreads rapidly across a number of countries and continents

70
Q

What is herd immunity

A

When a high percentage of the population (usually 90% or above) is protected through a vaccine against a virus or bacteria which prevents the disease from spreading.
Protects people who can’t have the vaccine like children or ill people because the disease can’t spread.

71
Q

where did penicillin derive from and what does it do

A

mould - originally from melons

antibiotic against many common bacterial diseases

72
Q

where did docetaxal/paclitaxel derive from and what does it do

A

yew trees

breast cancer treatment

73
Q

where did aspirin derive from and what does it do

A

willow bark

painkiller, anti-pyretic, anti-coagulant, anti-inflammatory

74
Q

where did prialt derive from and what does it do

A

venom of cone snail from Australian oceans

pain-killing drug which is 1000 X more effective than morphine

75
Q

where did vancomycin derive from and what does it do

A

soil fungus

one of the most powerful antibiotics

76
Q

where did digoxin derive from and what does it do

A

foxgloves

heart drug - treats heart failure and atrial fibrillation

77
Q

what do antibiotics do

why are they useful

A

kill or inhibit the growth of bacteria

they don’t damage body cells

78
Q

what is antibiotic resistance and overall what causes it

A

when bacteria is no longer killed by antibiotics

caused by overuse leading to mutations

79
Q

what is the evolution of antibiotic resistance

A
  1. a mutation or pre-existing genetic variation gives the bacteria resistance
  2. antibiotics acts as a selection pressure, killing non resistance bacteria , resistant ones are able to survive
  3. the resistant ones survive and reproduce
  4. they pass on the allele for resistance
  5. an example of natural selection because the best adapted survives
80
Q

how do we prevent antibiotic resistance

A

reduce doctors overprescribing antibiotics because it reduces the likelihood of resistance developing

finish the course of antibiotics because it ensures all bacteria is killed which reduces the likelihood of resistance developing

81
Q

what are examples of superbugs and give details about each one

A

MRSA - bacteria in skin or nose carried by 30% of population. causes boils or abscesses and fatal septicaemia. treated by methicillin but a mutation has produced methicillin resistant chains

C. difficile - in the guts carried by 5% of population. produces toxins that damages the lining of the intestines leading to diarrhoea, bleeding and death. it reproduces rapidly and kills off healthy bacteria in the gut.

82
Q

what are some other sources of antibiotics that we may have to use in the future

A 
soil microorganisms
crocodile blood
fish slime
honey
deepest abysses of oceans
83
Q

what are personalised medicines

A

medicines that are tailored to your DNA so it is most effective for you
eg. 30% of breast cancer is due to a mutation in HER2 gene which can be stopped by Herceptin

84
Q

what is synthetic biology

A

using technology to make artificial proteins, cells and microorganisms
could engineer bacteria to destroy cancer cells while leaving body cells intact

eg. nanotechnology are tiny non-natural particles that can deliver drugs to specific sites

85
Q

What’s the MHC in phagocytosis

A

The MHC (major histocompatibility complex) moves the antigens which have been absorbed in the phagocyte to the surface membrane to form an APC

86
Q

define parasite

A

an organism which lives in or on another organism (its host) and benefits by deriving nutrients at the other’s expense

ABHAYS A-LEVEL BIO FLASHCARDS (24 decks)

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