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Biology > Communicable Diseases 2 > Flashcards

Communicable Diseases 2 Flashcards

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1
Q

Bacteria

A

Prokaryotes
Classified by basic shapes ( rod shaped/spherical/spiralled) or by their cell walls

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2
Q

Gram staining

A

Gram + look purple/blue under microscope
Gram - appear red
Useful because type of cell wall affects how bacteria react to antibiotics

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3
Q

Viruses

A

Non living infectious agents
Genetic material surrounded by protein
Invade cells and genetic material takes over and replicated viruses
Use bacteriophages to identify and treat disease

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4
Q

Protoctista

A

Eukaryotic
Single cell or cell in colonies
Parasitic require a vector to infect host

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5
Q

Fungi

A

Eukaryotic often multicellular
Digest food extracellularly
Affect plant leaves prevent photosynthesis and plant dies
Produce spores which spread

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6
Q

Modes of action against host

A

Damaging host tissues directly
Producing toxins which damage host tissues

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7
Q

Damaging the host tissues directly

A

Viruses take over cell metabolism viral dna insert into host dna replicate virus and burst out cells
Protoctista take over cells and break them open digest and use contents to reproduce
Fungi digest living cells and destroy them

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8
Q

Producing toxins

A

Most bacteria produce toxins - damage cell membrane or inactivate enzymes and some interfere with genetic material so cells cannot divide
Some fungi produce toxins

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9
Q

Plant diseases

A

Ring rot- gram + bacteria damages leaves and tubers no cure cannot grow for 2 years
TMV- virus infects tobacco plant stunt growth and reduce yield no cure resistant crop strains
Potato blight- Protoctista - hyphae penetrate host cells chemical treatments reduce risk
Black Sigatoka- fungus attacks and destroys leaves 50% reduction in yield

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10
Q

Animal bacterial diseases

A

TB - damages and destroys lung tissue and suppress immune system hiv/aids more likely infected with TB prevent via vaccination and antibiotics
Meningitis - infection of meninges which can lead to blood poisoning and rapid death - antibiotics cure if caught early vaccine to prevent

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11
Q

Animal viral diseases

A

HIV/Aids- targets T helper cells gradually destroying immune system rNA is transcribed and dna then interacts with genetic material of cells
Passed via unprotected sex and no cure
Influenza- infection of ciliates epithelium leads airways open to 2nd infection. Mutate regularly no cure

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12
Q

Animal Protoctista diseases

A

Malaria - spread by mosquito vector reproducing in female mosquitoes as need to take blood meals before laying eggs invades liver cells RBCs and the brain
Controlled by preventing vectors

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13
Q

Animal fungal diseases

A

Ring worm- cause grey/white crusty infectious circles of skin antifungal cream cure
Athletes foot- human ring worm digests moist areas around toes causing cracking anti-fungal cream=cure

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14
Q

Transmission between animals

A

Direct transmission:
Contact of bodily fluids
Skin to skin
Faeces on hands
Break of skin - bite/needle
- Indirect :
Fomites(inanimate objects)
Droplet infection
Vectors

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15
Q

Factors affecting transmission

A

Overcrowded living
Poor nutrition
Compromised immune system
Poor waste disposal
Climate change
Infrastructure
Socioeconomic factors

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16
Q

Transmission between plants

A

Direct - contact between plants
Indirect:
Soil contamination - leave pathogens or spores
Vectors (wind/water/animals/humans)

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17
Q

Factors affecting transmission in plants

A

Planting susceptible crops
Overcrowding
Poor mineral nutrition
Damp and warm conditions
Climate change

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18
Q

Plant defences catergories

A

Recognising attack
Physical defences
Chemical defences

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19
Q

Recognising attack (plant)

A

Receptors in cell respond when plant wall is attacked
Stimulates release of signalling molecules that switch in genes in the nucleus - trigger responses chemical production /alarming other cells etc

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20
Q

Physical defences

A

Produce high levels of callose polysaccharide - thought to deposit between cell wall and membrane preventing pathogen entering
-lignin is added making barrier thicker
- callose blocks sieve plates sealing of infected part
- callose deposited in plasmodesmata between infected and healthy cells

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21
Q

Chemical defences

A
  • insect repellent / insecticides eg caffeine
    -antibacterial compounds- phenols
  • defensins- disrupt pathogen membrane
    -lysosomes break down cell walls
  • antifungal = saponins interfere w membrane chitinases break down chitin fungal walls
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22
Q

Non specific animal defences

A
  • skin /sebum oily sub inhibits growth
    -body tracts lined w mucus
    -lysozymes in tears and urine
  • expulsive reflexes
23
Q

Wound repair

A

Blood clotting platelets first to scene secrete several sub:
-thromboplastin enzyme that triggers reactions causing clot
- serotonin makes smooth muscle contract so narrow and reduce supply of blood to area
Collagen fibres deposit under scab

24
Q

Inflammation response

A

Mast cells activated releasing histamines and cytokines
Histamines- blood vessel dilate raised temp prevent path reproducing and make vessels more leaky so plasma is forced out (swelling)
Cytokines attract white blood cells to site and dispose of pathogens by phagocytosis

25
Q

Getting rid of pathogens (nonspecific)

A

Fevers- cytokines stimulate hypothalamus to increase body temp to inhibit pathogen growth and immune system works faster

26
Q

Phagocytosis

A

Pathogen produce chemical attracts phagocytes
Phagocyte engulfs the pathogen and encloses in phagosome
Combine w lysosome and enzymes digest the pathogen

27
Q

Neutrophils and macrophages

A

Neutrophils under 10mins digestion
Macrophages= longer combines antigens to surface w special glycoproteins- become antigen presenting cell
Stimulates specific immune response

28
Q

Cytokines

A

Cell signalling molecules inform phagocytes and can also increase body temp and stimulate specific immune response

29
Q

Opsonins

A

Chemicals that bind to pathogens and tag so can be recognised easily by phagocytes

30
Q

Antibody structure

A

Y shaped glycoproteins- immunoglobulins complementary to specific antigen
2x long polypeptide chains (heavy)
2x short polypeptide chains light
Held together via disulphide bridges

31
Q

Antibody mechanism

A

Lock and key
Binding site is an area of 110 as which is the variable region
When binds forms antibody antigen complex

32
Q

How antibodies defend

A
  • act as opsonins to engulfed easily
    -pathogens can’t invade cells once complex forms
  • acts as agglutinins causing pathogens to clump together - prevent spread
  • act as antitoxins making toxins harmless
33
Q

Lymphocyte types

A

B lymphocytes- mature in bone marrow
T lymphocytes- mature in thymus gland

34
Q

T lymphocytes

A

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

35
Q

B lymphocytes

A

Plasma cells
B effector cells
B memory cells

36
Q

T helper

A

Bind to surfaces on apcs
Produce interleukins - type of cytokine
Stimulate activity of B cells increasing antibody production and other T cells

37
Q

T killer

A

Destroy the pathogen carrying antigen
Produce perforin which makes holes in cell membrane of pathogen

38
Q

T memory

A

Immunological memory
If meet antigen second time rapidly divide into T killer and destroy pathogen

39
Q

T regulatory

A

Suppress and control immune system
Stop immune response once pathogen eliminated
Prevents autoimmune response
Interleukins are important in this process

40
Q

Plasma cells

A

Produce antibodies specific to antigen and release them
2000 antibodies per second

41
Q

B effector cells

A

Divide to form plasma cell clones

42
Q

B memory

A

Provide immunological memory
Programmed to remember specific antigen and enable a v rapid response

43
Q

Cell mediated immunity

A

Important against viruses and early cancers
1. Macrophages engulf and digest pathogens form APCs
2. Receptors on T helpers fit the antigen producing interleukins stimulating production of T cells
3. T cells may develop into memory cells produce interleukins for phago. Or b cell stimulation or develop into T killers

44
Q

Humoral immunity

A

Responds to antigens outside cells eg bacteria and fungi
1. B cell w complementary antibody bonds to antigen and then engulfed and becomes APC
2. T helper cells bind to APC - clinal selection
4. Interleukins activate b cells which divide via mitosis forming plasma cells and b memory cells - clonal expansion

45
Q

Autoimmune disease

A

When immune system stops recognising self cells and starts to attack healthy tissue
Genetic/T reg cells don’t work

46
Q

Natural immunity

A

If already met a pathogen T and b memory cells trigger rapid response destroying pathogen
Milk from mother passes antibodies through first dose of milk called colostrum - natural passive immunity

47
Q

Artificial immunity

A

Passive- antibodies injected into the blood stream - doesn’t last long
Active- vaccine pathogen is inactivated or weakened and injected into blood which triggers immune system
May need repeat vaccinations to increase immunity help memory cells

48
Q

Sources of medicine

A

Penicillin- mould secondary metabolite
Bioinformatics
3D models of molecules in body allows drugs to be created which target specific area of pathogen
Plants eg foxgloves - atrial fibrillation

49
Q

Pharmacogenetics

A

Personalised medicine that work with your combination of genetics and disease
Breast cancer mutation in gene this can be shut down by specific drugs

50
Q

Synthetic biology

A

Using genetic engineering can enable bacteria to make specific drugs
Nanotechnology to deliver drugs to specific sites in the body

51
Q

Antibiotic resistance

A

When using antibiotics may leave mutated strain of bacteria which can rapidly reproduce
Concern that overuse accelerates natural selection of resistant strains

52
Q

MRSA

A

30% of the population
Boils abscesses and septicaemia
Has methicillin resistant strains

53
Q

Antibiotic resistant reduction

A

Minimise use of antibiotics - every course is fully completed
Good hygiene in hospitals aseptic techniques

Biology (24 decks)

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