topic 6 Flashcards
1
Q
[6.1]
Why must we use aseptic techniques when handling cultures of microorganisms?
A
To prevent:
● potentially harmful microorganisms escaping from your cultures into air + infecting humans
● microorganisms in the air entering and contaminating your cultures
2
Q
aseptic techniques:
A
● all equipment (including agar + petri dishes) should be sterile
● flaming equipment in a bunsen flame ensures sterility
● inoculation should be done with a flamed instrument
● lids should be replaced as quickly as possible
● work near a bunsen burner flame
● disinfect surfaces
3
Q
Culture?
A
when microorganisms are provided with the nutrients, level of O2, pH + temp they require to grow large numbers, so they can be observed + measured.
4
Q
steps + techniques involved when culturing microorganisms:
A
- obtain culture from microorganism
- provide it with right nutrients + environment (eg carbon,nitrogen,protein,minerals) needed to grow
- transfer to the nutrient medium (nutrient broth [liquid] / nutrient agar [jelly] ) using sterile inoculating loop
- close dish airtight
5
Q
inoculating when using a nutrient broth..
A
-make a suspension of the bacteria to be grown + mix a known volume of it with the sterile nutrient broth in the flask
- close quickly (cotton wool) to prevent contamination w air
- flask incubated at suitable temp + is often shaken regularly to allow O2 to the growing bacteria
6
Q
inoculating when using nutrient agar….
A
if inoculating agar, either:
- Make a streak plate
- Make a spread plate
7
Q
streak plate?
A
Sterilise inoculating loop by flaming, dip in culture, sterile plate, at least 3 streaks straight / zig-zag, turn, streak which must overlap with first streak, turn, streak to try to obtain single colonies.
: aim to obtain single colonies by rotating the plate to build layers of the culture on at least 3 separate streaks.
8
Q
Spread plate?
A
distributing microorganisms evenly with a sterile spreader.
spread the sample evenly over the entire plate –> allow sample to absorb thoroughly (at least 5 minutes) before inverting the plate for incubation.
9
Q
selective mediums?
A
medium containing a very specific balance of nutrients = only very specific microorganisms with those particular requirement will grow in it = mutant strains won’t
= SM important in identifying particular mutant strains of microorganisms + antibiotic resistance
10
Q
+ / - of using broth medium over agar?
A
+ Broth can provide anoxic conditions as well as oxygen closer to the surface = can provide information about what kind of oxygen requirements the microbes have.
+ They can also grow a much larger volume of bacteria.
- However, u can’t get a single, discrete, pure colony from a broth to inoculate with/study.
11
Q
Different methods of measuring growth of bacteria?
A
- cell counts
- dilution plating
- turbidity (mass + optical methods)
12
Q
In Cell counts, bacteria + single-celled fungi can be counted directly using a haemocytometer.
What’s a haemocytometer?
A
bacteria + single-celled fungi can be counted directly using a haemocytometer
= a thick microscope slide engraved with a grid + a rectangular chamber which holds 0.1mm3 volume of liquid.
13
Q
- cell count
How to conduct a cell count?
A
- Cells counted using a haemocytometer
- The sample of broth is diluted 1:1 with trypan blue , which stains dead cells blue = so u can identify + count only the living cells.
- cells viewed + counted using microscope.
count cells in each of the 4 sets of 16 squares + take a mean.
Haemocytometer has been pre-calibrated so number of bacteria cells in 1 set of 16 squares = number of cells x 10^4 per cm3 pr broth. - This is repeated at regular intervals throughout growth = shows changing cell numbers.
14
Q
+ / - of using cell count
A
+ useful because it counts only viable (living) cells + is accurate.
- slow
- equipment involved is expensive
- large margin for human error
15
Q
- Diluting plating
A
- Dilution plating works on the principle that every colony is grown from a single, viable microorganism .
- Immediately after culturing, colonies cannot be counted because a single mass is often present.
= So that single colonies can be seen, the original culture is serially diluted, a lawn plate made and the colonies counted.
-This is then multiplied by the dilution factor to obtain a cell count.
16
Q
dilution plating is used to find the total viable cell count.
What’s the total viable cell count?
A
A measure of the number of cells that are alive in a given volume of a culture.
17
Q
+ / - of using diluting plating
A
+ only counts viable / living cells
+ no complex / expensive equipment needed
- slow as incubation period needed + serial dilutions needed
18
Q
What’s turbidimetry?
Turbid?
A
Turbidimetry:
- Is a specialised form of colorimetry
= measures the concentration of a substance by measuring the amount of light passing through it.
Turbid:
- Is opaque, or thick with suspended matter (bacteria cells)
19
Q
- Optical methods
[Turbidity]
A
- As turbidity⬆= transmission⬇+absorbance⬆ (measured in Au).
- This value can be linked to cell count by measuring absorbance of samples with a known cell count (by counting cells with haemocytometer / dilution plating), + using a calibration graph to obtain the cell count in an unknown sample.
20
Q
+ /- of using turbidity measurement:
A
+ Quick + can be conducted in the field
- expensive equipment
- counts both living + dead cells
- Requires calibration curve from known samples
- Assumes density of cells is equal across culture
21
Q
How to assess growth when fungi is used instead of bacteria?
A
measure diameter of the patches of mycelium
= used to compare growth rates in different conditions + find the optimum
22
Q
Generation time?
A
The time between bacterial divisions
23
Q
Analysing the data:
What are the different phases of a bacteria growth curve?
A
- Lag phase
- Log Phase / Exponential phase
- Stationary phase
- Death phase / Decline phase
24
Q
- Lag phase
A
- when bacteria are adapting to new environment = not yet reproducing at their maximum rate
25
2. Log phase
- When rate of bacterial reproduction is close / or at it's theoretical maximum
- After EVERY round of division, population size doubles (exponential growth).
26
3. Stationary phase
- When total growth rate is zero
- As number of new cells formed by binary fission = number of cells dying
Reproduction rate = Death rate
;so population size stabilises at its maximum
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4. Death phase
- when reproduction has almost ceased + death rate of cells is increasing
28
In death phase why does exponential growth in bacteria culture not continue?
(why do bacteria die?)
1. reduction in amount of nutrients available - level of nutrients available = not sufficient/enough to support more growth + reproduction
2. Build up of waste products - inhibits further growth + could poison + kill culture.
- CO2 produced by respiring bacteria cells build up = pH of colony falls to point where bacteria can no longer grow.
29
[6.2]
Pathogens?
Types of pathogens?
microorganism that causes diseases + harm to other living organisms.
1. Bacterial
2. Viral
3. Fungai
4. Protozoa
30
Systemic infections?
Localised infections?
systemic: pathogen has spread through bloodstream = can affect many different organs = dangerous
Localised: pathogen is in 1 area only = less widespread effect
31
Why are bacteria described as agents of infections?
Bacteria can be agents of infections via production of
- endotoxins
- exotoxins
- invasion + destruction of host tissues / cells.
32
1. Endotoxins:
Are **lipopolysaccharides** in outer membrane of **gram negative bacteria** cell wall
-The lipids (in lipopolysaccharide) act as the toxin
- The polysaccharide stimulates an immune response
- Endotoxins **released** from a bacterium **if it breaks down** (wall) + have **effects local** to the site of infection = effects show **LATER** (more time than exotoxins as bacteria cells needs to be destroyed first so they can leave)
Diseases caused by endotoxins are not fatal BUT symptoms they cause which can indirectly cause death. (eg dehydration due to severe diarrhoea)
33
Why don't all antibiotics work with bacteria which release endotoxins?
Antibiotics which target cell wall, can cause more endotoxins to be released from gram negative bacteria, as the lipopolysaccharide component of cell wall is damaged + releases them.
= adverse effect
34
Case study of Endotoxin: Salmonella?
- bacteria invades lining of intestines + endotoxins cause inflammation
= the cells no longer absorb water = faeces become liquid + gut goes into spasms of peristalsis = results in diarrhea
35
How is salmonella spread?
- through ingestion of contaminated food + water
- salmonella bacteria live in guts of many food animals + can contaminate meat = if not cooked properly bacteria survive + pass into ur gut when u eat it
they survive stomach acid + pass into small intestines
36
Treatment / reduce transmission
- ensure meat cooked well
- washing hands after handling raw meat
- avoid contaminated water
- antibiotics reduces symptoms = feel better but act as a carrier for longer
37
2. Exotoxins:
- soluble **proteins** produced + **released from living bacteria** as they metabolise + reproduce in cells of host
- produced by both **gram +/-** but mostly **gram positive**
- effects **more widespread** than endotoxins
- some damage cell membranes causing cell breakdown or internal bleeding
- cause most dangerous + fatal bacterial diseases
38
Case study of exotoxin: Staphylococcus?
- many have them in skin + gut flora = only cause disease if get inside tissues, if normal skin flora is changed or if person has compromised immune system due to other disease
- produce exotoxins which cause skin infections which can be fatal
- S. aureus: boils + styles (localised) + toxic shock syndrome (systemic)
39
3. Host tissue invasion
bacteria can invade + damage cells of a host
40
Case study of host invasion: Mycobacterium tuberculosis
TB most commonly caused by Mycobacterium tuberculosis, spread by **droplet infection**.
TB often **affects respiratory system**, damaging + destroying **lung tissue** + **suppresses immune system** = body less able to fight disease
-⬆affects immuno-compromised individuals
symptom = **coughing up blood** + weakness
got 2 stages:
1. primary infection (no symptoms, just carrier)
2. active infection
41
The primary infection stage?
- Initial stage when M. Tuberculosis is inhaled into lungs, **invades cells** of lungs + **multiplies slowly**
- **Immune system activated** = **localised** inflammatory response - causes a **tubercle** (a mass containing dead bacteria + macrophages) = stays for 8 week in lungs
- often **no symptoms** in primary infection stage
42
The active infection stage?
- some bacteria are resistant to immune system by developing waxy outer cuticle = resist macrophage enzymes
- Hide deep inside tubercles in lungs + **grow slowly** for years until person is weakened and immune system doesn't work well = **immuno-compromised**
- most effective bacteria passed on, once they become active again = **grow + reproduce rapidly causing serious damage + disease**
43
[6.3]
What are antibiotics? 1st one?
What's selective toxicity?
- medicines that either destroy microorganisms (bacteria) or prevent them from growing + reproducing.
- 1st antibiotic: Penicillin
- Selective toxicity means that whilst antibiotics are toxic / interfere with the metabolism or function of pathogen, there's minimal damage to cells of human host.
44
Antibiotics are split into 2 main groups:
1. Bacteriostatic antibiotics
2. Bactericidal antibiotics
45
Bacteriostatic antibiotics?
Example?
- Inhibits growth + reproduction of bacteria
EG: **tetracyclines** : inhibits protein synthesis by interrupting / preventing transcription /+ translation of genes = protein production affected + prevents formation of ribosomes
46
Bactericidal antibiotics?
Example?
- Destroys / kills bacteria
EG: **Penicillin**: damages cell wall = water moves in = osmotic lysis = kills bacteria
47
What does the effectiveness of any antimicrobial drugs depend on?
- Conc of drug in area of body infected
- the local pH
- Whether the pathogen or host tissue destroy the antibiotic
- The susceptibility (sensitivity) of the pathogen to the particular antibiotic used
48
[6.4]
Antibiotic-resistance?
When the microorganism is not affected by an antibiotic even if it was effective in past, it becomes resistant due to natural selection.
49
How does antibiotic resistance arise?
1. Random genetic mutations (eg makes the cell wall impermeable to drug) = alleles
2. selection pressure of drug
3. Due to natural selection, more bacteria possess these selective advantages as they're (alleles) passed on = more common in pop = increasing resistance to drug
50
what's the 'evolutionary race' ?
constant evolutionary race between pathogens + us (their hosts)
- we keep developing new drugs + bacteria keep evolving to resist these drugs
= as different antibiotics used to tackle increasing resistance = increases selection pressure for evolution of bacteria that're resistant to all them = creates ' superbugs' eg MRSA.
51
How to prevent this from continuing?
by reducing selection pressure for resistance by using antibiotics less often.
52
How do hospitals control the spread of antibiotic resistant infections?
● New patients screened at arrival, isolated + treated if infected = prevents spread of bacteria between patients.
● Antibiotics only used when needed + entire course of antibiotics is completed to ensure that all bacteria are destroyed + minimise selection pressure on bacteria to prevent resistant strains from forming.
● All staff must follow the code of practice which includes strict hygiene regimes such as washing hands with alcohol-based antibacterial gels + wearing suitable clothing which minimises the transmission of resistant bacteria.
53
[6.5] Viruses as pathogens
1. Influenza virus:
Transmission?
- Droplet infections (cough/sneeze)
- Direct contact (mucus/animal droppings /surfaces)
54
Mode of infection?
- Virus enters cells by binding to proteins (spikes) on surface of cells in lungs.
- Paralyses cilia on ciliated epithelial cells
- Viral RNA takes over biochemistry of cell + replicates (RNA) inside cell = viral proteins + capsids made = produces new virus particles = cell lyses = many virus particles released
55
Pathogenic effect?
- Nasopharynx (runny nose/sore throat..)
- headache, fever, coughing
- Secondary bacterial infection may occur when epithelial tissue becomes damaged = (immunocompromised)
56
Treatment / control?
[no cure for this disease]
- isolation = reduce transmission to others
- rest, plenty of fluids to avoid dehydration, warmth
- Antiviral drugs may reduce symptoms but doesn't cure + not always effective
- antibiotics for secondary bacterial infections
- Vaccine regularly to prevent infection
57
Fungi as pathogens
2. Stem rust fungus on cereal crops:
Transmission?
- wind carries spores from infected cereal plants to young crop plants
- infected plant fragments in soil
58
Mode of infection?
- spores germinate in water on plant
= produces hyphae which enter the plant through the stomata
= hyphae grow into mycelium + surround all tissues in the plant
= produce enzymes (eg cellulase) which digest the plant + nutrients are absorbed into the fungus
59
Pathogenic effect?
- nutrients lost to the fungus =⬇yield of grain
- weakened stem = plant more likely to collapse in wind
- weakened stem = less magnisium ions for chlorophyll
- pustules break epidermis = plant can’t control transpiration = water loss + dry out
60
Control?
- larger spaces between plants = less spores reach other plants
- reduced fertilisers use = stop growth
- soil disturbed little as possible = spores don't move
61
Protozoa as pathogens
3. Malaria (from plasmodium spp. parasites) :
Transission?
- Female anopheles mosquito act as vectors (transfer from person to person)
- Transmission occurs in both directions during it's 'blood meal' in human
- Feeds on person A with Malaria = takes parasite in from blood stream
- Feeds on person B (unaffected) = releases parasite out into blood stream
62
Mode of infection?
(life cycle of malaria parasite)
1. Female Mosquito takes 'blood meal' + takes parasite in
2. Parasite replicates in guts + releases more inside mosquito (HOST 1)
= 'blood meal' 2 - transmits to person
3. In human (HOST 2) - parasite travels to liver + remains for 2-3 days replicating
4. travels to, enters + invades red blood cells (asymptomatic until this point)
5. Parasite reproduce asexually + burst out of RBC, destroying them, releasing into the blood = symptoms show
63
Pathogenic effect?
- when malaria parasite burst out of RBC, they cause flu-like symptoms
- Fever, sweating, shaking, muscle pains + headaches = body's response to the lysis of RBC
- Long term damage to liver
+ steady reduction in blood cell numbers = severe anaemia = eventually death
64
Treatment / control?
- some drugs can kill the parasite + prevent it recurring, but only effective if given very soon after infection [but it's becoming resistant]
- get vaccinated
- Avoid contact with mosquito ( mosquito nets impregnated with insecticide, insect repellents, mosquito screens on windows, long sleeve clothing )
- Preventing mosquito breeding (proper disposal of sewage = foul water not left for mosquitoes to breed in / spraying local water sources with pesticides to kill eggs - chemical control)
- biological control - introduce predators
65
[6.6]
- Issues with treatment for endemic disease Malaria
Social implications:
- ppl have to be persuaded to change behaviour to reduce endemic disease
- eg persuading families to sleep under mosquito nets in affected countries
66
Economic implications:
- treatment, control + prevention involve economic investment
- need to decide is cost of action (eg nets) is worth the gain or if it should be used elsewhere (food) as most countries affected by malaria are poor
67
Ethical implications:
- issues with informed consent in medical trials for vaccines, as ppl may not know full risks involved
- spraying insecticides in water to kill mosquitoes eggs will also affect other species + affect the natural food chain
68
What's an endemic disease?
A disease which is constantly present in a particular country/area.
(EG: Malaria in countries were Anopheles mosquito survives)
69
Treating any endemic disease raises problems:
- disease is often widespread = eradication programmes covers large areas + difficult to track down + remove source of infection
- requires cooperation of large population numbers to eradicate pathogen/vector / vaccine community / use effective drugs
- Costs a lot of money to treat / control as they involve a lot of ppl
70
Role of the scientific community in controlling malaria:
- develop + test evidence based effective treatment
- Provide evidence for best prevention methods - insecticide impregnated mosquito nets can reduce cases by 50%, whilst untreated nets give only half that protection
- develop accurate diagnostic tools using microscopes to avoid overuse of expensive drugs
71
[6.7]
Physical barriers to infection?
● Skin is a tough physical barrier consisting of keratin
● Stomach Acid (hydrochloric acid) kills bacteria
● Gut + skin flora – natural bacterial flora competes with pathogens for food and space
72
Immune system has 2 responses:
What do they involve?
1. **Non-specific response**
- triggered by any pathogen
- Inflammation
- Fevers
- Phagocytosis
( neutrophils, macrophages)
2. **Specific response**
- Is antigen specific + produces responses specific to 1 type of pathogen only
- Cell mediated / humoral response
- B cells
- T cells
73
Cell recognition?
- all cells of 1 organism have a **specific** genetically predetermined surface protein on membrane (**glycoproteins**)
- Functioning immune system recognises these proteins as 'self' if cell can bind with glycoprotein
- Glycoproteins of 'non-self' (can't bind) act as antigens + are recognised by WBC, Leucocytes during specific response
74
What are antigens?
any substance (glycoprotein/ protein/ carbohydrates) which stimulate an immune response
75
Non-specific response:
1. Inflammation
- response to **localised** infection (1 area)
- tissue damaged = mast cells + Basophils (type of leucocyte WBC) release chemicals - histamines
- **Histamines** cause arterioles to dilate =⬆blood flow = local heat + redness
- Histamines = **leaky capillaries** -walls separate slightly = plasma with antibodies + neutrophils (leucocytes) forced out
- **Antibodies** = disable pathogens
+ the **Neutrophils** + **macrophages** destroy them (**phagocytosis**)
- ⬆ local temp = reduces effectiveness of pathogen reproduction in area
76
Non - specific response:
2. Fevers
issues?
- response to **systemic** infection
- infection detected - **hypothalamus** ⬆ body temp above normal 37°C = fever
= reduces ability of pathogens reproducing effectively = less damage
- If fever temp gets too high (⬆40°C) = enzymes denature + dehydration due to loss of fluid + electrolytes lost in sweat
77
2 main groups of leucocytes?
eg?
1. Granular / granulocytes :
Have granules which can be stained in their cytoplasm
(neutrophils)
2. Agranular / agranulocytes :
Don't have granules.
( macrophages + lymphocytes )
78
What's phagocytosis?
2 main groups of phagocytes ?
Phagocytosis- when phagocytes (leucocytes) engulf + digest pathogens + foreign matter in blood/tissues.
- 2 main types of phagocytes:
1. Neutrophils:
-70% of leucocytes in blood
-Ingest few pathogens before dies
-Granulocytes
-Can't renew their lysosome = once enzymes used up = can't break anymore pathogens
- short lasting
2. Macrophages:
- 4% of leucocytes in blood
- ingest many pathogens
- Agranulocytes
- Can renew their lysosomes
- long lasting
79
Non-specific response :
3. Phagocytosis
- Phagocyte engulfs pathogen
- Pathogen enclosed in vesicle called a phagosome
- Phagosome fuses with a lysosome
- Enzymes in lysosomes break down pathogen
(puss - phagocytes + build-up of dead cells (neutrophils) )
80
What happens after phagocytes have engulfed pathogen?
= they produce chemicals: Cytokins, in surrounding tissues
= cell signalling molecules that stimulate other phagocytes to move to site of infection + ⬆ body temp + stimulate specific immune response.
81
What are opsonins?
chemicals that bind to pathogens to make them more easily recognised by phagocytes
Phagocytes have receptors on cell membrane which bind to opsonins
strongest effecting opsonins are antibodies such as:
- immunoglobulin G (IgG)
- immunoglobulin M (IgM)
( these are produced in response to specific antigen)
82
Key characteristics of the specific immune response:
1. can distinguish 'self' from 'non-self'
2. It's specific = responds to specific foreign cells
3. It's diverse = can recognise ~10 million different antigens
4. Has immunological memory = once met + responded to pathogen = can respond rapidly if met again
83
where are lymphocytes produced?
The 2 different types of lymphocytes?
- Lymphocytes + macrophages 2 main WBC involved in specific immune response.
- Lymphocytes made in bone marrow + travel in blood + lymph
- recognise + respond o foreign antigens
- B cells + T cells
84
B cells:
- made in bone marrow
- found in lymph glands + free in body, when mature
- Have membrane bound globular protein receptors on surface = identical to antibodies they'll later produce
- Lots of B cells produced as embryo grows = each divide to from clone = potential to recognise soo many pathogens
85
When B cells bind to an antigen, which types of B cells are produced?
1. B effector cells: divide to form plasma cell clones
2. Plasma cells: produce antibodies
3. B memory cells: Provide the immunological memory to a specific antigen
86
T cells:
- made in bone marrow
- mature in thymus gland
- display thousands of identical T cell receptors, which bind to antigen on infected body cells
87
When T cells bind to an antigen, which types of T cells are produced?
1. T killer cells: produce chemicals to destroy pathogens
2. T helper cells: activate B plasma cells to produce antibodies against the antigen + secrete opsonins to 'label' the pathogen for phagocytosis
3. T memory cells: provide immunological memory + divide rapidly to form more T killer cells if meet pathogen again
88
Specific immune response:
- The humoral response
reacts to antigens found OUTSIDE the body cells (eg on pathogens)
split into:
1. T - helper activation stage
2. Effector stage
89
Humoral response:
1. T-helper activation stage
1. Macrophage engulfs bacteria + separates the antigen from the pathogen
2. It combines the antigen with the MHC protein + forms antigen/MHC complex
3. Antigen/MHC complex move to surface of macrophage outer membrane (as antigen has to be found OUTSIDE for humoral response)
4. cell = APC (antigen presenting cell) = T-cells bind to antigen on antigen/MHC complex on the APC = complimentary to receptors on T cells = triggers division + cloning of T cell
5. most become T helper cells for immune system + some inactive T memory cells = active rapidly if same antigen encountered again
90
Humoral response:
2. Effector stage
1. complimentary antigens from **APCs** bind to complementary **antibodies** on **B cells** + B cell engulfs pathogen by **endocytosis**
2. Vesicle formed fuse with lysosome + enzymes break pathogen down into fragments of antigen
3. Fragments attach to MHC protein + MHC/antigen complex transported to cell surface membrane = antigen displayed
4. An activated T helper cell (from T helper activation stage) with complementary receptor protein to the antigens binds to the APC + produces cytokines .
5. Cytokines stimulate the B cell to divide by mitosis (clonal selection) + forms clones of B memory cells + B effector cells .
6. B effector cells differentiate into plasma cells .
7. Plasma cells produce antibodies.
91
These antibodies bind to specific antigen on a pathogen + destruct it through:
1. **Agglutination**: causes pathogens to clump together = prevent them spreading + easier to be engulfed by phagocytes
2. **Opsonisation**: antibody acts as opsonin - makes antigen/pathogen easily recognised by phagocytes
3. **Neutralisation**: antibodies neutralise effects of bacterial toxins when bind to them
92
Specific immune response:
- Cell-mediated response
- when antigen is INSIDE host cell
1. Pathogen **invades** host cell = T lymphocytes respond to cells which've been changed / 'acting differently'
2. The host cell displays the antigens on its **MHC** = becomes an **APC**
3. **T helper cell** bind to the **complimentary antigen** on surface of APC (body cell)
4. **Cytokines** secreted by active **T Helper cells** stimulate the T Killer cell to divide by **mitosis**. = clonal division
5. T Killer cell divides to form **active T Killer cells + T Killer Memory cells**
6. Active T Killer cells bind to infected body cells (APC) + secrete **enzymes** which cause **pores** to form in the cell membrane.
7. = allows free entry of water + ions - cell swell + burst = infected cell **dies**
93
Primary immune response
- involves production of antibodies by plasma cells (from B effector cells)
- takes days/weeks for response to become fully active against pathogen = get symptoms of disease
94
Secondary immune response
- Quicker, greater, long-lasting
- B memory cells: allow body to respond rapidly to 2nd invasion by same antigen as antibodies produced rapidly to destroy it before symptoms show
- T memory cells: release flood of active T killer cells to engulf + destroy infected cells if same pathogen invades again
95
What are the different types of immunity?
1. Natural active immunity
2. Natural passive immunity
3. Artificial active immunity
4. Artificial passive immunity
96
1. Natural active immunity
When body comes in contact with foreign antigen + immune system activated + forms antibodies + pathogen destroyed.
Active: because ur body makes the antibodies
97
2. Natural passive immunity
When antibodies are passed from mother to fetus through placenta + to newborn from breast milk
Passive: because ur body does not make antibodies
- short-lived as antibodies not replaced
98
3. Artificial active immunity
Through immunisation
- small amounts of antigen (vaccine) used to produce immunity in person
- use non-invective pathogen = inactivated virus/ dead bacteria / DNA segments
= immune system produces antibodies + memory cells formed
99
4. Artificial passive immunity
when antibodies formed in 1 individual are extracted + injected into another individual
- from person who's already immune to a disease / or from different species (horse)
= prevents development of disease, but doesn't give prolonged immunity
100
How vaccination / immunisation can be used to control disease?
- protects individuals against disease which would've harmed them
- eradicates/eliminates/controls diseases that cause large numbers of deaths/illnesses in population
- herd immunity
101
Herd immunity?
benefits?
- occurs when significant proportion of population is vaccinated against a disease
- varies from 82-94% for different diseases
= difficult for disease to spread as individuals are protected against it + protects ppl who can't be vaccinated (old/ young/ compromised immune systems) as less exposure to it.
102
Benefits / Pros of vaccination:
- Individuals protected against disease that could kill / harm them
- Society benefits as potential pool of infection is reduced - protecting those who can't be vaccinated
- Cost of treating serious disease + caring for those left permanently damaged by them kept to minimum
103
Cons of vaccination:
- small minority of children become extremely ill after vaccination due to extreme immune response = some died + permanent brain damage
- Some vaccines cultures in eggs = some children suffer violent allergic reactions = not given vaccine + protected by herd immunity rather
- some scientists suggest mass vaccination programmes are linked to rise in children asthma + allergies
- some vaccines are given more for benefit of society rather than direct benefit of child. (rubella for boys)
