Communicable Diseases 2 Flashcards

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
Getting rid of pathogens (nonspecific)
Fevers- cytokines stimulate hypothalamus to increase body temp to inhibit pathogen growth and immune system works faster
26
Phagocytosis
Pathogen produce chemical attracts phagocytes Phagocyte engulfs the pathogen and encloses in phagosome Combine w lysosome and enzymes digest the pathogen
27
Neutrophils and macrophages
Neutrophils under 10mins digestion Macrophages= longer combines antigens to surface w special glycoproteins- become antigen presenting cell Stimulates specific immune response
28
Cytokines
Cell signalling molecules inform phagocytes and can also increase body temp and stimulate specific immune response
29
Opsonins
Chemicals that bind to pathogens and tag so can be recognised easily by phagocytes
30
Antibody structure
Y shaped glycoproteins- immunoglobulins complementary to specific antigen 2x long polypeptide chains (heavy) 2x short polypeptide chains light Held together via disulphide bridges
31
Antibody mechanism
Lock and key Binding site is an area of 110 as which is the variable region When binds forms antibody antigen complex
32
How antibodies defend
- 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
Lymphocyte types
B lymphocytes- mature in bone marrow T lymphocytes- mature in thymus gland
34
T lymphocytes
T helper cells T killer cells T memory cells T regulator cells
35
B lymphocytes
Plasma cells B effector cells B memory cells
36
T helper
Bind to surfaces on apcs Produce interleukins - type of cytokine Stimulate activity of B cells increasing antibody production and other T cells
37
T killer
Destroy the pathogen carrying antigen Produce perforin which makes holes in cell membrane of pathogen
38
T memory
Immunological memory If meet antigen second time rapidly divide into T killer and destroy pathogen
39
T regulatory
Suppress and control immune system Stop immune response once pathogen eliminated Prevents autoimmune response Interleukins are important in this process
40
Plasma cells
Produce antibodies specific to antigen and release them 2000 antibodies per second
41
B effector cells
Divide to form plasma cell clones
42
B memory
Provide immunological memory Programmed to remember specific antigen and enable a v rapid response
43
Cell mediated immunity
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
Humoral immunity
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
Autoimmune disease
When immune system stops recognising self cells and starts to attack healthy tissue Genetic/T reg cells don’t work
46
Natural immunity
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
Artificial immunity
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
Sources of medicine
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
Pharmacogenetics
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
Synthetic biology
Using genetic engineering can enable bacteria to make specific drugs Nanotechnology to deliver drugs to specific sites in the body
51
Antibiotic resistance
When using antibiotics may leave mutated strain of bacteria which can rapidly reproduce Concern that overuse accelerates natural selection of resistant strains
52
MRSA
30% of the population Boils abscesses and septicaemia Has methicillin resistant strains
53
Antibiotic resistant reduction
Minimise use of antibiotics - every course is fully completed Good hygiene in hospitals aseptic techniques