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Biology Alevel > Communicable Diseases > Flashcards

Communicable Diseases Flashcards

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1
Q

What is a disease?

A

Illness or disorder of the body or mind that leads to poor health

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2
Q

Diseases caused by bacteria?

A

TB (affects animals) - infect lungs causing cough/bloody mucus
Bacterial Meningitis (humans)- inflammation of meninges
Ring rot (potatoes/tomatoes) - infect vascular tissue/prevent water transport, causing plant to wilt/die

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3
Q

Diseases caused by viruses ?

A

HIV/AIDS (humans) -
Influenza (animals ) - flu - high temp/body ache
TMV (plants) - yellow leaves creates mosaic pattern

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4
Q

Diseases caused by fungus?

A

Black Sigatoka (banana plants) - reduces ability to photosynthesise , causing black streaks
Ringworm (cattle)
Athlete’s foot (humans)

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5
Q

Disease caused by protoctists ?

A

Potato/tomato late blight (potatoes /tomatoes) - dark brown marks on leaves , leaving it inedible
Malaria (animals) - plasmodium

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6
Q

What is direct transmission and eg of diseases caused by direct transmission?

A

When disease is transmitted directly from one organism to another (droplets, sex , touch)

E.g HIV/AIDS - sexual intercourse/needles
- blood donation
- from mother to child across placenta /breast milk
Athletes foot - touch
TB- droplets
Milk/meat

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7
Q

What is indirect transmission and eg of diseases transmitted this way?

A

When a disease is transmitted from one organism to another via an intermediate (air,water,food,vector)

E.G

Potato blight - caused when spores carried between plants , in air/water
Malaria- via mosquitoes or via blood transfusion (unsterile needles)
- mother to child across placenta

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8
Q

What factors affect disease transmission?

A

LIVING CONDITIONS:
- overcrowded living conditions increase transmission
TB is transmitted more in overcrowded places, indirectly/directly
- Farmers use monocultures to maximise yield/profit - large number of crop plants in a small area
the leaves of different plants touch each other, make transmission of pathogens like TMV easier

CLIMATE :
potato blight is common in wet summer bc spores need water to spread
- malaria - common in humid/hot conditions , bc mosquitoes can breed in these conditions

SOCIAL FACTORS: risk of HIV is high in places where there is no access to:
Good health care - less diagnosis/treatemnt, so will be passed on
Good health education - to inform ppl of risks/safe sex
Migration - spread from infected area to non infected area
Poverty - less sanitation/hygiene and more crowded

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9
Q

Non specific Animal barriers to pathogens?

A

SKIN: blocks pathogens from entering /chemical barrier producing chemicals that are antimicrobial/lower pH
MUCOUS MEMBRANES: protect body openings exposed to environment - secrete mucous to trap pathogens/antimicrobial enzymes
BLOOD CLOTTING : prevent pathogen entry
INFLAMMATION
WOUND REPAIR
EXPLUSIVE REFLEXES : coughing/sneezing expel pathogens
PHAGOCYTOSIS

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10
Q

How does inflammation protect against pathogens?

A

Mast cells respond to tissue damage by releasing HISTAMINE, which increase permeability of blood vessels
- so start to leak fluid into affected area —> cause SWELLING/help isolate pathogens
- histamine also causes VASODILATION , increasing blood flow into area - bring WBCS to area to fight off pathogens

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11
Q

How does wound repair prevent infection?

A

Surface of skin is repaired by skin cells dividing /migrating to edges of wound
- tissue below wound contracts/brings edges of wound closer tgt
- repaired using collagen fibres—> scar

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12
Q

PASSIVE Plant physical defences ?

A

WAXY CUTICLE on leaves/stem - physical barrier to pathogens
- stop water collecting on leaf , reducing risk for infection transferred between plants in water

CELL WALLS : physical barrier
CALLOSE - polysaccharide produced by plants
- gets deposited between plant cell walls/plasma membranes —> PREVENT PATHOGEN ENTRY
- callose deposition at plasmodesmata limit spread of viruses between cells

BARK : impermeable to pathogens

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13
Q

PASSIVE Chemical plant defences?

A

Can produce SAPONINS - destroy plasma membranes of fungi/pathogens
Produce toxic chemicals to insects - reduce insect feeding —> less risk of infection by vectors

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14
Q

4 stages of immune response?

A
  1. Phagocytes engulf pathogens
  2. Phagocytes activate T. Lymphocytes
  3. T lymphocytes activate B lymphocytes, which divide into plasma cells
  4. Plasma cells make more antibodies to a specific antigen
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15
Q

How do phagocytes (neutrophils and macrophages) work ?

A

Carry out phagocytosis
- carry out NON SPECIFIC IMMUNE RESPONSE

  1. Phagocyte recognise antigens on pathogen
  2. Cytoplasm of phagocyte moves around pathogen , engulfing it
    - OPSONINS make this easier, as they’re molecules that attach to foreign antigens to aid phagocytosis
  3. Pathogen now contained in PHAGOSOME (vesicle in cytoplasm of phagocyte )
  4. Lysosome fuses with phagosome (PHAGOLYSOSOME) —> BREAKS DOWN PATHOGEN - digestive enzymes
  5. NEUTROPHILS : digestive enzyme kills and digests pathogen
    MACROPHAGES : presents pathogen’s antigens /sticks antigens on surface to active immune system cells (ANTIGEN PRESENTING CELL APC)
    - don’t destroy pathogen completely
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16
Q

What are neutrophils? Structure?

A
  • type of phagocyte
  • first WBCs to respond to pathgens in body in response to signals from cytokines
  • cytokines are released by cells at site of wound

Multi lobed nucleus

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17
Q

How do T lymphocytes work?

A
  • surface covered with receptors
  • receptors bind to antigens presented by APCs
  • each T lymphocyte has a different receptor on its surface / when meets complementary antigen , it binds to it
  • this activates T lymphocyte —> process called CLONAL SELECTION (activated T lymphocytes include T helper/killer and regulatory cells)
  • then undergoes CLONAL EXPANSION - divides to produce clones of itself
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18
Q

What are the different types of activated T lymphocytes ?

A

T helper cells- release substances to activate B lymphocytes / T killer cells (release INTERLEUKINS, a type of cytokines)
T killer cells - attach to/kill infected cells - secrete toxic substances
T regulatory cells - suppress immune response of other WBCs , to prevent immune system attacking host cells

Can become memory cells too

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19
Q

How do B lymphocytes work?

A

Covered with antibodies
- antibodies bind to antigens - ANTIGEN-ANTIBODY COMPLEX
- each B lymphocyte has different shaped antibodies on surface / binds to complementary antigen , so each B lymphocyte binds to different antigens
- this and substances released from T helper cells - INTERLEUKINS , activates B lymphocytes —> process called CLONAL SELECTION
- activated B lymphocyte divides by mitosis , into PLAMSA CELLS /MEMORY CELLS (CLONAL EXPANSION)

Interleukins bind to specific lymphocyte/cause it to divide by mitosis - produce clones

20
Q

Structure of antibodies?

A

Glycoproteins made of 4 POLYPEPTIDE CHAINS - 2 heavy and 2 lightchains
- each chain has variable region - antigen binding site ,so complementary to particular antigen

Hinge region - Allow flexibility when antibody binds to antigen
Constant region - allow binding to receptors on immune system cells (eg phagocytes ) - same in all antibodies
Disulphide bridges - hold polypeptides chains tgt

21
Q

Function of antibodies ?

A

Can act as antitoxins , opsonins , agglutinins

AGGLUTININS : antibody has 2 binding sites , so can bind to 2 pathogens at once /clump them tgt
- phagocytes bind to antigens /phagocytose pathogens at once

ANTI- TOXINS: antibodies called antitoxins bind to toxins produced by pathogens/neutralise them
- toxin antibody complex also phagocytosed

OPSONISATION: antibodies attach to bacteria making them recognisable to phagocytes - opsonisation
Then phagocytosis can occur

22
Q

Explain the primary and secondary response ?

A

PRIMARY RESPONSE : antigens of pathogen activate immune system
- SLOW BC takes time for clonal selection/expansion of T and B cells
- not many B lymphocytes to make complementary antibodies
- in the process of making antibodies to combat infection, patient gets SYMPTOMS

After exposed to pathogen once , T and B lymphocytes produce MEMORY CELLS - remain in body
- memory T cells recognise pathogen on reinfection/ memory B cells record specific antibodies needed

SECONDARY RESPONSE : on reinfection, quicker, stronger immune response
- memory cells activated
CLONAL selection happens faster-
B lymphocytes —> plamsa cells for antibodies
T lymphocytes —> different types of T lymphocytes
- NO SYMPTOMS , bc pathogen combatted faster

23
Q

What is active immunity? 2 types

A

When immune system makes own antibodies after stimulation of antigen
NATURAL : immune after catching disease
ARTIFICIAL - immune after a vaccine

24
Q

What is passive immunity? 2 types?

A

Immunity from being given antibodies made by different organism

NATURAL : from mother to baby through placenta /breast milk
- baby becomes immune

ARTIFICIAL: immune after injected with antibodies from someone else

25
Q

What is autoimmune disease? Examples?

A

A disease resulting from an abnormal immune response
- when immune system can’t recognise self antigens, it treats them like foreign antigens /launches immune response against own tissues

LUPUS : immune system attacks cells in connective tissue —> cause damage to tissue/inflammation
RHEUMATOID ARTHRITIS: immune system attacks cels in joints —> pain and inflammation

26
Q

What is a vaccination and immunisation? EG of vaccines given to everyone?

A

Vaccination - Administration of antigens into the body
Immunisation - process by which you develop immunity
Vaccination causes immunisation

Common vaccines offered to everyone:
MMR - measles, mumps , rubella - given in schools
Mengingitis C vaccine - first given as injection to babies at 3mnths /booster given at 1 year and teens

27
Q

How does vaccines work? And how does it cause herd immunity?

A
  • contain antigens that produce memory cells against particular pathogens , without the pathogen causing disease
  • if most of pop is vaccinated, spread of pathogen is less likely —> HERD IMMUNITY ‘
  • prevents EPIDEMIC
28
Q

Why is the influenza vaccine always being changed?

A
  • antigens on virus change regularly —> NEW STRAINS
  • memory cells won’t recognise new antigens —> IMMUNOLOGICALLY DISTINCT
29
Q

How has antibiotic resistance arisen? Eg of antibiotic resistant bacteria?

A

Genetic mutations make bacteria naturally resistant to antibiotic
- more likely to survive so alleles for resistance get passed on to offspring

E.g : MRSA - cause serious wound infections
CLOSTRIDIUM DIFFICILE - harmless bacteria in digestive system killed by antibiotics but C.difficile isn’t

30
Q

How is antibiotic resistance prevented?

A
  • reduce use of antibiotics (don’t use for minor infections/prevention)
  • finish course of antibiotics
  • dont use for viral infections
  • use more specific antibiotics for the infection
  • use less in agriculture
31
Q

Possible Sources of medicines? And can they be protected?

A

From natural compounds in plants, animals and microorganisms
E.g PENICILLIN obtained from fungus

Maintaining biodiversity for survival of animals/plants that are sources

32
Q

What are personal meds?

A

Medicines tailored to individual’s DNA
- bc genes effec how ppl respond to different drugs

  • can predict ur response to drug/prescribe right one for you
33
Q

What is synthetic biology?

A

Using tech to develop molecules that mimic biological systems
- synthesis of new genes/organisms

34
Q

Compare passive and active immunity?

A

ACTIVE IMMUNITY: requires exposure to pathogen
- takes longer for protection to develop
- long term protection
-memory cells produced

PASSIVE IMMUNITY IS OPPOSITE

35
Q

How does blood clotting prevent infection?

A

A break in mucous /skin membranes causes release of molecules that trigger chemical CASCADE
- platelets collect together/release clotting factors
This , via cascade of events, results in formation of FIBRIN
- this forms a network - trapping platelets/forming a clot

CLOT ACTS AS BARRIER to pathogens getting into wounds (allows scabs to form - barrier)

36
Q

Role of opsonins/cytokines?

A

Opsonins - binds to antigen on pathogen
- increases phagocytosis by increasing recognition by phagocytes

Cytokines - attract phagocytes

37
Q

What is clonal selection?

A

The binding of a B cell/T cell to a pathogen’s antigen, an the subsequent activation is CLONAL SELECTION

38
Q

How is resistance different to immunity?

A

When resistant - don’t develop disease or suffer any symptoms
When immune - suffered symptoms of disease and recovered - less likely to suffer symptoms of disease again

39
Q

What are passive and active defence mechanisms?

A

Passive defence mechanisms always PRESENT - some are physcial , some are chemical

Active defence mechanisms activated when pathogens INVADE

40
Q

Active plant defence mechanism?

A

Hypersensitivity: rapid death of tissue surrounding infection sites. - deprive pathogen of host tissue/nutrients/energy

Create physcial barriers to reduce spread of pathogen
- invasion of pathogens stimulates release of callose and lignin - deposited between plasma membrane and cell wall
Callose reduces size of plasmodesmata that connects plant cells
Cytoplasm of cells grows into the xylem to create wall made of callose - TYLOSES
Sieve pores filled with callose - prevent phloem asap from being transported

41
Q

Important Signalling molecules in plant defense ?

A

Can produce PHYTOALEXINS- inhibit growth of fungi/other pathogens
Salicylic acid - activates defence mechanisms that protect plant against pathogens for some time
Ethylene - allows plants to communicate - if under attack , they secrete ethylene onto leaves
- vaporises , stimulating other leaves on plant/other plants to react

42
Q

2 types of vaccine?

A

Live Attenuated - contain whole pathogens that have been ‘weakened’
- reduce stronger and longer lasting immune response

Inactivated - contain whole pathogens that have been killed - cannot cause disease
- dont trigger long lasting and strong immune response

43
Q

What is ring immunity?

A

Involves vaccinating all people who have been in contact with infected person

44
Q

E.g of common antibiotic? Who discovered it ? And how does it work?

A

Penicillin
From Sir Alexander Fleming 1928
- inhibits synthesis of bacterial cell wall

45
Q

How do toxins differ in immunologically distinct strains?

A

Toxins produced by each strain will be different
Toxin will have different amino acids acid sequence
- toxin acts as a antigen

46
Q

How does genetics and environment vary immune responses ?

A

Genetics : inherit genes that code for antibodies
- different alleles code for different versions of immune cells
- alleles code for different variable regions on antibody
- mutation can produce new alleles* for immune cells
- autoimmune disease caused by genetics effect immune response

Environment : exposed to different pathogens
- may have memory cells - better immune response
- have access to vaccination
- poor diet can weaken immune system - lack of protein

Biology Alevel (25 decks)

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