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Biology Alevel > Communicable Diseases > Flashcards

Communicable Diseases Flashcards

(47 cards)

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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 from pathogens 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?

Study These Flashcards
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?

Study These Flashcards
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 ?

Study These Flashcards
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 ?

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
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
What is autoimmune disease? Examples?
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
What is a vaccination and immunisation? EG of vaccines given to everyone?
**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
How does vaccines work? And how does it cause herd immunity?
- 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
Why is the influenza vaccine always being changed?
- antigens on virus change regularly —> NEW STRAINS - memory cells won’t recognise new antigens —> IMMUNOLOGICALLY DISTINCT
29
How has antibiotic resistance arisen? Eg of antibiotic resistant bacteria?
**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
How is antibiotic resistance prevented?
- 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
Possible Sources of medicines? And can they be protected?
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
What are personal meds?
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
What is synthetic biology?
Using tech to develop molecules that mimic biological systems - synthesis of new genes/organisms
34
Compare passive and active immunity?
ACTIVE IMMUNITY: requires exposure to pathogen - takes longer for protection to develop - long term protection -memory cells produced PASSIVE IMMUNITY IS OPPOSITE
35
How does blood clotting prevent infection?
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
Role of opsonins/cytokines?
Opsonins - binds to **antigen on pathogen** - increases phagocytosis by **increasing recognition** by phagocytes Cytokines - attract phagocytes
37
What is clonal selection?
The **binding** of a B cell/T cell to a pathogen’s antigen, an the **subsequent activation** is CLONAL SELECTION
38
How is resistance different to immunity?
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
What are passive and active defence mechanisms?
Passive defence mechanisms **always PRESENT** - some are physcial , some are chemical Active defence mechanisms **activated when pathogens INVADE**
40
Active plant defence mechanism?
**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
Important Signalling molecules in plant defense ?
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
2 types of vaccine?
Live Attenuated - contain whole pathogens that have been ‘weakened’ - produce stronger and longer lasting immune response In suitable for those with weaker immune system as pathogen may divide before sufficient antibodies produced Inactivated - contain whole pathogens that have been killed - cannot cause disease - dont trigger long lasting and strong immune response
43
What is ring immunity?
Involves vaccinating all people who have been in contact with infected person
44
E.g of common antibiotic? Who discovered it ? And how does it work?
Penicillin From Sir Alexander Fleming 1928 - inhibits synthesis of bacterial cell wall
45
How do toxins differ in immunologically distinct strains?
Toxins produced by each strain will be different Toxin will have **different amino acids acid** sequence - toxin acts as a antigen
46
How does genetics and environment vary immune responses ?
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
47
Blood smear
1. Use a pippette to place blood on the slide 2. Place blood near one end 3. Use coverslip to spread blood across slide

Biology Alevel (30 decks)

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